Comments most of which emanate from an Asian short wave station are contained in a separate complaint entitled “ An addendum to the violation of Vickis Wilsons Human Rights “

  I am a 72 year old pensioner .    For over 40 years I have been subjected to an unprecedented campaign of human rights abuse, discrimination and negligence perpetrated by an international/local communist/terrorist satanic cult in not so democratic New Zealand. I had previously been employed by the New Zealand Security Intelligence Service  (NZSIS) during the years 1976-1981 from whom I received a reference signed by former Director Paul Molineaux subsequent to my formal resignation.  The campaign which began in Karori Wellington in 1979 was supplemented by a saga of “remote viewing-black psych ops” which began in Khandallah in the early 1980s but was not a feature previously in Karori where I had lived since the 1950s. These tactics were obviously initiated by the security services. I have always been a quiet living solitary individual .-hardened criminals are not subjected to these tactics.   The situation continued in Auckland and Whangarei and most recently in pensioner units in Takapuna Auckland where I have been subjected to insulting comments from some of the geriatric tenants. I emailed my complaint to Ms Clezy CEO of Haumaru Housing however while  she chose to discuss the matter over the phone she did not address the problem of insulting comments  suggesting that I might like to consider alternative accommodation providers.  Shifting to an alternative community within the Haumaru was not considered to be an option

(b) I was denied any information by two NZSIS Directors, presumably at the instigation of NZ Security’s psychological representative, and was advised to take my concerns to the police by Director Brigadier Lindsay Smith.  In addition the NZSIS made enquiries during my period of employment I was also subject to some rather unusual/ derogatory comments from  NZSIS staff. These and other comments pertaining to NZSIS staff from a public source are detailed below: ( Most  of these comments are projected via satanic/electronic? voyeuristic remote viewing procedures ex transcripts from the short wave service)      In recent times there have been international complaints  concerning ( (apparently unproven) “sonic attacks” however my complaint has been met with blatant indifference and suppression. Hardened criminals are not subjected to these types of tactics

©  Standover /intimidatory and tactics involve the projection of often ruthless comments by electronic/ultrasonic  means into every room of the house on a 24 hour basis. Were there ulterior motives in respect of my employment at NZSIS and if so was there also collusion on the part of staff with other influences outside the NZSIS.    ( In some quarters the security services are regarded as  “front organisations”)   Likewise  members of the British and American Security Services  (including the aristocracy) are  also dominant,  involved , and implicated in this regard.  Certainly none of the security services should have had any further involvement with my personal life subsequent to 1981. An opinion from an Internet site stated that  “external reinforcement by the intelligence community includes destruction of the target’s property ruining their financial affairs and vicious rumour mongering” The extensive apartheid which I  have been subjected to for the last 40 years must obviously be the result of serious mendacity instigated by the security services resulting in destructive apartheid.   In addition the wives of two NZSIS staff members were/are?employed in medical practices the one in Karori the other in St Heliers which might also be considered to be somewhat unethical.

(d) Mental Health: Much of the detail pertaining to the process is contained in the section entitled “Mental Health Issues”. It is a process which essentially sets up totally sane victims for an insanity diagnosis in order to use the hapless victim for experimental purposes.  I think I have provided sufficient evidence to prove my sanity . In 2007 Neurologist Dr Barry Snow advised that I had an essentially structurally normal and  non-schizophrenic brain. Subsequent EEG and (Dopamine)/Metanephrine tests were also normal. One aspect concerned the provision of a police escort when I was classified as “ neither suicidal nor dangerous “ on the committing certificate in 1985. In August 2011 I received the following advice from Ian Bradshaw, the Police Department’s privacy advisory officer “ that I have searched the police database and there is no reference to you on the database”

(e) In 1986 psychiatrist Dr Ogg advised ” I presented in a completely normal fashion ..It was clear that her effect was quite coherent and compatible with her effect…found no evidence of any formal thought disorder” Ashburn psychiatrist  Dr Carradock Davies advised ” cognitively she is functioning well and is of superior intelligence according to our psychological test”. However Ashburn Hall psychiatrist Dr Dr Fresne claimed that the test didn’t exist! – the response from the Privacy Commissioner was similarly unhelpful. The District Inspectors of Mental Health including now Justice Helen Cull  refused to assist .Whangarei  QC Ms J Young erroneously stated “the basic contention is that you were not unwell at times you have been treated by clinicians in the past”!  A local British woman from Onerhai aged in her 60s and possibly a member  of the local psychiatric or psychological fraternity commented   “why I got rid of nut case” while seated behind me on the local Onerahi  bus!.  Since returning to Auckland  there have been  frequent comments from a well spoken British woman ( psychiatrist?)   .

(f) Infiltration of and relationship between the security services and police departments would also need to be investigated as well as the involvement of the former Minister of Police Mr Clem Simich and his wife.  Have they also been running a rear-guard action ? Comments pertaining to “behavioural problems”   attributed to Mr Simich were overheard at the practice of a senior cardiologist Dr Ted  Clarke nd also a female staff member in the carpark.   I have never met either Mr or Mrs Simich and it isn’t entirely clear how they appear to have taken a degree of control of this situation without my knowledge or consent. Coercive comments attributed to Mrs Anne Simich are a common feature.  There is also apparently collusion between Mrs Simich and Mr LB of NZSIS and the Kassler family    There has been intermittent police harassment some of it apparently initiated by Mr LB ( including derogatory comments/remote viewing ) for many years.

(g) The dominance and 24 hour harassment of the Kassler relations in particular .  Apparently there is also a Nazi/terrorist/Soviet? influence to contend with in that family.   Presumably they have been tasked by NZSIS in particular psychology major Ms JE. They are apparently in collusion with a group of aggressive, salacious, and rather odious young men and women and apparently controlled by an unscrupulous psychiatrist.  There have been references to unusual terrorist/torturing activities in respect of the Kassler women.    An almost quasi-incestuous mania and mendacity seem to be endemic in the Kassler  family. They seem to have a close affinity with police/security staff/medical and legal personnel and also the british group.  The controller tactics which involve an obsession with my domestic minutiae would  obviously be supervised by a psychiatrist.  They also seem to involve interference in my personal affairs which would seem to represent an abuse of power on the part of psychiatry as I was formally discharged as a psychiatric patient in 1985.  The situation is now one of international apartheid involving the media and politicians. Derogatory comments  from passersby on the street and department store staff are also  commonplace. Relatives on both sides of the family including the Blake and Hawke families together with my brother Bruce Wilson and his family in the USA are also implicated. 

(h) The involvement of the immediate family. Was pressure applied to my parents to incarcerate their sane daughter -was blackmail possibly an issue in respect of either parent ( blackmail was quietly mentioned by my mother) and/ or blatant complicity?   Were “changes or substitutes” in the family/relations also an issue?

(i) An unusual morse type transmission from a phone in the home of a state department employee which was rented by my family in the early 1970s. The transmission was a regular feature for some months in the early hours of the morning. A complaint was made by my father Alan Wilson to the security representative at the NZ Embassy Mr Hensley and the transmission ceased. The owners of the home one of whom was an Australian had been posted to Ethiopia. There may have been repercussions from the owners and possibly Mr Henry Kissisnger who was Secretary of State at the time.

(j) Bearing in mind that a former director of the CIA is on record as stating “ you can never have enough guinea pigs” – is covert experimentation/eugenics prevalent throughout the security services generally in conjunction with the medical and psychiatric professions.  One of the pathogens I diagnosed in the early 2000s namely Serattia Marcescens  was also used by the American and British  authorities for  experimental purposes in the 1950s and 1970s.

 (k) The identity and credentials of the psychiatrists and/ or psychologists who are spearheading this campaign.

(l) Is there scientific involvement.? There have been suggestions of covert scientific analysis.  Mr Bensemann a DSIR scientist resided in central Karori in the 1950s and 1960s.  Mr LB of NZSIS lived in the vicinity in the 1970s as did Treasury Director Mr Shales. A male neighbour near my previous address in West View Crescent in Onerahi was pIs genealogy/lineage an underlying issue.

(m)  Legal Profession: Complaints to members of the New Zealand legal profession and media have been largely ignored. ( see : police/legal incidents

ALTERNATIVE CONTACTS

Former Karori neighbours the Beaumonts ( also of middle eastern  heritage) have some involvement in this case as do the Throll family.  A number of diplomats foom the US Embassy Mr Reddington?) Australians, New Guineans, and the Israeli Ambassador.The Irish Secretary of the Electrical Workers Union namely Mr Anthony Neary was an immediate neighbour .  His wife, a Nealander of Yugoslav extraction, was prone to making occasional abusive comments of an anti-semitic/lavatorial nature. I attended St Mary’s College in Wellington in the 1960s’s with their daughter Catherine Stella .

Since moving to Auckland in the mid 1980’s a fanatical British group( including respresentatives of the security service, british neighbours the Bishenos, and  former neighbours  the Colebrooks together with  members of the aristocracy)  seems to have predominated supplemented by the Americans and Australians. Others involved include New Zealand, Middle Eastern, Asian, Italian, Russian and German nationalities together with the occasional  politician, general officialdom including security service staff and the police.  A small group of Russians shifted into a nearby address in Devore St St Heliers several years ago. 

Also involved are the local Maoris, clergy and members of the medical/ psychiatric/psychological  and legal fraternity. No doubt members of the scientific community are also represented Others who are apparently also involved include Ben and Jenny Shipley,  and Mr Michael Burleigh  ( a British  psychologist?) who was previously resident in St Heliers and( psychologist?) Ann Wilson.  Lawyer Michael Begley and his radiographer wife Deryn,  Dr Graeme Sewell and his wife Karen Sharon Cederman and  Robert Sim his wife Sharon and family  also apparently have an interest in this case  The Sinatra family also appear to be involved.

 

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There is also representation by the local gay community.  Asian contacts of the Soka Gakkai Bhuddist group lived nearby.  A former Minister of Police Mr Clement Simich ( a gentleman of Maori /Yugoslav extraction) is a resident of St Heliers.  Both he and his wife also have a long association with this situation including the sex industry and are no doubt also members of the bio-hazardous ring. They also appear to have a significant influence. I have never met the Simichs and as I don’t have a criminal history it isn’t entirely clear how they came to be involved. I met representatives of the police in Auckland in 1988 and they advised that my situation was not within their jurisdiction. Despite this advice there have been years of police harassment.   A female Maori academic Miriama Evans who is a director of the Maruehi Fisheries company purchased 2 properties in Amapur Drive Khandallah including  our former home at No. 43. The house has since been on-sold.   I moved to Whangarei in 2014 where there is also a quasi-hostile attitude among members of the community including the unit complex where I reside.

Relations from both sides of the family divide including The Halls from Alabama, the Blake and Hawke families are involved.  My brother is resident in North Carolina.

My mother Patricia was a fully trained nurse who graduated from  Napier Hospital in the 1940s. Apart from working as a nurse/receptionist for Drs Gluckman Snr and Wright –Sinclair on Auckland’s North Shore in the 1940’s she did not continue with her nursing career. She had a number of health problems and undertook office work in later years

There are 3 nursing relations living in Auckland namely Mrs Cathy Howard of Bombay, Mrs Janet (Blake) Stokes of Bayswater and Mrs Christine Hawke of St Heliers. The latter once passed a quick aside on the street concerning the need for an assassination. Her brother is Dr Naden who has  a practice at Mt Smart.  In the late 1970’s and early 1980’s there was a rather curious scenario concerning a middle aged nurse Nancy Trengrove. She appeared to living apart from her family in Tawa and was apparently residing in an old block of flats in an adjoining street in Karori Wellington.

 I departed Karori and shifted to Khandallah where Trengrove reappeared on a regular basis in the afternoon driving past our house and up the hill to a nearby suburb.  My family moved to Auckland as apparently did Trengrove and her family.  She died in The north shore hospice a few years ago at almost the time as a former companion nurse-receptionist of my mother’s in Auckland during  the 1940’s namely Mrs Elsie Hannah. Pat was nurse receptionist at the practices of Dr Wright-Sinclair and Dr Gluckman Snr.

Standover /intimidatory and tactics involve the projection of often ruthless comments by electronic/ultrasonic  means into every room of the house on a 24 hour basis. Female cousins and particularly nieces from the the Kassler family who have adopted a particularly aggressive virtual  24 hour campaign of harassment including derogatory comments concerning sanity in conjunction with a group of young women. Members of the group also apparently have involvement with the local sex industry( including the members of the Kassler family) and seem to be comprised of a seriously non-eclectic bunch of dominatrix controllers including ruthless young men and women .  By contrast, I am a lady of feminist persuasion who is accustomed to living a quiet solitary existence with no liasions. 

The attitude to women seems to exploitative and retrogressive. The group are essentially a coven of socio/sexual psychopaths trying to obscure an obvious experimental case.An almost quasi-incestuous mania and mendacity seem to be endemic in the Kassler  family. They seem to have a close affinity with police/security staff and the british group.  The controller tactics which involve an obsession with my domestic minutiae would  obviously be supervised by a psychiatrist.  They also seem to involve interference in our personal affairs which would seem to represent an abuse of power on the part of psychiatry as I was formally discharged as a psychiatric patient in 1985.  The situation is one of international apartheid involving the media and politicians.

The process could be best described as a form of maniacal, ubiquitous satanic levitational group voyeurism or a variation of remote viewing with particular emphasis on harassment in the the bedroom and bathroom areas Derogatory comments  from passersby on the street and department store staff are also  commonplace.

Presided over by psychiatry/psychology it is a one off saga of unusual satanic remote viewing  procedures being utilised for the purpose of harassment /destabilisation/ experimentation/training in conjunction with the local bio/hazardous ring .A preoccupation with thought patterns is also evident . This behaviour can only be described as pathologically debased, obsessive if not necrophiliac obsession with sick elderly women. ( see also mental health )

There also seems to be an almost mugabesque obsession with property dispossession/displacement even swindling. A contemptuous /derogatory/sacrificial attitude toward the mentally and physically  impaired also seems to prevail. It does appear that a torturing ring was also operating in the area which is one of Auckland’s upmarket suburbs. Many pets have disappeared with often dubious reasons provided for their disappearance. Screams and screeches used to be quite commonplace in years gone by. Gunfire is often heard in the evening hours.

In May 2014 I shifted to Onerahi in Whangarei where there the same situation prevails with the womens group and  the British and Americans dominating the situation.  There is also a significant Maori/Islander group and also evidence of an attitude problem in respect of some of the other locals . The owners of the rental  property are Mr and Mrs Kesai and Yukio Watanabe of Auckland. (Wikepedia advises:  “Mutsuhiro Watanabe (Japanese: 渡邊睦裕, January 1, 1918 – April 1, 2003) was an Imperial Japanese Army sergeant in World War II who served at POW camps in Omori, Naoetsu (present day Jōetsu, Niigata) and Mitsushima (present day Hiraoka). After Japan’s defeat, the US Occupation authorities classified Watanabe as a war criminal for his mistreatment of prisoners of war (POWs), but he managed to evade arrest and was never tried in court. He was later granted Amnesty by the US in an effort to make peace. [1]”))

Due to a serious depletion in my finances at the end of 2017 I vacated my rental premises and took up residence in a local hotel. At the end of one month I was advised by the Maori owner that  ” and I would be required to leave which I did.  The Ministry of Social Development advertise that they provide emergency housing by way of paying a half share of local motel accommodation  however this option was not offered to me. Instead I was relegated to Karawai lodge at Ruakaka which was somewhat rundown but otherwise comfortable.   It is a rather impractical option if you don’t have a car as there is no local bus service and one has to rely on the intercity bus at a cost of $40.00 return to Whangarei. This is an additional problem if your finances are depleted. The Manager of the lodge Mrs Howard was always very obliging in driving the tenants to the bus stop on the main highway or elsewhere.  The other tenants were a Maori trio and a group of Filipinos who were employed at Marsden Point.   Any assistance either legal/financial would be gratefully received.

OTHER ASPECTS 

There were one or two unusual incidents in previous years which might also be relevant. On December 15 1969, my first trip to the US, I travelled from Los Angeles to Washington DC on an American Airlines overnight flight. A young black American gentleman locked himself in the lavatory and refused to exit despite the efforts of the pilots and staff .  The plane stopped at Fort Worth in Texas at 2.00am in the morning the gentleman was removed by the police.

My family rented a home in Chevy Chase Maryland in the early 1970s from an American employee of the State Department Mr Martin Carroll  and his wife who was Australian.  We were regularly awakened in the early hours of the morning by a type of morse code transmission emanating from the telephone .  It eventually ceased after the matter was mentioned to Mr Hensley at the NZ Embassy in Washington DC. An unusual feature of this scenario was the visitation of a black gentleman sporting a State Department identification card to our front door some months after the couple had departed for Ethiopia.  He was enquiring as to whether the couple were still resident at this address.

I was employed by Columbus Overseas Services a German shipping company in Sydney from 1972-1975.Unfortunately for reasons unknown to me the company attempted to swindle me out of my correct salary .  The matter was subsequently rectified by the union.  I did not leave the company at that time and subsequently received a reference from them when I finally departed for New Zealand.  I am constantly regaled with electronic comments about another German gentleman namely Mr Hartmut Krtschil  and his family. Mr Krtschil was a close personal friend of my employer Mr Hartmut Schwartz however I had only limited social contact with the gentleman. Krtschil is also apparently an acquaintance of Mrs Anne Simich.

 I visited Sydney in the early 1980’s however the the only job available was a temporary position at an insurance company where there was also evidence of discrimination. I was ignored by the staff and the Canadian female supervisor repeatedly passed asides to the effect that I could not remain there. After finally existing on a subsistence diet and selling some of the furniture  I returned to New Zealand.  Although I applied for many positions on Seek job interviews did not eventuate. I did have an interview with a company which specialised in selling therapeutic massage units. Apart from having been subjected to “nut case” comments from the staff  I was not selected.  Another unusual aspect of my stay involved a rather swarthy ( Italian?) gentlemen with a scar on his face who  drove past me in on a few occasions at different Sydney locations.

Several  ago there was a sighting of an old mercedes in a Panmure car park with the car registration “ Atta?/ata? . An elderly couple were seated in the car.  The couple who were seen again at a later date seated at a waterfront café in St Heliers mentioned my name as I passed by.?  (Mohammed Atta was  one of the ringleaders of the September 11 attacks who served as the hijacker-pilot of American Airlines Flight 11, crashing the plane into the North Tower of the World Trade Center )

 On another occasion a  middle eastern group were temporarily resident in an adjoining street in St Heliers . There were loud odd comments including a reference to my name. The harassment culminated in a broadcast using a megaphone -the sound of a cockerel followed by about a minute of an Isil war chant !

POLICE

There has been no offer of assistance or information from any source including two former Directors of NZSIS Paul Molineux and Brigadier Lindsay Smith. In 1985 Smith advised that his department was unaware  of any campaign  directed against my person and referred me on to the police. I met police officers Tozer and Batchelor at Auckland Central in 1988. Subseqent to their discussion with the police commissioner I was advised to re-refer my complaint to my former employer or alternative officials.  Appeals to  Human Rights Watch New York  and British Human Rights lawyer Geoffrey Robertson were of no avail. I finally received from the office of the United Nations commissioner for human rights in late July 2011.  They were unable to assist  ( A former neighbour of ours in St Heliers was a former cleric Julian Batchelor who was also a possible relative of one of the two police officers I had met in 1988.)

Late in 2006 months ago my beloved cat which had been missing for 6 weeks was found by the owners inside the gates of an empty property for sale in an adjoining street.  The property is protected by high walls and gates and situated immediately below the home of Mrs Standidge.  The cat was blind and brain damaged and died at the local veterinary clinic the following day.  Just how the animal came to be found inside the property remains a mystery .  There were two comments from within the neighbourhood, both from female neighbours. The two ladies in question were Miss Maria Sewell ( her father is a medical practitioner at Panmure) and Mrs Marie Standidge. One comment ( the day after the cat’s disappearance) suggested that the cat might have been taken by a Satanist and the other comment that she had been sent to terrorism .My written complaint to the police met with a measure of indifference.  During a conversation with a female police assistant I was advised that even if video coverage was available it probably would not have been monitored , nor was I likely to receive a written reply from the police department, which in fact proved to be the case. 

 

There are similarities between my case and that of an eighty two year old woman( Mrs Lymburn ) reported by the Sunday Times  in March 2005. “She was suing the police for $250,00 for alleged cruel treatment over a period of 10 years. She said the police would not help her when she called for assistance and treated he “ like a mental case” Her concerns were about a group of people abusing her at her Pt Chevalier home over several years in the1980s and 1990s. People would cut down trees, smash her gates, push her in the street and verbally abuse her in the neighbourhood.  A neighbour Arnea Adams admitted that some people had intimated Lymburn over the years  and that she had done the haka in front of Lymburn when she walked down the street “ to rev her up”

 Documents obtained under the official Information Act showed a constable considered Lymburn as unbalanced and her concerns were a figment of her imagination. Another officer labelled her as schizophrenic and a senior police officer said that  any police response to a letter from her would only give her more opportunity to select exaggerate twist and distort what is said. She would only become more upset . I therefore suggest that no response be made . Up to six officers made the comments. In 2001 Inspector Rob Marshall who headed an inquiry into her concerns apologised to her and acknowledged comments officers had made about her were inappropriate. Anthony Lymburn was “gutted” to learn that the police had regarded his  mother as mentally unwell and backed her attempt to clear her reputation.” Mrs Lymburn died in April 2009. .  One wonders if perhaps, irrespective of any other considerations, the lady in question also had a prime site property and was considered a suitable case for unscrupulous treatment by the authorities. 

A Dominion Post article of October 2010 reported on the arrest of a detective’s wife.  “Vicki Lee McCaskie the wife of police officer  Rob Mcaskie stole nearly $18,000 from an elderly woman and $8,000 from her employer Westpac to cover a gambling addiction.”

In June 2014 the Sunday Herald reported:

“An Auckland real estate agent has been censured and fined for putting pressure on an elderly widow to sell her Sandringham  property after it failed to meet the reserve at auction.  The Real Estate Agents Authority found agent Mark Birdling and his firm Bayleys engaged in unsatisfactory conduct over the sale. Birdling was fined $2000 and Bayleys $1500. Birdling and Bayleys last night declined to comment on the finding, saying the decision was being appealed.   Birdling, failed to notice his client was in “extreme distress” during the auction of her Sandringham property in March 2012 and that she had to be taken to a private room to calm down, the authority found. The auction was put on hold as she was “agitated, distressed and crying”. The authority’s finding said Birdling — a former police officer and soldier — claimed he didn’t see his client because he was on the phone to a bidder, who eventually bought the three-bedroom townhouse for $451,000. The owner had anticipated a sale price of $550,000. 

Our own home was sold earlier this year . Although not “ top of the range” it was a large well maintained sunny home with expansive views including a view of the island of Rangitoto. I had previously had the property advertised as a private sale with no interest. Although there was a large gathering at the auction, they were, apart from couple who bought the house, not people who had previously visited during the open homes. The opening price at auction was $100,000 less than the council valuation and the auctioneer appeared to struggle to get a bid. The house was probably worth at least $100,000 more than the eventual selling price . The female agent namely Ms Stewart  from real estate agency  Ray White was unfortunately prone to making occasional derogatory comments concerning “Mossad’s sacrifice of a mental case”! to clients. The property was re-sold for $1,490,000 a profit of over $300,000 in 6 months.

 The property has been retained as a rental by its present owner Professor Grinlinton with an assortment of unsuitable tenants including the Kassler women whose “stomping” parties were a source of concern for the neighbours..

The campaign has also included public harassment from the authorities particularly the police and fire service. This has included police cars parked outside our home, (one of the officers was identified as Mr Richards a local police officer) presumably as the result of defamatory complaints.  On another occasion a bomb threat resulted in the evacuation of shoppers at the Glenfield Mall  

In another incident a blond female police officer visited the local St Heliers police station and then reappeared in a shop in Takapuna on the North Shore directly opposite the law practice which I had been visiting. A short time later the name of a certain NZSIS officer who was also a former police officer was mentioned by a smirking young man who was a member of a middle eastern group seated in a coffee shop.

 More recently a woman presumed to be a female police officer has on more than one occasion used electronic harassment to project occasional derogatory anti-schizophrenic comments. There were similar derogatory electronic comments concerning mental health from a male police officer again at a North Shore Glenfield mall in December 2011.  The officer was accompanied by a well spoken young man. The officer was seen entering the mall in his car earlier in the day.

 In June 2012 a young male police officer turned off the main road and drove past me down a driveway adjacent to a popular discount store . Later the same day a male officer and his female companion drove down past my home.  On another occasion Maori police officers appeared in another large shopping complex with one middle aged Maori male officer turning into the complex in front of me and the other seen entering a large discount store nearby ahead of me.   Harassment from the police has continued to this day -in April 2018 I was subjected to  three police drive pasts in the vicinity of Whangarei’s Okara centre and the bus terminal in the city together with  “ alternative remote viewing” tactics including my bedroom and bathroom. Some of these comments were attributed to Mr LB of NZSIS.  

In August 2011 I received the following advice from Ian Bradshaw, the Police Department’s privacy advisory officer “ that I have searched the police database and there is no reference to you on the database

 In the past the fire brigade was also seen quite regularly in the car park of our local mall during our weekly shopping expedition.  My name was mentioned by one of the fire officers as I walked past the brigade while it was parked beside the kerb on a local street one Sunday morning . 

 On Christmas Eve 2006 my elderly mother had a trolley of groceries stolen from outside a pharmacy in a local shopping mall.   I observed at least 4 surveillance monitors including one strategically placed above the entrance to the mall .  In an attempt to establish which company was responsible for video monitoring in the the mall I had telephone conversations with 3 different managerial and security staff, however no information was forthcoming nor was there any written response to my letter to the manager of the supermarket.  

 Harassment from the police has continued to this day. I lived in Whangarei from 2014 until 2019. In April 2018 I was subjected to three police drive pasts in the vicinity of Whangarei’s Okara centre and the bus terminal in the city. I was subjected to a number of comments primarily from medical and police personnel some of which were attributed to NZSIS staff member and former police officer Mr LB.   . Some of these comments attributed to Mr LB of NZSIS are as follows:  “LB” (laughing manager of my storage unit in Raumanga)/// “ LB is getting rid” ( medic at A & E medical practice)// “LB told us to watch nut case” ( police officer -remote viewing technique -in my bathroom)///”LB arresting” ( quiet comment from a female medic Kamo practice)// “This commander does not like wandering” ( assumedly a new police commander in Whangarei)// “LB says its nasty pictures”(as I sat on a bus waiting to return home after a colonograpy procedure).

In June 2021 a young police officer recently commented via remote viewing “ police say its stolen goods”  In 2022( possibly a young police officer) advised that he was in possession of a silver kodak camera which contained scenes which would seem to be identical to a camera which should be in my storage unit in Whangarei.  In addition details of  book and record titles ( formerly my property) appeared a few years ago in the transcripts from the Asian shortwave station and would appear to be in someone else’s possession –possibly the relatives.

The discrimination about which I have complained has occurred as a result of collusion between my former employer , the police the medical, psychiatric, and legal professions together with  the general  public, which  was further exacerbated by the wrongful incarceration in a mental institution.. The situation subsequently deteriorated  into a sinister case of psychiatric/psychological  “black ops “and experimentation.”

The discrimination about which I have complained has occurred as a result of collusion between my former employer , the police,  medical, psychiatric, and legal professions together with  the general  public, which was was further exacerbated by the wrongful incarceration in a mental institution.. The situation subsequently deteriorated  into a sinister case of psychiatric/psychological  “black ops “and experimentation.”

 

LEGAL/GOVERNMENT/ CONTACTS

At a meeting with criminal barrister Mr Tomlinson in 2004 he stared rather fixedly during the consultation and repeatedly advised that he was unable to assist.I n July 2005 the former assistant to the President of the Auckland District  Law society Miss Malcolm advised  “that none of my concerns could be considered a legal matter”Miss Malcolm subsequently became  assistant to the National Party’s former  Minister of Justice Whereas in previous years although I did not receive any offers of assistance from senior members of the legal profession , I did at least receive the courtesy of a reply.  There were difficulties in obtaining legal assistance in respect of both my Human Rights complaint and also family trust matters.   

I In response to my complaint to the Minister of Justice Amy Adams I received a reply from Swati Bhim Private Secretary Justice and Courts dated 23 April 2015 He advised that  “the Minister of Justice ….has asked me to thank you for your correspondence regarding your concerns.  Please be assured that your correspondence …has been noted by this office. Thank you for keeping the Minister informed”   It isn’t entirely clear how my complaint to Mrs Adams was handled by Swati Bhim.

 A complaint to Chief NZ Human Rights Commissioner David Rutherford dated 30 March 2015 resulted in no reply.  In a subsequent  response to my complaint to the Human Rights Commission Mediator Sue Smith stated  in her letter dated 4 September 2015 that “ the commission will not take any further action on it because the matters you describe do not meet the required criteria for a complaint of unlawful discrimination”

Two criteria specified by the commission are  “ happened in an area of public life such as government activity” and “ disability –(apartheid as a result of  previous employment and  (inappropriate) psychiatric treatment) might be deemed most pertinent and  not to be disregarded.  Once again assistance has been denied.Two attempts to  involve a Queens Counsel Paul Davison and and barrister Mr Dan Gardiner both of whom specialise in criminal law and other senior members of the legal profession either elicited no response or rejection.  Davison’s secretary advised that he had other commitments.  (My email  had initially been consigned to spam!)  A further attempt to contact Davison in December 2014 resulted in no response..  There was no response at all from Gardiner. 

Other prominent members of the legal fraternity who were also unable to assist were Anthony Rogers  (barrister), Mr R Stewart (QC), Justice Asher ( formerly QC), J Billington (QC), G Illingworth(QC), Colin Pidgeon (QC)J Anderson ( barrister), RB Stewart (QC) criminal lawyers  Annabel Ives and  Karen Harding  and J Haigh (QC). In 2010 Barrister Graeme Newell  responded ‘that he hadn’t opened the attachment because he didn’t know what it was”  and in September 2016 Mr J Corby Barrister of Auckland failed to reply .There was no assistance offered from either David Neutze of Brookfields or Shane Tait.  

The comments detailed below are in respect of trust matters:

In 2009 a senior lawyer Mr J Kirkby of Remuera charged us $1800.00 for compiling and perusing documents the compilation and assessment of which probably wouldn’t have taken more than a couple of hours.   Another Remuera solicitor Mr Ellis who was about my age suggested that I might like to see a younger man as he was near retirement. He also quoted a rather exorbitant amount for the resettling of a trust . As of January 2013 he still practicing law.

A routine enquiry to Mr Duncan of Fortune Manning resulted in a delayed reply of almost 2 weeks as my enquiry had apparently been put into junk mail,

 Comments have included “ watch revolting” from a retired corporate lawyer (Mr G Jones of Orakei,) — “ get rid of her” (Mr Taylor of Galbraiths of Howick), and “committed” ( Harold Kidd of Glenfield )—- “ smells a bit //pain in the ass /breathing down the neck” from Barry Hopkins of Auckland city and  “there has to be a subsidy drama” –ultrasonic comment (Mr Walter Graham of Mt Eden) .–“ your email doesn’t appear to have surfaced” ( Mahon and Sumpter on the North shore)- “ Israelis say its mental derangement”/Its Maureen” (partners John Armstrong and Neil Murray of Takapuna). Graeme Newell  responded ‘that he hadn’t opened the attachment because he didn’t know what it was”

 A comment from lawyer  Mr Howard Smith suggested that both my brother and I might predecease our elderly mother!   When I enquired as to the hourly rate of senior partner  Mr R Craig he replied “ what is yours”!  ”. There have also been derogatory comments in the past from local lawyers including Mr Callaghan and his wife, and an “ arrested” comment from Mr Bone. Mr Stephen Anderson advised that he was “ overcommitted” and  Mrs Wood of Patterson Hopkins suggested that  “you could put the trust documents into the bank and then send them on to us”

 In 2013  I first arranged an appointment at 11.00 the following day with the  wife of lawyer Gavin Cocroft . Mr Cocroft advised me by phone that he needed to change the appointment time to 1 pm on the same day.

 When I visited their home at 1 pm I could see Mr Cockroft  in the lounge. A womans voice could be heard inside the house saying “ you are not wanted here”.  The dog was barking loudly at the front door- Cockroft called the dog away from the door but did not attempt to open it. I departed. I subsequently received an email from the gentleman advising that “I am sincerely sorry for your wasted trip yesterday. I have been having problems with blocked ears, which have severely affected my hearing, and am seeing the doctor today. Also, I found out only yesterday afternoon that our front door bell was not working, and I was listening for that. I did come out to the front about 11 but obviously missed seeing you”!  (My deceased mother was deaf!)

There was no response from criminal lawyer Mr Fairley of Thomson Wilson Law Whangarei in February and March 2016 nor from Dr Henderson of Henderson Reeves in May 2016.  A follow up query with Mr Reeves in November 2017 and 2018 was also ignored. In March 2018 Mr Eaton QC advised that “ he was unable to assist in this matter”  

 In September 2017 Ms E Priest of Blackstone Chambers Auckland advised “ It sounds like you have had a terrible time. It sounds like you are seeking compensation? I’m afraid I cannot take on your case as I am simply too busy. I am also purely a criminal barrister. It sounds like you need a civil lawyer with medico-legal experience”.  There was no response from Gerard McCoy QC of the same practice.  On February 2019 Barrister Ron Mansfield stated:   “I am not sure what you require or how I might assist. I am also very busy at the mk capacity to assist, if it is urgent.”   In May 2019 Mr Clarke senior partner of Bell Gully rejected my complaint and there was no reply from  from Mr Paul Dacre QC in June 2019 or April 2020.

.Murray Kirkness the Editor of the NZ Herald failed to reply to my emailed complaint in August 2016. There was no further communication from Stuart Dye Deputy Editor of the NZ Herald in February 2018 nor reporters K Johnston and J Savage in May 2018.

In his letter dated 23 april 2013  Mr Ilott advised “that the Ombudsman would exercise his discretion not to take your concerns any further”

The following are extracts from correspondence between myself and the Office of the Ombudsman from 4 July 2018  until 10 October 2018.

‘The underlying concern in my complaint was that of discrimination or apartheid and any probable negligent consequences. I am not requesting the Ombudsman’s review of Health and Disability’s decision. If complainants are not satisfied with the response they receive from one investigative body then they should be entitled to obtain another alternative opinion including from the Office of the Ombudsman

Scott Martin Acting Manager – Intake and Early Assistance Team advised:

‘The Ombudsman is not an appeal body, empowered to exercise the functions of the original decision maker, but considers whether the decision maker acted in a lawful and administratively reasonable manner regarding the relevant decision or action. I must advise that an Ombudsman does not have the authority to consider complaints about the standard of service provided by a health provider. This is the role of the Health and Disability Commissioner (HDC) under the Health and Disability Commissioner Act 1994.It may assist you to explain that an Ombudsman does have the authority to consider complaints about HDC. However, I must advise that this jurisdiction is limited, and an Ombudsman does not review HDC’s professional judgement about a complaint.

You have raised concerns about the assessment of your complaint by the Health and Disability Commissioner (HDC). You state that you are not seeking that an Ombudsman review HDC’s decision on your complaint, but that an Ombudsman provide ‘another alternative opinion.’ As previously explained, an Ombudsman has no authority to consider complaints or form opinions about the standard of service provided by a health provider . This is the role of the HDC.

You have noted that District Health Boards (DHBs) are subject to the Ombudsmen Act 1975, and therefore are within an Ombudsman’s jurisdiction. However, I must emphasize that an Ombudsman can only consider complaints about administrative acts or decisions of District Health Boards. Concerns about any health service provided by an organisation operated by a DHB remains a matter for HDC.

I should also reiterate that, if you have any concerns, in an administrative sense, about HDC’s consideration of your 2007 complaint, or your 2009 request for your complaint to be reopened, then you would need to outline clearly what these concerns are, and explain the reasons for your delay in approaching this Office

 If you wish to pursue this matter further, then I suggest that you discuss your concerns with a lawyer. You can contact your local Community Law Centre for free legal assistance. ”

There does seem to be some overlap with regard to investigative procedures of the Ombudsman’s office and Health and Disability. Perhaps the only difference is that H & D are acting in accordance with a code of rights, In the case of incarcerated mental patient Ashley Peacock a complaint was responded to by the Ombudsman’s office as opposed to Health and Disability.  ( There was no reference to the Peacock case in the replies from Scott Martin) . In your letter you advised that “ an Ombudsman does not have the authority to consider complaints about the standard of service provided by a health provider. This is the role of the Health and Disability Commissioner- but considers whether the decision maker acted in a lawful and administratively reasonable manner”. The latter statement would by implication involve an assessment of “the standard of service provided by a health provider”

You further advise that “ Ombudsman has the authority to investigate complaints about the administrative actions and decisions of the central and local government agencies listed in the Ombudsman Act. This does seem to contradict your statement concerning health providers in the previous paragraph. Local government agencies include District Health Boards who in turn have oversight over their Primary Health Organisations (PHOs)/ general practices.

Unfortunately you ignored a significant part of my complaint pertaining to the last 10 years. I have attempted to obtain assistance from a number of lawyers over the years but my complaint including mental health issues has been generally ignored including District Inspectors of Mental Health. .

On 13 December 2018 an email was onforwarded to PM Jacinda Ardern:

 “Dear Prime Minister,

Please find enclosed two complaints pertaining to human rights.  One complaint is abbreviated  including  some images and the while the other is a much lengthier version .An additional attachment sent under cover of a separate email contains files..  The level of discrimination in my case would seem to be unprecedented and unlikely to occur in any other country in the western world . Compensation/damages should be a consideration.

Acknowledgment of the receipt of this email would be appreciated.

Yours sincerely, Vicki Wilson”

On 17 December 2018 Dinah Okeby of the Prime Minister’s office advised : “Many thanks for your emails to the Prime Minister Jacinda Ardern.  I have passed your emails to the Minister of Justice Hon Andrew Little for his information”  On 14 December 2019  a subsequent email was sent  to the Prime Minister The Rt Hon Jacinda Ardern.  Apart from an automatic response there was no further reply.

On February 2019 Barrister Ron Mansfield stated:   “I am not sure what you require or how I might assist. I am also very busy at the moment and lack capacity to assist, if it is urgent.” A second attempt on 11 June 2020 was ignored.  In May 2019 Mr Clarke senior partner of Bell Gully rejected my complaint.

On 21 February 2019 I make an enquiry at the office of the Minister of Justice :

The Minister of Justice   The Hon. Andrew Little

“Dear Minister,

My lengthy email and attachments dated 17 December 2018 onforwarded to you from the office of the Prime Minister the Hon. Jacinda Ardern refer.An acknowledgment of the receipt of same and/or a reply would be appreciated. Copies of the emails are detailed below. There was no reply.

My complaint to National MP the Hon Gerry Brownlee in August 2019 was ignored.

Complaints were also emailed to M Laracy Inspector of Security and Intelligence on 19 March 2020 and an unsigned reply dated 23 March is as follows:

“Kia ora Ms Wilson  

Thank you for your correspondence. 

The Inspector-General is able to investigate complaints from a New Zealand citizen or a person ordinarily resident in New Zealand who has, or may have, been adversely affected by an act, omission, practice, policy, or procedure of the New Zealand Security Intelligence Service (NZSIS) or the Government Communications Security Bureau (GCSB).  The matters raised in the material you have sent to my office do not relate to the activities of the GCSB or NZSIS.  As a consequence, the Inspector-General does not have jurisdiction to investigate the matters you have raised. To the extent that the matters you raise relate to electronic and/or electro-magnetic activities, we are able to inform you that the Director-General of the NZSIS has previously informed the Inspector-General that the NZSIS does not use or deploy any electro-magnetic harassment technologies.??This will not have been the response you were hoping for but we trust that this advice from the Service is able to provide you with a small measure of reassurance. 

Regards

M Laracy Inspector General of Security and Intelligence 

Murray Kirkness the Editor of the NZ Herald failed to reply to my emailed complaint in August 2016. There was no further communication from Stuart Dye Deputy Editor of the NZ Herald in February 2018 nor reporters K Johnston and J Savage in May 2018. A further complaint to Emma Russell Health Reporter on 5 April 2021 was ignored.

 There was no eailed  reply from Paul Dacre QC in June 2019 or 21 April 2020 and a brief phone conversation in april 2022 did not result in any further contact. On 10 July 2020 Criminal lawyer Rosemary Thomson advised “Thank you for your email. Your complaints do not come within my role as District Inspector for Mental Health. Rosemary L. Thomson District Inspector for Mental Health 

MEDICAL / POLITICAL CONTACTS:

In November 2012 my complaint was onforwarded to the Associate Minister of Health Mr Peter Dunne.  A reply from his staff member A Portis recommended contact with both the Obmudsman and the District Inspector of Mental Health. In his letter dated 23 april 2013  Mr Ilott advised “that the Ombudsman would exercise his discretion not to take your concerns any further”

An emailed complaint to the former associate minister of Health Joe Goodhew in August 2014 was not replied to . In his letter dated 27 April 2016 the Minister of Health the Hon Dr Jonathon Coleman advised  “It is not appropriate for me as Minister of Health to intervene in the delivery of health care to individual patients . You should make your complaint to the provider of the services in the first instance”

On 22 February 2018 I onforwarded an email to Dr Roberts Chief Medical officer of Health for Whangarei expressing my concerns about respiratory, manmography  neurology, cardiology, matters and a local general practitioner Dr Detjen.. In his reply dated 22 March Dr Roberts advised  “I did not reply to your earlier mail because there did not appear to be a question for me to address. It seemed simply to pass on a considerable amount of information about your past medical care . Having reread that email today I remain unclear of your reason for contacting me. I would be most grateful for your advice in this regard.”

 My reply dated 2 April 2018 stated  “I  would have thought it obvious that the general nature of my email was that of a complaint which was sent to you in the hope you might be able to rectify some of these issues.” The complaint was also onforwarded to NDHB CEO Dr Chamberlain on 13 April 2018 and was in turn onforwarded to Quality and Control and finally the General Manager, Medicine, Health of Older People, Emergency and Clinical Support  Mr Beney. On 30 April he advised “ due to the number of services involved it is taking time to get the required information to respond to your concerns” There has been no further communication from Mr Beney.

  A reply was eventually received from Mr Beney dated 28 October 2018. He referred to “ your email and attachments which were received by Dr Bradley on 18 September 2018-as you raised a concern that was outside of her area Dr Bradley forwarded your email on so a coordinated approach to your response could be provided. Dr Bradley declined the request for a clinic review and reinforces that there is no evidence for bronchiectasis. (“ very minor right lower lobe bronchiectasis” was reported in an ADHB CT scan of 2011) “ The nodule has been under surveillance for well beyond the recommended timeframe. She does not believe there is a reason for a review in the respiratory clinic.” ( see also respiratory Vickis NZ Health Human Rights)

In respect of mammography “ On receiving your concern Dr Kim Shepherd requested Dr Walker ( Clinical Director for Breast Screening Waitemata-Northland) review the images and she agrees with Dr Shepherd’s email to you  on 19 June 2017- I have looked at this mammogram with my colleague Dr Wild. The appearance you have shown on your first magnified image is normal skin and subcutaneous tissue.  I would like to reassure you that I can see no areas of concern on your mammogram” .  This still does not appear to be a satisfactory explanation.

My complaint was emailed to Andrew Simpson Chief Medical Officer of Health at the NZ Ministry of Health . A reply was received on 6 June 2018 :

“As Chief Medical Officer, it is not appropriate for Dr Simpson to comment or give clinical advice on individual cases. I note that you have been in contact with the Health and Disability Advocacy Service and the Health and Disability Commissioner which are the correct places for consumers to raise concerns they may have about the care or treatment they

receive.

Kind regards

Clare Possenniskie | Principal Advisor to the Chief Medical Office

Ms Possenniskie does not seem to have read my Human rights complaint and seems to have ignored the unsatisfactory aspects associated with my previous complaint to Health and Disability.

 Neither a reply nor an acknowledgment of the receipt of my email dated 25 June was received from  the NZ  Health practitioners Disciplinary Tribunal.

An email was also sent to the NDHB cancer and blood service on 13 September 2018.  Staff member Toni Andrew replied : “Sorry we cannot accept this as a referral, you need to see your GP and get referred through the system to either the breast clinic or us (if confirmed cancer).” 

An email was received from the office of the Minister of Health David Clark on 18 December 2018 in response to my two complaints including an abbreviated version.

“Kia ora  Jordan Andrews <Jordan.Andrews@parliament.govt.nz>

On behalf of Hon Dr David Clark, Minister of Health, thank you for your correspondence.

The Minister has noted your comments and has asked the Ministry of Health to respond to you directly about the

issues you have raised. Please be aware, there may be a delay in responding to your correspondence due to the Christmas close down

period.

Ngā mihi

Jordan”

On 25 February 2019 he further advised “please be assured your correspondence is being treated seriously and you will receive a response. I sincerely apologise for the delay in responding to your correspondence.”

Correspondence from the Ministry of Health is detailed below:

MINISTRY OF HEALTH

March 2019                                                                                                                                                                                        Ref DR 19915

“Dear Ms Wilson,

Thank you for your correspondence of 17 December 2018 and 25 February 2019 to the Minister of Health, Hon Dr David Clark, regarding your experiences.  The Minister has referred your correspondence to me and asked that I respond to you directly.  I understand that you have made a complaint to the Health and Disability Commissioner ( HDC) and the Ombudsman.  The High court can also review the process used by the HDC to reach a decision.  If you are not satisfied with the process used by the HDC or the Ombudsman to investigate your complaints, you may wish to seek independent legal advice on this course of action.

Community Law offers free legal advice throughout New Zealand.  You can find he contact details for your nearest Community Law Centre on its website ( communitylaw.org.nz)

I am sorry this not the response you were hoping for .  I wish you the very best.

Yours sincerely, Hina Davis Manager Ministeral Services”

On 8 May 2019 I emailed my complaint to the Medical Council of NZ and on 24 May  received a reply from Anna Yardley Team Leader Professional Standards advising that  “A member of the Professional Standards Team will be in touch with you shortly regarding your concerns”.

A reply was received from Megan Williams Professional Standards Adviser for the MCNZ on 10 July 2019. She advised “ Unlike the HDC the Medical Council of New Zealand does not  have he ability to investigate care provided to an individual.  The HDC may refer concers to the Council for consideration under our juridsdiction however, Council  is only able to consider the case in the context of whether the matter indicates wider competence or conduct concerns about an individual doctor whch may require further action by Council”. Since the HDC investgates and  publicises its decisions one wonders how many of their cases are actually referred to the MCNZ for further consideration and how much duplication there may be between the MCNZ and the Medical Disciplinary Committee.   The MCNZ could have been an alternative backstop for those patients who are dissatisfied with the decisions of the HDC however unfortunately that is not the case.

In response to my email which also contained respiratory images I received a reply from  Professor J Zalcberg Head of Cancer Research at Monash University  on 13 July 2019. He advised:  

“Thank you for your correspondence but I am unable to help.  

I do not provide medical opinions over the internet and as respiratory medicine is not my area of expertise, it would not be appropriate for me to comment. I’m sorry I’m cannot assist 

Regards  

Professor John R Zalcberg OAM MB BS, PhD, FRACP, FRACMA, FAHMS, FAICD 

Tony Charlton Chair of Oncology Alfred Health Head, Cancer Research Program”

On 28 January 2020 I emailed Dr Mcauliffe Director of Labtests: “On occasions, and in respect of laboratory sputum tests microscopy details can be identical i.e.” mixed organisms seen- predominantly gram negative bacillus” in different reports but only one report will specify a culture.  In my case it is most often pseudomonas aeruginosa. An example of this are the two labtest reports dated  29/7/2019 and  7/12/2019. If no culture is reported then medication not provided by the general practitioner.The labtest report dated 14 October 2019 seemed to represent a departure from the norm ” mixed organisms seen- predominantly gram negative coccus including mixed gram negative organisms “.   The coccus was not specified as a culture however that group can include meningitis ( previous MRI scan- undiagosed and untreated) and Haemophilus influenzae . I have been afflicted with both of those infections in the past.    Aeruginosa might also have been present.” In addition I also provided images of 2 chest sputums dated 30 December 2019. 

 Dr Mcauliffe’s reply dated 28 January 2020 is detailed below:

“Labtests laboratory is accredited by IANZ ( Interntional Accreditation New Zealand).  All our tests are carried  out and reported according to established international guidelines.  This includes sputum testing and resulting. Unfortunately we are unable to comment on your specific clinical questions.  Such comments are only appropriately given by the medical practitioner who has the full clinical record of your symptoms and clinical examination.  We are always happy to discuss individual results with referrers if there is query on interpretation  of results  or treatment schedules. We advise that you would be best seeking advice and care from your medical practitioner.

Yours sincerely,

Dr Gary MCauliffe

Clinical Microbiologist Labtests Auckland

Medical Director Labtests and Northland Pathology Laboratory”

During my previous consultation with Dr Cunningham on 17 December 2019 he seemed to be disinterested in the question of disparities concerning the lack of reporting of  cultures and was not prepared to provide a prescription for antibiotics despite my symptoms of head chest and back pain.and a very sore throat. Dr Miller had adopted the same attitude with regard to the previous test dated 7 December.   In the week after the consultation with Dr Cunningham I developed a severe chest and sinus infection which lasted for a week and resulted in copious amounts of dark yellow sputum from both the chest and sinuses.The test of 9 January 2020 reported  “large numbers of polymorphs-culture: mixed gram negative organisms-  no predominant organism seen?”    One would have assumed that the sputum indicated yet another significant growth of Pseudomonas aeruginosa.    I managed to reduce the severity of the symptoms with natural remedies. 

I also cited the lack of treatment of  of my mother during the last week of  her life in ADHB in November 2013.

 ADHB hospital labplus report for P Sexton dated 27 October 2013 advised  “Muco-purulent large numbers of gram positive cocci seen-  large numbers of gram negative bacilli seen  Culture: a moderate growth of mixed oropharyngeal flora///gram negative organisms  (mixed species) ////at least three different organisms present” ( Al Anbuky)  The lack of a significant culture seemed to be totally inadequate. 

 Patricia  had previously been treated for staph aureus with flucloxacillin a few months earlier and one might assume that the gram negatiive organism was pseudomonas aeruginsoa most often associated with cancer patients in hospital.   A month before she died  in November 2013 she was diagnosed with lymphangitis carcinamatosis secondary to lung cancer. Despite the fact that mother was complaining of pain in her chest and back ( she also had a heart condition) and that her nursing notes indicated “productive cough with greenish sputum“ she was not provided with antibiotics .  When I enquired of hospital staff  I was advised there was no infection.   Gerontologist  Dr Spriggs considered ” that antibiotics were a waste of time as she was at the end of her life” and Dr Lim wrote on the day of her death. ” ‘I explained that she is unable to swallow in her recent condition and to put in an intravenous line would be cruel and inappropriate: sputum culture Nil infection,”   She literally groaned her way to her death on her final day until she quietened down with with morphine.

MENTAL HEALTH/PSYCHOLOGICAL OPERATIONS

In October 1985 I had barely recovered from an undiagnosed illness only to be incarcerated in a mental  hospital at the instigation of my own parents.  My mother ( a former nurse) in particular seemed to have a rather obstructive attitude toward my evidence gathering either my  attempting to record the electronic comments or the distorted diatribe emanating from a certain short ave station which broadcast all aspects of this case.

The reason for the obvious complicity of my parents has yet to be explained.   The reason was my complaint about harassment from a local satanic cult.  I was, as you would expect, classified as a delusional and paranoid schizophrenic.

Although my parents were the instigators neither my own General Practitioner ( Dr Delaney) nor my parent’s General Practitioner ( Dr Waite) were involved in my  incarceration into a psychiatric institution in 1985.  Instead a locum( Dr Brown)  appeared at the house and subsequent to discussions I was coerced into visiting a psychiatrist ( Dr Delahunt) at Wellington  public hospital.  It was obvious that the psychiatrist in question was not interested in any explanations and I was committed to a public mental hospital. I was quite shocked.  Regardless of the the committal order which quite plainly stated that I was “neither suicidal nor dangerous” I was treated like a common criminal and given a police escort with 3 police officers.

 I was consigned initially to a secure ward, my personal possessions were taken away and put into a cell with only a mattress on the floor . I had nothing to eat or drink from 3pm of the previous afternoon until the day after my arrival at the hospital.  I was confined to this ward for a few days wearing a chenille dressing gown and oversized men’s slippers.  After approximately a week I was consigned to the open ward –surely an indicator that an incorrect assessment had been made in the first instance.  The presiding psychiatrist was (Dr Averi.)

My parents then decided to send me to another privately run institution Ashburn Hall  in Dunedin. Ironically the psychiatrist ( Dr Carradock Davies) at this establishment did not see fit to place me into the equivalent of the public hospital’s open ward and I was confined to the schizophrenic ward for virtually the duration of my stay there.  Subsequent to my release and consultation with another psychiatrist in Auckland I discovered that my status was that of a “committed patient on trial leave”.

We were certainly not advised that this was my status prior to departure from the hospital in early 1986 however the matter was rectified by my subsequent  psychiatrist (Dr Ogg of the Bexley Clinic in Auckland ).   Interestingly his assessment was somewhat at variance with that of hospital psychiatrists stating that “ I presented in a completely normal fashion..it was clear that her effect was quite congruent with what she was saying ..her account was entirely coherent and compatible with her effect…found no evidence of  any formal thought disorder”

Advice from a Mental health officer provided some rather contradictory advice, namely that while  it was  the  usual practice to use the police force for the purposes of escorting patients from the Wellington Psychiatric Unit to Porirua in the 1980’s the officer in question  was unable to locate any information concerning the reason for the use of a  police escort in my case. In February 2009 The Clinical Director of Capital and Coast District Health Board Dr Masters advised thus :: “the file does not provide adequate detail to comment on your complaint regarding the initial treatment that you received on admission to hospital…from the perspective of today these practices can appear to be inappropriate at the least..I can assure you that the use of a police escort would not result in a police record”

I had complained  about the electronic projection of comments into the house on a twenty hour basis for the purpose of harassment and destabilisation. Voyeurism, which resulted in an immediate reduction in sound, negated any attempts to record the comments . Obviously the establishment of my sanity is a priority and to this end there is public evidence available . A certain short-wave station broadcasts a diatribe concerning all aspects of this case . With technical assistance extracts could be presented as evidence and the psychiatrist’s diagnosis reassessed accordingly. There are anomalies when it comes to matters of a spiritual nature-haunted house syndrome, programs devoted to the supernatural, even visions are classic examples.   Most of these claims are heresay and unprovable . Rarely however, do these revelations result in incarceration for the individuals involved.  I am surely nothing more than the victim of brilliant set-up/entrapment –“black psychiatry” In August 2017 media reported “ that mysterious  incidents caused physical symptoms-hearing problems  in at least 16 American linked to the American embassy in Cuba in what has been described as “ an acoustic attack”

An EEG report from Wellngton Hospital dated 22 October 1985 advised : “EEG obtained from a tense patient with constant flickering of eye movement shows a symmetrical alpha rhythm at 8-9 Hz of variably moderate amplitude attenuating on eye opening .  Low amplitude ill-defined theta activity at 6-7 Hz is recorded pre-centrally.  Hyperventilation well done and photicstimulation caused no significant changes. Comment: the EEG shows no significant abnormality.”  However the Hospital apparently had no trace of my CT brain scan undertaken in the same year.

MEDSCAPE:

 Normal EEG Waveforms

The frequencies most brain waves range from are 0.5-500 Hz. However, the following categories of frequencies are the most clinically relevant:

• Alpha waves – 8-13 Hz
• Beta waves – Greater than 13 Hz
• Theta waves – 3.5-7.5 Hz
• Delta waves – 3 Hz or less

MENTAL HEALTH DAILY:

“Alpha Waves

This frequency range bridges the gap between our conscious thinking and subconscious mind. In other words, alpha is the frequency range between beta and theta. It helps us calm down when necessary and promotes feelings of deep relaxation. If we become stressed, a phenomenon called “alpha blocking” may occur which involves excessive beta activity and very little alpha. Essentially the beta waves “block” out the production of alpha because we become too aroused. Frequency range: 8 Hz to 12 Hz (Moderate)

• Too much: Daydreaming, inability to focus, too relaxed
• Too little: Anxiety, high stress, insomnia, OCD
• Optimal: Relaxation
• Increase alpha waves: Alcohol, marijuana, relaxants, some antidepressants

“Theta Waves

This particular frequency range is involved in daydreaming and sleep. Theta waves are connected to us experiencing and feeling deep and raw emotions. Too much theta activity may make people prone to bouts of depression and may make them “highly suggestible” based on the fact that they are in a deeply relaxed, semi-hypnotic state. Theta has its benefits of helping improve our intuition, creativity, and makes us feel more natural. It is also involved in restorative sleep. As long as theta isn’t produced in excess during our waking hours, it is a very helpful brain wave range.

Frequency range: 4 Hz to 8 Hz (Slow)  Too much: ADHD, depression, hyperactivity, impulsivity, inattentiveness

• Too little: Anxiety, poor emotional awareness, stress
• Optimal: Creativity, emotional connection, intuition, relaxation
• Increase theta waves: Depressants´”

Scottsdale Neurofeedback Institute: “Normal Occurrence of Theta Waves

• Theta waves oscillate about 3.5 – 7.5 times per second (Hz). Some consider Theta to be from 4 – 8 Hz. Theta is normal in small very amounts in the healthy waking adult EEG. Theta in the adult waking EEG should be symmetrically distributed. Theta at the scalp surface in the adult EEG is normal as part of the early stages of drowsiness.
• Excessive Theta activity in the waking raw EEG of adults is considered abnormal. It can represent reduced metabolism cortical grey matter (too little oxygen uptake). Theta that is asymmetrically distributed in the waking adult EEG is considered abnormal (more on one side than the other)
• Spike and slow wave complexes that occur in seizure disorder often occur in the Theta frequency range.Excessive Theta on quantitative analysis is often seen in conditions such as…
  • ADHD
  • Learning disabilities
  • Head injuries or brain lesions
  • Certain neurological disorders”

SCHIZOPHRENIA BULLETIN:  To conclude, we found evidence that high-frequency activity in resting state EEGs may function as an endophenotype for schizophrenia. Schizophrenia patients and first-degree biological relatives of schizophrenia patients exhibited increased beta activity in their resting state EEGs during an eyes-open condition. Excessive EEG high frequencies in schizophrenia may relate to anomalies of the prefrontal cortex that are neural manifestations of genetic liability for the disorder. The present study also provides evidence for augmented low frequencies in resting state EEGs of schizophrenia patients as reflective of the disorder’s pathophysiology. Consistent with the presence of disorder-specific resting state functional brain abnormalities, schizophrenia patients exhibited increased activity in delta, theta, and alpha ranges, while similar anomalies were absent in bipolar disorder patients

Machine-learning-based diagnosis of schizophrenia using combined sensor-level and source-level EEG features :

“In this study, we used both sensor-level and source-level features extracted from EEG signals recorded during an auditory oddball task for the classification of patients with schizophrenia and healthy controls. EEG signals were recorded from 34 patients with schizophrenia and 34 healthy controls while each subject was asked to attend to oddball tones. Our results demonstrated higher classification accuracy when source-level features were used together with sensor-level features, compared to when only sensor-level features were used. In addition, the selected sensor-level features were mostly found in the frontal area, and the selected source-level features were mostly extracted from the temporal area, which coincide well with the well-known pathological region of cognitive processing in patients with schizophrenia. Our results suggest that our approach would be a promising tool for the computer-aided diagnosis of schizophrenia”.

Most patients classified as schizophrenic exhibit diminution in grey matter. In December 2007 a neurologist ( Dr B Snow) classified my MRI brain scan as normal or structurally non-schizophrenic. “ The cerebral hemispheres and ventricles were of normal size .  There was no evidence  for ventricular hypertrophy or temporal lobe atrophy which has been reported in schizophrenia. There were a few minor T2 hyperintensities in the cerebral white matter of no clinical significance” (Dr Snow) recommended  that I should consult a psychiatrist as refuting of the diagnosis of schizophrenia solely on the basis of a normal MRI scan would not be likely.

Wikepedia advises “In addition, significant cortical grey matter volume reductions are observed in this disorder. Specifically, the right hemisphere atrophies more, while both sides show a marked decrease in frontal and posterior volume. disorder.

Most schizophrenics also  have three times the normal amounts of dopamine receptor in their brains . “Schizophrenia has been shown to involve elevated levels of dopamine activity in the mesolimbic pathway and decreased levels of dopamine in the prefrontal cortex’^[5].Dopamine is part of the catecholamine  group also known as metanephrines.” A urine metanephrine test dated  21 January 2013 was essentially normal  @ 260 nmol/d ( 0-1150 ). I can confirm that the urine collection was collected over a 24 hour period  despite a qualification from the laboratory that “The low creatinine output suggests  this may be an incomplete 24 hour urine collection unless this patient has a very low muscle mass.”

Attempts to obtain the results of psychological tests and brain scans from 1985 have to date proved unsuccessful.    The former Director of the psychiatric institution Ashburn Hall ( Dr Du Fresne) was unable to locate my psychological test in 2007.  The psychological tests were referred to in a psychiatric report from Dr Carradock Davies to Dr Basil James in which Davies advises  “Cognitively she is functioning well and is of superior intelligence according to our psychological testing”.  The tests were provided by a former American  staff member psychologist/ psychotherapist  Dr Bernhardt of Kansas/Chicago. As I recall they not indicate any significant abnormality either. Since March 2013 my emailed requests for the psychological report have met with singularly unhelpful replies . On 28 May 2013 the Administration Manager of Ashburn Hall  Kate Ryan advised “ we also advised you by letter in 2007 that we were not holding the Psychological tests/report that you refer to . I am sorry we cannot assist further with this”

I then lodged a complaint with the Privacy Commissioner –the reply is thus:

Dear Vicki Wilson,

Your email was forwarded to the Complaints team and it was determined that as your  requests were made in 2007/08 – and you were  told the report doesn’t exist, the Office of the Privacy Commissioner would not be able to address especially as that issue as it was  too long ago.

In regard to the use of psychological testing apparatus: that would  not raising a privacy issue, in terms of the Privacy Act, the Privacy Act did not exist in 1985.

Regards

Fred Henderson

 Psychiatrist  Dr Carradock Davies clearly indicated that psychological testing had occurred . Irrespective of the fact that the agency is unable to assist because of the time limit  Principle 5 of the legislation states “ that an agency that holds personal information shall ensure that the information is protected …..against loss ……”   It is a matter of concern surely that either medical or psychiatric records can go astray without further investigation.

The Mental Health Act (1992) advises:

75 Complaint of breach of rights

• (1)Where a complaint is made by or on behalf of a patient that any right conferred on the patient by this Part has been denied or breached in some way, the matter shall be referred to a district inspector or an official visitor for investigation.

(2) If, after talking with the patient, the complainant (where that is not the patient), and everyone else involved in the case, and generally investigating the matter, the district inspector or official visitor is satisfied that the complaint has substance, the district inspector or official visitor shall report the matter to the Director of Area Mental Health Services, together with such recommendations as the district inspector or official visitor thinks fit, and the Director of Area Mental Health Services shall take all such steps as may be necessary to rectify the matter.

(3) On concluding any investigation under this section, the district inspector or official visitor shall also inform the patient or other complainant of his or her findings.

(4) If the patient or other complainant is not satisfied with the outcome of the complaint to the district inspector or the official visitor, he or she may refer the case to the Review Tribunal for further investigation; and, in any such case, the provisions of subsection (2), with any necessary modifications, shall apply.

My attempts to obtain assistance from two district inspectors of mental health proved unsuccessful with in my opinion further evidence of blatant disregard by the legal profession. I can see no time limit imposed in the legislation particularly section 75 that precludes an investigation prior to that time.

In his email dated 18 September 2013 District Inspector Andrew Molloy advised:

Dear Vicki

The legislation under which you were treated was the Mental Health Act 1969. That Act was repealed upon the coming into force of the 1992 Act. My appointment is as a District Inspector under the 1992 Act. Section 75 of that Act covers complaints that have arisen since the 1992 Act came into force.  It does not cover anything that happened to you, or to anyone, under the 1969 Act. However, it may not surprise you to learn that there are many people who have a sense of grievance arising out of the manner of their treatment under the 1969 Act. As a result of this the government has established what is called the Confidential Listening Service, which is under the leadership of a District Court Judge, Judge Henwood. It may be that this can provide you with the best means of making sense of what happened to you, and provide you with a clear sense of what you can do about it.

The service has a freephone , 0800 356 567.

If you wish to telephone me to discuss any of this please feel free to do so.

Andrew Molloy

District Inspector for Mental Health

In her email dated  April 2014 senior Queens Counsel and senior advisory district inspector of mental health Helen Cull  stated: 

“I note your complaint with regard to your incarceration in Porirua Hospital and Ashburn Hall, Dunedin in October 1985 to January 1986.  In n my role as Senior Advisory District Inspector, I am not permitted to provide opinions to former patients under the Mental Health Act.  If however you wish to seek legal advice, may I suggest you contact the Community Law Office, which will recommend lawyers practising in the area of Human Rights Law.”   Apparently Ms Cull was not au fait with her role in relation to patient complaints.

I attempted to enlist the assistance of yet another QC/ District Inspector of mental health namely Ms J Young of Whangarei  in December 2014. In her email dated 12 January 2015 Ms Young advised “As you are probably aware I am a lawyer and not a doctor so would be unable to answer the medical questions that you pose. I can help with jurisdiction and also complaints under the Mental Health act as they pertain to a patient in the legal sense of matters.”

In her email dated 27 February 2015 Ms Young further advised “I have had the time to consider the complaint you forwarded. It seems that you have brought this to the attention of a number of other professionals including Helen Cull the senior District Inspector and Andrew Malloy a district Inspector in Auckland. I am unable to assist with this request as I believe that it requires consideration from a medical point of view as the basic contention is that you were not unwell at times that you have been treated by clinicians in the past. I hope that you do find the assistance you require”.

Ms Young’s comment “as the basic contention is that you were not unwell at times that you have been treated by clinicians in the past” can only be regarded as nonsense.

In my email to Ms Young dated 19 January 2015 I expressed my concern that “ The repercussions of this erroneous incarceration have been significant and  include apartheid, and in respect of the medical profession , scant regard, even falsification. It is a blatant experimental case of psychological operations which incorporates unusual technology for the purposes of voyeurism and harassment, incorporating  elements of ritual abuse, and the use of the mentally impaired for bio hazardous exposures.

Obviously I would appreciate your assistance in having that original diagnosis of schizophrenia revoked by psychiatry. One might also need to take into account  the interrelationship between the instigators – the security services, medical, psychiatric and legal professions and the involvement of relatives amongst others”

 The Mayo Clinic advises that in respect of schizophrenia “ a person must  have at least two of the common symptoms of the disorder — delusions, hallucinations, disorganized speech, disorganized or catatonic behavior, or presence of negative symptoms for a significant amount of time during one month

• Experience significant impairment in the ability to work, attend school or perform normal daily tasks
• Have had symptoms for at least six months”

If one accepts the veracity of the use of ultrasonics and masers ( synthetic telepathy)in psychological operations as specified in this and other websites then this aspect should exclude the diagnosis of delusional and paranoid  schizophrenia. Since schizophrenic patients must normally exhibit a minimum of two symptoms of the disorder and since none of the other criteria such as disorganized speech, catatonic behaviour,or significant negative symptoms are applicable in my case it might be inferred that I am now,and have always been mentally normal and the victim of a wrongful incarceration in 1985.

Despite many bouts of physical ill health I am a generally well organised and coherent person who has been largely responsible for the administration maintenance and décor of the family home including the welfare of an elderly and failing parent.

 Of interest is  “Schizophrenia: Reliability and Validity of diagnosis”  Professor Rosenhan ((deceased) was a professor of psychology and law at Stanford University conducted a  an extract from a study entitiled  ‘Sane in Insane places” study   “To illustrate how clinicians can wrongly diagnose schizophrenia.   Rosenhan conducted the this study with   8 volunteers (including Rosenhan himself and 5 doctors/psychologists) arrived at several hospitals reporting only one symptom, that they could hear voices saying ‘hollow’ and ‘thud.’ All 8 were admitted into the hospitals that they arrived at and while they were there they acted as model patients in a bid to be released as soon as possible. The results showed that the average length of stay was 19 days with the longest person staying 52 days. Every single volunteer was diagnosed as suffering from schizophrenia in remission even though there was absolutely nothing wrong with them. This shows that validity of diagnosis was poor as the volunteers has been wrongly diagnosed”Acccording to website Helpguide.org a common delusion is the “ Delusion of control – Belief that one’s thoughts or actions are being controlled by outside, alien forces. Common delusions of control include thought broadcasting (“My private thoughts are being transmitted to others”), thought insertion (“Someone is planting thoughts in my head”), and thought withdrawal (“The CIA is robbing me of my thoughts”).

 However evidence concerning  mind control activity much of which I have experienced personally  and which is downloaded from  different sources is detailed below:

Lone star consulting( lonestarconsultinginc.com/mindcontrol.htm) advise “ hearing voices or sounds in your head or your thoughts being repeated back to you that are not caused by a medical condition and appear to be emanating from external sources that you can’ t seem to pinpoint? You may have tried to record these sounds but with no luck. This is because the most modern and popular audio digital recorders and tape recorders are not designed to record faint sounds sound bursts ultrasounds and infrasounds.  Lone star consulting provide a SSSD specially designed interface unit that plugs into the mike input of a digital recorder –it uses automatic gain control  (AGC) which is invaluable because it results in maximum amplification of faint sounds but automatically adjusts for less amplification for louder sounds . Ultrasonic signals by themselves, carriers,  infrasonic modulating ultrasonic carriers and audio signals modulating ultrasonic carriers are highly characteristic of electronic attack and mind control technologies”`

At Walter Reed Army Hospital of Research in 1973 Dr Joseph Sharp strapped inside an isolation chamber heard “ words” beamed at him in a pulsed microwave audiogram. An audiogram is a computerizied analog of the spoken voice  ARPA’S Robert O Beck  foresaw in the experiment obvious applications in covert operations. Becker imagined a barrage of voices driving an enemy insane .

 A psychoanalyst Carole Smith (soleilmavis spaces live.com/Blog) expressed some concern over the American Psychiatry Association’s Diagnostic Criteria for Schizotypal personality. “The third Edition ( 1987) of Diagnostic and Statistical Manual of Mental disorders ( DSM) required that there be at least four of the characteristics set out for a diagnosis of schizophrenia and an approved selection of four could be: magical thinking, Telepathy or sixth sense limited social contact, odd speech and over sensitivity to criticism.  By 1994 the required number of qualifiying characteristics were reduced to 2 or more. Including hallucinations and  “negative” symptoms such as affective flattening , or disorganised or incoherent speech- or only one if the symptoms were bizarre or the hallucination consisted of a voice keeping up a running commentary on the persons behaviour or thoughts.  But if the accounting of bizarre experiences more or less guaranteed you a new label or a trip to the psychiatric ward there is even more reason for a new group of people to be outraged about how their symptoms are being diagnosed.  A doubly cruel sentence is being imposed on people who are the victims of the most appalling abuse by scientific-military experiments and a totally uncomprehending society is indifferent to their evidence.  For the development of a new class of weapons now has the capability of entering the brain and mind and body of another person by technological means.

 Satellite technology is used not only for surveillance and communication systems but also to lock on to human beings manipulating brain frequencies by directing laser beams, neural partical beams, electro magnetic radiation sonar waves  radiofrequency radiation soliton waves torsion field . In particular pulsed radio frequency radiation is used for manipulating and disturbing the human mental process and for causing  negative effects on human health and thinking. The beam is administered from space.  The development over the last decades since the Cold War arms race has included as a major strategic category psycho-electronic weaponry the ultimate aim of which is to enter the grain and mind.  The only witnesses to this terrible technology are the victims themselves and those who are given the task of diagnosing mental illness are attempting to silence them by classifying their evidence and accounts as the symptoms of schizophrenia, while the dispensers of psychic mutilation and programmed pain continue with their work unopposed.

 It was always crucial under the threat of psychiatric sectioning to carefully screen out any sign of confused speech negativity coldness suspicion bizarre thoughts sixth sense telepathy premonitions but above all the sense that “ others can feel my feelings and that someone seemed to be keeping up a running commentary on your thoughts and behaviour” then reporting these to a psychiatrist or anyone else for that matter who was not of a mind to believe that such things as mind control could exist, would be the end of your claim to sanity and probably your freedom.   For one of the salient characteristics of mind control is the running commentary which replicates so exactly and surely not without design the symptoms of schizophrenia  Part of the effort is to remind the victim that they are constantly under control or surveillance.  Programmes vary but common forms of reminders are electronic prods and nudges body noises twinges and cramps to all parts of he body increasing heart beats applying pressures to internal organs all with a personally codified system of  comments on thoughts and events designed to create stress panic and desperation. This is mind control at its most benign.

There is reason to fear the use of beamed energy to deliver lethal assaults on humans including cardiac arrest and bleeding in the brain. In 2001 congressman Dennis Kucinich introduced a bill to the House of Representatives which it was hoped would be extremely important in the fight to expose and stop psycho-electronic mind control experimentation on involuntary non-consensual citizens . The Bill was referred to the committee on Science and in addition to the committee on Armed  Services and International Relations.  There was however no mention in the revised bill of any of the aforementioned mind-invasive weaponry nor any other technology designed for deployment against the minds of human beings.

 In England on May 25 1995 the Guardian newspaper in the UK carried an article based on a report by Nic Lewer, the peace researcher from Bradford University, which listed “ more than 30 different lines of research into new age weapons.  There are according to Lewer plans for pulsed microwave beams to destroy enemy electronics and separate plans for very low frequency sound beams to induce vomiting, bowel spasm, epileptic seizures and also crumble masonry.  There are also plans for mind control with the use of psycho –correction messages transmitted by subliminal audio and visual stimuli.  There is also a plan for pychotronic weapons apparently the projection for consciousness to other locations.

Another article entitled ” Mind control and ritual abuse” describes methods as follows:

Dysfunction: methods causes memory loss blocking of awareness ( disassociation) and mindless obedience

Densitisation:  Diminished thoughts emotions and behaviors are replaced with induced responses.Individuals are manipulated isolated and debilitated. Physical biological and psychogical attacks weaken individuals. Tactics and drugs employed destroy self-sufficiency and force reliance on manipulators. Cruelty and confusion techniques create depression uncertainty numbness fear and rage.  Controllers manage the people and situations . Imposed behaviors are reinforced and events covered up. 

In Essays on Mind Control by Allen Barker (Mental Firewalls) ( jbhfile.com/Part III Mental Firewalls .htm) advises “ there truly are some people with mental illnesses which occur naturally. There are also people with mental illness which were externally and purposely inflicted for example by harassment operations  It is common knowledge that the mentally ill have used as guinea pigs in mind control experiments precisely because they would tend to be disbelieved and are relatively powerlesss victims for torturers to experiment on.  Abuse includes psychosurgery, microwave harassment etc.which can cause organic problems in addition to psychological problems. The victim is under constant surveillance.The victim is harassed overtly and covertly . All forms of taunting and goading tend to occur.  The victim soon has to wonder about everything that breaks or goes wrong in their lives.  The victim is purposely isolated .  People close to them are threatened or deceptions are created to make the victim suspect those closest to him or her. Unfortunately in the despicable circles of mind control it is sometimes the neighbour or even a close family member that  is truly responsible.

The victims mind  is under assault with voice projection voice cloning  The Village Voice in an article from July 2001 titled “psycho warfare” described an Air Force report uncovered by Nick Begich. Quoting from the article “ twenty four hours a day the victim is subjected to commands ridicule and distractions inside his or her private mind. Finally the victim’s supposedly private subvocalized thoughts are somehow read or inferred and analysed .  There are various levels at which this can occur from remote heartbeat up to and including brain implants telemetering EEG signals. Sex, defecation, burping etc and normal human emotions such as worrying and anxiety are turned against their victims.   The perpetrators  constantly attempt to demean their victims and turn all of these human properties against their victims.”  Ultrasonics views homeless people as a  definite threat to neighbourhood communities and are actively running homeless people out of the community with sonic weapons .

Law enforcement can easily brush off the complaints by the targeted homeless because the general public assume that most homeless people are mentally ill. In my opinion there is a massive organized effort being mounted against mentally ill people in this country to drive them out of neighbourhood communities and force them into mental institutions and onto prescribed medications.  Ultrasonics attack you relentlessly and will attempt to get you to turn violent thus precipitating forcible placement in a mental institution.

 The American Psychiatric Association does not recognize the possibility that high technology may be used to create or mimic symptoms of mental illness in a person. Therefore a psychiatrist does not have to consider the possibility of high technology when diagnosing mental illness. There is a safety net for psychiatrists doctors lawyers and law enforcement if somehow the use of this technology becomes public. This is plausible deniability or simply denying any knowledge of what they did thus enabling them to continue to damage and destroy people’s lives indefinitely and not be accountable for anything.

Another article entitled “ What is mind control?” advises that when serious lies are used to cause carefully scripted harassment and electronics used to destroy faculties the target’s life is virtually worthless. The symptoms of mind control can include:

Excruciating pain///// blanking of recent memories////sudden enforced wakening at precisely the same time in the middle of the night//// the  “injection of air from nowhere” inside the upper lip when the lips are firmly closed, and the tongue and cheeks are blocking air from the lungs – this injection is used to keep the target awake as it results in a loud noise like flatulence////sudden clumsiness////attacks of extreme fatigue////wildly racing heart without any cause//// artificial and powerful sexual stimulation///, around the clock  transmissions usually insulting and/ or threatening  to indicate that you are under surveillance. The external symptoms can include: many wrong number calls///theft of personal papers and records particularly those which the target doesn’t access often////tradesmen botching the job or overcharging///chronically erratically performing computers//spreading rumours that the victim has a criminal record////non-stop attempts to crush religious faith//

A quote from Dr José Delgado, Director of Neuropsychiatry, Yale University Medical School Congressional Record, No. 26, Vol. 118 February 24, 1974 states:  “We need a program of psychosurgery for political control of our society. The purpose is physical control of the mind. Everyone who deviates from the given norm can be surgically mutilated.” “The individual may think that the most important reality is his own existence, but this is only his personal point of view. This lacks historical perspective. Man does not have the right to develop his own mind. This kind of liberal orientation has great appeal. We must electronically control the brain. Someday armies and generals will be controlled by electric stimulation of the brain.”

A specific reference to the involvement of the intelligence community personnel in mind control is contained in an article entitled “ Microwave Mind Control” by Tim Rifat (whale.to/b/rifat/html.)   “Transducers are used to modify the spoken word into ELF audiograms that are then superimposed on the pulse modulated microwave beam.  There are also the laser equivalent of microwave beams. These MASER beams have been used to develop something called synthetic telepathy.  This is the ability to read people’s minds from a distance   Electronic scanning of victim’s brains by monitoring the electromagnetic (EM) emissions from people’s brains and using among other things the brain waves ( as measured on a EEG) to read the victims subvocalised thoughts.

Secondly, the police have been granted the exclusive use of the 450 MHz microwave frequency range. This is exactly the frequency used by Dr Ross Adey, the CIA mind control expert, in his experiments on behavioural modification. It seems the police have the exclusive use of this mind control frequency and a vast array of antennae to broadcast this frequency all over the country. Very useful for mass mind control in times of emergency. Adey found that by using 0.75mW/cm² intensity of pulse modulated microwave at a frequency of 450 MHz, it was discovered that an ELF modulation could be used to control all aspects of human behaviour. The Sussex police headquarters is connected to CCTV, closed circuit television cameras throughout the town. Some of these cameras have microwave telemetry devices that could easily be used to broadcast this frequency. The large antennae that bracket the town could also be used.

The most insidious aspect of this, is that the entire mobile phone network could easily be used to control the behaviour of the phone users. By use of my microwave detector, I have found that mobile phones of the newer type, give off a pulse modulated microwave signal of around 0.75mW/cm² at the earpiece. This may be coincidence, but it is exactly the intensity required for behavioural control as found by Dr Ross Adey, the pioneer of microwave mind control. So in theory, an ELF signal could be added to the microwave network to feed a precise behavioural pattern into every mobile phone user in the UK.

 If there were widespread riots, the ability to broadcast behavioural stimuli to mollify all the mobile phone users in the country would prove useful. Since mobile phone users are generally middle class, it means authority has a useful method of controlling the behaviour of the key voters. Microwave carrier beams are perfect for transmitting the excitation potential of docility to the phone user to keep them servile in times of trouble. When no ELF signal is broadcast the phone acts in a completely different manner on behaviour in humans. In this case the microwave phones causes the neurones to release calcium ions which makes the user tired irritable and when stresses likely to emotional outbursts such as road rage.

In Brighton, the local MI5 headquarters has a large microwave array on its roof. Secret bunkers in the area also have large microwave arrays above them. It is child’s play to transmit an ELF modulated signal to be broadcast by the entire mobile phone network – if need be. By this means the entire mobile phone users can be behaviourally modified. At the cost of developing cancer from low level microwave exposure from the phones they constantly use, stressing the neural network by constant calcium ion efflux and interference with bioelectric fields.

It seems strange that a few milliCuries of ionising radiation will get the National Radiological Protection Board excited, whilst high intensity cancer inducing non ionising microwave radiation, goes unchecked. So high are levels near transmitters, that litter the countryside, that light bulbs will explode near them. If the intelligence community is using microwaves on a large scale as mass mind control weapons, then the NRPB’s silence is easily explainable. To add to this, the numerous microwave detectors that were cheaply available to check leakage from microwave ovens are no longer made by any company in the country. It seems the UK authorities do not want the population to be able to detect when they are being microwaved.

In conclusion, it can be seen that the UK intelligence and police, have a dizzy array of high-tech mind control devices. They regularly target their own populations and thousands of people are made ill by microwave weapons. With the advent of synthetic telepathy, ‘CCTV of the mind’ becomes a reality.  External reinforcement by the intelligence community includes destruction of the target’s property ruining their financial affairs and vicious rumour mongering. “

 NAZISM

It’s a rare occasion in a democracy when legal recourse is denied .  This is surely nothing more than odious conspiracy and a gross abuse of power imbued with more than a touch of Nazism.  .  The association of an elderly female relative Miss Marianne Kassler (now resident in Epsom Auckland) with a former French nazi war criminal Mr Jacques Correze might be of relevance. Miss Kassler’s initial harassment involving derogatory comments concerning my intelligence and mental health continues occasionally to this day. She returned to Auckland in 1997 previously having lived in London since the mid 1950s.    A summary of the background of Mr Correze is provided in Wikepedia and  is also  detailed in the book written Michael Bar-Zohar is as follows:

 Bitter Scent  The Case of L’Oreal, Nazis, and the Arab Boycott by Michael Bar-Zohar:

“A powerful   expose that unmasks a giant cosmetic firm’s long history as a haven for French Nazis—sanctioned at the highest levels of the French government.

This is the true story of scandal and skullduggery in high places that rivals the intrigue of any fiction thriller. Set in the contemporary world of the glamorous cosmetics industry, its roots are in the Nazi occupation of France during World War II, and it involves leading political figures and business executives who are accused of protecting high-ranking French Nazis for the last five decades. It also involves a genuine hero, Jean Frydman—a man who as a teenager fought the Nazis in the French underground, and who as a contemporary media wizard and multimillioniare has made it his crusade to expose the French collaborators who have provided a haven and fortress for war criminals.

World famous as the symbol of beauty and glamour, L’Oreal became the target of an Arab boycott when it swallowed another cosmetic giant, Helena Rubinstein, whose founder had been a prominent Zionist. When Frydman was forced off the L’Oreal board with a letter of resignation apparently forged to satisfy the Arabs, he found himself confronted with the anti-Semitism he had fought against all his life. Determined not to let his L’Oreal partners get away with it, he learned that the forgery was made on the orders of one Jacques Correze, chairman of L’Oreal’s marketing group in New York and a former Nazi collaborator who had been convicted of war crimes after the Liberation. Frydman then filed suit against L’Oreal for financial malfeasance, fraud, forgery, racial and national discrimination.

It was one lone individual up against the powerful L’Oreal and the French establishment. But despite L’Oreal’s indignant denial of the charges, papers were found that revealed the whole dark story of negotiation between the cosmetics firm and the Arab Boycott Bureau. And as Frydman continued to dig into the records of L’Oreal’s past, he discovered more Nazi collaborators on their payrolls and a chain of connections that reached the highest level of the French government-President Francois Mitterand.

With the complete cooperation of Jean Frydman himself and rare access to other people involved in the scandals as well as to the legal documents, Michael Bar-Zohar has written an exciting, suspenseful book that proves once again how much stranger truth is than fiction.

LOreal has an unwholesome past regarding Nazi collaboration. Jacques Correze a convicted Nazi Collaborator, was hired by L’Oreal in 1950 after his release from prison and was assigned to the United States in 1954 and appointed Chairman of Cosmair in the late 1960s. He died in 1991. shortly after his past as the No. 2 man in the Nazi & French terrorist squad The Cagoule was exposed. Correze was also alleged to have belonged to several pro- Nazi groups during the war, including the Mouvement Social Revolutionnaire (MSR). But L’Oreal’s Nazi ties go deeper still: the companys founder, Eugene Schueller, is reported to have helped finance the MSR and later  joined the pro-Nazi Rassemblement National Populaire.”

http://www.farinc.org/newsletter/v8_n3_-4_94/gleanings.html

My former rental home in whangarei is owned by the Japanese Watanabe family who are apparently resident in Auckland.  Wikipedia advises that “ “Mutsuhiro Watanabe (Japanese: January 1, 1918 – April 1, 2003) was an Imperial Japanese Army sergeant in World War II who served at POW camps in Omori, Naoetsu (present day Jōetsu, Niigata), and Mitsushima (present day Hiraoka). After Japan’s defeat the US occupation authorities classified Watanabe as a war criminal for his mistreatment of prisoners of war (POWs), but he managed to evade arrest and was never tried in court .

HEALTH MATTERS

During 2007/2008 I lodged complaints with the Advocacy Service of the Office of  Health and Disability Commissioner. Obstructive tactics seemed to be in evidence.

HOn  25 June 2008 I emailed a complaint to Ms Strid of Health and disability about the  unnecessary and sometimes disjointed and incoherent  attempts at editing my complaints by HDC advocate Aaron Morten.

In his letter dated 25 June 2008 Aaron advises “ Firstly, you make numerous reference to concerns about reports but you do not reference the authors and the relevance of including these and in future identify first your actual concerns and then reference the reports /consultations/research relevant to each of the concerns that you feel  I have not been responded to.  Furthermore a more structure approached that easily understood in terms what it is you are trying to address that is structure and straight- forward i.e. the background of the concern identify the issue what it is you want resolved and what do you believe is the best approach is the provider able to respond”

Dr Henrys:   In respect of Dr Henrys, who  despite Medlab’s diagnosis of a gram negative bacterial infection and a recommendation for drug treatment  was initially reluctant to prescribe. This might also be considered to be significant as there has been a similar pattern/response from other general practitioners.   Aaron’s response was“this is irrelevant” In the same letter I referred to the non-diagnosis of a broken toe by radiology and the non-reporting of some other  incidental findings . Aarons response was “ Umm is there really a complaint who diagnosed the boken toe”.   Regardless of the non-diagnosis, presumably I would not have been referred to radiology if a broken toe had not been suspected-I also experienced prolonged pain.

Dr Whyte: With regard to my letter to Respiratory Physican Dr Whyte I stated “ that pain and tiredness ( possibly indicative of a mild form of meningitis )are a common feature”. Aaron queried ( was Dr Whyte aware of the meningitis). In fact there was no specific diagnosis of meningitis, just my own suggestion,particularly as meningitis can be associated with gram negative infections.  I quoted 2 paragraphs from Dr Whyte’s report. The paragraph concluded “ if the evidence points to the chest infection then she should consider admission for assessment and IV antibiotic therapy”.  Aaron stated “ who advised you of this ,reference from another practitioner ? Report? E Journal?.  I was quite obviously quoting from the report of Dr Whyte. 

The Complaints Co-Ordinator ////Dr Pardy In respect of my complaint to the Auckland District Health Board there seemed to be confusion as Aaron changed/ juxtaposed the addressee namely  the Health complaints Co-ordinator Auckland District Health Board  cc. Gynaecological Clinic Greenlane Clinical Centre with a letter to Dr Respiratory Physican Dr Pardy. Aaron had ( correctly?) amended the addressee from Health complaints co-ordinator to Quality and Safety Unit. His notation was thus:  “( was this referral to the DHB therefore the above contact details would suffice or did you attend an appointment at the Auckland Medical Specialists Respiratory Services who are in Newmarket”.  My consultation with Respiratory Physician Dr Pardy at the Greenlane Clinical Centre occurred in  March 2002. My written complaint to Julie Byers Complaints Co-Ordinator at the Auckland District Health Board concerning a gynaecological scan was dated 23 May 2005.  I had also referred to Greenlane Radiology reports dated 30 November 1999 and 29 June 2002.  In respect of the latter report Mr Morten stated ( was this report a result of the March 2002 performed Dr Pardy or someone else)  

Dr Hartley :In my complaint concerning Dr Hartley I advised that when I tried to discuss a change in the symptoms in the late1980s.  Dr Hartley curtailed the consultation. Hartley clearly specified in his report that “ when she was unwilling to listen to an alternative explanation as to what was going on I terminated the consultation”  Aaron stated ( is this what Dr Hartley said, seems inconsistent and similar to a previous response to another General Practitioner complaint”)  Inconsistency isn’t really the issue- if anything the consultation might be regarded as somewhat consistent  and certainly similar to a consultation with General Practitioner Dr Tom Marshall who also aborted his consultation.

Dr Coral Fonseca: With regards to Dr Coral Fonseca I was concerned about her prescribing of allergy medication rather than antibiotics . Aarons response was : “ to resolve this complaint would to request whether these records were made available at the time during that consultation and whether there was any record of these.  Concerns of access to these and if they were available at the time might be more relevant  questions and since this Doctor is no longer at this clinic , and these questions would need to be posed to the Clinic itself, about whether they were present at that time”. I think this is a case of overstating the obvious- even though Dr Fonseca is now practicing at Great North Road Avondale medical records should be available concerning the date of the consultation date of  5 November  2005 at East Tamaki Health Care 5 Mayfair Place Glen Innes. Access to those records should not be a problem for Dr Fonseca.

Dr Kolbe : In contradiction the Medlab allergy tests which indicated allergies to rye grass silver birches and peanuts Dr Kolbe stated that I had no known allergies. Mr   Morten stated (  do you want these detail  amended if so request as a further desired outcome in the final paragraph). My final paragraph had specifically asked for an explanation as to this incorrect biographical detail. In respect of Kenneth Todar an American bacteriologist whose assessment contradicted that of Kolbe Morten asked ( who is Kenneth Todar  why has he been included only in the last paragraph)

Dr Garrett :  I quoted from Garrett’ report including a reference to his spirometry testing” a study of peak flow and expiratory scans……although she did have 61/2 ribs exposed anteriorly”  FEV1 and peak flow measurement were considered to be within the normal range.   Mr Morten’ statement ( are these the actual comments made by Dr Garrett –are your able to explain this furthermore did he  have copies of these reports).  Anyone with a rudimentary medical knowledge would be aware that spirometry testing is generally carried out by the specialist himself.  It seems rather nonsensical to enquire whether the specialist had copies of the reports. In respect of the photos from bronchoscopy Morten enquired ( what photos yours, medlines  Are they part of the report?)  I  had quite clearly stated that the photos were from the bronchoscopic procedure.   Lavage results indicated a difference in the neutrophil cell  levels between the left and right lungs. Morten stated ( Is this what Dr Garret stated or a reference to Mediline) Lavage results are obviously provided by Diagnostic Medlab. I had stated that on occasions “crackles” and “ rales” which are often associated with a diagnosis of pleurisy had been detected by general practitioners. Mr Morten commented  (who said this reference to who? –from my understanding rales ( ostensibly crackles is a symptom-am querying the rationale for include the above two paragraphs and paragraphs with reference to Dr Todar).   Todar had stated “that gram negative bacteria Pseudomonas Aeruginosa almost exclusively afflicts patients who are compromised in their lower respiratory tract or defence mechanisms and almost never infects uncompromised tissues” Despite  subsequent detection of “ rales” by practitioners there has never been a repeat pleurisy diagnosis.  While of interest the pleurisy diagnosis is not specifically relevant to Todar’s comments.  

Dr Simcock:  I had quite clearly specified that an Auckland Radiology report of a CT scan of the sinuses stated “ that the nasal septum is deviated slightly to the right…..which might predispose to oesteal obstruction …………” Mr Morten stated ( was this what the Radiologist report or Mr Simcock?)   I also clearly quoted from  Internet site E Med.  Mr Morten stated ( you need to lead in from here with reference to the following i.e. from own independent research”) The comment “ from own independent research” might be considered extraneous and unnecessary –a case of overstating the obvious.  Dr Simcock’s  exclusion of the  nose and sinuses as the source of my symptoms is contained in my  letter of complaint.  Mr Morten neverthless enquired ( Had he diagnosed bacteria?)  Any bacterial diagnoses  are provided by Diagnostic Medlab.  Mr Morten’s comments once again indicates  of comprehension.   Mr Morten further states ( (ostensibly you are seeking his professional opinion about the diagnosis and further information about the condition and reports”   I was obviously  not seeking his professional opinion about the diagnosis. I obviously am concerned that a despite a 30+ year  history of serious chest and sinus infections and on one occasion a laboratory diagnosis of  gram negative cocci in sinus sputum coupled with occasions of  frequent discharge from the nostrils Dr Simcock dismissed the sinuses as the source of my symptoms. 

Dr B Snow:   In respect of a C-Reactive Protein test  Mr Morten enquired ( was this also included in Dr Snow’s report or is this an additional comment made by you?) This reference is an additional comment and was not referred to in Dr Snow’s report. I certainly discussed the thermography reports of 2003 which indicated a generalized inflammation and also the diagnosis of Myalgic Encephelomyelitis (ME). However neither of these 2 conditions were alluded to in Dr Snow’s report. His only reference to my history of gram negative bacterial and chest and sinus infections was a reference to” intermittent chest and sinus infections” Dr Snow reported “no carotid bruits” . Morten stated ( reference to the carotid is bruit  is this relevant to the above topic or is this separate?)  A carotid bruit is an abnormal sound heard with a stethoscope when checking the carotid artery in the neck. The artery carries blood  to the head.  It can indicate atherosclerosis.   Checking for carotid bruits might therefore obviously also be considered relevant .

Dr Ng:  I referred to the removal of a fibroadenoma from the breast measuring approximately 1 cmm.  Although it is obvious in the script Mr Morten queried ( 1 cmm or mm). At the end of the last paragraph in which I stated “ I would appreciate your advice as to why excisional biopsy of the existing fibroadenomas/cyst aspiration had not been recommended “ Mr Morten stated (did you have an appointment with Dr Ng if so when –to remind you I can only assist if this is a complaint about the quality of treatment received by a practitioner but you do not specifically outline an appointment with Dr Ng at any time” Although I didn’t specifically refer to the consultations with Dr Ng I recall one possibly 2 consultations with him five or six years ago .  Dr Ng was Director of the Breast Clinic at that time. and regardless of whether I had consulted with him personally or not presumably the ultimate decision concerning surgical procedures would rest with him.   I had a large fibroadenoma removed at Auckland Hospital in 1997 and ultrasound scans were undertaken at the hospital in 2002 and 2003.

Dr Theakston:  I advised that in 1988 Dr Simpson of the University of Otage had diagnosed Myalgic Encephalomyelitis . A blood test which had established an increase in the surface changes of the cells. Mr Morten queried ( were these blood tests the same blood tests that were requested by Dr Simpson).  It would seem unlikely that Dr Simpson would have made that diagnosis without the assistance of a blood test.  With regard to the non-reporting of red blood cells as” general practitioners did not think it provided any useful additional information to the haemoglobin concentration” Mr Morten queried ( the relevance of this statement in relation to the first paragraph or the second or is there still additional information required?)  Non reporting of the red blood cells might be considered a serious matter particularly in view of the diagnosis of red  blood cell abnormalities in 1988 .  In view of the fact that haemoglobin is a component of the red blood cell the non-reporting of the latter might be considered unusual if not suggestive of concealment of a disorder.  

Dr Lane:  In my complaint I made reference to your  upper endoscopy and colonoscopy reports dated 21 May 2003 .  Mr Morten stated ( who performed the colonoscopy report ? What is the relevance to the endoscopy report ? Did Dr Lane make this statement i.e. lining of the bowel attributed to the overuse of laxatives”) I think Mr Morten is being somewhat obtuse –an endoscopy examines the upper digestive area and the colonoscopy the large bowel. Advice attributing melanois coli to the overuse of laxatives was provided by both Dr Lane and on the internet from the West Shore Colonoscopy Centre in Philadelphia .   I concluded my letter of complaint by stating that “ I would appreciate your explanation as to why details  from earlier scans concerning mural polypi and the condition of the oesophagus were  not detected”  Mr Morten stated  (reference to what report? Was this outlined in the endoscopy report by Dr Lane ) Mural polypi were referred to in an Auckland Radiology report of 8 April 1988 and the oesophagus in a CT scan of the lung dated 20 June 2002. Dr Lane advised that images of the endoscopy/colonoscopy procedures had not been retained at Auckland  public hospital after the procedure.  Mr Morten stated ( more specific questions would be relevant to why they are not retained).  I don’t see quite how I could have been any more specific in my query as to the non-retention of hospital procedural.film.

Dr  Marshall: Mr Morten stated ( elaborate how you felt you were discriminate)  As I recall there was no significant acrimony evident during the course of the consultation.  Dr Marshall seemed to take umbrage at my comments concerning gram negative bacterial infections hardly a reason to terminate the consultation. The fact that he suggested I seek medical care closer to home would seem to indicate that my presence wasn’t wanted at his practice i.e. discrimination. Dr Marshall was a Chairman of Procare and a senior member of the medical fraternity.

Dr  Knill  I do not have a record of the exact date of the consultation which occurred in 2004  I had incorrectly stated the year of the consultation as 2005.

Dr Corbett:  I contrasted the attitude of this practitioner who during one consultation diagnosed “rales” and prescribed antibiotics with her strange comment and change in attitude in a subsequent consultation . Mr Morten seems to missed the point (what is your reasoning for the above comment in relation to the following paragraph is it because she diagnosed rales or because she prescribed antibiotics . I do not recall the exact date of the consultation however I believe it was in 2004.

Dr Julie  Hancock:  During a consultation with Dr Hancock in December 2004 she suggested that a reason my red blood cells had not been reported by Diagnostic Medlab was because they were being reported in an alternative way. Mr Morten commented ( are you suggesting he explain how they report this information) Obviously this was not an accurate statement  by Dr Hancock as Dr Theakston the Clinical  Director of Haematology at Medlab subsequently advised that reporting of the red blood cells had ceased altogether-“ because general practitioners did not think that it provided any useful additional information to the haemoglobin concentration” Mr Morten queried ( is this relevant to the complaint). Non-reporting of red blood cells might be construed as seriously negligent.  .In respect of a diagnosis by Diagnostic Medlab of a gram negative bacterial infection during 2 consecutive months Mr Morton stated ( (was this by Dr Hancock).   Dr Hancock provided an alternative prescription of  nasal spray and paradex tablets during the consultation of June 2005.  Mr Morten queried  (is this what he prescribed in June).  I described a comment overheard from Dr Hancock’s office as discriminatory. Mr Morten suggested that the word (disrespectful ”) might be more appropriate. I don’t agree.

Dr Dan Anderson:  I attended a consultation with Dr Dan Anderson on 27 January 2006.  On my way out the door at the end of the consultation Dr Anderson passed a derogatory sexual comment “ doesn’t like f….king “   Mr Morten commented ( are you certain that Dr Anderson made these comments) As I recall I suggested  to Dr Anderson that it might be a matter for the police however my comment met with a measure of  indifference.

Dr Van Roekel:  I considered that Dr Van Roekels twice repeated “ committed” comments in the reception area of the practice was discriminatry.  Mr Morten stated ( not necessarily that perhaps where unnecessary)  Whatever that means! 

Dr  Ron Jones: It is quite clear from the chronology of my text that I underwent a hysterectomy in 1988 and some 2 years later as a result of experiencing severe contractions in the groin an investigative laparascopy procedure was performed by Dr Ron Jones. Mr Morten appears to have juxtaposed  the details from the laparascopy with the hysterectomy i.e. (“ a hysterectomy had been performed in 1988 and you reported  “that a loop of small bowel was adherent to the stump of the right infundibulo pelvic ligament ………-do you believe that this could have contributed to the laparascopy in 1991 –further elaborate about these details) Subsequent to the laparascopy I was advised by the nurse/receptionist that I would experience only a little referred pain however the pain proved to be very severe and long lasting. Mr Morten stated  (was this in 1988 or in 1991 more importantly the complaint should be directed to the Nurse in concern and more specific details would required to determine which Nurse had advised you at that time)   Any complaints concerning the procedure should be directed to the gynaecologist who performed the procedure not the receptionist /nursing staff.

I also expressed concern about the closure of my complaints by a female staff member (Miss K Tu) prior to the receipt of replies from the medical providers.  The stated reason was  “ your  complaints to the following health providers had been closed with our service-the majority of your concerns requested explanations from Doctors regarding reports written about  your health concerns…I am unable to pressure or convince Health Practitioners to change  what they reported on completion of examination into your health however this should not stop you from continuing your campaign to seek full explanations about your ongoing health concerns” 

This attitude was later affirmed by HDC’s legal representative Ms T Baker who apparently chose to ignore salient facts and concurred with the replies of most the providers.    Right 4 of the Health and Disabilty Code of Rights is advises “every consumer has the right to have services provided in a manner that minimises the potential harm to and optimises the quality of life of that consumer”  Right 6 entitled the “ Right to be Fully Informed”  includes  an “explanation of his or her condition///an explanation of the options available ///the results of tests and procedures. “  The replies from the medical providers often tended to be evasive sometimes discriminatory and in the case of at least one respiratory physician seriously erroneous.   A summation of some of these complaints are detailed below in a letter received from Theo Baker dated 23 February 2009 on behalf of the then acting HDC Commissioner Ron Paterson.

I

BIO HAZARDOUS EXPERIMENTATION

Wikipedia advised that “ From 1946 to 1953, at the Walter E. Fernald State School in Massachusetts, in an experiment sponsored by the U.S. Atomic Energy Commission and the Quaker Oats corporation, 73 mentally disabled children were fed oatmeal containing radioactive calcium and other radioisotopes, in order to track “how nutrients were digested”. The children were not told that they were being fed radioactive chemicals and were told by hospital staff and researchers that they were joining a “science club”

In another study at the Walter E. Fernald State School, in 1956, researchers gave mentally disabled children radioactive calcium orally and intravenously. They also injected radioactive chemicals into malnourished babies and then pushed needles through their skulls, into their brains, through their necks, and into their spines to collect cerebrospinal fluidfor analysis

In 1941, at the University of Michigan, doctors Francis and Jonas Salk and other researchers deliberately infected patients at several Michigan mental institutions with the influenza virus by spraying the virus into their nasal passages.^[17] Francis Rous, editor of the Journal of Experimental Medicine wrote the following to Francis regarding the experiments:

“It may save you much trouble if you publish your paper … elsewhere than in the Journal of Experimental Medicine. The Journal is under constant scrutiny by the anti-vivisectionists who would not hesitate to play up the fact that you used for your tests human beings of a state institution. That the tests were wholly justified goes without saying.”

The History of Bioterrorism in America
By Richard Sanders, Coordinator, Coalition to Oppose the Arms Trade.

“Who is behind the recent spate of Anthrax attacks? Who would intentionally expose Americans to such deadly germs? To answer these questions, it is useful to know that there have been previous cases bioterrorism in the U.S. Previous incidents of bioterrorism in America since WWII, although more widespread than this year’s anthrax-related incidents, received very little media attention. 

The identities of those who planned and perpetrated decades of bioterror attacks on Americans is known. Although they have admitted their guilt – in written confessions to Congress – they remain immune from prosecution. They are above the law.

In a 1977 special report to Congress, the U.S. Army admitted conducting hundreds of chemical and biological warfare tests, including at least 25 that deliberately targeted the unsuspecting public. The military disclosed evidence that it had released disease-causing germs in at least 48 open-air tests. (U.S. Army Activity in the U.S. Biological Warfare Programs, 1942-1977. Vols 1 and 2, February 24, 1977) In 1994, Senator John D.Rockefeller’s report (Examining Biological Experimentation on U.S. Military) further revealed that over the previous 50 years, the U.S. military intentionally exposed hundreds of thousands of their own soldiers to dangerous microbes, mustard and nerve gas, radiation, hallucinogens and psychochemicals. 

Recent bioterror attacks have prolonged the national crisis sparked on September 11. Widespread concerns about anthrax have served those who wish to promote the draconian laws that are descending upon the U.S. Curiously, the strain of anthrax bacteria being used most likely originates from the U.S. military (Debora MacKenzie, New Scientist, October 24)

The following quotations, compiled from various sources, summarize the shameful but little-known history of the U.S. military’s responsibility for exposing Americans to the terror of biological weapons.

——————-
1943 Fort Detrick:
The U.S. began research on biological weapons at Fort Detrick, MD.1 They studied anthrax, brucellosis, Botulinus toxin, plague, Sclerotium rolfoil, late blight, late blast, brownspot of rice, rinderpest, tularemia, mussel poisoning, coccidioidomycosis, rickettsia, psittacosis, neurotropic encephalitis, Newcastle disease and fowl plague.

1945 Recruiting Nazis: 
The U.S. State Department, Army intelligence and the CIA initiated Project Paperclip to recruit Nazi scientists and offer them immunity and secret identities in exchange for work on top secret, U.S. government projects [including bio-warfare experiments on unwilling human subjects].1

1946 Japanese war criminals: 
The U.S. began negotiations with Japan to acquire their germ warfare data. In exchange, Japanese scientists received immunity from prosecution for their war crimes. Dr. Shiro Ishii, a physician and army officer who began experiments in germ warfare in 1932 when Japan invaded Manchuria, formed a biological-warfare unit (Unit 731) that used Chinese soldiers and civilians as test subjects. About 9,000 died of bubonic plague, cholera, anthrax and other diseases. U.S. soldiers captured in the Philippines were sent to Unit 731 so the Japanese could test biological weapons on them.2

1948 Cttee. on Biological Warfare:
The Secretary of Defense’s Research and Development Board, requested an evaluation of biological agents as weapons of sabotage. The Committee on Biological Warfare recommended that methods be assessed for disseminating biological agents, with emphasis on special operations. It recommended research to test “innocuous organisms” in ventilation systems, subways and public water supplies. This influenced administrations for 20 years and the U.S. conducted highly-classified scientific tests on unknowing populations throughout the country.

The biological warfare research program in the early 1940s and 1950s involved antipersonnel, anticrop and antianimal studies. Field trials included open-air vulnerability testing, and contamination of public water systems with live organisms such as Serratia marcescens. Covert programs were conducted by the CIA. Pathogenic organisms were tested in Florida and the Bahamas in the 1940s. Chemical anticrop studies evaluated defoliation and crop destruction.

1949 Germ bombs: 
Explosive munitions tests with pathogens were begun.

1950 The First “open air tests”: 
The first open-air tests with biological agents were conducted in various locales, including off the coast of Norfolk, Virginia.

1950 Spraying San Francisco: 
The first large-scale, aerosol test was conducted in San Francisco Bay in September 1950, using two species of bacteria (Bacillus globigii and Serratia marcescens). Many experiments used various Bacillus species because of their similarities to B. anthracis.3 

On September 26 and 27, 1950, the U.S. Army sprayed S. marcescens from a boat off the coast. On September 29, patients at San Francisco’s Stanford University Hospital began appearing with S. marcescens infections.4 Many residents came down with pneumonia-like symptoms and one died. A military, follow-up study showed that nearly every single exposed person became infected with the test organism.

The death of Edward J. Nevin was associated with this release of S. marcescens.4 (The first lawsuit against the U.S. government was filed by his family [in 1981]. The court decided that the U.S. government could not be sued, under the Federal Tort Claims Act, since the decision to spray S. marcescens was a part of national defense planning.)

1951 Racist Germs: 
Army researchers deliberately exposed a disproportionate number of black citizens to the fungus Aspergillus fumigatus, to see if African Americans were more susceptible to such infection, like they were already known to be to coccidioidomycosis (Coccidioides immitis). Similarly, in 1951, unsuspecting [black] workers at the Norfolk Supply Center, Norfolk, VA, were exposed to crates contaminated with A. fumigatus spores.3

1955 Whooping Cough: 
Tampa Bay, FA, experienced a sharp rise in Whooping Cough cases, including 12 deaths, following a CIA bio-war test in which bacteria from the Army’s Chemical and Biological Warfare arsenal was released to the environment.5

1951-1969 Dugway Proving Ground: 
Hundreds, perhaps thousands, of open-air tests using bacteria and viruses that cause disease in human, animals and plants were conducted at Dugway Proving Ground, a military testing facility about 80 miles from Salt Lake City, Utah. These tests were to determine how the agents spread, survive and effect people and the environment.

It is unknown how many people in the vicinity were exposed to potentially harmful agents during these open-air tests. In 1969, concerns were expressed at a congressional hearing about the possible public health implications of the VEE virus tested there.

University of Utah scientists and doctors are greatly concerned about the potential health consequences not only for military personnel who work and train at Dugway, but also for civilians who live in a nearby small town and Indian reservation. Utah Medical Society physicians complained about the lack of information provided to the medical community.According to Rutgers University political science professor Dr. Leonard Cole, the use of potentially harmful chemical and biological agents continues at Dugway. He testified that the U.S. Army uses Bacillus subtilis “which is is recognized as a potential source of infection and can cause serious illness in some people when they are exposed to it in large numbers and they inhale large numbers of those microorganisms.”4

Mid1950s-early 1970s Project Shad:
The Dugway Proving Ground and Fort Douglas had a secret navy, called Project Shad. Their ships sailed through clouds of germ and chemical agents. Some sailors blame these tests for the cancer and other diseases that they suffer from.6

1956 Operation Transit III: 
One of Project Shad’s first tests occurred in San Francisco Bay as part of Operation Transit III. In September 1956, plans called for a 40-foot munitions boat to create clouds of Bacillus globigii germs that the Eastman would travel through. Plans called for enough germs to ensure that “a minimum respiratory dose of 10,000 organisms is received on deck.” Planners considered B. globigii a safe “simulant” of more dangerous germs. (The U.S. Army still uses it for field testing.)
The tests included dropping “20,000 gallons of BG (B. globigii) slurry” from helicopters.

1956 to 1958 Testing on Blacks: 

The U.S. Army did field tests in the poor black communities of Savannah, Georgia, and Avon Park, Florida, in which mosquitoes were released into residential neighbourhoods from ground level and from planes and helicopters. Many were swarmed by mosquitoes and developed unknown fevers; some even died. After each test, Army personnel posing as public health officials photographed and tested the victims and then disappeared from town. It is theorized that the mosquitoes were infected with a strain of Yellow Fever. Details of the tests remain classified.5

1950s to 1970s Operation Whitecoat:
Many experiments that tested various biological agents on human subjects, referred to as Operation Whitecoat, were carried out at Fort Detrick, MD. The human subjects originally consisted of volunteer enlisted men. However, after the enlisted men staged a sitdown strike to obtain more information about the dangers of the biological tests, Seventh-Day Adventists who were conscientious objectors were recruited for the studies. Because they did not believe in engaging in actual combat, they became human subjects in military research projects that tested various infectious agents. At least 2,200 Seventh-Day Adventists were used in biological testing during the 1950s through the 1970s.

1962 More on Project Shad: 
Training outlines show that Project Shad sailors were briefed on work with germs causing some of the deadliest diseases known, including tularemia, anthrax, parrot fever, Q fever, African swine fever, the plague and botulism.

1963-1965 Project Shad ships “participated in 111 tests” using nerve agents GB and VX, and biological agents Bacillus globigii, Serratia marcescens and Escherichia coli. (Letter from Maj.Gen. L.J.Del Rosso, Army director of space and special weapons, to Senator Steve Symms, R-Idaho, 1992)

1966 New York Subway: 
From June 7-10, the U.S. Army’s Special Operations Division dispensed [Bacillus subtilis var niger3] throughout the New York City subway system. The Army’s justification for the experiment was the fact that there are many subways in the USSR, Europe and South America. Details of the experiment are still classified.5 More than a million were exposed when army scientists dropped lightbulbs filled with the bacteria onto ventilation grates.

1987 Continued Research:
The Department of Defense admitted that, despite a treaty banning research and development of biological agents, it continues to do research at 127 facilities and universities in the U.S.1”

In 1955, the CIA conducted a biological warfare experiment where they released whooping cough bacteria from boats outside of Tampa Bay, Florida, causing a whooping cough epidemic in the city, and killing at least 12 people.

In 1953, the CIA placed several of its interrogation and mind-control programs under the direction of a single program, known by the code name MKULTRA, after CIA director Allen Dulles complained about “not having enough human guinea pigs to try these extraordinary techniques”.^[113] The MKULTRA project was under the direct command of Dr. Sidney Gottlieb of the Technical Services Division.^[113] The project received over $25 million, and involved hundreds of experiments on human subjects at eighty different institutions.

In a memo describing the purpose of one MKULTRA program subprogram, Richard Helms said:

We intend to investigate the development of a chemical material which causes a reversible, nontoxic aberrant mental state, the specific nature of which can be reasonably well predicted for each individual. This material could potentially aid in discrediting individuals, eliciting information, and implanting suggestions and other forms of mental control.

—Richard Helms, internal CIA memo

In 1954, the CIA’s Project QKHILLTOP was created to study Chinese brainwashing techniques, and to develop effective methods of interrogation. Most of the early studies are believed to have been performed by the Cornell University Medical School’s human ecology study programs, under the direction of Dr. Harold Wolff.^{[101][115][116]} Wolff requested that the CIA provide him any information they could find regarding “threats, coercion, imprisonment, deprivation, humiliation, torture, ‘brainwashing’, ‘black psychiatry’, and hypnosis, or any combination of these, with or without chemical agents”. According to Wolff, the research team would then:

…assemble, collate, analyze and assimilate this information and will then undertake experimental investigations designed to develop new techniques of offensive/defensive intelligence use … Potentially useful secret drugs (and various brain damaging procedures) will be similarly tested in order to ascertain the fundamental effect upon human brain function and upon the subject’s mood … Where any of the studies involve potential harm of the subject, we expect the Agency to make available suitable subjects and a proper place for the performance of the necessary experiments.

—Dr. Harold Wolff, Cornell University Medical School

Details of Pseudomonas Fluorescens are as follows: Chemtrail Sky Samples Analyzed

 By William Thomas with Erminia Cassani
http://educate-yourself.org/ct/ctarticle12.shtml
April 21, 1999

VICTORIA, British Columbia, Canada, April 21, 1999 (ENS) – As unmarked tanker-typeaircraft continue spraying sky-obscuring chemtrails over regions of the U.S. and Canada,this writer and American journalist Erminia Cassani have obtained laboratory tests of fully documented samples of aerial fallout.

 The samples were tested by aU.S.Environmental Protection Agency (EPA) licensed facility. The two samples were taken from aluminum-sided structures in separate states nearlya year apart after their respective owners went outside in the wake of low-flying aircraft to find dwellings and outbuildings splattered with a brown, gel-like substance.

Trained in the health sciences, Cassani carefully took samples from the second incident which occurred at 2:00 pm on November 17, 1998. The samples were taken from property directly under the flight approach path to Thomasville airport, an old airport once used for commercial flights but now used only for small planes. This facility is located a 45 minutes drive from the Harrisburg International Airport in Pennsylvania.

Noting nearby military hangars filled with big helicopters, Cassani videotaped a house splattered on all sides, as well as the driveway. The reporter also interviewed a man living near the main runway who claimed that a similar goo had hit his house the previous October. Cassani became ill with flu-like symptoms and was sick for four days after obtaining the sample. When a marine biologist at a nearby university started working with the gel material, he too immediately developed upper respiratory symptoms. The woman whose house had been struck also caught the”flu.” Two weeks before Christmas 1998 she suffered a heart attack.

Coliform tests by the state Department of Health were negative. But when the university Ph.D. biologist turned his microscope to high power, he found the glass slide teeming with a protozoan life form he said was “very resilient to very cold temperatures.” The laboratory staff who eventually received our sample for a complete analysis had never seen cell cultures bloom so fast. Cell cultures normally take several days to grow; ours flowered into brilliant colors within 48 hours of being placed in petri dishes. Exclaiming that, “It was all over the plate,” the biologist who examined our first sample wanted to know where we had obtained this “bio-hazard” material.

No markers for jet fuel were evident. But the TNT and fuel-eating Pseudomonasfluorescens found in our sky sample is listed in 163 Pentagon patents for bioremediation. Sometimes employed against oil spills, Pseudomonas fluorescens can consume jet fuel as a primary food source. This bacteria can cause upper respiratory illness and serious blood infections in humans.

Serratia marcescens was found in yet another gel sample obtained in Idaho in late March, 1999. Often causing upper respiratory infections resulting in pneumonia, Serratia marcescens was sprayed into the New York subway system in 1953, and over Dorset, England from early 1966 to 1971 by the military in both countries. Serratia marcescens was supposedly withdrawn as a biological warfare stimulant in the 1970s when this infectious agent was deemed too hazardous for  use on friendly test populatioE.coli, Serratia marcescens, and Bacillus globigii were sprayed over UK population centers to stimulate bio warfare attacks in the 1960s and 1970s, the London Telegraph reported in May of 1998. All three agents can cause disease in humans including pneumonia and chest  infections. According to recent admissions by the British Defense Ministry, a Canberra jet bomber was modified with spray tanks to “attack as a spray aircraft for research into defence against biological warfare.”

 Serratia marcescens was used by the American Army for experimental purposes over San Francisco in the 1950s.  There was a significant increase in both respiratory urinary infections thereafter.   The same bacteria also contaminated the American flu vaccine of 2004.’

Mr Graeme Malaghan, a businessman, who is the Chairman of the Malaghan Biomedical research institute in Wellington, resides in an adjoining street in St Heliers .  A former resident of St Heliers was an  Iranian woman Hideh Harger  who previously taught biological sciences at the international school in Jakarta Indonesia. She owned a small local shop specialising in Iranian imports and on one or two occasions and was prone to making comments of a sexual nature while standing beside me in the local supermarket. ESL biosciences is also located in St Heliers.   Another local woman Dr Adriana Gunder has a doctorate in biological sciences and is a member of the national ethics advisory committee.   In 2005 an Iraqi local resident Mrs Hamdi  advised the local press that her son, a microbiologist, had secured a work permit for New Zealand. Soviet microbiology might also be relevant-there is a soviet group resident in the neighbourhood.

A neighbour in Whangarei was also apparently involved in a bio experimental program controlled by an individual  possibly named Kissling. Anthrax and diptheria were 2 diseases mentioned in the short wave transcripts in respect of Melitia (?) nee Jenkins.  Melitia had experimented on her cats two of which had shaved areas on their legs-the one an inverted triangular shaved area with a classic split lip and the other a small round area with what appeared to be a light coloured pustule. Photos were sent to the Whangarei SPCA. The number of cats was also increased and they seemed to spend most of their time outside. 2 cats would sleep in my unit at night from time to time  I fed 4 of Melitias cat twice a day for 12 months.

 

RESPIRATORY

Addtional health problems began in Wellington in the early 1980s .  I had been unemployed for approximately 18 months.    I was first afflicted with a cloracne type condition affecting the lower portion of both legs .A prescription cream proved to be almost useless and the condition disappeared the next summer.  I don’t recall any specific any specialist diagnosis however it is quite probable that that condition was erythema nodosum  (sometimes indicative of sarcoidosis and /or TB) . The following year I experienced sudden pains in the side of the neck coupled with blocked and painful ears together with pain extending down the left side of the body and subsequent extreme exhaustion after exertion. A dark red discolouration  (erythema  palmar) appeared under the skin at the edge of both hands.  There was neither medical diagnosis nor treatment . This particular condition has been shown to a number of medical practitioners in subsequent years but has otherwise been ignored.    

  I have been afflicted with severe chest and sinus infections for approximately 40 years- first  diagnosed in the early 2000s. In recent years I have been diagnosed with different gram negative bacteria often in conjunction with gram positive strains.  They include Pseudomonas Aeruginosa with which I have been almost exclusively afflicted in recent years. Other pathogens include Serratia liquefaciens. Serratia marcescens   Stenetrophomonas maltophilia. Pseudomonas Fluorescens  Haemophilus Influenzae and in August 2011 Streptococcus Pyogones.     S Maltophilia has been described as  “opportunistic-infecting patients with predisposing risk factors including malignancy”  Serratia marcescens was used by the American Army for experimental purposes over San Francisco and elsewhere  in the 1950s.  There was a significant increase in both respiratory urinary infections thereafter.   The same bacteria also contaminated the American flu vaccine of 2004. 

Details of pathogens with which I have been afflicted are as follows:

Date 7/3/2003: Heavy growth pseudomonas aeruginosa and Serratia liquefaciens  4//4/2005 heavy growth of serratia marcescens /////////3/5/2005 large nos of gram negative bacilli//////25/1/2006 Heavy growth of Stenotrophomonas maltophilia/////// 6/1/2007 Heavy growth of serratia liquefaciens//////30 /7/2009 Heavy growth of pseudomonas fluorescens///////24/11/2009 moderate growth of haemophilus influenzae///////24/8/2009 No acid fast bacilli seen no mycobacteria species isolated after six weeks//////9/7/2010 large nos of gram negative bacilli small nos of gram positive bacilli//////27/8/2010 heavy growth of non-fermenting gram negative bacilli////4/3/2011 mixed gram negative organisms////31/8/2011 Streptococcal antibodies ASOT 116 IU/mL (<240)- aDNase B 600U/mL(<200)H Interpretative range aDNase 200-680 equivocal

 24/1/2013 large nos of epithelial cells- large nos of gram negative bacilli –mixed gram negative organisms///  ////16/5/2013 large nos of gram positive cocci- small nos of gram positive bacilli- and small nos of gram negative bacilli///////2/9/2013 large nos of gram negative bacilli- small nos of gram positive bacilli- large nos of gram positive cocci-heavy growth of psesudomonas species////////24/2/2014 large nos of gram negative bacilli heavy growth of pseudomonas species////11/9/2014 large nos of gram negative bacilli heavy growth of pseudomonas species//// 21/10/014 large nos of gram negative bacilli small nos of gram positive cocci small nos of gram positive bacilli////////31/12/2014 Fungal culture of sputum : no fungal elements seen: TB culture : no acid fast bacilli seen -no mycoba////bacteria isolated after six weeks/////////3/3/2015 Large nos of gram negative bacilli moderate nos of gram positive cocci-heavy growth of pseudomonas species////////3/7/2015 large nos of gram negative bacilli small nos of gram positive cocci -heavy growth of pseudomonas species/////// 5/9/2015 large nos of gam negative bacilli -heavy growth of pseudomonas species////////16/12/2015 Large nos of gram negative bacilli small nos of gram positive bacilli heavy growth of pseudomoas species////////23/2/2016 Large nos of gram negative bacilli heavy growth of pseudomoas species/////4/1/2017 Large nos of gram negative bacilli light growth of pseudomonas species///////

27/3/2017 Large nos of gram negative bacilli -mixed gram negative organisms/////15/5/2017 Large nos of gram negative bacilli small nos of gram positive bacilli  heavy growth of pseudomonas species//////////4/7/2017 Large nos of gram negative bacilli small nos of gram positive bacilli heavy growth of pseudomonas species////26/7./2017 moderate nos of gram positive cocci- small nos of gram negative bacilli- small nos of gram positive bacilli culture:-growth of respiratory flora?//////////28/8/2017 large nos of epithelial cells- Large nos of gram negative bacilli-small nos of gram- positive cocci – heavy growth of pseudomoas species////////2/10/2017 moderate nos of epithelial cells Large nos of gram negative bacilli-small nos of gram- positive cocci – mixed gram negative organisms////////15/12/2017 small nos of epithelial cells Large nos of gram negative bacilli-small nos of gram- positive cocci -occasional gram positive bacilli-mixed gram negative organisms//////////

 5/1/2018  No streptococci A C G or Arcanobacterium isolated///////27/1/2018 moderate nos of gram positive cocci moderate nos of gram negative bacilli -mixed gram negative organisms////////19/2/2018 Large nos of gram negative bacilli—heavy growth of pseudomonas species////////7/3/2018 moderate nos of gram positive cocci small nos of gram negative large nos of gram negative bacilli bacilli-mixed gram negative organisms///////20/3/2018 large nos of gram negative bacilli heavy growth of pseudomonas species/////////20/4/2018 moderate nos of gram positive cocci/////// large nos of gram negative bacilli- heavy growth of pseudomonas species///////18/5/2018///////  moderate nos of epithelial cells large nos of gram negative bacilli occasional gram positive cocci////////19/6/2018  large nos of gram negative bacilli small nos of gram positive cocci- heavy growth of pseudomonas species//////20/7/2018 large nos of gram negative bacilli small nos of gram positive cocci- heavy growth of pseudomonas species//////20/7/2018 large nos of gram negative bacilli small nos of gram positive cocci////////14/9/2018 moderate nos of polymorphs and epithelial cells mixed organisms predominantly gram negative bacillus-heavy growth of pseudomonas specie 28/12/2018 s/////////18/2/2019  mixed organisms predominantly gram negative bacillus-culture growth of respiratory flora////// 28/12/2018 large  nos of polymorphs and  small nos  epithelial cells- mixed organisms predominantly gram negative bacillus heavy growth of pseudomonas species//////8/4/2019 mixed organisms predominantly gram negative bacillus/////27/5/2019 mixed organisms predominantly gram negative bacillus  heavy growth of pseudomonas species///////14/10/19 Culture : Mixed gram negative organisms seen predominantly gram negative coccus?  ( Wikepedia advises : “Medically relevant gram-negative cocci include , a meningitis (Neisseria meningitis) and respiratory symptoms (Moraxella catarrhalis, Haemophilus influenzae”.)// 7/12/2019 Mixed organisms predominantly gram negative bacillus-culture mixed gram negative organisms//////9/1/2020 Mixed organisms no   predominant organism seen culture: growth of respiratory flora including mixed gram negative organisms//20/11/2020 Heavy growth of serratia liquefaciens////18/3/ 2021 Throat Swab Labtests: “Group A Strep not detected. Culture: No beta-haemolytic streptococci group A C and G or Arcanobacterium isolated//////3/6/2021 heavy growth of serratia species//2/8/2021 Moderate nos of epithelial and polymorphs-heavy growth of stenotrophomonas maltophilia -mixed organisms predominantly gram negative////12 /10/2021 small nos of polymorphs and epithelial cells-mixed organisms predominantly gram negative bacillus 

For many years I have been afflicted with severe sinus and chest infections. On one occasion over 20 years ago a GP diagnosed  pleurisy.  Shortly after my arrival in Sydney in the early 1980s  I was afflicted with the most potent chest and sinus infection I had ever experienced which almost caused me to almost  lose consciousness and affected my balance.  I was confined to a motel room for 2-3 weeks taking prescribed antibiotics.

 Chest x-rays of 1989 and 1991 reported ‘over expanded lung space commensurate with chronic obstructive airways disease”. This was somewhat  contradicted as a result of later specialist spirometry  testing. A study of peak flow and expiratory scans indicated small airways disease. “The diaphragm was not flattened and as I had only 2.5 metres of air in front of the aortic arch the lungs were not categorised as being over expanded although I did have 6 1/ 2 ribs exposed anteriorly”  CT scans of 1999 reported  “several lymph nodes lying adjacent to the main trachea however there was considered to be no pathological lymphadenopathy”

.In 2001 I was afflicted with a particularly severe but undiagnosed chest infection. A senior respiratory physician  Dr Pardy) at public hospital appeared to be indifferent and referred me back to my GP.  He also suggested that the CT scans could be discontinued .  However in a report dated March 2002 Radiologist David Milne recommended “ that further consideration could be given to a further examination in 12 months time”  As I was  concerned about  Pardy’s  verbal recommendation  I then decided to attend an alternative respiratory physician  Professor Garrett in a private capacity . 

 A  report dated 20 June 2002 stated  “very minor atelectasis in  the right medial aspect of the right middle lobe and the lingular segment of  left upper lobe . Fluid is seen within the oesophagus which is a little thick-walled.  There is no pleural fluid or mediastinal lymphadenopathy.”

In 2002 respiratory  physician  ( Professor Garrett) performed spirometry testing which indicated small airways disease i.e. “ bronchiolitis cum asthma”  In 2002 “the peak flow was 370 litres per minute which although low is within the normal range…..couldn’t maintain a particularly good forced vital capacity manoeuvre but neverthless FEV1 was 2.71 litres which is well within the normal range…there was no downward scalloping of the expiratory flow volume loop as would be expected in someone with obstructive disease.The diaphragms are not  flattened and as I had only 2.5 metres of air in front of the aortic arch the lungs and therefore does not fulfil criteria for over-expansion though she does  have 6 1/ 2 ribs exposed anteriorly

 In May 2004 respiratory physician Dr Kolbe advised   “–she has no known allergies and has no significant exposures”  and claimed that    “that the presence of this organism(aeruginosa) is often associated with antibiotic use and it is likely that this generally resistant organism is selected out by antibiotic use….the best course of action would be to stop all antibiotics  Under the circumstances of chronic airway colonization the Pseudomonas Aeruginosa very, very, seldom invades and thus systemic anti-pseudomonal antibiotics are generally not indicated in the non-CF population, even during periods of  exacerbation”

This assertion would seem to be at odds with the assessment of an American bacteriologist Kenneth Todar of the Madison Department of Bacteriology at Wisconsin University who stated that “ pseudomonas aeruginosa was toxinogenic  invasive  and notorious for its resistance to antibiotics and  almost never infects uncompromised tissue.It  almost exclusively affects those who are compromised in their defence mechanisms or lower lobes . . Pseudomonas aeruginosa causes meningitis and brain abscesses. The organism invades the CNS from a contiguous structure such as the inner ear or paranasal sinus, or is inoculated directly by means of head trauma, surgery or invasive diagnostic procedures, or spreads from a distant site of infection such as the urinary tract.”

 Incorrect biographical details began to be evident in reports. In 2004  Physician Dr Whyte advised “no history of significant childhood chest problems///she denies major problems with rhinosinusitis”….. He continued:  “that the culturing of an out of the ordinary bacteria in a patient who has received many antibiotics does not prove that the out of the ordinary bacteria is doing any harm… the presence of antibiotics can inhibit the growth of bacteria on the culture plate leading to other innocent bacteria growing and being mistaken for the culprit”  One would  assume that if the strain is virulent it would be predominant and the likelihood of innocent bacteria being mistaken for the culprit would be remote . 

 Prior to bronchoscopy in 2004  respiratory physician  (Professor Garrett)  advised that  “a bronchoscopy would also allow us to do a BAL  which would allow us to better understand the inflammatory cells present within her lower airways and allow a more pure collection of mucus from the lower airways for bacterial culture.  I would undertake a bronchial biopsy to assess whether she has inflammation within her airways” The subsequent  Hospital bronchoscopy report  stated “that there was no evidence of bronchitis  so no biopsies attempted . No evidence of bronchitis or sinusitis”

There was some bleeding from the lungs ( not entirely abnormal after this procedure). The specialist concerned was not present immediately after the procedure –I was left in the care of the nurses.  The bleeding from the lungs was not referred to in the specialist’s  report –there was only  one notation namely that  “ I tolerated bronchoscopy well-I  had bronchitis and requested antibiotics”( which contradicts the hospital report) The day after bronchoscopy  I was  in fact afflicted with a chest infection producing coloured sputum.    Specialist’s bronchoscopy report advised that there was “no evidence of inflammation or mucous in the airways”  The two sputum samples-the one as a result of the lavage and the other the following day were at variance  i.e Medlab  report for the former  indicated “no white cells organisms nor epithelial cells” while the the lab report for the latter indicated “mixed bacterial flora large number of white cells and a heavy growth of normal respiratory flora   Although no pathogen were specified the white cell count is in itself indicative of infection. There were a few bright pin pointed areas evident in the trachea adjacent to the bronchi which may be significant?

The bronchoscopy  report continued – “that cell differentials were normal the results are against chronic infection in view of the fact that the neutrophils are not elevated” Lavage results indicated that there was a difference in the neutrophil levels between the left and right lungs i.e. 31% ( 0.31)  in the left and  and 72% ( 0.72) in the right  A decreased percentage of neutrophils can indicate overwhelming infection and aplastic anemia. Lymphocytes in the left lobe were 9% and 10% )in the right. A significant decrease in lymphocytes might  indicate HIV infection, leukemia Radiation or sepsis.  

“Bronchial epithelial cells were 58% in the left and 14% in the right. Photos from the bronchoscopy included, the vocal chords. bifurcation of the trachea and the origin of the right lower lobe only.   Photos of the bronchoscopy did not include a photo of the left lower lobe – the specialist’s written explanation concerning the missing photo advised  “that the left lower  lobe was normal and no photograph was taken.  The right was photographed just to show you how normal the appearance was in general’   Prior to bronchoscopy the physician  initially expressed concern about the contamination of the lower lobes but was subsequently at a loss to explain further infection . The entire bronchoscopic procedure is now available on YouTube.

I visited Respiratory Physician in Dr Christmas in   November 2007 . He expressed some concern about the gram negative bacterial infections however he regarded the oropharyngeal flora to be the main culprits The four gram negative bacteria have been cultured from chest sputum have resulted in  some quite severe chest infections . I  was also concerned that in view of the gram negative infections an underlying condition might be responsible e.g. in the case of Pseudomonas Aeruginosa it exclusively affects patients who are compromised in their defence mechanisms or lower lobes .  The respiratory physician stated that he   “ agreed that it i unusual to have these sorts of organisms in immunocompetent hosts but the reports would suggest these are mostly oropharyngeal flora and the only procedure which  is sampled from the lower airways has not grown these organisms so I suspect that they are in fact predominantly oral contaminants” ?

 I assume that the procedure referred to was a bronchoscopy which was undertaken in 2004. In fact I was afflicted with a chest infection the day after the bronchoscopy however there was no identification of any specific bacteria.   The lack of diagnosis on that occasion coupled with the fact  that there is frequently  oropharyngeal flora contamination in my chest sputum samples should not detract from the fact that I have a history of serious chest infections ranging in intensity from low grade to severe with  accompanying head /neck/ chest/sinus pain with congestion ,significant sputum and generalised  severe inflammation

A high resolution CT scan of the chest was undertaken at Ascot Hospital on 7 January 2008 reported that   “ there was no evidence of bronchiectasis nor small or large mucous plugging .  There was mild bronchial wall thickening.-also minor patchy decreased attenuation involving less than 10% of the volumes of both lower lobes –no mediastinal abnormality –no evidence of gastro-oesophageal reflux.  An 8 mm slightly lobulated nodule in the lateral basal segment of the right lower lobe has radiologically benign characteristics –it may have a small hilum increasing the chance that the nodule is a lymph node.  Mild bronchitis and minimal functional small airway disease-no other specific cause for cough is seen.  A limited surveillance scan was recommended for 6-9 months”  A solitary nodule can sometimes be indicative of sarcoidosis.

 On 24 July 2009 I consulted with Respiratory Physician Margaret Wilsher.  While there was no  mention of  my smoking history of 20 years in her report her  assessment of my  history  was generally  correct.  In respect of the discomfort that I have experienced in the left side of the chest during infection Ms Wilsher advised  “Miss Wilson admits that one of her most depressing symptoms is of the left inframammary chest pain  which although not typical of pleuritic pain is worse when she has chest infection. The pain always recurs in the same place and is not associated with haemoptysis. She has had this for many years and no explanation and hence no treatment has ensued. “On examination she presented as a well looking lady of flat effect.”

 ( Note: a General Practitioner once diagnosed Pleurisy in Wellington in the 1980’s. Crackles and rales( specific sounds indicative of pleurisy) have been reported once or twice as a result of stethoscope examinations by general practitioners in Auckland.  One practitioner thought he detected a “ dullness” on the left side.

Wilshers comments concerning my thyroid condition seem to be somewhat contradictory   “She takes carbimazole for hyperthyroidism  under the supervision of Brandon Orr Walker ….she  was clinically euthyroid and there were no signs of Grave’s disease.   In 2007 I was diagnosed by Orr Walker with “thyrotoxicosis probably secondary to autoimmune thyroid disease ( probably Graves disease) She was  not clubbed. Oxygen saturation was normal (96%) predicted and auscultation of the chest revealed no findings of note ( I am frequently afflicted with lung congestion however sputum is generally produced on a daily basis). There was no spontaneous cough.  She is in sinus rhythm rate 80 blood pressure 140/85 with dual heart signs the JVP is not raised . Her spirometric lung volumes are normal with  an FEV  1/FVC of 2.34 /2.72 litres and her peak flow rate is normal.” ( normal predicted values for a 60 year old woman of 168 cm in height are FEV1 2.75/FVC 3.55)   I am afflicted with chest sputum on an almost continuous basis however this was not apparently detected in Wilsher’s examination 

There has always been a disparity between the oxygen saturation levels, the spirometric results and the readings of the more rudimentary peak flow meter undertaken at the local medical practice which has often been recorded in the early 300’s. ( Normal peak flow values would seem to range from the late 300’s to mid 400’s)  The minor atelectasis  (collapse ) in 2 areas of the lung were briefly discussed –Wilsher did not think the condition was entirely abnormal after a history of asthma/bronchitis. She did not refer to the condition in her report.  I pointed out to Dr Wilsher what appeared to be a disparity in the cell levels in the broncoscopy procedure undertaken in 2004 by Dr J Garrett. In particular I referred to bronchial epithelial cells 14% in the right and 58 % in the left- .also the neutrophils 72%  in the right and 31% in the left  .  Lymphocytes were 10% in the right and 9% in the left. 

The subheading on the Medlab report clearly specifies “cytology-bronchoalveolar lavage right and left lower lobes”. Ms Wilsher reported “ bronchoscopy undertaken by Jeff Garrett showed no anatomical abnormality and no excess secretions .  There were some excess neutrophils in the wash but I pointed out to Miss Wilson that this was not a bronchoalveolar lavage and thus differential cytology is of less value”!!!  Dr Wilsher clearly ignored any disparity in the cell levels between the left and right lungs and quite incorrectly claimed that the differential cytology was not part of a bronchoalveolar lavage  when it was quite clearly annotated as such in the Medlab report.

With regard antibiotic treatment for chest infections Wilsher virtually reiterated the opinion of Dr Whyte a respiratory of the same practice.  “we know that even normal individuals will eventually have replacement of normal respiratory flora with gram negative pathogens following heavy use of multiple courses of antibiotics”  In respect of gram negative pneumonic strains medical websites advise that patients afflicted with these types of pathogens are compromised in some way either in their lower lobes or defence mechanisms. One might assume that a previous history of bronchitis asthma and some 20 years of smoking might have been considered pertinent in this regard. Unlike her counterparts Wilsher did not refer to my history of smoking in her reports. She advised   “that one needs to be judicious in the prescription of antibiotics …shorter courses of simple broad spectrum antibiotic are just as likely to be effective.”

 Gram negative bacterial infections are notoriously antibiotic resistant and a specific regime of drugs (including intraveneous Gentamicin) are generally recommended by Medlab At this late stage and with a current history of permanent chest infections and with resistance an obvious problem one would have considered that containment /treatment would be the priority and to that end longer courses of antibiotic would be  necessary.   A sputum specimen result dated 30 July 2009 reported a diagnosis of pseudomonas fluorescens with the recommended antibiotic treatment of Ciprofloxacillen or Gentamicin. 

The test was requested by Dr Wilsher and presumably she received the result .  She did not see fit to send me a script for antibiotic treatment.  I emailed her on 13 August requesting same.  Despite the Medlab report which stated a “ heavy growth of Pseudomonas Fluorescens” Dr Wilsher stated  in a letter dated 17 August 2009 that  “antibiotics are not recommended on the basis of sputum culture results alone and frequent use of antibiotics will not eradicate Pseudomonas  and will only result in the growth of increasingly resistant and atypical organisms….if you have a change in symptoms then it may be that you have an exacerbation but if you symptoms are unchanged then the benefits of antibiotics are less clear and the risks may well outweigh such.”

 I don’t know what alternative diagnosis Ms Wilsher might be referring to in respect of obtaining a diagnosis but a heavy bacterial growth would surely equate with  significant infection. Why else would the laboratory also recommend specific drug treatment ? When I first consulted Wilsher on 24 July I had congestion in the lungs, pain in the left lung and pains in the neck and head. The sputum was viscous, impacted and yellow/ golden in colour

 A study by the Respiratory Institute of the University of Milan in 2004 advised thus: “Our study indicates that purulent sputum is strongly associated with bacterial growth in COPD exacerbations. Deepening sputum color (from yellowish to brownish) was associated with increased yield of Gram negative and P. aeruginosa/Enterobacteriaceae”.  Another sputum sample yellow/golden in color, some of which appeared to be viscous and was adhering to the side of the plastic receptacle, was analysed by Labtests on 24 August 2009 . Microscopy reported “ no acid fast bacilli seen”! 

 Ms Wilsher should have provided a script for antibiotics after receiving the sputum result on the 30 July and particularly as I have a heart condition –my blood pressure was recorded as 170/98 in July 2009 and 170/90 in August 2010.   Wilsher advised    “regrettably I do not offer a prescription service without seeing the patient….this is poor clinical practice……if you have an exacerbation that requires the antibiotic then I am happy to see you and evaluate the situation-alternatively you can see your regular practitioner”  A second consultation was surely unnecessary at that stage since only 4 days had elapsed between the date of the first consultation and the medlab report .  I am a beneficiary and although I have health insurance, the cost of a consultation would have been $300.00.

In November 2009 I was diagnosed with Haemophilus Influenzae and appropriate antibiotic treatment was prescribed. The blood test performed by Labplus on 19 November indicated a higher than usual neutrophil count of 7.84 ( norm 1.90-7.50) and monocyte count of 1.10 ( norm 0.20-1.00). The lymphocytes remain a constant 1.63 (norm 0.90-4.00) which might be considered borderline low. Frothy sputum together with large air bubbles were indicated in a photo of the haemophilus sputum. This can be indicative of a number of conditions including  bronchiectasis,  bronchoalveolar cancer, aspiration pneuomonitis  pulmonary edema or abscess.   

For the first 2 weeks of March 2011 I was again afflicted with a severe infection of the chest and sinuses with severe coughing sometimes involving a croup-like cough accompanied by purulent yellow coloured sputum. I was prescribed romicin and doxycycline

The labplus test results dated 4 and 7 March 2011 only specified “small numbers of gram positive cocci and mixed gram negative organisms-moderate numbers of gram positive cocci and moderate growth of respiratory flora”The significant  sputum specimens of 2009 and 2011 appear to be similar if not identical i.e. dark yellow in colour, frothy, layered, together with large air bubbles.  .

A chest  x-ray undertaken by Auckland Radiology on 7 December 2010 reported “FINDINGS: The heart is normal in size and shape and the pulmonary vessels, lungs and pleura show no evidence of any pathology .IMPRESSION: Normal chest examination. ( see cardiomegaly reference below) 

 On 21 December 2010 I met respiratory physician Dr Stuart Jones for an early evening appointment.    He checked my lungs with a stethoscope but otherwise could find nothing significantly amiss. An x-ray monitor was not available so Dr Jones resorted to holding  the x-ray plates up to the light! 

I pointed out to Jones what appeared to be an enlargement in the area of the heart. He made no comment.   The measurement of the heart area has increased approximately 3cm from 1989 to  2010. “The cardiothoracic ratio (CTR) is the ratio of the transverse diameter of the heart to the internal diameter of the chest at its widest point just above the dome of the diaphragm as measured on a PA chest film. An increased cardiac silhouette is almost always the result of cardiomegaly, but occasionally it is due to pericardial effusion or even fat deposition.”

 Jones did not check the x rays from previous years for comparative purposes.  I explained that I had been experiencing pain in the left side and the centre of the chest extending around to the back causing extreme discomfort in the chest for approximately the first 20 minutes or while walking up a hill  however Dr Jones ignored this complaint.  The latter symptoms were having a deleterious effect on my walking capacity for some months  .  A spirometry test was not performed.

 While he noted that “ the bronchoaveolar lavage from the right lower lobe demonstrated neutrophilia with neutrophils accounting for 72% of the cell count compared to 31% from the right lower lobe” he ignored the cell differentials for the bronchial epithelial cells in both the lobes.  “On examination there was no particular abnormality. Her lung fields were resonant throughout and her breath sounds were normal with no added crepitations. Miss Wilson obviously has an abnormality with her defence leading to a recurrence of gram negative infections. It is likely that she has a degree of small airways disease and chronic bronchitis’ 

The BAL from the right lower lobe had demonstrated significant neutrophilia consistent with a degree of airway inflammation….I am struggling to come up with a diagnosis as to what the underlying abnormality might be  …macrolides have proven to be very beneficial both for the anti inflammatory effects as well as the effect on the pseudomonas biofilm and have been shown to significantly reduce the number of gram negative infections despite the organisms not being specifically sensitive to roxithromycin and culture growth…recommend try 300mg for several months….antinflammatory medication such as non steroidal or colchicine are potential options”

 He initially considered that no further investigations were necessary other than another CT of the lungs and an induced sputum. This course of action was abandoned –it was then suggested that I might consider a CT scan a “ waste of  time” and as  I agreed that might be the case a referral was not provided.    At the end of the consultation he decided not to proceed with the the sputum test and and the form was ripped up.    A   thermography report dated 2003 which provided a full body scan and illustrated areas of  inflammation. was disregarded by Jones. He suggested that I could perhaps see him again in 3 months. .  As I departed he passed a quick aside namely “why you are kaput”!!!

I met respiratory physician Dr Christmas  at Greenlane Clinical Centre on 5 October 2011. He  acknowledged receipt of my email with attachments including previous chest sputum results and the latest labtest result dated 31 August 2011 indicating probable (equivocal 600H) streptococcus pyogenes infection.  The physician’s report stated that “pharynx was clear and chest examination was unremarkable……she complains about some intermittent pains in the chest and sputum has shown respiratory flora and no pathogens recently”   Dr Christmas briefly alluded to past   “sputum samples have grown gram negative and gram positive organisms including pseudomonas aeruginosa and serratia ……but did not refer in his report to the recent streptococcus infection diagnosed in August 2011  He“ doubted that antibiotics are helpful with Vicki and I think I would avoid them as much as possible except during definite infections and not simply to eradicate organisms which you will not achieve-she appears to be quite obsessed with the organisms she has grown in the p ast and feels that these need to be treated and it will be difficult to convince her other wise” 

 I think this is also a very spurious argument if not a seriously negligent attitude  particularly in  respect of the recent streptococcus diagnosis which the specialist  apparently chose to ignore and the long history of unusual gram negative pneumonic strains diagnosed in the last several years.  It it’s a rare occasion when I am not infected.. I have suffered for about 12 months with severe inflammation in the upper part and centre of the chest together with  a severe cough and simultaneous pain occasionally extending around to the back, the severity of which, on a number of occasion, has impacted on my mobility.

According to Kenneth Todars “Online textbook of bacteriology”  “Streptococcus pyogenes is one of the most frequent pathogens of humans. It is estimated that between 5-15% of normal individuals harbor the bacterium, usually in the respiratory tract, without signs of disease. As normal flora, S. pyogenes can infect when defenses are compromised or when the organisms are able to penetrate the constitutive defenses. When the bacteria are introduced or transmitted to vulnerable tissues, a variety of types of suppurative infections can occur.

In the last century, infections by S. pyogenes claimed many lives especially since the organism was the most important cause of puerperal fever (sepsis after childbirth). Scarlet fever was formerly a severe complication of streptococcal infection, but now, because of antibiotic therapy, it is little more than streptococcal pharyngitis accompanied by rash. Similarly, erysipelas (a form of cellulitis accompanied by fever and systemic toxicity) is less common today. However, there has been a recent increase in variety, severity and sequelae of Streptococcus pyogenes infections, and a resurgence of severe invasive infections, prompting descriptions of “flesh eating bacteria” in the news media. A complete explanation for the decline and resurgence is not known. Today, the pathogen is of major concern because of the occasional cases of rapidly progressive disease and because of the small risk of serious sequelae in untreated infections. These diseases remain a major worldwide health concern, and effort is being directed toward clarifying the risk and mechanisms of these sequelae and identifying rheumatogenic and nephritogenic strains of streptococci.

Acute Streptococcus pyogenes infections may present as pharyngitis (strep throat), scarlet fever (rash), impetigo (infection of the superficial layers of the skin) or cellulitis (infection of the deep layers of the skin). Invasive, toxigenic infections can result in necrotizing fasciitis, myositis and streptococcal toxic shock syndrome. Patients may also develop immune-mediated post-streptococcal sequelae, such as acute rheumatic fever and acute glomerulonephritis, following acute infections caused by Streptococcus pyogenes.”

Christmas alluded to the “ mild bronchial wall thickening” reported in the CT scan of 2008 but did not refer to the two areas of minor atelectasis (collapse) in the right and left lungs nor to the bronchial epithelial cell levels specified in the bronchial lavage of 2004  (58% L and 14%R).

His report continued: “ Vicki coughs up about a half pot full of purulent looking sputum per day and she had pictures of this to demonstrate. It was brownish in colour and there was no blood  -interestingly she did not cough once when she was doing the consultation-she complains about intermittent pains in the chest’  Contrary to his statement a brownish tinge can be indicative of old blood / pneumonia in the sputum.

In fact I subsequently experienced difficulties with the spirometry test conducted by an island female staff member after the consultation.   Blowing into the device caused severe coughing fits including a deep seated cough on one occasion.  There was no discussion on the significance of the sputum. My mother has complained about my halitosis  however the physican claimed to be unaware of it.

A police car passed by with a flashing light and siren  heading in the opposite direction as I was travelling to the clinic . After my consultation at Greenlane clinical centre  a male police officer aged 30s of  medium build short dark hair carrying a blue folder walked  past  me while I was seated at the bus stop. A tall female medical  staff member with  slightly curly grey hair and wearing a  plastic identity  tag around her neck appeared a few minutes later and  stood a short distance from the bus stop looking on, then walked away.

A CT of the sinuses and chest ( high resolution) was performed on  14 November 2011 at Greenlane Clinic. FINDINGS: “At the right lung base there is an 8mm nodule which has a sclerotic rim with central density approximately 90 HU and peripheral density approximately 200 HU.  It is not calcified.  There are calcified mediastinal nodes in the anterior superior mediastinum but  no enlarged nodes throughout the mediastinum or axilla. Mediastinal structures and organs below the diaphragm all appear normal. There is very minor right  ower lobe bronchiectasis, without evidence of current inflammation.  There is mild air trapping on the expiratory views.  No pleural fluid.  No bony abnormalities.

CONCLUSION: Solitary pulmonary nodule. Requires follow up and the first follow up should be in 3 months.”

A CT scan of 2008 described the nodule as “slightly lobulated and radiologically benign” .In respect of solitary pulmonary nodules Wikipedia reports: “to distinguish benign conditions from possible lung cancer. The first parameter is the size of the lesion: the smaller, the less risk for malignant cancer.Benign causes tend to have a well defined border, whereas lobulated lesions or those with an irregular margin extending into the neighbouring tissue tend to be malignant.

If there is a central cavity, then a thin wall points to a benign cause whereas a thick wall is associated with malignancy (especially 4mm or less versus 16mm or more).^[4] In lung cancer, cavitation can represent central tumor necrosis (tissue death) or secondary abscess formation. If the walls of an airway are visible (air bronchogram), bronchioloalveolar carcinoma is a possibility.

An SPN often contains calcifications. Certain patterns of calcification are reassuring, such as the popcorn-like appearance of hamartoma.^[1] An SPN with a density below 15 Hounsfield units on computed tomography tends to be benign, whereas malignant tumors often measure more than 20 Hounsfield units. Fatty tissue inside hamartomas will have a strongly negative value on the Hounsfield scale”

The Hounsfield unit (HU) scale is a linear transformation of the original linear attenuation coefficient measurement into one in which the radiodensity of distilled water at standard pressure and temperature”

Radiological Rounds a newsletter of Massachusetts General Hospital advises that:

“Pulmonary nodules ≤4 mm have a low risk of being cancerous; nodules between 4-8 mm are of intermediate risk for cancer; follow up CT scans for both categories are recommended on different schedules

Pulmonary nodules >8 mm and mixed solid/ground glass nodules are suspicious for cancer; percutaneous needle aspiration biopsy (PNAB), positron emission tomography (PET), or video assisted thoracic surgery (VATS) should be considered”

The expiration frame of  the  2011 scan indicates a possible mosaic pattern in the lung’s  lower left lobe and upon magnification  a group of small irregularly shaped nodules possibly identical with  popcorn shaped hamartomas? which  are evident in the lower lobes of both lungs and somewhat larger in the right lower lobe. The expirational view wasn’t repeated in the 2012 scan.

According to Radio Graphics website “The “crazy-paving” pattern is a common finding at thin-section computed tomography (CT) of the lungs. It consists of scattered or diffuse ground-glass attenuation with superimposed interlobular septal thickening and intralobular lines. This finding has a variety of causes, including infectious, neoplastic, idiopathic, inhalational, and sanguineous disorders. Specific disorders that can cause the crazy-paving pattern include Pneumocystis carinii pneumonia, mucinous bronchioloalveolar carcinoma, pulmonary alveolar proteinosis, sarcoidosis, nonspecific interstitial pneumonia, organizing pneumonia, exogenous lipoid pneumonia, adult respiratory distress syndrome, and pulmonary hemorrhage syndromes”

On 27 March 2012 I met Dr Sexton at Greenlane respiratory clinic who I assumed was a registrar.  He ignored the DVD containing the most recent CT scans. He did not check my throat , however ,  however check my chest with a stethescope including a manipulation of the upper part of the  central area of the chest which is quite painful to the touch-likewise the sinuses. I am still afflicted with a “croup” –like cough.  He made no comment concerning the examination.  I expressed my concern about the 8mm nodule in the right lower lobe particularly the peripheral density HU of 200 and the possiblilty of malignancy however seemed to be rather dismissive of that notion did not discuss the subject in any detail and suggested that he might take the matter up with radiology. 

He adopted an attitude similar to Dr Christmas in respect of antibiotics i.e.  “ I advised her to  work toward coming off all regular antibiotics and only using antibiotics when she has a clear cut respiratory infection – that I suspect the main driver for the presence of these organisms is her ongoing use of an inappropriate regimen of long term extremely broad  spectrum antibiotics which are distorting her normal respiratory flora and causing various unusual organisms to thrive”

He agreed –that in respect of the pathogens that I have been afflicted with over the last several years one might expect evidence of more significant structural damage in the lungs however this opinion was not contained in his report. His report did refer  to my having  been  diagnosed with  “asthma /bronchiolitis and   “mild right lower lobe bronchiectasis” in the most recent  CT scan dated 14 November 2011

 A CT ( Inspiration only) of the chest was performed at Auckland hospital on 16 May 2012.  The scan merely confirmed the previous diagnosis of a “ well defined rounded 8mm nodule within the lateral basal segment of the right lower lobe is unchanged in size and morphology.  No new suspicious pulmonary masses or nodules are seen . No collapse or consolidation.  No  interstitial infiltrate. Stable appearance of the solitary 8mm right lower lobe pulmonary nodule.  It remains indeterminate in this high risk patient and further CT follow up in 6 months time is recommended .

Any reference to the previous houseman unit measurements of the 8mm nodule in the right lower lobe seemed to lacking in this particular report.

A labtests sputum report dated 24 January 2013 stated:  “ Large numbers of polymorphs , large numbers of epithelial cells, large numbers of gram negative bacilli and moderate numbers of gram positive cocci: Culture : growth of respiratory flora-including mixed Gram negative organisms” A culture was non-specific.

A report dated 16 May 2013 advised that “ large numbers of gram positive cocci, small numbers of gram positive bacilli and small number of gram negative bacilli” were present in the sputum sample.

Labtests further reported on 2 September 2013: Large numbers of polymorphs seen Moderate numbers of epithelial cells Large numbers of Gram negative bacilli, small numbers of Gram positive bacilli Large numbers of Gram positive cocci

Culture :Heavy growth of Pseudomonas species//Moderate growth of mixed Gram positive and Gram negative bacteria .Susceptibilities : Ciprofloxacin S Gentamicin S Ceftazidime    S = Susceptible, R = Resistant, I = Intermediate  The test dated 24 February 2014 reported: Moderate numbers of polymorphs , no epithelial cells and large numbers of negative bacilli. Culture:  Heavy growth of Pseudomonas species

A sputum test assessed by Northland Microbiology in September 2014 reported “occasional gram positive cocci large numbers of gram negative bacilli Culture: heavy growth of Pseudomonas species. Ciprofloxacin in conjunction with alternative antibiotics has normally been prescribed.

My elderly mother who had a bowel –resection in early May 2013 was diagnosed in June with staphylococcus aureus . In both our cases previous laboratory tests had specified gram positive cocci only.   One might have assumed that if aureus was infecting one member of a family that cross-infection would be a possibility .

A chest HRCT was performed at Whangarei Hospital on 21 October 2014.  “ Findings:  Multiple bilateral axillary supraclavicular and mediastinal lymph nodes are present largest in the mediastinum with short axis diameter approximately 8mm.  These are non specific and may be reactive.  No pulmonary hilar lymphadenopathy is identified.  Bilateral apical pulmonary fibrosis and scarring.  Right posterior basal lower pulmonary lobe 8mm well defined opacity is present. No pulmonary consolidation or signs of cardiac failure .  No signs of chronic interstitial lung disease.  Trachea and major bronchi are patent. No bronchiectasis.  No pleural effusion or calcification.  No destructive bone lesions.

Conclusion:  In respect of respiratory matters  and a recent CT of the chest, Dr  Kennedy a physician of Whangarei stated in his report dated 23 October 2014:  Vicki  had an HRCT scan undertaken on 21 October 2014 and I have reviewed this.  There were no signs of bronchiectasis though there was minor bronchial wall thickening consistent with bronchitis.  .  . The oesophagus appeared unremarkable with no thickening or air fluid level and there were no signs of interstital or pleural disease ( which seems to be at variance with the HRCT report of  June 2002 which specifies “ fluid is seen within the oesophagus which is a little thick walled ” There was a stable 8mm well defined non-calcified right lower pulmonary nodule with no significant mediastinal or hilar lymphadenopathy- the right lower lobe pulmonary nodule  has been stable over many years and through its lack of growth has proved to be benign in nature.  No radiological surveillance of the pulmonary nodule is required . “

The radiologist classified  the nodule as  “representing  a primary benign or malignant lesion”  and recommended  -“ a repeat Ct scan in approximately 3 months time”  His comments  seems to be at variance with the comments of both Kennedy and  Dr Impe of the Northland DHB who in his report dated 24 October 2014 advised “ I looked upon her previous scans from Auckland and this nodule has been present since 2011. It has remained stable in excess of 2 years (since 1999) and therefore requires no further evaluation. The radiologists had not taken note of her previous scan reports.” It would appear however that the radiologist had at least consulted the previous CT report from ADHB.   It is unclear whether Dr Mpe had consulted the  previous reports.

The “Bilateral apical pulmonary fibrosis and scarring” reported in this latest scan also seems to have been ignored  by both physicians.  Medicine net .com advises that in respect of pulmonary fibrosis : “Pulmonary fibrosis is suggested by a history of progressive (worsening over time) shortness of breath with exertion. Sometimes, during examination of the lungs with a stethoscope, the doctor can hear crackling sounds in the chest. These crackles have a very characteristic sound and are very similar to the sound heard when Velcro is pulled apart. These are often referred to as “Velcro crackles (or rales)”. The chest X-ray may or may not be abnormal. However, a special X-ray test called a high resolution CT scan will frequently demonstrate abnormalities”

  A spirometry test undertaken by Dr Kennedy reported “ spirometry today showed  minor restrictive picture FEV1/FVC  1.92/2.66 ( 72%) and PEFR 325L/min with predicted values of 2.46/3.18  and 370 L/min.  FEV1 was 78% predicted FVC was 83% predicted.”.

 Some large horse shoe shaped cells appear to be evident  ( but not reported) in an expiratory sequence of  the right lung CT scan of 21 October 2014.  Wikepedia advises that “they are formed by the fusion of epithelioid cells (macrophages), and contain nuclei arranged in a horseshoe-shaped pattern in the cell periphery  and  are probably identical with Langhans cells. Although traditionally their presence was associated with tuberculosis, they are not specific for tuberculosis or even for mycobacterial disease. In fact, they are found in nearly every form of granulomatous disease, regardless of etiology. Clinical significance: Langhans cells are often found in transbronchial lung biopsies or lymph node biopsies in patients suffering from sarcoidosis.”^[5]

The American Lung Association states: In sarcoidosis, immune system cells that cause inflammation overreact and cluster together to form tiny lumps called granulomas. If too many of these granulomas form in one organ, it may not be able to work correctly. For example, if the granulomas damage healthy tissue in the lungs, scarring and stiffness may occur and limit how much air the lungs can hold. This condition is known as pulmonary fibrosis. The problems caused by sarcoidosis differ depending on which organ is affected.

According to Medicine.net.com: Blood tests can measure a blood substance called angiotensin converting enzyme (ACE). Because the cells that make up granulomas secrete large amounts of ACE, the enzyme levels are often high in patients with sarcoidosis. ACE levels, however, are not always high in sarcoidosis patients, and increased ACE levels can also occur in other illnesses

In the early 1980’s I was afflicted with a probable case of erythema nodosum on the calves of both legs. “Erythema nodosum may occur as an isolated condition or in association with other conditions. Conditions that are associated with erythema nodosum include medications (sulfa-related drugs, birth control pills, and estrogens), strep throat, Cat scratch disease, fungal diseases, infectious mononucleosis, sarcoidosis, Behcet’s disease, inflammatory bowel diseases (Crohn’s disease and ulcerative colitis), and normal pregnancy.

Erythema nodosum (also called EN) results in reddish, painful, tender lumps most commonly located in the front of the legs below the knees. The tender lumps, or nodules, of erythema nodosum range in size from one to five centimeters. The nodular swelling is caused by a inflammation in the fatty layer of skin

In addition I was also affected by erythema palmar a distinctive dark reddish discolouration at the edge of the hands which is still evident todayWebsite Patient UK states: Secondary palmar erythema can be attributed to:  

• Liver cirrhosis and its many causes including alcohol abuse.^[4](Palmar erythema develops as a result of abnormal oestradiol levels.)^[1] 
• Hereditary liver disease such as Wilson’s disease and hereditary haemochromatosis.^[1]
• Rheumatoid arthritis (associated with a favourable prognosis).^[1]
• Systemic lupus erythematosus.^[5]
• Thyrotoxicosis.^[6]
• Diabetes mellitus.^[1]
• Sarcoidosis.^[7]
• Gestational syphilis.^[1]
• Human T-lymphotropic virus type 1 (HTLV-1)-associated myelopathy.^[1][8]
• Neoplastic disease (as a paraneoplastic disorder), particularly primary or metastatic brain neoplasms.^[1][9]However, also associated with ovarian carcinoma.^[10]
• Drug-induced (amiodarone, gemfibrozil, cholestyramine, topiramate and salbutamol have all been implicated).^[1][11]
• ^[1]
• Chronic mercury poisoning.^[1]
• Polycythaemia
•  
• Kennedy further reported : “Spirometry shows no features or airflow limitation. Vicki had mild asthma and bronchitis during childhood though seemed to grow out of this. Tirals of inhaled corticostseroid were unhelpful”.  ( My asthma was quite severe requiring the use of an inhaler in the 1960s and occasionally in recent years)  Vicki has been bothered by troublesome cough  and recurring epsodes  of bronchitis and sinus infection….a variety of organisms grown from sputum.  She is a distant ex smoker having smoked an average a packet of of cigarettes a day for over a 30 year period ceasing in 1992″ Most of the organisms are gram negative pathogens and in 2003 I was infected with a severe case of probable bronchial pneumonia to the extent that my general practitioner Dr Holton had suggested that I might be hospitalised.

There are recurring episodes of bronchitis with multiple different organisms having been cultured in the past ….I would recommend sputum clearance techniques and I have referred Vicki through to the physiotherapy department under whangari hospital for help with this.  …One option for patients with recurring infective episodes in COPD and bronciectasis is a prolonged ( 6-12 ) months course of Azithromycin three times a week.-she tell me that a variety of organisms have been grown from sputum ..there  has been some question as to whether some of these organisms have been oral bacteria that have contaminated sputum cultures” 

This appears to be a somewhat irrelevant concern as the Laboratory frequently specifies  “Heavy growth of  pseudomonas species” with a recommended drug treatment.    I frequently experience quite severe pain in the centre and lower part of the chest and occasionally the thoracic spine dependent on the severity of the infection. I did advise Dr Kennedy in our consultation however he doesn’t appear to have referred to it in his report.

 While a suspicion of minor right lower lobe bronchiectasis was reported on an HRCT of 2011 this has been excluded in the latest scans. “There was minor generalised lymphadenopathy not reaching levels of significance One option for patients with recurring infective episodes in COPD and bronchiectasis is a prolonged ( 6-12 ) months course of Azithromycin three times a week”. Pseudomonas Aeruginosa  is resistant to Azithromycin.

 A number of irregularly and spherical shaped cells in the lower lobes of the right and left lungs which do not appear to have been reported Despite the stability of the nodule it does have characteristics namely that is non calcified, has a sclerotic rim and extremely high central and peripheral densities as reported in 2011 which were not referred to by either respiratory physician

A test for serum IgE ( allergy) of 7 November 2014 was 23 kIU/L ( norm: <100).

I visited Dr Kennedy at Whangarei Hospital at the Respiratory Outpatients clinic on 13 March 2015.  . His report dated 16 March stated “ Ciprofloxacin 500 mg –about to cease -I have not recommended a further course of antibiotics at this time.  I suggested that after 10-20 years the more appropriate concern might be treatment and containment of the pathogen .  I explained that I experience pains in the lungs from time to time depending on the severity of the infection and I also have a heart condition.  He referred to the “ occasional and long standing bibasal pleuritic type chest  pains though this is not a prominent feature” (Gram negative infections can precipitate heart attacks.)

 During the consultation Kennedy claimed that the scarring and fibrosis evident in the latest scan  was only minimal –however he did not refer to same in his report. My query that sarcoidosis might also be a possible diagnosis resulted in no response from Kennedy.  I referred to the notations in the CT report of 2011 concerning the high houseman unit readings – and the characteristics of the nodule in the base of the right namely that it was sclerotic and  non calcified. He suggested that some benign nodules were non calcified and vice versa.!  As there had been no change in the size of the nodule in over 2 years then “no further CT surveillance  was required”.   He disregarded the radiologist’s recommendation of October 2014  for a follow-up CT scan in three months and his assessment  that the nodule might be either “ malignant or benign”. Kennedy  claimed “that the radiologist who reported the most recent CT chest did not have the luxury of access to the earlier scans”!  This seems to a rather odd if not evasive statement –one would assume that it would be almost mandatory for physicians and radiologists to  gaining access to the details of previous CT scans and reports.

 Kennedy advised that there would be further CT scans.  An ECG was performed which indicated “ a possible inferior infarct- abnormal ECG” . This was not discussed during the consultation however Kennedy did refer to it in his report “ A resting 12- lead ECG today showed sinus rhythm 70/min normal QRS axi, small Q waves in the inferior leads , not reaching levels of significance no left ventricular hypertrophy or strain minor T wave flattening in the anterosepetal leads.”  “A chronically occluded left circumflex” which was also referred in the report is still outstanding from an initial diagnosis in 2003.

“ Spirometry today showed sub-optimal  technique with a poor start which will have influenced the FEV, value with FEV1/FVC  1.76/2/2.61 (67%) with predicted values of 2.21/2.64 . FEV 1 was  80% of predicted ( though likely under-estimated ) and FVC was 99% of predicted.”  I was not advised that anything was amiss with the spirometry testing by the presiding nursing staff .   A spirometry test performed by Dr Wilsher in 2009 reported “Her spirometric lung volumes are normal with  an FEV  1/FVC of 2.34 /2.72.

In respect of my enquiry concerning missing set of images from a CT lung scan of October 2014 I received the following reply from Tracey Hildreth Release of Information Officer Northland District Health Board on 18 March 2015: “ I have discussed with our PACS office (Picture Archiving and Communication System) in our Radiology dept.   It is normal that there will be Reports and Images missing. In your case it being No.6. This is due to when a series of Images are taken there will always be certain ones that do not require reporting on, in your case No.6 did not require to be reported on and thus is why it is missing.” This was confirmed by radiology staff in a phone conversation on 23 March 2015.

I subsequently  emailed a complaint to Mr Potts the general Manager of Clinical Services about my nodular concerns. His reply dated 12 October 2015 : “ I write to provide an update on my investigation of your concerns regarding your follow-up. Following discussion with Dr Kennedy and Dr Mpe, we have agreed to seek the opinion of a tertiary specialist radiologist regarding what the most appropriate follow-up would be in the light of your scan images. I will reply formally to your complaint when we have obtained this opinion. Kind regards. Andrew Potts General Manager Clinical Services

As a result of Mr Potts initiative I received a copy of a reply from senior radiologist Dr David Milne of AD HB. In his  letter dated 14 October 2015 he stated that “ I have reviewed the CT imaging from 7/1/2008 performed at ascot Radiology and from Northern Radiology from 21/10/2014.  There is a solid 8mm lobulated nodule in the lateral basal segment of the right lower lobe.  This has no calcification or fat with in it and  has no particular distinguishing features.   ( Dr Milne seemed to be unaware of the characteristics of the nodule detailed in the CT report of 2011 and specified  in my letter to Mr Potts Clinical Director of Northland DHB) ) Our experience of having biopsied thousands of lung lesions over 20 years is that the yield from biopsy of nodules this size is less than 50% positive diagnosis. The current CT imaging from Northern Radiology  was clearly reported without knowledge of the prior scans and  has been considered as a new finding with further surveillance imaging recommended.  If this was indeed a new finding  then in 2014 CT PET could also be considered in the management of this nodule along with surveillance scanning…..the nodule is clearly not new and  is entirely unchanged between the scans of 2008 and 2014. the stability satisfies all current criteria for the nodule being benign and further follow up of this nodule is not required.  We can be certain that this nodule is benign.   There is no bronchieactasis and the mediastinal adenopathy demonstrated is normal and no abnormal nodes are seen on the most recent CT imaging.   No follow up imaging of any type is recommended based on the findings of the CT examination of 21 October 2014.”  The longevity of the nodule would seem to be an irrelevant consideration in view of its specified possibly malignant characteristics.

As the latter might be suggestive of malignancy one might have considered it prudent to have instigated further investigation such as fine needle aspiration.   I have a 20 year history of smoking , am  now permanently afflicted with Pseudomonas Aeruginosa and frequntly afflicted with pain in the lower lobes and a have a regular cough.  I would not  have thought it appropriate to  have curtailed regular CT scanning.  There seems to be a difference in medical standards between New Zealand and their overseas counterparts.

Sputum tests performed by Northland DHB( Labtests Auckland)  on 26 February 2015 and 3 June 2015 reported “ large number of gram negative bacilli moderate numbers of gram positive cocci Culture: Heavy Growth of Pseudomonas species” and an identical subsequent diagnosis with “occasional polymorphs present”  Ciprofloxacillin was prescribed in February and August 2015. Pseudomonas continued to be diagnosed by Northland pathology on 6 September and 16 December 2015    Only a limited supply of Ciprofloxacin was prescribed in December 2015.  ( see general practitioners) . The pathology test dated 23 February 2016 reported  “moderate number of polymorphs , small numbers of epithelial cells, large numbers of Gram negative bacilli, moderate numbers of gram positive cocci: Culture: heavy growth of Pseudomonas species. A prescription for 10 days of Cipro (1,000 mg per day)  was provided  in  early March 2016.

On 14 October 2016 Northland Pathology reported a “ heavy growth of Pseudomonas species “ evident in a chest sputum sample.  AFB (TB) tests have been undertaken at Medlab on 21 June 2002, Labtests on 9 October 2009, and Labtests on 31 December 2014.   All tests reported “ no mycobacteria species isolated after six weeks”.

A consultation was arranged with Dr Megan Cornere on 18 April 2016. Dr Cornere is Director of respiratory Services at Waitemata DHB.   I had emailed Cornere a number of relevant images and reports. She did refer to them briefly but they were not otherwise discussed at length..  They clearly showed the lung nodule in the right lobe and what appeared to be another smaller nodule in the left lobe. While Cornere referred to my having been previously afflicted with erythema nodosum in the early 1980’s she omitted any reference to the simultaneous diagnosis of erythema palmar an image of which was shown to her in the consultation.

Dr Cornere advised “ It remains likely that Vicki has an underlying small airways inflammatory disorder with very little to see on high resolution CT scanning and excessive sputum production.  She has recurrent Pseudomonas and the question remains as to whether or not this has colonised her lungs.  Despite my attempt at reassurance she remains worried that the right lower lobe nodule could be cancerous and was questioning whether or not a CT PET would be appropriate.  In the first instance I think it would be appropriate to repeat a high resolution CT scan of her lungs to see if there has been any development of bronchitis/bronchiectasis or small airways inflammatory disease.

  She will also have a CT scan of her sinuses to ensure that significant sinusitis is not contributing to her symptoms.  If pseudomonas remains a concern we could consider 3 months treatment with nebulised aminoglycosides as she has had multiple courses of ciprofloxacin in the past. As the nodule remains an ongoing concern despite reassurance we could pose the question as to whether or not the nodule would be amenable to FNA.  Although it is sub-centimetre a skilled radiologist may be able to perform this which would at least put paid to her concerns as to its malignant potential.  I suspect this would be a difficult procedure with low yield.  As such I have referred her to Green Lane imaging as they have significant expertise.   I do not think at this point that a CT PET would be appropriate and I have explained my rationale to Vicki.” I consulted Dr Cornere as a private patient.  I did not attend at Green Lane imaging.

I had expressed my concern over the status of the lung nodule in the right lower lobe and the cancelling of t he CT scans by Dr Kennedy.  Dr Cornere was not prepared to discuss the significance of the characteristics( high houseman unit readings)  of the nodule specified  in an ADHB report of 2011 which might be suggestive of malignancy. Dr Cornere reiterated the statements of Kennedy and radiologist David Milne that the sole criterion conerning a slow growing nodule of 8mm was that it had remained unchanged in size for 2 years. 

I had complained about the inflammation in the centre of the chest and the pains  in the lower lungs the dependent upon the severity of the infection. The discomfort was often sufficiently debilitating to make walking difficult . “ Bilateral  apical pulmonary fibrosis and scarring “ together wi th “ multiple bilateral lymph nodes described as non-specific and possibly reactive” were reported  by  Northland DHB in 2014 but again were not alluded to by the Cornere. 

 I had advised her of a previous consultation with neurologist  David McCauley and my dissatisfaction that he had apparently ignored the subsequent  MRI brain scan report of October 2015.  Gyral or serpentine leptomeningeal enhancement and thickening of the meninges were clearly evident in the MRI scan of 2015 but were not diagnosed and the report apparently ignored by Dr McAuley.  An erroneous assessment was also made by neurologist Dr Charleston who claimed to have consulted neuroradiologists at Auckland Hospital. I had also provided Cornere with a copy of an image clearly depicting leptomeningeal enhancement however she did not consider that it was a matter for her to deal with  despite my advice that the first bout of probable meningitis occurred in the late 1980s’s in conjunction with a severe sinus and chest infection.

 Nevertheless Cornere incorrectly stated “ that Vicki  was seen by David McCauley last year and continues to remain concerned that the MRI and CT images demonstrate evidence to support chronic meningitis despite his reaassurance that this is not the case”. 

A CT Chest and Upper Abdomen( high resolution of the chest without intravenous  contrast) was performed at Whangarei Radiology on 27 October 2016.  Findings:  “ Right lower lobe lobulated well-defined soft tissue density 8m nodule is better defined  on today’s CT scan and then on the previous CT  scan but does not appear to have changed in size or shape since the previous CT scan.  Anterior and lateral right upper lobe 3 mm well- defined nodule is also present and restrospect and is unchanged.  Bilteral apical fibrosis is unchanged.  Trachea and major bronchi are patent and there is no bronchiectasis .  No pleural effusion.

Numerous small axillary and mediastinal lymph nodes are unchanged.   No pulmonary hilar lymphadenopathy. 

No abnormality is identified on these unenhanced images of the upper abdominal viscera that are included within the field of view of this examination.  There is a hiatus hernia.  No destructive bone lesion.

Conclusion:   right lower lobe 8mm and  right upper lobe 3 mm nodules are unchanged.  Suggest follow-up CT scan in 6 months.  Lymph nodes are unchanged”. Once again the clearly defined characteristics of this 8mm nodule specified in an ADHB Radiology report of 2011 have not been referred to.

With regard to laboratory tests, although microscopy details are sometimes the same ( large numbers of gram negative bacilli which are the equivalent of a heavy growth of pseudomonas ) a culture is  not always specified and as a consequence the general practioners won’t prescribe ciprofloxacillin.  That seems to be rather remiss in respect of a chronic long term sufferer with a heart condtion. I also experience pain in the centre of the chest and lower lobes which at times can make walking very difficult  As a consequence I have had no ciprofloxacillin  prescribed from September 2017 until  February 2018.   I did email my concern to Labtests however I was advised that the matter would need to be referred by a general practitioner.  Dr Sprague seemed somewhat reluctant to pursue a further enquiry.

A mammogram was performed at Mauri Ora mammography on 17 January 2017.   In one frame a small bright line extends under the breast . When it is magnified a dense cotton wool type of infiltrate/opacities are depicted in the chest wall possibly extending into the breast.   An email requesting further advice and with accompanying images was sent to Breast surgeon Dr Shan on 8 June 2017 but there was no reply from either Shan Emails were also sent to Dr Cornere director of the  Waitemata Respiratory and Dr Dawber NDHB radiologist.

 In her email dated 22 June 2017 my general practitioner Dr Henderson stated: “Hi Vicki Thank you for the films.  I am not a radiologist but from my training I cannot see any features on your imaging that would raise alarm bells for me.  The patchy changes in your screen shot are normal findings on many x-rays – particularly when looking through dense tissue due to the variable uptake of the x-ray radiation.  Dr Kim Shepherd is a very skilled radiologist who reads the vast majority of breast imaging and I have faith that she would have reported any changes of concern.  Regards Dr Henderson”

On 8 June 2017 NDHB radiologist Dr Dawber advised : I am unable to comment on the Mercy Radiology MRI and the Mauri Ora Breast Screen mammogram and would advise you to contact them if you require any further information about these two studies. With regards the CT Scan of 2014 I am not sure what “horseshoe shaped cells” you are referring to, but individual cells are too small to appreciate on CT Scan. The somewhat “horseshoe shaped” structures in the lungs on the image that you have included with your email are lung blood vessels a little blurred by movement from breathing.

In her emailed reply dated 3 July 2017 Dr Cornere stated: “Dear Vicki I am sorry I can’t be more helpful but I have absolutely no experience in interpreting mammography.Hopefully you will get a reply from the radiologist and breast physician who should be able to assist as they have the expertise

Kind regards Megan Cornere” 

A chest x ray was performed at whangarei hospital on 8 January 2018.  Radiologist Jan Walsh reported  “ Nodular density evident at the right base with further lesion in the right upper pole and possibly also the left base.  I  note the patient is under care of the chest team.  The lungs otherwise appear clear.  Normal  heart size, mediastinal outline and hila”. ( the possible presence of a nodule also in the left base has not been referred to previously)

On 14 February 2018 a reply was received at the Onerahi Medical practice from Dr Tan a respiratory physician in response to a request from Dr Detjen of Onerahi Medical  “I see her CT scan in 2016 being quite normal and devoid of bronchiectasis.  I make note of her previous review with Mark Kennedy . I suggest she has a chronic cough previous smoker with a normal CT.  I would agree with you that regular antibiotics is not required in this patient in this particular case.  She is not even growing pseudomonas species. Consider changing the ACE-1 to an ARB in case this is an ACE induced cough.  Approach to her chronic cough as outlined in the cough pathway-routine spirometry +/- trial of ICS.”  (See also general practitioners)

This seems to be a somewhat erroneous assessment by both Dr Detjen and  Dr Tan- I have a long history of gram negative chest infections, scarring and fibrosis in the lungs and a nodule which is possibly malignant.  Any coughing is related to my chronic long term chest infections and is not ACE induced.  Dr Detjen should have been able to access my previous laboratory reports -her actions might be  construed as obstructive in respect of obtaining appropriate medical treatment.

On 22 February 2018 I onforwarded an email to Dr Roberts Chief Medical officer of Health for Whangarei expressing my concerns about respiratory, manmography  neurology matters including a local general practitioner. In his reply dated 22 March Dr Roberts advised   “I did not reply to your earlier mail because there did not appear to be a question for me to address. It seemed simply to pass on a considerable amount of information about your past medical care . Having reread that email today I remain unclear of your reason for contacting me. I would be most grateful for your advice in this regard.”

My reply dated 2 April 2018 stated  “I  would have thought it obvious that the general nature of my email was that of a complaint which was sent to you in the hope you might be able to rectify some of these issues.”  

My complaint was also onforwarded to NDHB CEO Dr Chamberlain on 13 April 2018 and was in turn onforwarded to Quality and Control and finally the General Manager, Medicine, Health of Older People, Emergency and Clinical Support  Mr Beney. On 30 April he advised “ due to the number of services involved it is taking time to get the required information to respond to your concerns”! 

In June 2018 a response was received from Respiratory Physician Christine Bradley:  “ Thank you for this referral.  This lady has been seen recurrently in Auckland and here.  Her right lower lobe nodule has been unchanged since 1999 her last CT was in 2017 so there have been 18 years of stability and t his does not require a repeat CT at any point.  Her prior breathing tests indicated mild obstructive disease likely secondary to a 30  pack year smoking although remote.  She has intermittently grow Pseudomonas species Haemophilus influenzae, Serratia (2003,2005 and 2007) Stenotrophomonas maltophilia ( 2006),  Ongoing antibiotics  lead to development of resistance species so they would only be indicated when true infection is indicated-marked  increase  in  sputum with colour change plus or minus fever. My initial approach would be to treat as any bronchitis using augmentin , Roxi or doxy .would stop culturing unless she was clearly not responding. She has declined three day weekly azithro  in the past.  Her last CT does not show bronchiectasis .  I do think she is likely a very challenging patient but I am not sure how I can add further to my colleagues over the years.  Thanks Christine

My emails, which contained respiratory images, including the dense opacities evident in a mammography frame, were sent to to Dr Bradley on 28 September 2018 and to Dr Mpe Senior Respiratory Physician NDHB on 31 July 2018.  I had requested  a re-consideration of the decision not to continue with CT chest scan however there was no response.

A reply was eventually received from Mr Beney dated 28 October 2018. He referred to “ your email and attachments which were received by Dr Bradley on 18 September 2018-as you raised a concern that was outside of her area Dr Bradley forwarded your email on so a coordinated approach to your response could be provided.  Dr Bradley the declined request for a clinic review and reinforces that there is no evidence for bronchiectasis. The nodule has been under surveillance for well beyond the recommended timeframe. She does not believe there is a reason for a review in the respiratory clinic.” 

In respect of mammography(respiratory) “ On receiving your concern Dr Kim Shepherd requested Dr Walker ( Clinical Director for Breast Screening Waitemata-Northland) review the images and she agrees with Dr Shepherd’s email to you  on 19 June 2017- I have looked at this mammogram with my colleague Dr Wild. The appearance you have shown on your first magnified image is normal skin and subcutaneous tissue.  I would like to reassure you that I can see no areas of concern on your mammogram”    . This would seem to be an erroneous assessment pertaining to the original frame not the magnification.

In respect of mammography(respiratory) “ On receiving your concern Dr Kim Shepherd requested Dr Walker ( Clinical Director for Breast Screening Waitemata-Northland) review the images and she agrees with Dr Shepherd’s email to you  on 19 June 2017- I have looked at this mammogram with my colleague Dr Wild. The appearance you have shown on your first magnified image is normal skin and subcutaneous tissue.  I would like to reassure you that I can see no areas of concern on your mammogram”

I attended ED at North Shore Hospital on 6 May as I was afflicted with a chest infection. I was attended by Dr Etienne De Beer .( Senior Medical Officer)> “ History of presenting complaint: cough productive of yellow tinged sputum x 1 week. Sore throat now resolved and coryza ( inflammation of nasal mucous membranes) headache and sinus pains.  No fever.  No dyspnoea- Primary diagnosis : RESLRTI  LRTI uspecified -includes bronchitis- the trachea was central and the lungs clear. Initial impression/Assessment Acute LRTI .  “ RR : 16 bpm////02Sat 98%/////Fi02: 21%(  oxygen flow rate)///////// General exam: alert and appears well. Colour, hydration,   perfusion normal. No oedema.  CXR normal.   Public Health subsequently advised by text that the result of the nasal swab for COVID 19 was “negative”  Dr De Beer provided a prescription for a repeat of most of  my usual medications ( not including omeprazole) and a 2 weeks supply of ciprofloxacin normally previously  prescribed for pseudomonas aeruginosa.  A covid 19 test from a nasopharyngeal swab was negative, 

A mobile chest x ray report: cardiac and mediastinal contours normal. The lungs and pleural spaces are clear. ( Richard Beedie Radiologist),  Dr De Beer also assessed the lung scan as ne Waitemata Respiratory Clinic on 17 July 2020. Nursing staff assessed my height and weight but did not check my blood pressure. I discussed the x ray dated 6 May 2020 which contained evidence of previously diagnosed lung nodules iPP Pn the base of the right lower lobe and a  previously undiagnosed but probable somewhat obscured nodule/mass evident in the left lower lobe  While nodularity in both lower lobes was evident in the latest x ray it was not diagnosed .The latest x ray was not available fo r viewing in the consultation however Dr Cornere did take note of those nodular details.   Dr Cornere  referred me for another CT lung scan which is scheduled for early August. I asked for her opinion about the frame indicating dense opacities which seemed to involve the chest wall  and the breast  extracted  from a mammogram dated 2017 . The  frame was disregarded by Dr Cornere. She provided a stethoscope chest check , a referral for blood and sputum tests, and  a prescription for roxithromycin. We had discussed nasal saline sprays however Dr Cornere prescribed teroclear nasal spray to be used in conjunction with saline douche.  A medical  recommendation is generally required in respect of a steroid spray particularly if a nasal or sinus infection is present.

Dr Corneres report dated 16 July 2020 is as follows:

:  Problem Chronic productive cough with  recurrent respiratory tract infections  and  history of recurrent  bronchitis and Pseudomonas colonisation.     

Bronchitis since childhood, with associated asthma. Longstanding  issues with bronchitis since the 1970s -20- to 30-pack-year smoking history, having stopped in 1992. Previous hypertonic saline challenge negative-.BAL 2004 72% neutrophils- HRCTs at multiple sites dating back to 1999.  CT chest 27 October 2016 documenting right lower lobe 8 mm nodule, right upper lobe 3 mm nodules are unchanged- Bilateral apical fibrosis is unchanged.- pTrachea and major bronchi are patent and there is no bronchiectasis- numerous small axillary and mediastinal lymph nodes are unchanged. No pulmonary hilar lymphadenopathy .CF mutations negative. Variable response to macrolide therapy in the past. No significant improvement in symptoms with inhaled corticosteroid.  History of erythema Pnodosum but no suggestion of sarcoidosis on HRCT.P

 Multiple  sputum  cultures  since  2003  including  Haemophilus,  Staph  aureus,  Serratia,Stenotrophomonas, Pseudomonas aeruginosa to name a few (Vicki  has an extensive and comprehensive list of all pathogens cultured Aspergillus serology negative 2014.  Low-level IgA 0.7 in 2009, 0.6 2014 – no known immunology review. 1990s Letters documenting normal lung function    Clinic spirometry April 2016 FEV1 1.79 (77%).

  Previous respiratory physicians seen to date include Adrian Harrison 1995, Jeff Garret April/May 2002 and July 2004, John Kolbe in May 2004, Margaret Wilsher in 2009, Stuart Jones in December 2010, Tim Christmas 2011, Paul Sexton March and June 2012, Mark Kennedy October 2014, myself April 2016   History of TB contact with father suffering from TB. (It is uncertain as to whether my father was ever afflicted with TB as opposed to his father who was seriously ill with TB No AFBs cultured in the past. Multiple cultures of Pseudomonas in the last 18 months, treated with ciprofloxacin.  

 A full blood count 7 May 2020 -normal, lymphocytes reduced at 0.7. COVID negative.  Chest x-ray 7 May 2020 cardiac and mediastinal contours are normal. Lungs and pleural spaces are clear    Right lower lobe pulmonary nodule present since 1992 CT scans x 2 in 1999, 7 May 2008, 14 November 2011, 16 May 2012, 21 October 2014 and 2016 all  demonstrating stability of the nodule.  Family history of lung cancer .   

 Rhinosinusitis. CT in 2014 documenting no significant sinusitis . Escalation in sinus congestion, obstruction and headache. History of dyslipida .Hyperthyroidism, on long-term carbimazole . Previous gastric ulcer related to nonsteroidals with haematemesis requiring transfusion.    lschaemic heart disease –  Coronary angiogram 26 November 2013 severe stenosis distal LAD with further DES, severe ostial   PDA disease, chronically occluded left circumflex ..Last reviewed by Cardiology :Northland August 2018  

 History of chronic fatigue and fibromyalgia.  Systemic. hypertension with episodes of hypotension, presyncope and generalised bilateral visual abnormality in December 2013.  CT MRI performed .reviewed by David McAuley in 2015. Concern regarding chronic meningitis, thrombosis and connection to Pseudomonas colonisation seen by Alison Charleston May 2016 ? result.

 Medications:  Aspirin 100 mg daily. Salbutamol 200 mcg inhaled prn.   GTN spray as direct  .Cilazapril Plus 1 tablet daily. Atorvastatin 40 mg daily Omeprazole 40 mg daily.  Carbimazole 5 mg daily. Roxithromycin 150 mg orally bd for six weeks.

Therapy as above:  HRCT chest and CT sinuses  Repeat full blood count.  Sputum for culture if necessary,  Baseline lung function including FeNO.  Outpaiient Clinic Repeat blood count CRP and immunoglobulins.   

 It was a pleasure to review Vicki in clinic. I have not seen her since 2016. In this time she has continued to have a chronic productive cough with recurrent respiratory tract infections. She has had multiple courses of ciprofloxacin for sensitive Pseudomonas. When I saw her in 2016 our thoughts had been that this was a colonisation as opposed to pathogenic—?however, Vicki does report feeing unwell with these infections. Vicki also describes discomfort in her chest and feels fatigued. She also experiences sino-nasal symptoms which have escalated and she now has obstructive and congestive symptoms with associated headache. She does take her salbutamol inhaler, which she uses occasionally when required. Vicky continues to cough the purulent-appearing sputum and has recently finished a course of ciprofloxacin.

Vicki last had a CT scan in 2016 which demonstrated the right lower lobe nodule, upper zone fibrosis and no other findings of concern. This has been summarised as above.Vicki’s past medical history is extensive and again I have endeavoured to summarise the pertinent points of her history above.

Examination:

On examination today, she looked well. She was not breathless at rest. There is no digital clubbing or cervical lymphadenopathy. Heart rate was 80 per minute and regular. Heart sounds dual, chest clear to auscultation. 

Comment:

In summary, Vicki is known to have recurrent respiratory tract infections. interestingly she has had a low serum IgA, which may predispose her to recurrent respiratory tract infections. To my knowledge she has not had a previous immunology review.  She has had a variable response to macrolide in the past but I think in view of ongoing congestion this should be considered. She has a sputum pot for culture should her sputum change in colour and given that she now has more in the way of sinus symptoms, the above therapy. She will have a repeat CT scan of her chest and sinuses to exclude significant sinusitis and also to review the recurrent infection to ensure that she has not developed significant bronchiectasis in the interim.This will also review the lower lobe pulmonary nodule which has been present since 1999 and also the upper lobe fibrosis which was concerning also to Vicki.

Vicki will have the above blood tests for completeness and to recheck her immunoglobulins and ensure the mild lymphopaenia has resolved.  She will also have baseline lung function as we may consider optimising inhaled therapy if this is what Vicki wishes.

Moving forward one consideration in view of the recurrent Pseudomonas would be nebulised gentamicin. I will, however review Vicki with the results of her investigations and formulate a management plan accordingly.

Addendum: Blood work: Normal immunoglobulins, FBC, CRP

Dr Megan Cornere MBChB, FRACP, PhD Respiratory Physician

A few extracts from Dr Corners report are detailed below”

a) “history of recurrent bronchitis and Pseudomonas colonisation-when I saw her in 2016 our thoughts were colonisation as opposed to pathogenic” . I never agreed to an assessment of colonisation as I have been afflicted with serious chest and sinus infections extending back to the 1970s.

(b) “BAL 2004 72% neutrophils” – The Bronchoalveolar lavage also reported twice the number of bronchial epithelial cells in the left lobe (58%) as opposed to the right. (14%)

© “Chest CT 27 October 2016 documenting right lower 8mm nodule”……. The CT report dated 14 November 2011 reported “ at the right lung base there is an 8mm nodule which has a sclerotic rim with central density 90HU and peripheral density 200 HU.  There is very minor right lower lobe bronchiectasis-there is mild air trapping on the expiratory views”

(d) “Numerous small axillary and mediastinal lymph nodes” The ADHB report dated 21 October 2014 referred to the lymph nodes as “ non specific and may be reactive”

(e ) “ No significant improvement in symptoms with inhaled corticosteroid”  I have found the steroid inhaler very helpful in respect of inflammation.

(f) History of erythema of nodosum but no suggestion of sarcoidosis in HRCT:  Erythema palmar occurred simultaneousely with erythema nodosum in the early 1980s.

(g) “Coronary angiogram 26 November 2013 …..distal LAD with further Des severe ostial PDA disease chronically occluded left circumflex”  Stenting of the left main and left descending arteries occurred on 15 November 2011.

(h) “CT MRI (brain) performed -reviewed by David McAuley in 2015……….seen by Alison Charleston May 2016? Result.”  There was no further communication from Dr Mcauley subsequent to the first consultation nor was there any assistance from Dr Charleston. There were some unsatisfactory aspects concerning non-reporting in  the scan.

CT HRCT Vicki Wilson NHI GRD 8664 5 August 2020

Clinical: recurrent infections with multiple pathogens including pseudomonas. Continues to expectorate purulent sputum . Sinusitis nonsmoker. Hx of 8mm nodule RLL previously under surveillance and upper lobe scarring and fibrosis.   Question: ? bronchiectasis ? atypical infection?other? interval change in pulmonary nodule.   Comparison made with prior HRCT latest dated October 2014.

The 8mm nodule in the lateral basal segment of the right lower lobe is stable unchanged compared with prior examinations back to 2012. No other lung nodule is seen. There is no bronchiectasis,emphysema, interstitial lung disease or evidence of small airways disease. There is stable minor scarring in the inferior division of the lingula segment of the upper left lobe. Trivial apical pleural thickening noted bilaterally with no evidence of underlying adjacent pulmonary parenchymal scarring. No hilar or mediastinal lymphadenopathy and no pericardial or pleural effusion.  There is a small sliding hiatal hernia approximate 5 cm height.

John Gunn Radiologist North Shore Radiology

Website Radiopaedia advises that   “Apical pleural thickening: Thickening of the top-most portion of the pleura. This type is benign unless the pleura has thickened more than two centimeters. Focal pleural thickening: Thickening confined to one or more specific areas of the pleura. Pleural thickening can be serious, especially when it reaches more advanced stages. The presence of pleural thickening is not enough to confirm a pleural mesothelioma diagnosis, but it can be a sign of serious and significant asbestos exposure. . Healthtop questions advises: “There are many causes for apical pleural thickening, including: bacterial pneumonia; chemotherapy; infection; lupus (an important factor because it can cause infl body” The CT report of October 2016 stated:  Bilteral apical fibrosis is unchanged”  

Consultation with Dr Chapman on 4 November 2020:

 Dr Chapman was also probably unaware?of the details of ADHB reports of 1999 and 2002 which specified “several lymph nodes lying adjacent to the the main trachea -no pathological lymphadenopathy” or the report of 2002 –“ very minor atelectasis in the right medial aspect of the middle lobe and the lingular segment of the left upper lobe”.  Chapman did refer to the “BAL of 2004- 72% neutrophils” but not the reference to “twice the number of bronchial epithelial cells in the left lobe as opposed to the right”  As with Dr Cornere’s report there was no mention of the characteristics associated with the 8mm lung specified in a 2011. What appears to be a small nodule in the left lower lobe was also evident in the 2014 scan but not reported.    

CT report of October 2014 states “Conclusion: Well defined 8mm opacity in the posterior basal segment of the right lower  pulmonary lobe is non-specific and may represent a primary benign or malignant lesion and CT scan surveillance of  this is advised with repeat CT scan in approximately 3 months time.  Non-specific axillary, supraclavicular and mediastinal lymph nodes possibly reactive . No bronchiectasis. Chapman described the recent CT  sinus scan of 5 August 2020 as showing “minimal nasal disease”. I am however almost permanently afflicted with sinus infections.

Chapman commented “ she does not have faith that recent sputum cultures particularly looked for relevant pseudomonal infection and that the mixed gram negative organisms which were commented on she feels is her culprit infection of pseudomonas. Currently she complains of having a croaky voice and coughing up dark yellow coloured phlegm -she does not particularly report breathlessness or wheeze but was very focused on the fact that she required antibiotics particularly ciprofloxacillin. Conversely cardiologist  Dr Glenie later reported “She has occasional crepitation at the left base but otherwise the chest was clear”

  We have not seen any pseudomonas on sputum culture for over a year now despite multiple testing and the CT scan does not show any bronchiectasis. I did not think antipseudomonal antibiotics were indicated but that we should consider that if we found pseudomonas going forward.  I am usually in favour of treating pseudomonal infection aggressively with intraavenous antibiotics and possibly nebulised gentamicin in my bronchiectatic patients.  It is interesting to me why she has cultured such an array of bacterial pathogens which we would normally see in a cases of bronchiectasis yet she had no development of bronchiectasis over the years” “Minor right lower lobe bronchiectasis and mild air trapping in the expiratory view” was reported in a NDHB report of 2016.

I explained to Dr Chapman that I have a long history of chest infections extending back to the 1970s -diagnosed as primarily gram negative infections since 2003. I provided him with a list of pathogens diagnosed since 2003.  The most significant pathogen in recent years has been pseudomonas aeruginosa.  In respect of non-diagnosis in the last year the problem lies with the laboratory staff.   While the microscopy details of  two reports can be identical only one will provide a culture. For reasons best known to the laboratory staff no culture has been provided during the last 12 months.  In addition “mixed species”is also often reported but not specified .  If gram positive pathogens are also involved then alternative antibiotics would also be required. Neither the Director of Labtests nor the general practitioners seem prepared to assist in rectifying this irregularity.   In the last few months I have had courses of ciprofloxacillin and romicin and I am still producing sputum, experiencing a nagging cough and a sore chest.  .  In November 2020 I emailed Labtest scientists stating my concern but received an unsatisfactory response as was the case with the complaint to Labtest Director Dr McAuliffe..

Chapman referred to the recent CT scan as “reassuring….did not think that surveillance going forward for her lung nodule was indicated”

The CT report of October 2016 stated: “ Bilteral apical fibrosis is unchanged.”  From time to time I experience serious discomfort in the chest during a period of infection to the point where I have difficulty walking..  This may be attributable to fibrosis and scarring in the lungs and the condition would need to be monitored at least on a yearly basis.  Medications are available for this condition. I am afflicted with a cough on an almost permanent basis. My former history of smoking and lung pathogens should also be sufficient reason for continued yearly monitoring . 

There also was no significant response from Dr Chapman  in respect of the images and reports I had emailed.  He conducted an examination of my chest and abdomen but made no comment.  Unusually a nurse was present for the duration of the consultation.  Chapman advised my BP was “180/90” which seemed unusual in comparison with recent readings from my medical practice last recorded as 140/80 on 24 November 2020.

I had requested a change of specialist to Dr Brant however on 30 July 2021 I received a reply from Janice Kirkpatrick Operations Manager who advised  ‘ I can confirm that we have received your referral and that it has been graded as a Priority 3 to be seen within 4 months.  I note that this appointment will be with Dr Alex Chapman. Dr Brant has reviewed your history and is supportive of the current plan of care outlined by Dr Chapman and as such has declined to take over your care’. That is not a very satisfactory outcome.

ENT

I  have for as many years been afflicted with severe sinus infections and on-going pain some of which is attributable to allergies have for as many years been afflicted with severe sinus infections and on-going pain some of which is attributable to allergies 

T to allergies A nasal sputum  test in 2000 indicated “ large number of gram negative cocci  in conjunction with small number of  gram positive cocci” The CT sinus miniseries of December 2000 reported that “ “the nasal septum is deviated slightly to the right.  The maxillary sinus ostia are narrowed by lateral ethmoid cells Haller’s cells which might predispose to  oesteal obstruction with relatively mild degrees of nasal mcosal swelling”)

An tion by specialist Dr Dev Tandon at Green Lane hospital in June 2001 reported that  “ the nasal mucosa as looking remarkably healthy. He noted small Haller cells in the superior ps of the maxillary antra  that seem to have narrowed the oestomeatal complexes to some extent but there was considered to be no significant pathology as such”. The subheading  on his res “ delusional about bacterial infection throughout  the whole body”

Although he has initially categorically denied having written the comment it is quite clearly evident in the copy of his original report.  He did also apologise . However, in his letter to Ms B adviser to the Health and Disability Commissioner dated  4 February 2009  Tandon contradicted his earlier apology with the statement that “ the word “ delusion” was used in the context where it means an unshakable belief in something untrue where such a belief remains firm even when overwhelming proof is presented to dispute it”   The middle meati are clear-there was no infective mucous or polyps.  There was an accessory ostea bilaterally and the antral mucosa appeared healthy.  The nasopharynx appeared unremarkable.  The remainder of the upper airway looked healthy”  A subsequent MRI scan of the brain and neck was also unremarkable.  His recommended a change. in bedding (mattress pillow encasements) and he continuation of exisiting medication as prescribed by the respiratory physician.

 A physical check of the external sinuses by GP Dr Thomson in January 2006 indicated  “tender sinuses all over and T 36.6”) 

In December 2007 a somewhat contradictory CT scan to that of December 2000 reported “that the frontal and maxillary sis were clear with only mild scattered mucosal thickening in scattered anterior ethmoid air cells.

In 2007 during the course of a consultation with yet another ENT specialist( Dr Bartley) my medical history was annotated and areas of muscular tenderness or trigger points examined. .While the here was also brief instrumental check of the sinuses there was no external examination  to assess pain.

It seemed to be a matter of priorities . When I began to explain that I had begun to experience a change in the symptoms associated with infection in the late 1980s, namely additional pain in the sinuses, neck stiffness,  sleepiness, blood spotting and small blood clots, the specialist  suddenly took umbrage and suggested that if “ I was unwilling to listen to an alternative explanation as to what was going on then he  would  terminate  the consultation.” And that is what occurred.

Apart from a briefly referring to“ has grown Pseudomonas as well as Serratia Marcens” (Marcescens) there was no discussion of  the gram negative bacterial infections with which I have been afflicted with in recent years” Nor did he consider that another scan of the sinuses would serve much purpose.  

As an ENT specialist I would have that an investigation of these quite serious symptoms in the sinuses with possible further investigation of the pain and  narrowed maxillary sinus ostia would have been his initial priority with ME symptoms and diet secondary to the main concern  The aborting of the consultation was unjustified and tantamount to negligence.  

These findings also seem to be at variance with  thermography  reports of 2003 which specified  “focal areas of hyperthermia over both maxillary paranasal sinuses and the medial eye sockets”   I am afflicted with almost continuous sinus pain and on occasions have had to use an ice pack on the head . I am also often afflicted with a stiff neck and this  inflammation has also  been indicated in a thermography report .The latter symptoms can also be indicative of meningitis. Thermography scans  are not recognised by the medical profession.

The report of ENT specialist Simcock dated 20 December 2007 stated  “ Examination with the fiberscope showed that the nose nasopharynx pharynx and larynx were normal as were the ears. The nasal septum was slightly curved but with good patent nasal airways….. the symptoms were not attributable to infective sinusitis but were referred from myofascial trigger points in the  neck-that the post nasal mucus is from vasomotor rhinitis from alternation in the sympathetic nerve supply controlling the nasal membranes…. recommended treatment from either a physio or chiropractor. A CT (Mini Sinuses ) of the sinuses dated 19  December 2007 reported : “  The frontal and maxillary sinuses were reported as clear as were the posterior ethmoid and sphenoid sinuses.  There was mild scattered mucosal thickening in both anterior ethmoid air cells.   The frontal recesses and osteomeatal complexes are normal.  A bone lesion in the base of the  skull was not identified.’

The same specialist’s  second report was dated 22 January 2008  differentiated between the sinuses and the nose or nasal passages.  “ any mucous that you are producing is arising from the nasal passages and not from the sinuses the presence of microorganisms in nasal secretions is not necessarily an indication of infection either in the nose or in the sinuses.  In my opinion your symptoms are not arising from any pathology in the sinuses but are being refered to the area of the face in which they are situated.  Your tiredness forgetfulness and difficulty with thought processes are much more related to your ME and are not related to any problems arising from your nose or sinuses and are certainly not due to Meningitis. ……except to exclude the nose and sinuses as the origin of your symptoms” 

 Wikepedia advises that “Another possible complication is empyema .Bacterial or occasionally fungal infection of the skull bones or air sinuses can spread to the subdural space, producing a subdural empyema. The underlying arachnoid and subarachnoid spaces are usually unaffected, but a large subdural empyema may produce a mass effect. Further, a thrombophlebitis may develop in the bridging veins that cross the subdural space, resulting in venous occlusion and infarction of the brain. With treatment, including surgical drainage, resolution of the empyema occurs from the dural side, and, if it is complete, a thickened dura may be the only residual finding. Symptoms include those referable to the source of the infection. In addition, most patients are febrile, with headache and neck stiffness, and, if untreated, may develop focal neurologic signs, lethargy, and coma. The CSF profile is similar to that seen in brain abscesses, because both are parameningeal infectious processes. If diagnosis and treatment are prompt, complete recovery is usual.   It can be associated with sinusitis.^[2]

.EMed website  advises “ if disruption occurs that affects the normal host defenses inside the sinuses those defenses may allow bacteria which are normally present in the nasal passages to enter any of the sinuses . Once there the bacteria may stick to the lining cells and cause a sinus infection. Bacteria that normally cause acute sinusitis are Streptococcus pneumoniae and Staphylococcus aureus”

 I have a history of chest and sinus infections –in recent years I have been afflicted with 4 different gram negative strains often in conjunction with gram negative cocci. These details have been relayed to all  the ENT specialists that I have consulted. Antibiotics do normally alleviate the symptoms.   Specialist assessment would seem to be erroneous. Reference to a small lesion in the right nostril was also omitted from the report.

A CT of the sinuses at Greenlane Imaging on 24 November 2011 reported: “SINUSES. There is  no mucosal thickening throghout the paranasal sinuses, which are well aerated.and have  normal anatomy.  The OMU  are patent.  The nasal septum is midline and the airway open.  No bony or soft tissue abnormality.  A linear density in the roof of the mouth /tongue is possibly something  patient had in her mouth. Conclusion: No evidence of sinusitis

 I visited ENT specialist Mr Shetty of Whangarei on 4 November 2014. I had complained about a combination of symptoms which I h ave experienced most particularly since the late 1980s.  They included  falling asleep occasionally on public transport,  a stiff neck , discomfort  in the frontal lobes , mild headaches in conjunction with occasional memory loss.( see also ENT). I had suggested that Ameningitis, or empyema might be the culprits.

Mr Shettys report dated 5 November 2014 is thus:   “her most important complaints currently are facial maxillary and frontal pain along with multiple pain points on the scalp chronic postnasal drip and currently using  Fess nasal washes. There is no history of any nasal obstruction. She has also shown very mild signs of sinus inflammation in the CT scans which were done in 2000 and 2007” .( A physical check of the external sinuses by GP Dr Thomson of Glen Innes  in January 2006 indicated “ tender sinuses all over”   Thermography report of 2003 reported “focal areas of hyperthermia over both maxillary paranasal sinuses and indicated a pervasive inflammation over the back of the neck. Thermography is not recognized by the medical profession. 

 Shetty’s report continued: She does complain of memory loss dull  headaches and nasal congestion…(also sleepiness)has shown me the sputum culture which has grown pseudomonas aeruginosa which is sensitive to Ciprofloxacin…..Clinical examination today with anterior rhinoscopy also  did not show any polyps or mucopus in the nasal cavity.  The oropharynx was normal.  Neck palpitation was normal. Miss Wilson requested me to put her case to the public system for fiber optic nasal pharyngolaryngeal evaluation and also to order a CT scan of the paranasal sinuses to investigate further to the sinus pathology’.

I explained that I was virtually  prescribed ciprofloxacin on a permanent basis .Shetty erroneousely stated that it was primarily prescribed for chest rather than sinus infections:  Website Nature Communications advises : The opportunistic bacterium, Pseudomonas aeruginosa, is extremely skilled at both colonizing and persisting in the airways of patients with lung damage. It has been suggested that the upper airways (including the paranasal sinuses and nasopharynx) play an important role as a silent reservoir of bacteria”.  I advised that my previous GP also prescribed Curam Duo as a supplementary treatment however Shetty was not prepared to also prescribe penicillin.  Pseudomonas can also result in meningitis and abscesses.

The Centre for disease Control ( CDC) advises: “Because of the risks of severe morbidity and death, effective antibiotics should be administered promptly to patients suspected of having meningococcal disease. Multiple antimicrobial agents, including penicillins, are effective against N. meningitidis.[5] For patients who receive penicillin, eradication of nasopharyngeal carriage with rifampin, ciprofloxacin, or ceftriaxone is recommended prior to discharge from the hospital Shetty had a quick glance at some of the previous reports and took some copies.

On 23 October 2014   Physician  Dr Kennedy of Whangarei  Kennedy commented  “ CT scans of the sinuses in 2000 and 2007 failed to identify significant sinusitis with mild mucosal thickening of the anterior ethmoid air cells” A sinus sputum test has never been previously suggested by either physicians  or general practitioners.

ENT specialist  Mr Chris Seeley advised in his letter dated 23 January 2015 that “ I will see her in our clinic to discuss her symptoms and look at the scan”.   As of June 2015 the appointment had not eventuated and ENT administration as20sistant Ms Marsh apologised for the delay advising in her email dated 10 June2015 “ that we were not sent a copy by our typist” . and instead arranged an appointment with Dr Faumui in early July.  I further advised her of my preference for an appointment with Dr Seeley however this never eventuated.

There is a possible abnormality in the area below the sphenoid sinuses detailed in the MRI brain scan of 2015.( see images in neurology-abbreviated version of NZ Health Human Rights)

CT Sinuses: North Shore Radiology 5 August 2020  John Gunn Radiologist

“The maxillary antra are entirely clear with patent ostia bilaterally.  A thermography report dated 2003 referred to “ focal areas of hyperthermia over both maxillary paranasal sinuses whicm may correlate with  reported symptoms of sinusitis.There is very mild mucosal thickening in the ethmoid air cells and left frontal sinus. The sphenoid sinuses are normal.  The nasal airway is normal and the nasal septum deviated. No postnasal space mass.  Mastoid air cells and tympanic cavities are normal bilaterally. Conclusion: Minimal nasal sinus disease.”

On 24 September I was advised by the Otorhinolarynology Clinic “that the assessment of your clinical details did not meet the the criteria for an outpatient assessment appointment with a specialst”  I am frequently afflicted with both chest and sinus sputums from pathogenic infections.

NEUROLOGY

In May  1988 I received a report from Dr Simpson of  Dunedin providing a diagnosis of ME or Myalgic Encephalomyelitisalgic Encephalomyelitis –“ I enclose herewith the results of your blood sample whothe cup forms typical of most cases of ME. At present nothing is known about hocan be converted to normal. You will notice that cells with surface changes were abnormally have all o)

• painful lymph nodes (small glands of the immune system)
• stomach painand other problems similar to irritable bowel syndrome, such as bloating, constipation, diarrhoea and nausea
• sore throat
• sleeping problems, such as insomnia and feeling that sleep is not refreshing
• sensitivity or intolerance to light, loud noise, alcohol and certain foods
• psychological difficulties, such as depression, irritability and panic attacks
• less common symptoms, such as dizziness, excess sweating, balance problems and difficulty controlling body temperature

My history had included severe sunstroke on one occasion in the 1970’s . An MRI scan of the brain and spine was performed  in February 2004. “No brain lesions were shown. All regions were shown to have normal intensity on all sequences apart from a few minor T2 hyperintensities in the cerebral white matter described as of no clinical significance.  No abnormality was seen at the craniocervical junction. The spinal cord was normal in appearance with of sign of spinal cord or of any intrinsic spinal cord lesion. There are mild degenerative changes in the lower cervical discs without evidence of spinal cord or nerve root distortion.  No paraspinal lesion was seen (See also Orthopaedics)  )

On December 6 2007 I consulted a Neurologist Dr Snow.  He considered “ the neurological examination was normal.  I had a good view of normal fundi.  All reflexes were graded 1+ and symmetrical Her blood pressure was 170/90. There were no carotid bruits. I reviewed the MRI scan performed in 2004. The cerebral hemispheres and ventricles were of normal size.  There was no evidence for ventricular hypertrophy or temporal lobe atrophy, which has been reported in schizophrenia . There were scattered small T2 hyperintensities.  In summary, the  scan is essentially normal. Occasional T2 hyperintensities are commonly seen and seldom have pathological significance’. The specialist first viewed the plates on a monitor downstairs and then resting on his knee as he was seated beside me.

In his report dated 5 January 2008 the neurologist further advised “ it is important to understand that there are no specific MRI findings that make a diagnosis of schizophrenia.  Thus while there are features associated with schizophrenia, in this case ventricular hypertrophy or temporal lobe atrophy , these are not specific or diagnostic for the condition. In addition these changes are not always found in schizophrenia.  For these reasons the diagnosis of schizophrenia is clinical and not based on investigations such as MRI scanning.”

There are many case studies from both Neuro-scientists and Psychiatrists alike all of which, irrespective of any specific diagnostic criteria, clearly denote a significant reduction in grey matter as being a significant aspect of schizophrenia. Logically, behavioral aspects associated with schizophrenia would be non-existent if the brain structure were normal. In this regard MRI scans must be considered invaluable with regard to diagnosis.

 The neurologist was dismissive of the thermography scan of 2003 which reported both diffuse and focal areas of hyperthermia extending from the neck to the lumbar region claiming that inflammation was not evident in the MRI scan any any problems with memory loss etc were not entirely abnormal. He made no recommendations as to further investigation

E MedicineHealth advises that “ if a person experiences mild personality changes, headache, altered consciousness, visual problems or seizures infection may have spread to the brain . Coma or death may follow” 

An extract from an overseas studies entitled  PERIVENTRICULAR WHITE MATTER LESIONS by Timothy Hain stated that  ‘ “MRI studies of older person with disequilibrium and gait disturbances of unknown cause often show frontal atrophy and subcortical white matter T2 hyperintense foci” .Radiological findings of the head  and spine in neurofibromatosis 1 (Nf!) IN Northern Finland reported the localization of T2 hyperintensities in the cerebellum brainstem supartentorial white matter and optic areas. The supratentorial white matter was affected in 44%.  From the clinical point of view T2 hyperintenstities have been regarded as benign lesions. In rare cases malignant evolution of the lesions has also been reported ( Griffiths et al. 1999 Miaux et al. 1997, Crella et al 1997) and the borderline between neoplastic and non-neoplastic lesions has not always been clear ( Raininko et al 2001). Szudek and Friedman (2002) came to the conclusion that the presence of T2 hyperintensities correlated with central system neoplasms other than optic gliomas .In one of the present patients glioblastoma multiforme appeared at the site of a hyperintense lesion affecting partly the optic radiation which had remained unchanged for many years>” The correlation of T2 hyperintense lesions of the brain with learning difficulties behavioral problems seizures and mental  retardation has been widely studied but the results have been contradictory ( Ozonoff 1999

In January 2008 a second neurologist Dr Elizabeth Walker  reported “ Tests of gait and balance were normal. Cranial nervous system examination was normal. Peripheral nervous system was normal. Blood pressure was 125/75.  Normal heart sounds and no carotid bruits-cognitive function was not examined in detail. The scattered T2 hyperintensities are acceptable for her age She considered “ that a diagnosis of schizophrenia could not be refuted on the basis of a normal brain scan-that I should have a consultation with a psychiatrist or neuro-psychiatrist-the MRI scan of the brain performed in February 2004 is within limits of normal for her age”  She provided a rather cursory check of the MRI plates and did not have a monitor for viewing. My advice concerning previous severe sun stroke, and the more recent pain experienced in the head and neck together with bouts of memory loss elicited no response.

A study by neurologist and research fellow  Stephanie Debette of the BMJ Group dated  26 July 2010 advises: “In conclusion, our systematic review and meta-analysis provides strong evidence that white matter hyperintensities predict the risk of stroke, dementia, and mortality. This emphasises that white matter hyperintensities indicate increased cerebrovascular risk when identified clinically as part of diagnostic investigations and supports their use as an intermediate marker in a research setting. Further studies assessing the impact of progression of white matter hyperintensities on stroke and dementia are needed to help design therapeutic trials incorporating progression of white matter hyperintensities as an intermediate end point. Their discovery should prompt detailed screening for risk factors of stroke and dementia.

What is already known on this topic

• Studies have assessed the relation between white matter lesions and risk of stroke, cognitive decline, dementia, and mortality.
• The results are, however, partly conflicting
• Heterogeneity of study designs, imaging types, setting, sample size, and follow-up makes the interpretation of published data difficult

What this study adds

• White matter hyperintensities are associated with an increased risk of stroke, dementia, and death

For stroke and death the association was present in both community based and high risk populations, whereas for dementia the association was significant for community based patients only”

A fall down some concrete steps in the garage in December resulted in my  banging the right side of my head against the brick wall. I met neurologist Dr Willoughby on 5 February 2013.   He looked over the plates of the Brain and spinal MRI performed in 2004 together with the skull x ray of August 2012   A  monitor was not available to view the plates.  .

 Auckland Radiology’s report dated 24 august  2012 advised:   “That no fracture is seen. Alignment is normal. Aeration of the paranasal  sinuses is normal”. Subsequent to a fall in August 2012. His report stated  “ there was a bump on the right parietal scalp – a skull x ray showed no fracture.  There was no palpable abnormality at the site of the previous scalp haematoma.  Neck movements were normal except for mild restriction of lateral flexion.” (Neurologist David McCauley subsequently advised that in his opinion a venous lake was indicated)

I provided Willoughby with  a photo dated October 2012 of a rather large nasal blood clot however the neurologist made no comment . I provided the specialist with copies of ENT reports from the early 2000s’ and a report from a Dunedin haematologist  dated 1988 confirming a diagnosis of ME complete with drawings of malformed blood cells.  Although chronic fatigue fibromyalgia syndrome was mentioned in the specialist’s report any reference to the diagnosis of a Dunedin haematologist which specified myalgic encephalomyelitis and the accompanying diagram of malformed red blood cells was omitted.  The neurologist considered the diagnosis to be controversial .

In respect of my sinus head and neck pain the report further stated “CT scans of the sinuses in 2000 and 2007 did not show any evidence of significant sinusitis. ( see also ENT ).  In 2004 she had a normal MRI scan of the brain and spinal cord-there were mild degenerative changes in the lower cervical spine. ( see also orthopaedics-lumbar)……has had variable dull headaches  ….she has been concerned that her memory and concentration are reduced …there does not seem to any indication of a progressive problem …headaches which are variable  but perhaps mainly frontal without any particular pattern through the day or relationship to postural change.” 

 The temporal arteries were normal.  There were no significant abnormalities in the cranial nerves or limbs. Visual acuity was N4 in each eye with normal visual fields optic discs and eye movements.  There was marginal impairment of hearing on the left.  In the limbs tone was normal and there was no weakness or inco-ordination.  Reflexes were normal except for perhaps a slightly reduced left knee jerk.  The plantars were flexor.  Sensation was normal except for mild  impairment of vibration in the toes ( of no particular significance).  There was no rest tremor. BP was 140/75 lying and 130/80 standing .  Peripheral pulses were just palpable.  I do not see an indication for repeat brain scanning. Overall her complex symptoms are of the sort that commonly occur in the chronic fatigue/fibromyaliga syndrome.There seems to be little supporting evidence for recurrent sinusitis or serious URT infections associated with her symptoms….it is possible that L3 or L4  root irritation in the past is the cause of minor asymmetry of the knee jerks.  ….there are no features to suggest that recurrent or ongoing meningitis is the cause of her symptoms.”

I enquired about the type T2 intensities in the white matter which were reported in the MRI scan of 2004 however Willoughby gave the matter scant regard stating: “ we all have those” Any reference to them was omitted from his report.. With regard to the the dull headaches, memory wipes, stiff necks and sleepiness that I have been afflicted with  bacterial related inflammation  is obviously the culprit however he seemed to rather sceptical of this notion and suggested that a course of amtriptiline might be appropriate.!

I had previously met Dr Willoughby in February 2013 and again on 31 December 2013 . His report advised  “ Ms Wilson whom I saw in Neurology Day Stay today for assessment of a recent episode of visual disturbance with faintness – a suspected TIA ( Trans ischemic attack).

The recent episode occurred two weeks after an uneventful coronary stent which had improved chest pain. It occurred about an hour after rising in the morning when she was standing in the bedroom. She suddenly experienced patchy black blotches in both visual fields with a feeling of faintness (a symptom that she noted was similar to that experienced when she suffered bleeding from a gastric ulcer in August 2013). The symptoms settled within a few minutes on lying down and have not recurred. With the episode there was no focal weakness or sensory symptoms in the limbs, nor double vision or vertigo. She also did not have palpitations or chest pain and, subsequently, has not had any evidence of further bleeding from a gastric ulcer noted on gastroscopy.

 She gave a clear account of recent events. There were no carotid bruits. There were no significant abnormalities on neurologic examination of the cranial nerves or limbs. Visual acuity was N5 in each eye with normal visual fields, optic discs and eye movements. In the limbs there was no focal weakness or incoordination and reflexes were normal. BP was 180/95 mmHg sitting and 160/95 mmHg standing with a regular pulse

Comment:The recent episode of symptoms were of uncertain cause but sound most like a pre-syncopal episode. There were no typical features of a posterior circulation TIA although  it is difficult to exclude that – we can reasonably exclude a carotid territory TIA and I do not think there is an indication to repeat a carotid ultrasound although Ms Wilson has wondered about that. A carotid ultrasound in 2003 showed minor plaque in both common carotids withno stenosis. I do not think repeat brain imaging is indicated but we should re-consider that if her course is unsatisfactory.”

Dr Starkey assisted Dr Willoughby at the consultation and made reference to a slight drooping on one side of my mouth. Willoughby was somewhat dismissive in his attitude suggesting that it was probably a permanent physical characteristic. There was a quick aside “ its your brain” from willoughby at the end of the consultation. In addition his Irish assistant Mr Starkey advised me to “ go home and have a nice day and I would miss out on the carotid scans at 11.00 am!”

Website  “ Seconds Count” advises  “As we age, cholesterol and fatty substances build up in our arteries, causing the arteries to narrow and increasing our risk for cardiovascular disease, including both carotid artery disease  and coronary artery (heart) disease. The relationship between the two diseases is direct: if you are at risk for heart disease, then you are also at risk for carotid artery disease”

Wikepedia advises: “Syncope  also known as fainting or passing out, is defined as a short loss of consciousness and muscle strength, characterized by a fast onset, short duration, and spontaneous recovery. It is due to a decrease in blood flow to the entire brain usually from low blood pressure. Some causes have prodromal symptoms before the loss of consciousness occurs. These symptoms may include: light headedness, sweating, pale skin, blurred vision, nausea, vomiting, and feeling warm among others. Syncope may also be associated with a short episode of muscle twitching. If a person does not completely lose consciousness and muscle strength it is referred to as presyncope. It is recommended that presyncope be treated the same as syncope”^[1]

US library of Medicine (NIH) states: ” Carotid TIA’s are not accompanied by loss of consciousness.  Therefore Carotid Doppler ultrosonography is  not required in patients with syncope”

Medsafe website advises that subsequent to a TIA:

Imaging of the brain should be performed within 24 hours of symptom onset, as follows^{[4, 5]} :

• Magnetic resonance imaging (MRI) with diffusion-weighted imaging (preferred)
• Noncontrast computed tomography (CT; ordered if MRI is not available)

The cerebral vasculature should be imaged urgently, preferably at the same time as the brain. Vascular imaging for TIA includes the following:

• Carotid Doppler ultrasonography of the neck
• CT angiography (CTA)
• Magnetic resonance angiography (MRA)

Website UpToDate states that “SOURCE OF ISCHEMIA — The most common causes of posterior circulation large artery ischemia are atherosclerosis, embolism, and dissection. Dolichoectasia (elongation and tortuosity) of the vertebral and basilar arteries is another occasional cause.

• About one-third of posterior circulation strokes are caused by occlusive disease within the large neck and intracranial arteries, which are the vertebral arteries in the neck and the intracranial vertebral, basilar, and posterior cerebral arteries
• The proximal portion of the vertebral artery in the neck is the most common location of atherosclerotic occlusive disease within the posterior circulation. Atherosclerosis of the intracranial vertebral arteries and of the basilar artery is also common..)
• Dissection of the extracranial and intracranial vertebral arteries is another frequent cause of ischemia within the posterior circulation.

Wikipedia states “ Vertebral artery dissection (abbreviated VAD, often vertebral dissection) is a dissection (a flap-like tear) of the inner lining of the vertebral artery, which is located in the neck and supplies blood to the brain. After the tear, blood enters the arterial wall and forms a blood clot, thickening the artery wall and often impeding blood flow. The symptoms of vertebral artery dissection include head and neck pain and intermittent or permanent stroke symptoms such as difficulty speaking, impaired coordination and visual loss. It is usually diagnosed with a contrast-enhanced CT or MRI scan.^[1][2]

The UC Vascular Centre advises “Vertebrobasilar insufficiency is a condition characterized by poor blood flow to the posterior (back) portion of the brain, which is fed by two vertebral arteries that join to become the basilar artery. The vertebrobasilar arteries supply oxygen and glucose to the parts of the brain responsible for consciousness, vision, coordination, balance and many other essential functions.

Unlike the vertebral and basilar arteries, atherosclerosis and dissection of the posterior cerebral arteries is not common. Most infarcts in the posterior cerebral artery territory are due to embolism from the heart, aorta, or vertebral arteries.

A person with vertebrobasilar insufficiency may experience symptoms lasting for a few minutes or permanent symptom.  These symptoms my include: 

Loss of vision in all or both eyes Double vision, Vertigo ( spinning sensation),Numbness or tingling

Nausea and vomiting Slurred speech,loss of coordination, dizziness or confusion,,Trouble swallowing

Whangarei physician Dr Kennedy’s report dated 23 October 2014 was a fairly comprehensive  summation  of my medical history and recent consultations with other specialists,’ Kennedy alluded to Dr Willoughby’s examination and report of late 2013 concerning my collapse in December 2013 “” he felt that the symptoms in late 2013 were likely presyncopal in nature with no  features of posterior circulation TIA  or evidence of anterior circulation disease and he did not believe that neuroimaging or carotid Doppler would be helpful.  He believed there  was an overlay of chronic fatigue/fibromyalgia” I was diagnosed with myalgic encephalomyelitis in 1988 from a blood sample sent to Dr Simpson in Dunedin. Willoughbys report stated that there were no typical features of a posterior circulation TIA although it is difficult  to exclude that .

The presyncopal symptoms that Vicki experienced before Christmas 2013 are entirely in keeping with an episode of hypotensive presyncope with systemic symptoms and and absence of focal neurological signs.  Should there be further such typical episode it would be appropriate for Vicki to take evasive postural measures lying down elevating the lower limbs and using the musculovenous pump and isometric hand grip to quickly increase blood pressure and improve cerebral perfusion. It there were to be recurring episodes then her antihypertensive treatment should be reviewed. 

Vicki  has a long history of fleeting and variable tenderness over the scalp frontal temporal parietal and occipital on either side.  Vicki has attributed these headaches to low grade psesudomonas meningitis.. Willoughby reassured Vicki that t here was  no suspicion of Pseudomonas Meningitis or significant sinus disease and felt the symptoms in late 2013 were likely presyncopal  in nature with no typical features of posterior circulation TIA or anterior circulation disease and did  not believe that neuroimaging or carotid doppler would be helpful. I did not undertake a formal neurological examination. In view of the scalp tenderness I have arranged for an up to date check of ESR and CRP –reactive protein although I believe that giant cell arteritis is improbable.

According to Wikepeida :Giant-cell arteritis (GCA or temporal arteritis or cranial arteritis) or Horton disease is an inflammatory disease of blood vessels most commonly involving large and medium arteries of the head, predominantly the branches of the external carotid artery.

It is a form of vasculitis. It typically causes inflammation of the network of small vessels (vasa vasorum) that supplies the larger arteries. GCA affects arteries of the head and neck, including the three arteries that branch out from the arch of the ascending aorta, and their branches—the thoracic aorta, the axillary arteries, the vertebral arteries, and further on in the head in the ophthalmic and external carotid arteries (the temporal and occipital arteries). It can cause occlusion of the arteries and ischema (tissue death).^[1]

• LFTs, liver function tests, are abnormal particularly raised ALP- alkaline phosphatase
• Erythrocyte sedimentation rate, an inflammatory marker, >60 mm/hour (normal 1–40 mm/hour).
• C-reactive protein, another inflammatory marker, is also commonly elevated.
• Platelets may also be elevated
•  
• .Radiological examination of the temporal artery with ultrasound yields a halo sign. Contrast enhanced brain MRI and CT is generally negative in this disorder. Recent studies have shown that 3T MRI using super high resolution imaging and contrast injection can non-invasively diagnose this disorder with high specificity and sensitivity.

I don’t think that Dr Kennedy was aware that I also had a fall in 2012 banging the right side of my head hard against a brick wall .I also  had a significant nose bleed and produced a large nasal  blood clot about a month after the event.   More recently I have noticed that the bony areas of the skull are very sore upon manipulation however this aspect was not referred to in Kennedy’s report

Subdural haematomas are also of concern in the elderly. Taking into account this history one might it prudent to have erred on the side of caution and implemented a brain and/ or carotid scan particularly if the symptoms should recur. Type T2 hyperintensities in the white matter were reported in an MRI scan of 2004 however these are always disregarded by the specialists  as insignificant. 

A consultation was conducted with Dr Mccauley of 7 Clonbern road Remuera on 29 September 2015. .His report is as follows:

“ The patient looked depressed and sat through a lot of the consultation with her head bowed, avoiding eye contact.  She was inclined to mumble and at the same time spoke very rapidly sometimes making it difficult to understand what she was saying. ( I don’t recall this type of assessment in any previous specialist consultations)  There was a reduction of normal facial expressivity. but no other features of an extrapyramidal disorder  blood pressure was 120/80.  Pulse 80 per minute regular – full general examination was not performed.  (McCauley provided a fairly extensive testing of my reflexes and apparently did not find anything significantly amiss).

 Bilateral prominent palmar erythema was noted  over the hypothenar eminences.  The skull was normal . Neck movements wre mildly restricted but non-painful.  There were no cervical or cranial bruits.  There was no meningism.  Only minimal scalp tenderness was present requiring significant pressure to elicit it ( Although I requested it, Dr McCauley did not apply significant pressure in  his examination of the scalp preferring instead to  use only a very light touch!).   The temporal and occipital arteries were normal to palpitation with good pulsations. The cranial nervies were normal.  In particular her optic fundi were normal.  There was no motor or sensory abnormality in the limbs. The tendon reflexes were normal and symmetrical  with flexor plantar responses.  The patients gait and balance were normal.  She was able to stand steadily on a narrow base with her eyes closed, could tandem walk without difficulty and could stand on either leg alone with her eyes closed.”

I showed McCauley a rather poor quality copy of the rear view of a skull x ray undertaken by Auckland radiology when I hit my head against a wall in 2012. McCauley advised   “the patient mentioned a fall down stairs in 2012`which resulted  in a coccygeal haematoma. She hit her head at that time and began to experience soreness of the scalp particularly in the right occipital region. Ever since that episode the patient  has been experiencing “ terrible tenderness of the scalp” which is generalised. In addition she has constant dull pain in the head mostly at the vertex and in the high biparietal region. The patient provided me with photocopy of a plain skull x ray with a venous lake marking she had outlined on a PA view which she is worried is a fracture. I agree with the accompanying x-ray report which the patient provided states there is no fracture seen and I agree with this report based on the photocopy of the  single skull projection which she provided.” …

I think it is very unlikely that the patient has any serious underlying intracranial structural cause which accounts for her ongoing troublesome symptoms including scalp tenderness and chronic head pain. This has been present for many years and on that basis one can say with certainty that it is very unlikely here is any serious underlying cause which has not by now declared itself.

 I am in agreement with my colleague Dr Willoughby that her symptoms are part of her long-standing chronic fatigue syndrome and fibromyalgia with additional tension headache.” In respect of my collapse at the end of 2013 McCauley considered that “ this event was thought to have been a presyncopal episode rather than a posterior circulation TIA”

In his report dated 31 December 2013 Neurologist Willoughby stated :  “There were no typical features of a posterior circulation TIA although it is difficult to exclude that – we can reasonably exclude a carotid territory TIA and I do not think there is an indication to repeat a carotid ultrasound although Ms Wilson has wondered about that. A carotid ultrasound in 2003 showed minor plaque in both common carotids withno stenosis. I do not think repeat brain imaging is indicated but we should re-consider that if her course is unsatisfactory” .

McCauley stated “ that she has a long standing chronic cough of uncertain cause and has chronic rhinosinusitis. Previous sputum cultures at one time grew pseudomonas. He  attributed the symptoms of “ neck stiffness.. falling asleep at unusual times and periods of deficient memory  to ME or Chronic Fatigue syndrome”( ME syndrome was diagnosed by Dr Simpson of Otago from a blood test in the late 1980s).  I had advised McCauley that these symptoms, which I had never previously experienced, were in fact the result of a a particular sinus infection in the late 1980s. He did not refer to this in his report. I have a long history of chest/sinus infections over the last 30-40 years and multiple different  gram negative infections diagnosed since 2003. I have been permanently afflicted with pseudomonas aeruginosa during the last 12-18 months . I made a suggestion as to what might be afflicting me in the head and sinuses  i.e. possibly subdural empyema, or  meningitis. Other than to suggest that empyema was a condition affecting the  lungs there was otherwise no discussion as to the possible nature of the problem.

 I also discussed the possibility of another carotid  ultrasound which overseas sources suggested were generally recommended in conjunction with heart procedures. The specialist seemed  opposed to this.. I also showed the specialist the thermography body scan from 2003 which clearly shows  significant inflammation .The results of a few of  of the previous ESR and CRP tests have been  in excess of the maximum. McCauley made no comment.  I asked if he would be prepared to prescribe antibiotics however he considered that was the task of the general practitioner.

McCauley agreed to provide a referral for a brain MRI to Mercy radiology however it wasn’t until approximately 10 days later that the referral was confirmed by the radiology group. I had requested a change to a head /neck scan however this elicited no response. He refers to the “ normal MRI brain scan of  February 2004” – although he did not allude to “a few minor type T2 hyperintensities in the white cerebral matter of no clinical significance”

An article from the Journal of th e American Heart Association dated September 2015 states: “There is strong evidence that (White Matter Hyperintensities (WMH) are clinically important markers of increased risk of stroke, dementia, death, depression, impaired gait, and mobility, in cross‐sectional and in longitudinal studies. They associate with brain damage such as global atrophy and other features of small vessel brain damage, with focal progressive visible brain damage, are markers of underlying subvisible diffuse brain damage,and predict infarct growth and worse outcome after large artery stroke.hey could be considered as the neuroimaging marker of “brain frailty”.

 I had requested a head/neck scan from McCauley however he has a requested a brain scan only. Although he had advised me that he would be onforwarding a request for the scan to radiology the day after the consultation there seemed to be a delay of approximately 10 days before it was received at Mercy Radiology.  A brain MRI was performed at Mercy radiology on 27 October 2015 by Dr Gerard Deib.  His report is as follows: “ Comparison none ( I provided  plates from the former MRI performed in 2004 to the radiographer however apparently they were not consulted by Deib). Diffusion weighted imaging not performed as there is a mechanical fault with the sequence.

Findings: There are a few small foci of periventricular  and subcortical T2 FLAIR hyperintensity non- specific in appearance likely due to cerebrovascular small vessel disease.  Dilated  perivascular space is  noted in the lentiform nucleus bilaterally.  No evidence of  focal  intracranial abnormality with no definite evidence of infarct haemorrhage or space occupying lesion. Mild to moderate enlargement of the extracerebral CSF spaces with commensurate enlargement of the ventricles.  Orbits and globes  unremarkable.  Mastoid air cells and paranasal sinuses are clear.  Orbits and globes are unremarkable .  No abnormal contrast enhancement .

Impression: Non- specific white matter change- Mild to moderate involutional change-No focal intracranial abnormality to account for patients symptoms

There was no subsequent communication or report from the neurologist Dr McCauley subsequent to the MRI brain scan.   In addition it would appear that there are additional areas of non-diagnosis:.  Image 90/176 from the MRI scan  (the superior saggital  sinus?) would seem to indicate a possible small thrombus ( inverted small triangle-“ the delta sign”).  Likewise a diagnosis of  leptomeningeal enhancement ( indicative of meningitis)  and diffuse enhancement of the pachymeninges  also evident, seems to be lacking.  Upon recent reappraisal a greyish/white slightly variegated lesion?/intracerebral haematoma?//abscess?  in the upper left is also evident.  This is not however apparent in the CT of the head/brain performed at NDHB in January 2018.

Timothy Hain MD advises that treatment for periventricular white matter lesions include:

Treatment: Control vascular risk factors — especially labile (variable)

 hypertension Pyridoxine (vitamin) supplement 

Migraine prevention treatment — especially “vascular” agents such as verapamil and beta-blockers

 Physical therapy — especially fall counseling –Adjustment of medications

RADIOPAEDIA: Leptomeningeal enhancement Dr Bruno Di Muzio and Dr Hani Salam:  Leptomeningeal enhancement refers to a diffuse or focal gyriform or serpentine enhancement that can be seen in the following conditions:

Diffuse

•         meningitis
  • pyogenic meningitis
  • viral meningitis
  • tuberculous meningitis(can also be focal)
  • CNS cryptococcal infection
•         encephalitis
•         leptomeningeal carcinomatosis(e.g. from carcinoma of breast or lung, melanoma, ependymoma)
•         haemorrhage (e.g. post-subarachnoid)
•        post uncomplicated lumbar puncture (rare, less than 5%) ²
•       granulomatous conditionsneurosarcoidosis(can also be focal)
•       post-operative (late finding)
•      post-traumatic (late finding)

Focal

• leptomeningeal carcinomatosis(e.g. from carcinoma of breast or lung, melanoma)
• post-ictal hyperemia
• infarction: subjacent acute (leptomeningeal collaterals) or subacute
• lymphoma
• meningitis(e.g. tuberculous)
• encephalitis
• neurosarcoidosis
• postoperative scar
• vasculitis 

 Radiographics advises “ Vascular causes of serpentine (gyral) enhancement include vasodilation after reperfusion of ischemic brain, the vasodilatation phase of migraine headache, posterior reversible encephalopathy syndrome (PRES), and vasodilatation with seizures (19–21). Serpentine enhancement from breakdown of the blood-brain barrier is most often seen in acutely reperfused cerebral infarction, subacute cerebral infarction, PRES, meningitis, and encephalitis. The primary distinction between vascular and inflammatory causes of the serpentine pattern of enhancement relies on correlation with clinical history and the region of enhancement. An abrupt onset of symptoms suggests a vascular cause, whereas a more indolent history and nonspecific headache or lethargy suggests inflammation or infection. Gyral lesions affecting a single artery territory are often vascular, whereas inflammatory lesions may affect multiple territories. The most common vascular processes affect the middle cerebral artery territory (up to 60% of cases). However, PRES lesions usually locaize in the posterior cerebral artery territory (21–27).

Meningitis is usually characterized as acute, sub-acute and chronic. In respect of gram-negative meningitis caused by  pseudomonas aeruginosa infections Medsafe recommends that “ a gram stain and culture of CSF if meningitis is suspected”   Medscape’s recommendation are : “ Ceftazidime or cefepime Alternatives: Aztreonam, meropenem, ciprofloxacin”

The Merck manual advises :  “The symptoms of chronic meningitis are similar to those of acute bacterial meningitis, except that they develop more slowly and gradually, usually over weeks rather than days. Also, fever is often less severe. Symptoms may last for years. Some people get better for a while, then worsen (relapse).

Headache, confusion, a stiff neck, and back pain are common. People may have difficulty walking. Weakness, pins-and-needles sensations, numbness, paralysis of the face, and double vision are also common. Paralysis of the face, double vision, and hearing loss develop when meningitis affects the cranial nerves (which go directly from the brain to various parts of the head, neck, and trunk)”.

ASK .COM: The function of the lentiform nucleus involved in maintaining the muscular tone of the body and assisting in controlling movement, mainly of the limbs of the human body. In addition is it involved in making find precision movements by reducing any extraneous or unwanted movements.  The lentiform nucleus is formed by a cluster of neuron bodies deep within the brain. It is composed of two distinct structures: the globus pallidus and the putamen. The lentiform nucleus is part of a larger unit known as the basal ganglia. The putamen is thought to have an additional role in memory formation, more specifically, muscle memory. When you are learning to ride a bike you are using your putamen. The globus pallidus serves to help make fine movements and inhibit abnormal movements. Damage to this structure can cause involuntary limb shaking like that in Parkinson’s patients.

EM CONSULTE: Involvement of the lentiform nucleus occurs mainly in association with toxic, metabolic and chronic vascular disorders.

RADIOGRAPHICS: West Nile fever typically demonstrates bilateral involvement of the thalamus and the caudate and lentiform nuclei 

WIKEPEDIA: Dilation is most commonly and closely associated with aging. Dilation of perivascular spaces has been shown to correlate best with age, even when accompanying factors including hypertension, dementia, and white matter lesions are considered.^[13] In the elderly, such dilation has been correlated with many symptoms and conditions which often affect the arterial walls, including vascular hypertension, arteriosclerosis, reduced cognitive capacity, dementia, and low post-mortem brain weight.^[6].^[6] When dilated VRS are observed in the corpus callosum, there is generally no neurological deficit associated. They are often observed in this region as cystic lesions with cerebrospinal-like fluid.

 Symptoms of dilation: Extreme dilation has been associated with several specific clinical symptoms. In cases of severe dilation in only one hemisphere, symptoms reported include a non-specific fainting attack, hypertension, positional vertigo, headache, early recall disturbances, and hemifacial tics. Symptoms associated with severe bilateral dilation include ear pain (which was reported to have resolved on its own), dementia, and seizures. This data was compiled from case studies of individuals with severe VRS dilation.^[6] Considering the anatomical abnormality presented in such cases, these findings were considered surprising in that the symptoms were relatively mild. In most cases there is in fact to mass effect  associated with some VRS dilation. An exception to the mildness of clinical symptoms associated with VRS dilation is when there is extreme dilation in the lower mesencephalon at the junction between the substantia nigra and cerebral peduncle. In such cases, mild to moderate obstructive hydrocephalus was reported in most patients. Associated symptoms ranged from headaches to symptoms more severe than those just discussed in the cases of dilation in the cerebral hemispheres.^[6] Other general symptoms associated with VRS dilation include headaches, dizziness, memory impairment, poor concentration, dementia, visual changes, oculomotor abnormality, tremors, seizures, limb weakness, and ataxia.^[2] These symptoms are also similar to those experienced in 2013 which were classified as a probable pre-syncopal attack /or Trans-ischaemic attack (TIA).

Radiopaedia.org: Virchow-Robin spaces (VR spaces) also known as perivascular spaces, are spaces surrounding the walls of arteries, arterioles, veins, and venules as their course from the subarachnoid space through the brain parenchyma.

These spaces do not communicate directly with the subarachnoid space but they are filled wit  interstitial fluid which behaves similarly to CSF in MR.

Dilated perivascular spaces consist of regular cavities containing an artery. The mechanism that occurs is not well known but there are many hypotheses in study. It s considered to be dilated when the size exceeds 2 mm visualized better in T2 weighted images. Rarely the size of the space is so large that produces mass effect on the adjacent brain parenchyma and it can cause hydrocephalus. The prevalence increased with aging, and in some cases this perivascular atrophy of ccerebral tissue, generates lacunae and is called “ etat crible”

There are no flow restriction in diffusion-weighted images and they don’t enhance after the administration of contrast material. The key to differentiate it from other pathologies is that VR spaces are hypointense in sequence FLAIR unlike other entities in the differential diagnosis.

Associated disorders: Dilation is a typical characteristic of several diseases and disorders. These include diseases from metabolic and genetic disorders such as mannosidosis, myotonic dystrophy, Lowe syndrome, and Coffin-Lowry syndrome. Dilation is also a common characteristic of diseases or disorders of vascular pathologies, including CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), hereditary infantile hemiparesis, retinal arteriolar tortuosity and leukoencephalopathy, migraines, and vascular dementia. A third group disorders typically associated with VRS dilation are neuroectodermal syndromes. This includes polycystic brains associated with ectodermal dysplasia, frontonasal dysplasia, and Joubert syndrome. There is a fourth miscellaneous group of disorders typically associated with dilation which include autism in children, Megalencephalopathy, Secondary Parkinson’s Disease, recent-onset Multiple Sclerosis and chronic alcoholism. Because dilation can be associated with several diseases but also observed in healthy patients, it is always important in the evaluation of VRS to study the tissue around the dilation via MRI and to consider the entire clinical context.^[6]

WIKIPEDIA:

Cerebral edema or cerebral oedema is excess accumulation of fluid in the intracellular or extracellular spaces of the brain. Signs and symptoms: Symptoms include nausea, vomiting, blurred vision, faintness, and in severe cases, seizures and coma. If brain herniation occurs, respiratory symptoms or respiratory arrest can also occur due to compression of the respiratory centers in the pons and medulla oblongata. Certain changes in morphology are associated with cerebral edema: the brain becomes soft and smooth and overfills the cranial vault, gyri (ridges) become flattened, sulci (grooves) become narrowed, and ventricular cavities become compressed.

Cerebral edema can result from brain trauma or from nontraumatic causes such as ischemic stroke, cancer, or brain inflammation due to meningitis or encephalitis.^[1]The blood–brain barrier (BBB) or the blood–cerebrospinal fluid (CSF) barrier may break down, allowing fluid to accumulate in the brain’s extracellular space.

Altered metabolism may cause brain cells to retain water, and dilution of the blood plasma may cause excess water to move into brain cells. Fast travel to high altitude without proper acclimatization can cause high-altitude cerebral edema (HACE)

Another consultation was scheduled with neurologist Alison Charleston on 10 May 2016.  I had emailed Ms Charleston with  copies of images and reports on 1 April 2016 which I  had hoped she would discuss at the consultation however she claimed she was unable to find them on her computer .  Receipt of the emails were confirmed by the receptionist Helen Kilpatrick  at the practice on 1 April 2016  “Thanks Vicki. Received both of your emails and I have passed these on to Dr Charleston.”

I  had advised Charleston that In adddition to a diagnosis of myalgic encephalomyelitis in 1988 by Dr Simpson in Dunedin  I also experienced a  stiff neck, slight memory impairment, and drowsiness in conjunction with a bout of flu in about the same year.. I subsequently experienced quite severe headaches requiring an ice pack.    In her report dated 10 May 2016 Charleston referred to “a bout of “ influenza in the late 1980s-she felt  unwell with a stiff neck headache and excessive drowsiness. She had memory lapses”.   These symptoms have been attributed to chronic fatigue syndrome”  These symptoms would more likely to have been be synonomous with meningitis as opposed to encephalomyelitis and have been on-going in subsequent years.

I produced two copies of images from the MRI brain scan of October 2015 one of which clearly indicated “leptomeningeal  diffuse or focal gyriform or serpentine enhancement”  Charleston glanced at the image and suggested that “ veins” might be the cause!  She did not discuss the MRI report.

In adults and elderly patients, bacterial meningitis symptoms may include the following:

• Sudden high fever.
• Stiff neck.
• Confusion
• Headache
• Drowsiness
• Irritability
• Stroke 

“Miss wilson describes a dull discomfort felt  at the top  of and back of  her head-the discomfort is constant  she had a normal appearing scalp and I could not identify any tenderness despite firm pressure. She was disappointed that I was not prepared to press hard enough to elicit it” . The cranial vessels were all normal, pulsatile and  non-tender and there was no meningism.  She had discomfort on rotation of  her neck and lateral bending.  The range of movement was restricted consistent with her age”.  She examined my head but like Dr McCauley did  not resort to firm pressure as I  had requested declining on the basis “ that she might hurt me”.!   “On neurological examination she had a somewhat flat effect with reduced eye contact but there was no definite hypomimia or bradkinesia.  Her speech was normal . Cranial nerve examination was normal  There was no drift  or tremor.  Muscle tone was variable.  Power, rapid alternating movements and co-ordination were normal.  Reflexes were present and symmetrical.  She had a strong withdrawal reaction to the plantar test.

 She walked a little slowly with a slight stoop.  However she was able to pivot turn and could tandem walk well.  Romberrg’s test was negative and she was able to stand easily  on either  leg with her eyes closed. Miss Wilson presents with symptoms suggestive of tension type headache.  The neurological examination does not suggest any underlying neurological disorder.  The very long  history is in support of a benign cause.  I think there is some degeneration in her cervical spine and  this  may be contributing to the development of discomfort  in  her head as the day goes on. 

Miss Wilson is very concerned about apparent abnormalities that she has identified on her MRI scan.   As promised I  have spent time reviewing the MRI scan in detail with the assistance of the skilled neuro-radiologists at Auckland Hospital.  I can confidently say that they found no evidence of raised CSF pressure, venous sinus thrombosis  or cerebral abscess.  The appearance Miss Wilson interpreted as  indicating leptomeningeal enhancement is normal appearance after the administration of contrast .  Dilated  perivascular spaces mentioned in the report are a normal finding . In addition her nasal sinuses appeared normal . In summary there are no signs that Miss Wilson is suffering  from a chronic meningitis.z”

The MRI  report clearly specified “ mild to moderate enlargement  of the extracerebal  CSF spaces and  commensurate enlargement of the ventricles  which could indicate “Hydrocephalus  a condition in which excess cerebrospinal fluid (CSF) builds up within the ventricles.  of the brain and may increase pressure within the head’:

I had suggested that  intercranial pressure (ICP) might be an  obvious issue and that  a prescription  of prednisone or an alternative medication  to help reduce any swelling might be in order.    Charleston didn’t think it was necessary nor did the general practitioners.

I had advised that there is excellent comparative imaging available on the internet however Charleston cautioned against too much reliance on “ Google”.  Her hourly fee was $430.00!

On 20 December 2017 I was hit on the head by a brass table in my storage unit. I have suffered from mild to moderate headaches and twinges since then.  A Ct of the head was performed  On 8 January 2018 at NDHB ED .  On 8 January 2018 ED Radiologist Albert Eshun advised that “neither skull fracture nor haemorrhage were detected” However after studying the video of the scan it does appear that at least a fracture is evident with a possible small haemorrhage . I  emailed the images to Dr Cameron HOD of ED Whangarei Hospital whose reply is detailed below:

13 February 2018

Dr  Scott Cameron

Emergency Department

Whangarei Hospital

 Dear Sir,

 I received a blow on the head from a heavy brass table in a storage on 20 December 2017. A CT of the head was performed at ED

Whangarei Hospital on 8 January 2018. The report by radiologist Mr Eshun clearly stated that there were no fractures . I have enclosed frames from the video which clearly show fractures as well as a nodule in the lateral ventricle in the brain. I am still afflicted with mild headaches.

 An MRI brain was performed at Mercy Radiology in October 2015 and again it appears that neither leptomeningeal enhancement (synonomous with meningitis) nor a posssible thrombus in the superior sagittal sinus region ( also an obscure grey area above the thrombus )were not reported. The reports are enclosed.

 There was no communication from neurologist Dr McCauley subsequent to the scan and a later consultation with Dr Alison Charlesworth was also non productive.

 Yours sincerely,

 Vicki Wilson

 Scott Cameron (NDHB) Feb 13 (2 days ago)

 Hi Vicki 

I am sorry to hear about your ongoing symptoms. Thank you for sending me all of this information. I have looked over the images and I do see some vascular channels and some arachnoid granulations (where cerebrospinal fluid is created), but I do not see a fracture. I am happy that your MRI was normal, and that the report and exam from Dr Charlesworth was reassuring, and I wish you a full recovery.

 Where there any ED issues that I can address?

 Cheers

 Scott cameron

HOD, ED

I visited North Shore Hospital on 6 May 2020 with a chest complaint. The result of a neurological test is as follows:  “GCS 15 ( eyes verbal and motor responses-maximum 15-fully awake patient-nil focal”

Subsequent to a request from my General Practitioner Dr Thorpe I was referred to the Neurology Department at  ADHB.   I emailed copies of relevant reports and images including the MRI images of 2015 to both Dr Bergin and Dr Anderson.  I also received a reply from Dr Wong.

On 1 September Dr Bergin advised via email: “Dear Vicki  I have read through the letters you have provided and the e-mail below.I do not think there is any point in your coming to see me, as I do not believe my opinion will differ from those of the other neurologists you have seen in the past.   Despite your ongoing symptoms, I do not think it is likely that you have chronic meningitis, and I would be very unlikely to recommend any further investigations.  Kindest regards  Peter Bergin”

 On 18 September Dr Neil Anderson advised that “ I have asked for the letters to be forwarded to the triaging neurologist.” 

On 24 September 2020 neurologist  Dr Wong stated  “Thank you for your recent referral letter. The department of Neurology is currently receiving many more referrals than can be seen. Some patients cannot be seen at all, and some must wait many months to be seen, which delays treatment. Your referral has been triaged by two neurologists to a Non-contact Consultation. This means we have not arranged a clinic appointment, but instead provide the following advice based on the information in the referral letter. If Vicki Wilson’s condition is not addressed by the advice below, or if there are further developments please send a new referral letter and we will re-triage accordingly. You referred Vicki Wilson, a 71-year-old woman with a long history of headaches and head pains, which affect her memory. She fell and struck her head in 2012 and there is a possible history of meningitis. She had an MRI scan in 2015 at Mercy MRI and a CT scan in 2018 at Whangarei Hospital. Subsequently she had contacted our department by e-mail. She outlined a number of her concerns primarily regarding failure to report/pick up a skull fracture, a meningeal disorder including meningeal enhancement, a superior sagittal sinus thrombosis, and bleeding in the brain.

I have reviewed her MRI scan from 2012 and a CT scan from 2018 at our Neuroradiology meeting. The MRI brain scan and CT brain scan are normal for her age. There is no evidence of a skull fracture, meningeal enhancement or any other meningeal disease process, brain haemorrhage/bleed, or thrombus in venous system. Hence, we can confidently reassure Vicki Wilson that her two brain scans are normal and allay her of her concerns about missed diagnoses?. She included copies of her consultations with Dr McAuley, Dr Charleston, and Dr Willoughby in her e-mail. There is also a reference to an assessment by Dr Snow but a report was not included in her e-mail. She has been seen by three, possibly four, neurologists. I do not think there is anything further that our review will add to the reassurance we can provide after reviewing her brain imaging with a neuro-radiologist.   Yours sincerely Edward Wong Neurologist Department of Neurology “

I think Dr Wong has ignored salient facts concerning abnormal aspects of the MRI brain scan of 2015 which are evident in copies of the images extracted  from the MRI brain scan of 2015  and attached to the email.  ( See Facebook).  He has however left the way open for a re-referral.

On 8 December I received an email from Consumer Liaison ADHB:  “In respect to the email below the service has reviewed your  and they advise that from reading of the two GP referral letters 11/8/20 and 24/11/20 as well as your correspondence, your symptoms remain the same as those assessed by Dr McAuley and Dr Charleston.Given the chronicity and nature of the symptoms, normal brain imaging and two prior neurological assessments, the service does not believe further neurological assessment is likely to be beneficial.   However, please be reassured that if you are experiencing new symptoms then it is appropriate for you to see your GP.  The nature and duration of the new symptoms, along with relevant clinical findings, shoul”d be conveyed in a further referral letter.I   trust this information is helpful.

Kind Regards

Donna Deans
Consumer Liaison Coordinator, Clinical Quality & Safety
Auckland District Health Board” 

 A reply from Dr Kilfoyle neurologist dated 9 December 2020 is detailed below:

“Thank you for your referral letter dated 24 November. I have reviewed your referral letters of 24 November and 11 August. I have also reviewed email correspondence sent by Vicki to Consumer Liaison. From my reading of the referral letters and this correspondence, the symptoms are similar to those assessed by Dr McAuley and Dr Charleston. Given the chronicity and nature of the symptoms, normal brain imaging (we do not agree with the patient’s assertion that the MRI is abnormal) and two prior neurological assessments, we do not think that a further neurological assessment is likely to be beneficial. If there are new symptoms the nature and duration of the new symptoms, together with the relevant clinical findings should be conveyed in a further referral letter from the patient’s general practitioner. We do not believe       that the MRI in 2015 requires further investigation after reviewing this carefully in our combined               neuroradiology conference. Yours sincerely Dr Dean Kilfoyle Neurologist Auckland City Hospital”

 On 18 March 2021 GP Dr Thorpe agreed to request a consultation with Dr Snow at ADHB. Upon a subsequent enquiry I was advised by the scheduler that the referral had once again been placed in triage It is unclear whether the referral reached Dr Snow as I was advised by the scheduler that the referral had once again been placed in triage .I have received further advice of another rejection provided on this occasion by way of a letter dated 12 May 2021  from Neurologist  Dr Bose.

THYROID

In 1999  investigations were initated with  Dr Simpson of Epsom with regard to thyroid function. “The initial tests showed borderline elevation of the free T4 and a low TSH  and low titre antibodies..  The latter were not associated with a corresponding high T3 and were not considered to be necessarily representative of throtoxicosis..The accompanying serological investigations showed a raised rheumatoid factor –with the immunoglobulins, CRP and CSR as normal.  There was a suggestion that positive rheumatoid serology and low titre ANF  might be suggestive of a connective tissue disorder. An assessment of thyroiditis was made at this time.  No further investigations were undertaken at this time”

As a result of a consultation with a haematologist on April 04 further thyroid tests were undertaken resulting in the following results: ‘ Thryoglobulin antibodies  Negative (up to 1: 100) // Microsomal antibodies 1:100 ( up to 1:100) – small increase in auto-immune thyroid antibodies.”

 Thyroid antibodies are found in 90-100% of cases of thyrotoxicosis. Antibodies are present in less than 20% of cases of non-toxic goiter or thyroid tumour and fewer than 10% or normal persons.

Free T4: 22.0 pmol/l ( 10-24)
TSH 0.004 units/ml (0.4-4.0)
Free T3 5.1 pmol/L (2.5-5.5)

An ultrasound of the thyroid of April 2004 indicated ‘that both thyroid lobes were of normal size. Both showed slight heterogeneity of echotexture  Anteriorly in the midpole of the region of the right lobe there was a small hypoechoic nodule of 5 x 3 mm which showed no significant internal vascularity.  No other focal abnormality was seen in the right lobe. In the left lobe a smaller 2-3 mm hypoechoic area is also seen.  No other focal abnormality detected.  The isthmus was normal and no significant lymphadenopathy detected.  It was suggested that a follow-up be undertaken with regard to the hypoechoic nodules.  Subsequent to examination by Dr Orr-Walker my condition was described as  “thyrotoxic with mild resting tremor and tachycardia  of 90 /minute/  . The diagnosis also referred to moderate proximal myopathy.  There was no dysthyroid eye disease, with normal  examination of visual acuity, eye movements and fundoscopy .  The thyroid was normal to palpitation with no tenderness nodularity or bruit.  There was no lymphadenopathy. The diagnosis was thyrotoxicosis.and carbimazole was prescribed”

In June 2005 Orr Walker described the thyroid as being “minimally enlarged and clinically was not nodular”. There were no bruits”. Treatment with carbamazole was reinstituted in December 05. and I have continued with a daily dose of 10 mgs.  On 17 January 2012 Diagnostic Medlab reported “the free T4 as 12.8 and the TSH as 1.4  which are within the normal range.”

 In his report dated 19 February2008 Dr Orr Walker advised that “ the thyrioid is only mildly  enlarged fleshy with no palpable nodules. I think she would be a satisfactory candidate to proceed to surgery”  I advised him that I would be prefer the operation to be undertaken under the public health system however I decided against the procedure.

6 March 2017 Consultation with physician Nicole McGrath of Northland DHB’s  Endocrinology Department. Dr McGrath advised  “ that my weight was 65 kg heart rate 76 per minute regular and blood pressure 134/75.  She appeared clinically euthyroid.  The thyroid gland was not palpable. It is most likely  that Vickis thyroid nodules are incidental and of no clinical significance however given her obvious concern about this and the fact follow up was recommended I will request a thyroid ultrasound scan.  We talked today about thyroidectomy but really if she is tolerating Carbimazole well that seems to be the best treatment for her.   I  have not arranged to see Vicki again myself  in clinic and will leave the follow up to Dr Henderson.”

Thyroid function tests undertaken at Northland Pathology on 25 September 2017 were essentially normal with the exception of the TSH which was assessed “ as borderline low-sometimes temporary recovering from illness-repeat in several months”

Free T4   pmo1/L  13.8 ( Range 10.0-20.0)  TSH  Miu/L  4.5*  (Range  0.30-4.00)

Thyroid Function Tests dated 14 May 18 indicated TSH levels : 4.5* (25/9/18)  7.0* ( 23/3/18 ) 4.2* ( 11/5/18

If  on treatment dose /compliance review may be appropriate . A test dated 30 October 2018 indicated a normal TSH of 3.1 consistent with euthyroidism. TSH is again elevated at 4.4 on 6 May 2019. The only abnormality in the thyroid test dated 1a Free T4 reading of 11.00 ( ref range 12.00-22.0 // TSH 2.9 (0.30 – 4.00)

Thyroid function tests undertaken at Northland Pathology on 25 September 2017 were essentially normal with the exception of the TSH which was assessed “ as borderline low-sometimes temporary recovering fIn rom illness-repeat in several months”

TSH Miu/L (Ref range 0.30-4.00)*=H   4.5*25/9/2017 // 7.0*23/3/2018//  4.2*11/5/2018// 4.5*25/9/2018 ////3.1 30/10/2018/ /4.4*6/5/2019///  2.9 11/12/2020///4.7*18/2/2021

Free T4 MiU/L (ref range 12.0-0-22.0)  13.8 ( 25/9/2017///12.7 23.3.2018//12.5 11/5/2018///12.4 6/5/2019/// 11* /11/12/2020////12.6 18 /2/021

Continued borderline elevation of TSH.  If on treatment dose/compliance review may be appropriate .

ORTHAPAEDICS 

In 1999 an  x-ray ( RADSPEC)  of the spine and hip indicated ‘a moderate lumbar roto-scoliosis convex to the left. There was severe intervertebral disc degeneration at L5/Sl.. The other intervertebral articulations appeared well preserved.  The sacrociliac joints symphysis pubis and hips were normal .  No bony destruction was detected.”  A whole spine  (chiropractic-Auckland Radiology) undertaken in September 1999 reported “a minor scoliosis of the lower thoracic spine convex to the right and centred at T11/12.  There was no underlying cause. In the lumbosacral spine a marked reduction in height was again noted in the L5/Sl disc together with degenerative endplate”.

In November 1999 a left hip ultrasound ( ADHB) was undertaken as a result of extreme discomfort extending down the thigh. “A moderate amount of fluid was noted within the greater tronchanteric bursa on the left with increased blood flow in the peribursal tissues consistent with inflammatory changes and synovitis. The right tronchanteric bursa was normal in appearance without any evidence of inflammation or fluid. No abnormality was identified scanning down the iliotibial band to the knee joint. The diagnosis was significant left greater tronchanteric bursitis.”

A 2003 x ray report( Mercy Radiology) of both feet advised thus:  “ Indication of joint pain and swelling – Bone density and alignment are normal. There is no evidence of peri-articular erosions.  The joint spaces are well preserved.  No underlying bone abnormality is shown.” An enlarged bony growth on the inside of the left foot ( a probable bunion) was however  clearly evident but was not reported

In 2006 I appeared to have a broken toe on the right foot. .  The end of the toe had suffered a severe blow and was swollen and painful for some months. The female practitioner Dr Henrys recommended that I strap two toes together .  She did not examine the toe.  According to the American National Institute of Health  “buddy taping” of a broken toe is not always appropriate.   Neither an x-ray nor a specialist’s visit were suggested. At my instigation an x- ray was requested-and the accompanying  report from Auckland Radiology  advised  “that there was no evidence of any fracture or other abnormality”  The radiologist advised  “that we are aware that some  fractures are not  evident on x-ray- MRI scans demonstrate many fractures which are not evident on x-rays alone”

An x ray of  the thoracic spine was performed at Greenlane Radiology on 11 May 2011.  Findings were as follows:  “ there is normal alignment . There are no fractures or destructive osseous lesions. Vertebral body and intervertebral disc heights are maintained.  Minor anterior marginal osteophytes are present at T8 and at L2”   Quite dense patchy opacities  (also cavities??)  also seemed to be evident in the x ray but were not referred to in the report.

On  16 August 2012 I suffered a fall down some concrete steps and banged my head on the right side against the adjacent  brick wall . The female general practitioner considered that the small haematoma on the head and discomfort on the right side of the head was considered to be better left alone.   A CT scan was not deemed appropriate at this time based on my lack of significant symptoms since the accident a week earlier.  A skull x ray dated 24 August 2012 ( Auckland Radiology) reported “ No fracture is seen. Alignment is normal. Aeration of the paranasal sinuses is normal’    

The scan showed both the rear and front views of the skull with two duplicate images of the left lateral. . Subdural haematomas are always a possibility particularly in the elderly and can develop days or even weeks after after a head injury.

There was also extensive bruising at the base of the spine, the bursa and on the right buttock with accompanying swelling and haematoma .( Haemorraging from the gluteal artery can very occasionally be a concern) .    I attended a female general practitioner Dr Anna Thwigg  on 24 August 2012 . There was a cursory visual check of the buttock a but no general examination. If there is no reduction in swelling syringing of the area can sometimes be a consideration however the practitioner didn’t seem to be in favour of this course of action. There was no referral for a lumbar scan. I did also develop pain in the left lumbar area extending down the left leg but managed to rectify this with a home massage unit.

Ultrasound of the right buttock . An ultrasound of the right buttock at Auckland Radiology on 24 August 2012 reported:

Indication: “Haematoma secondary to fall on concrete Findings: extensive soft tissue bruising and palpable mass-there is a complex cystic lesion…measuring 78 x 28 x.83 mm with a volume of 96 mls. The mass is 6mm deep overlying the gluteus maximus muscle..no vascularity demonstrated  no collection seen in the underlying muscle…..appearance consistent with a large subcutaneous haematoma.”

Much of the severe bruising has disappeared due to the use of hirudoid and arnica creams. An orthopaedic specialist Mr Hucker syringed the haematoma on 14 September however by January 2013 most of the swelling had subsided although there was still some soreness if pressure is applied.

Neurologist Willoughby’s report dated 5 February 2013 advised : “a slightly reduced left knee jerk.  The plantars were flexor.  Sensation was normal except for mild  impairment of vibration in the toes  (of no particular significance)”

An x ray of the left knee was performed on 10 September 2014 at NDHB.  Findings: “There is mild osteoarthritis of the medial compartment. No fracture or focal bony lesion”

I attended North Shore Hospital’s ED Department with a chest complaint on 6 May 2020.  Subsequent to investigation  there was“ no leg pain or swelling”

X-ray Knee North Shore Radiology 17 September 2020

No previous imaging available for comparison. Findings:  moderate reduction in joint space in the medial compartment with mild changes in the medial aspect of the patellofemoral compartment. The lateral compartment is spared. No joint effusion. Normal alignment. No fracture.

Radiologist: Nina Umaria

An ultrasound of the left shoulder and arm was performed at TRG Radiology on 29 September 2020

SHOULDER (LEFT) ULTRASOUND

INDICATION

Pain going down the arm particularly when reaching back

FINDINGS

Long head of biceps: Intact. Subscapularis: Intact.Supraspinatus: Intact. 

There is a moderate insertional enthesopathy posteriorly.  
Infraspinatus: Intact Teres minor: Normal
Suprascapuar notch and spinogienoid notch: Normal.osterior glenohumeral joint: Normal.

Acromioctavicular joint:There is capsular thickening. on-tender to probe guided compression,Coracoacromial ligament:Normal. Subdeltoid bursa and dynamic imaging:                                        

Bursa:Mildly thickened.

Dynamic imaging: There is a painful arc commencing at 120 degrees There is mild bursal bunching during abduction.

CONCLUSION: Borderline thicken ing of the subacromiail bursa raises the possibility of early bursitis. if clinically’ relevant an ultrasound guided steroid injection can be offered. * No high-grade rotator cuff-tear detected.

Dr Franco:s Du Toit, Radiologistn

Tracie Phillips Sonographer

TG Imaging

 INDICATION
Painful left
arm and shoisulder.

FINDINGS

Mild sclerosis of the greater tuberosity.

No soft tissue mineralisation.

Glenohumeral  and  AC joint is congruent.

No destructive bony lesions.

Partially included chest is clear

GYNAECOLOGY 

In 1988 I attended a well-known female gynaecologist Dr Liggins who, subsequent to examination, advised that there was nothing significantly amiss..  I had suffered years of pain.  At the sole  instigation of my own  General Practitioner Dr Harries an ultrasound was performed  and a large uterine fibroid was discovered.8 showed a “large well-defined mass of around 8 cms in diameter with slightly heterogeneous echo texture. It appeared to arising in the right side of the uterus and was considered to be a large uterine fibroid.  Both ovaries appeared normal.  No free fluid was shown in the pelvis and the bladder appeared normal”. 

 Subsequent surgery in May 1988 by Dr Liam Wright at Mercy Hospital Auckland resulted in “a laparotomy which revealed a large fundal fibroid and a smaller one in the anterior wall. The right ovary was quite densely adherent to the back of the uterus with endemetriosi and there was a small endometriotic cyst. The left ovary was normal except for 2 tiny black dots. The latter may have been endometriotic or were perhaps the site of previous follicles. They were treated with diathermy. The remainder of the abdomen and pelvis were normal to palpitation.  A total hysterectomy and right salpingo oophorectomy were performed.   There were no complications.”

 In 1991 I experienced severe pain and contractions in the groin area in both the left and right sides after severe exertion. .  I subsequently was admitted to day surgery for an E.U.A. and diagnostic laparoscopy  performed by Professor Ron Jones–the report stated   “limited E.U.A. failed to reveal any abnormalities.  The left ovary appeared normal –and there was a a loop of small bowel adherent to the stump of the right ifundibulo pelvic ligament . There was no evidence of an obstructive element .”  I was reassured by the nurse that I might experience a little pain after the procedure  however I experienced very severe pain extending from the groin to the shoulders over a period of months! The gynaecologist jokingly commented that “ he had trampled over my insides with his boots on”!

A pelvic ultrasound was undertaken  in April 2003. . “The left ovary was described as being of normal size with a volume of 8.3 cc.  Arising from the ovary was a small oval unilocular simple cyst ( 2.4 x 1.4 x1.3/2.3 cc).  There were considered to be no significant findings nor there was any mass lesion or free fluid identified elsewhere in the pelvis.”  A subsequent scan of 15 February 2005. performed  at Green Lane Radiology from  advised “the left ovary was visualized and measured 19mm x 19mm x 15mm giving a volume of 3cc  No ovarian cysts were evident.  There was a large amount of adjacent fluid-filled bowel.  No free fluid .  There was no evidence of any cysts”

Tests undertaken in Jan 02 for LH FSH Oestraadiol and progesterone ( Post –menopausal) all seemed to be within the normal limits. A carcino-Embryonic Antigen test in April 03 also seemed to be within the normal range at 0.6 ( range 0-3.0)

 A pelvic ultrasound was performed at Ascot Radiology on 22 March 2012.  Findings:……… “Surgical abscence of the uterus is noted  Neither ovary is identified and no mass or free fluid is detected. The kidneys are of normal size shape position and echotexture.  The right kidney is 10.2 cm in length the left kidney at 10.8.  Summary:  Appearances are within normal limits with no sinister pathology.” The radiographer was of the opinion that an alternative type of pelvic ultrasound might have been more appropriate in respect of visualising the remaining left ovary however ultrasound scanning of the left ovary in 2003 was apparently achieved without any difficulty.

MAMMOGRAPHY:

 I have a 30 year history of breast fibroadenomas beginning in 1973 with the removal of an “ intra canalicular fibroadenoma in the right breast” in the USA. In November 1985 another fibroadenoma was removed from the right breast  at Wellington Hospital  – “ an irregularly nodular smooth surfaced lump of grey/white tissue measuring 1.6 1.5 x 1cm –sections show a fibroadenoma of intracanalicular type.  Several foci of aprocrine metaplasia are present within the adenoma.  A small amount of adjacent breast  tissue shows fibroadenosis”.  An Auckland Hospital Histopathology  report dated 3 July 1997 concerning a fibroadeoma in the left breast reported    ‘the mammogram suspicious”   I was not aware of that diagnosis until approximately a year later when I managed to obtain a copy of the report. 

 The same fibroadenoma  measuring 30 x 28x 24 mm  was removed from the left breast at Auckland Hospital  by surgeons (Hamil and MacCormick) on 3 July . It was described as “ a circumscribed and lobulated mass 30’ x 28’x 24’with a small amount of attached fatty tissue. The cut surface is firm and yellowish grey with small foci of haemorrhage…..there is no atypia or malignancy” (foci of haemorrhage and necrosis are sometimes associated with malignant Phyllodes tumour).  In 2003 a large cyst measuring 11 mm in the left breast was aspirated and produced 2 mls of yellowish fluid. In 2004  2 fibroadenomas were diagnosed in the left breast one measuring 10 mm and the other 5 mm. A solid isoechoic mass measuring 5 mm was also diagnosed in the right breast.

 24  October 2002 a breast ultrasound was performed by Margaret Adams of Mercy Radiology:“In the right breast in the 6 o’clock position just below the nipple there was a reasonably well defined mass of homogeneous low echogenicity  with some posterior shadowing measuring 5 x 7 mm which was consistent with a small adenoma.  In the 11 o’clock postion and adjacent to the nipple there was a small cystic mass ( 5 x 5 mm) with some internal echoes but through transmission.i.e. a small cyst. In the left breast there was a cyst measuring ( 14 x 10 x 14.5 mm )which was well defined –had good through transmission but contained internal echoes. This was in the 12 o’clock position again adjacent to the nipple.  There were smaller areas of uniform echogenicity with well defined borders and poor through transmission one measuring (8 x 10 x 3 mm)  and a small mass with identical characteristics measuring (6 mm. ) The latter were consistent with small fibroadenomas. There was recommendation of confirmation of benign histology by biopsy.”

Ultrasound of the breasts at the Mercy Breast Clinic in April 2003 showed “ a (3-4 mm )rounded cyst at the 11 o’clock position in the right breast.  In the 6 o’clock position there was an ovoid (5 mm) hypoechoic lesion possibly commensurate with a small cyst or adenoma. On the left side there was a cyst in the the 2 o’clock position measuring about( 11 mm) in diameter.  This was considered to be smaller than an earlier measurement.  The remainder of the breast looked normal to ultrasound review.A resulting aspiration of the large cyst in the 2 o’clock position on the left side resulted in a couple of  mls of yellowish fluid.  The lab report indicated a number of foamy histiocytes and lymphocytes consistent with a benign breast cyst”’

A mammogram and ultrasound  were  performed at Auckland Hospital in September 2003. “A small well defined lesion in the right breast just below the areola  was described as unchanged  as well as the 2^nd adenoma.  A small nodular lesion in the left outer breast was in keeping with a small intramammary lymph node.   In the right breast there a small oval isocheoic lesion at 6 o’clock .measuring 7 mm in size . 2 small cysts were noted at 11 12 o’clock measuring 4mm and 2mm in size.  Ultrasound of the left breast showed small cysts at 12 o’clock measuring 32mm and 4 mm respectively. 2 small ovoid lesions are seen at 12 o’clock deep to the areola measuring 6 and l0 mm.”   There was considered to be no significant interval change-2 yearly mammography was recommended. 

A bilateral breast ultrasound : Auckland Hospital on 14 October 2004 reported thus: “ In the left breast just superior to the nipple there is an ovoid 10 x 3 x 7mm solid benign appearing mass with a thin echogenic capsule and posterior through transmission.  Just to the right of this is a second solid lesion with similar characteristics which measures 5 x 2 mm . Also in the left breast around 11-12 o’clock there are two tiny cysts each measuring 3mm.  In the right breast there s a solid isoechoic mass at the 6 o’clock position a couple of centimetres inferior to the nipple. This is difficult to discern from the surrounding tissue as it is isoechoic to the adjacent fat.  It measures 5 x 4 x 5 mm.  In addition two 3 mm cysts are noted in the upper outer quadrant of the right breast”

I have previously had  a lengthy discussion with Dr Ng of the Greenlane Breast Clinic  concerning the removal of breast adenomas.  He advised that if they keep increasing in size then biopsy might be considered.   The NIH(National Institute of Health)  USA advises “ that most surgeons prefer to remove fibroadenomas to make sure they are benign. Excisional biopsy which is similar to  lumpectomy is currently the standard procedure for lumps that are smaller than an inch or so in diameter.  Not every lump  merits a biopsy –however, regardless of the fact that benign lumps rarely turn into cancer, cancerous lumps can develop near benign lumps and can be hidden on a mammogram.  Even if you have had a  benign lump removed in the past it cannot be assumed that any new lump would also be benign”

A breast ultrasound: Auckland Radiology in Kepa Road Mission Bay on.4 June 2009. During the course of the scan I advised the radiographer that I had inadvertently omitted to bring copies of the previous ultrasound reports and film. I did advise her that the most recent ultrasound was performed at Auckland Hospital in 2004 and I could email the report to Radiologist Ms Peart if necessary. However in her report dated 4 June 2009 radiologist Ms Peart advised “that previous mammograms from 2003 and 2005 and ultrasounds from 2003 and 2004 are available for comparison. There are no reports” 

 The only reported finding was “a  single  7 x 2 x 6 mm well circumscribed ovoid focal lesion in the right breast which has appearances most in keeping with a small intramammary lymph node.–no other focal or cystic sonographic abnormality is identified in either breast.

 This fibroadenoma of approximately 5 mm  was previously identified in a  Mercy Radiology’ report of 24 October 2002 together with   “two smaller areas of uniform echogenicity measuring 8 x 10 x 3  mm  and 6 mm respectively  with well defined borders and poor through transmission ….consistent with small fibroadenoma”.  These findings were further confirmed in an ultrasound report from Auckland hospital dated 14 October 2004-the 2 fibroadenomas in the left breast were described as having “posterior through transmission”

 In recent years the  only surgical procedures  have involved a 3cm fibroadenoma which  was surgically removed at Auckland Hospital in 1997 and a large breast cyst was drained at the Mercy Breast Clinic in April 2003 by Mr Cotter.   I requested an explanation from Ms Peart as to the  significant non-reporting of fibroadenomas in the left breast. Ms Peart advised “ that the sonographer did relay to me that you had previous breast cysts and fibroadenaomas with surgery for these and that she had looked very carefully for any solid lesions and failed to identify any other than those described above. ‘She also advised me that you had offered to make the reports of the previous imaging available to us. However as no sonographic features of any concern had been seen I felt that this was unnecessary.  With respect to the significant non reporting of fibroadenomas …..in the left breast these were not visualized on this study and therefore I could not describe them in the report .  There are two likely reasons that we did  not identify on ultrasound as they are very mobile and often move away from the transducer.  Thus it is possible that they remain there but we did not visualize them as presumably happened in the ultrasound in 2003. However fibroadenomas also involute over time and they may have decreased significantly in size or resolved completely since the most recent previous scan in 2004”.

Previous ultrasound scans of 2002-2004 did not encounter any of these difficulties with regard to  “visualizing”of  fibroadenomas. The ultrasound report  of the  Mercy Breast Clinic dated 24 April 2003 reported  “ on the left side there is a cyst in the 2 o’clock position measuring about 11 mm in diameter. The additional  annotation that   “The remainder of the left breast looked normal to ultrasound review” omitted any reference to the fibroadenomas.  Bearing in mind that the  reported  “visualised” fibroadenoma in the right breast had actually increased in size, the likelihood of the fibroadenomas having disappeared from the left breast is very remote. Diagnostic descriptions of fibroadenomas in the left breast have ranged from “a suspicious mammogram, to poor and posterior through transmission”. The reason provided concerning the ability of the fibroadenomas to move away from the transducer seems rather dubious.   The blatant failure to scan fibroadenomas is nothing short of negligence and is further compounded by the fact that clarification by way of a further investigative scan was not requested by the radiologist. It also raises questions as to whether similar failures have occurred in respect of other types of scans (e.g. CT scans of the lungs).

A recent bilateral breast ultrasound undertaken by the Horizon  radiology group  in August 2010 reported “ no fibroadenomas seen and multiple small cysts  seen throughout both breasts” !

I consulted with  the Director of  both Radiology and the Breast Clinic at public hospital on 3 February 2011 subsequent to A bilateral mammogram and breast ultrasound was performed at public hospital in February 2011. The consultant was Dr Ng. 

.The report of February 2011  is as follows: ‘Findings:  bilateral mammograms are stable in appearance with symmetrical mildly dense breast parenchyma with no suspicious masses microcalcifications or distortion.  The bilateral benign appearing masses are unaltered in size and number.  In the right breast the benign appearing 6 o’clock mass remains stable measuring 4 x 5 mm  (previously 4 mm).  No internal  vascularity demonstrated.  In the left breast the 12 o’clock benign appearing mass measures  11 x 3 x 8 mm( previously 10 x 6 mm).  No internal vascularity.   A 5 mm ovoid anechoic cyst is noted more superiorly.  Interpretation: stable mammographic and ultrasonographic appearances of the bilateral benign masses.  No evidence of malignancy.” This report omitted to mention a second solid lesion which measured  5 x 2 mm in 2004 also located in the left breast.

I later discussed the possibility of obtaining a dvd/cd of the scan with the receptionist who rather belligerently demanded to know why I would want it and what I intended to do with it !

 In 2011 it was agreed to surgically remove the fibroadenomas at public hospital in the near future depending on my health.   In the interim my latest chest x ray was also requested.  I discussed the matter of the disparity between the lack of diagnosis of fibroadenomas in the breast ultrasounds by two alternative private radiology groups in comparison with the findings of both public hospital and one other radiology group. I expressed my concern that it could have wider implications for other patients. . Dr Ng demurred and felt it was not within his jurisdiction to pursue the matter further unless perhaps a cancer was involved.  He suggested that I take the matter up personally with the Directors of the other Radiology groups.  The surgical removal of fibroadenomas had been delayed pending the completion of the course of antiplatelet   clopidogrel medication prescribed after arterial stenting.  A further consultation at public hospital is scheduled for February 2013.

On 11 August 2011 Surgeon Dr Puttick advised my former General Practitioner Dr Retford : “Your patient was unable to attend a follow-up appointment in the Breast Clinic today. From reviewing her notes she is on the list to have some breast lumps removed, but in the interim she has had some cardiac issues and is awaiting coronary artery bypass grafting. This is obviously more pressing that the breast problem and we would not proceed with general anaesthetic for a breast problem without the cardiac issues being sorted out first. We will send her an appointment to see us in six months’ time when hopefully things will be looking a bit better. I also note that she is seeing the dermatologists about some skin lesions and we could discuss these with her if she still wishes to have them excised, perhaps at the same time as her breast lumps, as we do quite a lot of skin surgery.

Kind regards .Yours sincerely Mr Michael Puttick MBBS MD FRCS (General Surgery)Breast and Endocrine Fellow to Messrs. Jones, Cranshaw, Ng & Prof. Shaw 021842940

I did not take up Mr Putticks offer as I was awaitng heart stenting procedures 

 A bilateral  mammogram and ultrasound were again performed at  public hospital on 15 March 2012.  Findings: “ comparison is made with previous mammogams of 2/11.  There is no significant interval change.  The breasts  are of mixed density   A small benign appearing nodule  in the central right breast is stable .   Other benign appearing densities  mostly skin lesions are also stable.  No new focal masses, areas of architectural distortion or suspicious microcalcifications are detected.   Bilateral ultrasound shows two small benign appearing masses in the left breast close to the nipple at 12 o’clock .  These are a few mm apart from each other and measure 9 x9 x3 mm ( previously  11 x 8x 3 mm) and 5 x 4 x 2 mm ( previously not perceived ). No other left breast abnormality is seen-the small cyst noted last year is not evident. In the right breast the lesion at 6-7 o’clock near to the nipple is stable at 5 x 4 x 4 mm ( unchanged).  Another subtle mass at  11 o’clock  measuring  5 x 3 x 3 mm is also likely to be a small fibroadenaoma and is benign  in appearance.  No other abnormality is seen. 

CONCLUSION:  No evidence of malignancy.  The two lesions seen last year are stable.  The Mammogram is stable.  A further lesion in each breast is seen today neither of concern-scans from year to year will vary due to different sonographic technique.”

I visited the breast clinic at Greenlane clinical centre on 25 february 2013.  I was first appraised by a young Asian female  registrar who also performed a breast examination She had Dr Ng’s report dated 22 March 2012 in which he advised “ that if she wishes to proceed with surgery then she can be assessed by the anaesthetists”.  Surgery had  initially been delayed until I had  completed a course of clopidogrel medication prescribed after a stenting procedure in late 2011.

The registrar however did not have the Radiology report dated 15 March 2012-I provided her with a copy!.  She was unable to detect any fibroadenomas and there was no discomfort during the examination.  A further examination was performed by an Indian specialist which caused quite severe discomfort and the the obvious  “tenderness” was noted.   I have now been rescheduled for surgery in the near future.

A referral was made to the Breast Clinic Whangarei in 2014 by Dr Henderson of Onerahi however apart from a phone call from a nurse querying whether I retained any reports a consultation never eventuated.

Subsequent to a referral from Dr Henderson to the Breast clinic at Whangarei hospital a reply was received from Dr Usha Shan breast surgeon:  “ I appreciate this is a very difficult situation for you. I have discussed with the breast team including  colleagues involved in screening and diagnostic services.  We have reviewed your referral and the Auckland clinic letter from Mr Ng and the consensus is that there is no indication for her to be seen in the breast clinic.  We have lack of resources, no capacity and a long waiting list for symptomatic patients.  It is very common to find incidental fibroadeonomas ( no palpable) on screening mammograms.  The standard treatment for non-palpable fibroadenomas is for observation and this is done at the time of 2 yearly mammogram via free breast screening program.  She had the option of seeing a private surgeon.”

A mammogram was performed at Mauri Ora mammography on 17 January 2017. .  A report from Dr Jenny Walker clinical Director of Breast Screen Wiatemata Northland advised “ No evidence of cancer.”  In one frame a small bright line extends under the breast . When it is magnified a dense cotton wool type of infiltrate/opacity is depicted in the chest wall possibly extending into the breast.  

 On 8 June 2017 NDHB radiologist Dr Dawber advised “ I am unable to comment on the Mercy Radiology MRI and the Mauri Ora Breast Screen mammogram and would advise you to contact them if you require any further information”  On  4 July 2017 Director of Waitemata DHBs respiratory clinic Dr Cornere advised: “ I am sorry I can’t be more helpful but I have absolutely no experience in interpreting mammography Hopefully you will get a reply from the radiologist and breast physician who should be able to assist as they have the expertise.”  As at 8 April 2018 I have not received any clarification.

An email requesting further advice with accompanying images was sent to Breast surgeon Dr Shan on 8 June 2017 but there was no reply from either Shan or radiologist Dr Shepherd  of Mauri Ora mammography .

 Ms Susan GERRED General Surgery Waitemata DHB

Copy To GP Dr Audrey Thorpe

Re. WILSON, Vicki NHI: GRD8664 DOB :02/07/1949

Exam performed at: North Shore Hospital Radiology Date of exam: 21/07/2020  Examination (s) included in this report: Mammogram Clinical Bilateral US Breast INDICATION: For follow—up of previous for breast fibroadenoma  

FINDINGS : Comparison is made with previous mammograms of at 2019 and 2012. There is no significant interval change.  Stable small bilateral benign appearing nodular densities. No spiculate masses, areas of architectural distortion or suspicious microcalcifications are detected.  Correlation made with the breast ultrasound 15/03/2012. In the right breast a well—defined hypoechoic nodule at 7 0’clock near the nipple measuring 6 x 2 mm. No further lesions identified in the right breast.  ( The breast ultrasound of 2012 reported  “In the right breast there is another subtle mass at  11 o’clock  measuring  5 x 3 x 3 mm is also likely to be a small fibroadenaoma and is benign  in appearance”)

In the left breast are two benign appearing nodules at 12 0’clock near the nipple measuring 10 x 2 mm and 5 x 2 mm. No other lesions in the left breast. Normal axillae bilaterally. COMMENT: No features suspicious for malignancy . Stable bilateral benign lesions which have the appearance of fibroadenomas .

DOUBLE READ BY: Dr C Paulus     Kim WILLIAMS Radiology Consultant Report status: Validated.

There are two  ( undiagnosed) smoky black irregularly shaped images of varying size with shadowing?in the scan which may be synonymous with  spiculated masses?). A second opinion was requested but the  the patient service centre of Waitemata DHB advised on 24 July and 12 August 2020” that you have undergone a triaging process that included an assessment of the referral by a Breast Surgeon and bgi Your breast imaging investigations showed no abnormality and you are not required to attend a clinic appointment.-unfortunately the assessment of your clinical details did not meet the criteria for an outpatient assessment appointment with the specialist.”

On 5 November I emailed copies of the breast scan to Dr Karen Amies oncologist at ADHB, and  brea surgeons Dr Mitlick  and Mr Harman for an opinion.  There has been no reply. On 27  I emailed The Quality Team at Waitemata DHB.

Dr Gerred Breast Surgeon telephoned me in early December to advise that the black images in the scan were “fat”! and followed up the phone call   with a letter dated 3 December 2020

Problems: “Reassurance regarding breast imaging. It was good to talk to you today regarding your feedback that you submitted to Waitemata District Health Board regarding your breast imaging. You underwent mammogram and USS on 21/07/2020. Today, I was able to reassure you that your imaging did not show anything of concern and that there were no spiculated masses which you were concerned about. I went through that fat appears black on mammograms and glandular tissue white. I have had yolms reviewed by our Head of Breast Radiology who has reviewed the films from 2019 and 2012 as well and there are no changes. You were quite aware that you have the fibroadenomas that have been stable for years. I reassured you today that this was all good news and there is nothing here that needs any further follow up or imaging.

Electronically sighted and approved by Mrs Susan Gerred General & Breast Surgeon

Although  the appearance of fat in mammograms is  a description which normally equates with the condition “ fat necrosis” Gerred  did not specifically refer to the ultrasound images. The images of fat necrosis in ultrasound seem to differ from the images in my ultrasound insofar as they tend to be generally rounded /oval  in shape. Dr Thorpe agreed to seek a further opinion of Breast Surgeon Mr Harman. As of 15 December 2020 no alternative  opinion  has been provided.

Dr Thorpe agreed to seek a further opinion from Breast Surgeon Mr Harman however it appears that a reply has not been received by the general practitioner either.  Dr Gale was emailed a query but there was no reply. Instead Helen Olsen operations manager General Surgery advised:

Hi Vicki:      Thank you for your email asking for an opinion on your breast imaging. We supplied a second opinion in December last year and  are unable to provide another one.                                                    

 If you have any concerns please don’t hesitate to follow up with your GP, or contact the Advocacy service or the Health and Disability    Helen Olsen| Operations Manager | General Surgery  |Waitemata District Health Board

Another bilateral l breast ultrasound was performed at the Auckland Breast Clinic on 27 May 2021 

BILATERAL BREAST ULTRASOUND 

Patient :Ms Wilson Vicki Referred by Dr Audrey Thorpe INDICATION

Concern about  ultrasound image of the left breast. Known presumed fibroadenomas in both breasts. The mammograms and breast ultrasound examination performed at North Shore Hospital on 21/07/2020 are available for review.

FINDINGS

Ultrasound examination of both breasts was performed. In the right breast 7 0’clock position, there is a circumscribed hypoechoic solid nodule measuring 5 x 2 mm (previously 6 x 2 mm). In the left breast 12 0’clock position, there are two adjacent similar appearing circumscribed hypoechoic solid nodules measuring 8 x 2 mm (previously 10 x 2 mm) and 5 x 2 mm (previously 5 x 2 mm). No solid or complex cyst is identified elsewhere in either breast. Both axillae are normal with no lymphadenopathy.

CONCLUSION

No suspicious abnormality is identified in either breast. The 3 hypoechoic nodules most likely represent fibroadenomas.  The Hypoechoic area deep to the left nipple seen on  the North shore Hospital breast ultrasound dated 21/7/20 is normal posterior acoustic shadowing caused by the nipple

Dr Mike Baker,Radiology Auckland Breast Centre 

The large dense black variegated image arising from the nipple in the ultrasound of 2020 is no longer evident in the latest scan of May 2021. The Journal of ultrasound in medicine advises “  Although posterior acoustic shadowing is a sonographic feature that is most commonly associated with mammary malignancies, this sonographic finding may also be seen with benign breast lesions. An enlarged lymph node was  evident in the ultrasound of 2020 but not in the scan performed at the Auckland Breast Centre in  2021. It was not diagnosed in either scan.

There is a significant difference in the procedures at the breast clinics of both ADHB and Waitemata DHB.  When I previously attended at  ADHB, subsequent to scanning the patient would then wait in a private room for a consultation with the attending specialist. Unfortunately subsequent to scanning, Waitemata DHB despatches a letter advising patients that they do not fulfil the criteria for a consultation with a breast specialist.  The last breast examination was at ADHB in 2012.

HAEMATOLOGY 

1988 I was diagnosed with  Myalgic Encephalomyelitis by Dr Simpson of Dunedin.  A blood test clearly esablished “ an increase in the cup forms together with an abnormal increase in the surface changes of the cells”. Simpson also referred to “surface changes” ( bumps and ridges). While he has listed  echinocytes and knizocytes it isn’t entirely clear whether they have also been incorporated into his assessment as there is no specific percentage measurement for either. 

‘Echinocyte (from the Greek word echinos, meaning ‘hedgehog’ or ‘sea urchin’), in human biology and medicine, refers to a form of red blood cell that has an abnormal cell membrane characterized by many small, evenly spaced thorny projections.^[1][2] A more common term for these cells is burr cells. Echinocytosis is a reversible conditin of red blood cells that is often merely an artifact produced by EDTA, which is used as an anticoagulant in dried blood.

In addition to appearing as an artifact of staining or drying, echinocytes are associated     with^[5]

• Uremia and chronic kidney disease
• Liver disease (e.g., cirrhosis)
• pyruvate kinase deficiency
• hypophosphatemia
• hyperlipidemia
• Phosphoglycerate kinase deficiency
• Disseminated malignancy
• Myeloproliferative disorders
• Vitamin E deficiency
• Early posttransfusion of RBC
•  

The term knizocyte describes a specific shape form of erythrocytes that deviates from the standard form. … Like normal red blood cells, knizocytes show a clear central area, but this is crossed by a thin strip of hemoglobin. It can be seen particularly in patients with thalassemia.

Thalassemias are inherited blood disorders characterized by  abnormal hemoglobin production.^[7] Symptoms depend on the type and can vary from none to severe.^[1] Often there is mild to severe anemia (low red blood cells).^[1] Anemia can result in feeling tired and pale skin.^[1] There may also be bone problems, an enlarged spleen, yellowish skin, and dark urine.^[1] Slow growth may occur in children.^[1]

Thalassemias are genetic disorders inherited from a person’s parents.^[2] There are two main types, alpha thalassemia and beta thalassemia.^[7] The severity of alpha and beta thalassemia depends on how many of the four genes for alpha globin or two genes for beta globin are missing.^[2] Diagnosis is typically by blood tests including a complete blood count, special hemoglobin tests, and genetic tests.^[3] Diagnosis may occur before birth through prenatal testing.^[8]

As of 2013, thalassemia occurs in about 280 million people, with about 439,000 having severe disease.^[9] It is most common among people of Italian, Greek, Middle Eastern, South Asian, and African descent.^[7] Males and females have similar rates of disease.^[10] It resulted in 16,800 deaths in 2015, down from 36,000 deaths in 1990.^[6][11] Those who have minor degrees of thalassemia, similar to those with sickle-cell trait, have some protection against malaria, explaining why they are more common in regions of the world where malaria exists.^[12]’

In 2004 I attended a haematologist( Dr Blacklock) as my haemoglobin  level had declined  from 145 in 2003 to 118 .   While the neutrophils were classified as marginal there was  no reference to the missing RBCs. There was considered to be no significant anaemia and it was suggested that further investigations should concentrate on the  lung and thyroid.  As a consequence I am now also being treated for hyperthyroidism or Graves disease.

In 2005 I received written advice from the Medlab Director Dr Theakston as to why my red blood cells hadn’t been reported for 7 years .i.e.  “reporting of this value had been discontinued as general practitioners did not think it provided  any useful additional  information to the haemoglobin concentration” As haemoglobin is a component of RBCs one would assume that an assessment of both would be necessary.  Size/shape of RBCs can be important in ME as can the number of RBCs.  Excessive numbers can lead to thickening of the blood and clotting. According to NIH  (American National Institute of Health)  RBCs are still being reported in every blood test.  In 2008 Theakston further advised that non-reporting of the red blood cell count was general practice in most New Zealand medical laboratories however a blood test undertaken by Labplus in September 2008 reported the RBC count as within the normal range .

The blood count , the serum B12 and Folate, also the iron studies tests performed at Northland pathology on 25 September 2017, were within the normal range.

A full blood Count as part of a panel at NDHB’s laboratory dated 2 August 2018 indicated a high count of Immature Granulocytes  0-10   E+9/L  H  0.0-06.

Healthline explains  “that granulocytosis happens when there are too many granulocytes in the blood.  Granulocytes are a type of white blood cells that seems to contain small granules when examined under a microscope. These tiny granules have proteins essential for immune system function.

 Some of the health problems associated with granulocytosis include leukemia, inflammatory bowel diseases, bacterial infections, sepsis, metastatic cancer, kidney failure, rheumatoid arthritis, heart attack and autoimmune disorders. Additionally, burn injuries, habitual smoking, physical and mental stress, as well as usage of medications such as corticosteroids may also result in high levels of granulocytes”

A blood count from Northland Pathology indicated a normal blood count. Since February 2019 lymphocytes have varied from 1.5-1.8 to 1.6 (ref range 1.0-4.0) “ Blood film examined -no immature granulocytes seen. Increased oval cells. Platelets appear normal”

Wikepedia advises:  “Elliptocytes, also known as ovalocytes, are abnormally shaped red blood cells that appear oval or elongated, from slightly egg-shaped to rod or pencil forms. Rare elliptocytes (less than 1%) on a peripheral blood smear are a normal finding. These abnormal red blood cells are seen in higher numbers in the blood films of patients with blood disorders such as:^[2Thalassemias: Iron deficiency  Myelodysplastic ndrome and myelofibrosis Primary myelofibrosis is a relatively rare “bone marrow/blood cancer” .^[1] It is currently classified as a myeloproliferative neoplasm, in which the proliferation of an abnormal clone of hematopoietic stem cells in the bone marrow and other sites results in fibrosis, or the replacement of the marrow with scar tissue.^[2][3]

Megaloblastic anemia is an anemia (of macrocytic classification) that results from inhibition of DNA synthesis during red blood cell production.^[1] When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to contivision, which presents as macrocytosis.”

As I was afflicted with a chest complaint I attended the ED Department at North Shore Hospital on 6 May 2020.  I was attended by Dr Etienne De Beer -Senior Medical Officer. Both a blood test and a general chemistry test were undertaken.  The blood test was normal with the exception of the lymphocyte levels : 0.7 xE9/L range (1.0-4.0 x E9/L) L.    General chemistry results were normal

A  blood test dated 18 February 2021 was essentially normal apart from : WBC 12.4 x10e9/L (4.0-11)H,  Neutrophils 9.0 x10e9/L (1 .9-7.5)H  Monocytes  x 10e9/L (0.2-1.0) H

 

GASTROENTEROLOGY

An ultrasound of 12 July 1991  reported  ‘a mural polypi adjacent to the gall bladder’.  In   2002 a CT scan of the lung stated that “fluid is seen within the  oesophagus which  .   The only finding arising out of a  colonoscopy / endoscopy in 2003 undertaken at public hospital was a diagnosis of “melanosis coli,”  a pigmentation of the lining of the bowel normally ascribed to overuse of laxatives). The oesophagus was reported as “ normal” Some overseas studies have indicated that some patients are afflicted with melanosis coli who have never taken laxatives  Melanosis coli can sometimes mimic ischemic colitis  Thermography also clearly showed a significant area of inflammation extending from below the breastbone to the stomach.

Irrespective of the diagnosis no film of the procedure was retained.  I was advised by the specialist Dr Mark Lane  that  “the images were not recorded –this is the norm in the situation where endoscopy reveals no abnormalities or the abnormalities are considered to be minor.”

One would have assumed that all procedural film was retained particularly in a public hospital for comparative purposes, if for no other reason.  In this case there was a diagnosis . Clear images of melanosis coli were of course available on the internet from an American colonoscopy centre. Endoscopic procedures are now available on YouTube.

An abdominal ultrasound of January 2011 was assessed as normal apart from identifying  “ 3 mm diameter gall bladder polyp”There has been no further investigation.

 The  GGT (Gamma-glytamyl transpeptidase) was reported by Labtests in January 2012  as 57 U/L  ( norm: <50) H .  GGT is an enzyme which is found in hepatocytes and biliary epithelial cells and  may be high in liver disease. In particular it is a feature of biliary outflow obstruction rather than hepatocellular damage. GGT serum measurement provides a very sensitive indicator of the presence or absence of hepatobiliary disease. However the usefulness of measurement of serum GGT is limited by its lack of specificity. Raised GGT levels have been reported in a variety of clinical conditions including (1): pancreatic disease, myocardial infarction, chronic obstructive pulmonary disease, renal failure diabetes, obesity, alcoholism

A  low eGFR .(The Estimated  Glomerular Filtration 68 mL/min/1.73m2 (>90)L was also reported.  It  is an indicator of kidney health. In adults, the normal GFR number is 90 or higher.

As a result of collapse preceeding an episode of haematemesis on 12 June 2013 I was admitted to Auckland Hospital. I remained in hospital for most of the day receiving fluids and an anti nausea injection.  I returned home the same day and felt much better however I collapsed again the following day and was unable to get out of bed.  I returned to hospital the following day. A Gastroscopy was performed by Dr Lane. The discharge summary dated 14 June 2013 reports as follows: 

“Clinical Management: 63 year old presenting with 2 episodes of haematemesis on the background of regular NSAID use. ( note: there was only episode of haematemesis ). Her Haemoglobin was 53 and hence was transfused 3 units of blood in ED. Remained haemodynamically stable.  Had a gastroscopy next day which showed gastric ulcer.  This has been biopsied and the results are pending.  She remained well following gastroscopy. Received a further blood transfusion of 1 unit.  Hb was 99 today and she has been discharged home.

 A gastroscopy was performed by endoscopist Dr Mark Lane and he reported “ the oesophagus was normal.  One non-bleeding cratered gastric ulcer with pigmented material was found on the posterior wall of the gastric body.  The lesion was fifteen mm by twenty mm in largest dimension.   Biopsies were taken…the duodenum was normal”

On 21 June 2013 my blood pressure was recorded at 120/60 by nursing staff at One Health.  A blood test result received from Labplus 20 June 2013 recorded the haemoglobin level as (94 g/L) ( 115-155) L/////////RBC: 3.23 x 10e 12/L ( 3.60-5.60) L///HCT: 0.29 l/l ( 0.35-0.46)  L.  Blood Film: Anaemia is present.

 A further test by Labtests on 30 June 2013 reported a haemoglobin level of 110* ( 115-155) RBC of 377 ( 3.60-5.60) and an excessive platelet level of 443* ( 150-400)

On 12 June 2013 I was admitted to Auckland Hospital.  The clinical summary dated 14 June 2013 reported “ …presenting with 2 episodes of haematemesis on the background of regular NSAID use.  Her Haemoglobin was 53 and hence was transfused 3 units of blood in ED…received a further transfusion of 1 unit…gastroscopy showed a gastric ulcer

Labplus gastric ulcer biopsy report dated 20 June 2013 stated:  “Macro: eight pieces of cream tissue that measure from 2mm to 4mm .  Micro: The sections sow multiple fragments of gastric bodytype mucosa with muscularis mucosa present. No ulceration is present. There is a mild increase in chronic inflammatory cells within the lamina propria accompanied by mild foveolar hyperplasia.  No active inflammation is seen . No H pylori organisms are identified.  There is no dysplasia or invasive malignancy.  Diagnosis: Suggestive of regenerative mucosa”

I did not meet Dr Lane after the gastroscopy however he did comment about “ the fate of Miss Wilson” prior to the procedure.  As has been the case in the past there were one or two unfortunate comments from the staff . While visiting my mother in her ward an unidentified person who was obviously Maori was overheard referring loudly to “ a bastard mental case” while standing in the corridor.  A Maori or Island Female nurse on night duty wandered into my ward and passed a “ kill Vicki” comment.  A gastric bleed was precipitated by an anti-inflammatory tablet.  A faecal occult blood test performed by Northland pathology on 16 December 2015 was “ negative”. 

In November 2015 there was evidence of some internal bleeding as evidenced in black stools precipitated by a once only anti-inflammatory tablet. On this occasion the problem was eliminated with a natural remedy namely cinnamon. Organic Facts  : “Healing:Cinnamon  acts as a coagulant and helps to stop excess bleeding. Therefore, it facilitates the healing process”.

Liver and Renal function tests performed at Northland Pathology on 25 September 2017, 11 May 2018 and 6 May 2019 were within the normal range.

 Egfr   m/L/min/1.732m2     61 ( Range >90)  An Egfr > 60Ml/MIN/1.73m2  suggests normal kidney function in the absence of other evidence .On 6 May 2019 eGFR was *57.  (>90).  Sodium potassium and creatinine levels were all within the normal limits.

In August 2018 I had  experienced a pain in the lower abdomen which resulted in a period of paralysis involving my legs- I was unable to lift my legs over the side of the bed. This condition lasted for a day and was not repeated. On 3 August 2018 I attended at the Emergency Department at Northland Hospital (I had been previously  hospitalised as result of a haemorrhage from a duodenal ulcer in 2013.)

 Blood and urine tests were undertaken and I was advised that were normal. A CT scan was scheduled but later abandoned.  I was in the care of an Irish female Dr Lyons.  ED Director Dr Cameron’s when scheduled visit did not eventuate. Subsequent to a physical examination Dr Lyons advised that my situation did not comply with ED criteria for further investigation “  she would have an inpatient scope if she was newly anaemia had haematemesis-an outpatient scope could be arranged if she does not fulfil these criteria” and she advised that a recommendation would be sent to my General practitioner for further investigation to be implemented at the Gastroenterology clinic  A  gastroscopy was performed at Whangarei Hospital on  16 September 2019.

Anion Gap reading of 17 mmol/L  H 8-16 was reported by Whangarei Hospital on 2 August 2018

Med line Plus states: The anion gap is a measurement of the difference-or gap-between the negatively charged and positively charged electrolytes. If the anion gap is either too high or too low, it may be a sign of a disorder in your lungs, kidneys, or other organ systems.

The anion gap blood test is used to show whether your blood has an imbalance of electrolytes or too much or not enough acid. Too much acid in the blood is called acidosis. If your blood does not have enough acid, you may have a condition called alkalosis.

  If your results show a high anion gap, you may have acidosis, which means higher than normal levels of acid in the blood. Acidosis may be a sign of dehydration, diarrhea, or too much exercise. It may also indicate a more serious condition such as kidney disease or diabetes.

Mild acidosis may not cause any symptoms or it may be associated with nonspecific symptoms such as fatigue, nausea, and vomiting. Acute metabolic acidosis may also cause an increased rate and depth of breathing, confusion, and headaches, and it can lead to seizures, coma, and in some cases death.

• Those that affect respiration and cause changes in pH due to changes in CO₂ concentration are called respiratory acidosis (low pH) and respiratory alkalosis (high pH). Respiratory acid-base disorders are commonly due to lung diseases or conditions that affect normal breathing.
• Disorders that affect metabolism and cause changes in pH due to either increased acid production or decreased base are called metabolic acidosis (low pH) and metabolic alkalosis (high pH). Metabolic acid-base disorders may be due to kidney disease, electrolyte disturbances, severe vomiting or diarrhea, ingestion of certain drugs and toxins, and diseases that affect normal metabolism (e.g., diabetes).

  Abnormal leucocytes  Ca 15 Leu/l were reported on 2 August 2018

  Anytestkits.com advise: “ Normal leukocytes range in urine  0 – 10 leu/ul///////Measuring range 0 – 500leu/ul

Leukocytes levels in urine This test indicates whether white blood cells are present in urine.///pathological concentration: more than 20 leu/ul.

abnormal leukocytes values may indicative of :

 Cardinal symptom of urinary tract infection///kidney infection///cystitis//urethritis///Contamination//vaginal secretion

Further action is required if leukocytes are found in urine’

The Albumin/Creatinine Ratio test performed on 5 July 2019 from a random urine sample was normal. 

ALBUMIN/CREATININE RATIO (Random Urine Sample)Date: 05/07/2019 Northland Pathology

Ref. Range

Ur.Albumin mg/L     < 3       (< 30)

Ur.Creatinine mmol/L   4.1

Alb/Creat ratio mg/mmol < 1.0    (< 3.

 Medline Plus advises: “A microalbumin creatinine ratio is most often used to screen people who are at higher risk for kidney disease. These include people with diabetes or high blood pressure. Identifying kidney disease at an early stage can help prevent serious complications.”

A Norpath midstream urine dated 11 September 2019 reported “Leucocytes and Erythrocytes : < 10 x 10 (6) L Ref Range (<40) and < 35)//(  Epithelial Cells 1 x 10 (6)/L culture is not routinely reported in the absence of pyuria.”

An upper GI endoscopy  report dated 16 September 2019 from NDHB Gastroenterology stated “The second portion of the duodenum, the duodenal bulb, the Pylorus, and the lower third of the oesophagus were all examined. “Findings : Oesophagus normal, stomach normal, the examined duodenum was normal. Scattered minimal inflammation was found in the stomach. A test for H Pylori Urease was negative.” Indications: suspected gastro-oesophageal reflux disease . A 2002 ADHB  report of a CT chest scan  stated that “fluid is seen within the  oesophagus which is a little thick walled”, and  a  CT of the chest dated 27 October 2016 reported “a hiatus hernia.” 

 In 13 June 2013 ADHB reported  “a cratered gastric ulcer with pigmented material was found on the posterior wall of the gastric body . The lesion measured fifteen by twenty mm in largest dimension” References to possible reflux disease  would obviously be of secondary concern to the main reason for the procedure namely an episode of haematemesis/coagulase in June 2013 which required a transfusion of 4 units of blood any reference to which was omitted from the 2019 report.  The latest NDHB images do not appear to be quite as specific as the original images of June 2013 which are somewhat enlarged , photographed from a different angle and clearly showed the duodenum’s posterior wall.

On 2 September 2019 Dr Miller of Bush Road Medical Kamo referred my to Gastroenterology at Whangarei Hospital for a colonography. Despite booking clerk Michelle’s advice that there was the likelihood of a strike on the day of my appointment and odd advice that the courier was NZ Van Lines, the procedure has been scheduled for late November.

CT COLONOGRAPHY:26 NOVEMBER 2019

CLINICAL DETAILS:  Change in bowel habits and constipation. No family history of colon cancer. TECHNIQUE: Unenhanced low dose, supine and prone acquisition following automated colonic insufflation with carbon dioxide  COLONIC FINDINGS: No colonic mass or significant polyp  . EXTRACOLONIC FINDINGS:(Extra colonic evaluation is limited by the low-dose CT technique and lack of intravenous contrast)  Solid Abdominal Organs: [No gross abnormality within the limits of the low dose unenhanced technique.]  Abdominal Aorta: [Normal calibre] Other: [No lymphadenopathy or ascites]

 COMMENT:

No colonic mass or significant polyp.

Repo ted by:

Dr Ziad Hamid

CARDIOLOGY

A follow-up Angiogram in June 03 instigated by cardiologist Dr Ellis  indicated “calcium within the left coronary artery an occluded proximal circumflex with one major OM branch which cross-filled from both the LAD and RCA territory, mild-moderate LAD lesions ,and  mild RCA lesions”. The general assessment was .of “an occluded proximal circumflex , mild-moderate LAD mild RCA lesions and generally good LV systolic function. There was no suggestion of  either LV systolic impairment or damage to the LV”.   The possibility of opening the heart vessel  wa considered a possibility but considered unlikely at the time of the investigative procedure.”

Ecchocardiography of 10 June 2003 indicated “ that the LV was not dilated  with LVEDD 4.9 cms and LVESD  at 3.4 cms.  There was normal Doppler indices through the mitral valve and pulmonary veins indicting good LV diastolic function.  The left atrium was not dilated at 3.3cms. The mitral valve was structurally normal  opening freely and closing with trivial MR>  The aortic valve is trileaflet, mildly thickened and calcified, opening freely and closing with trivial AR.. The aortic root is 2.9 cms and there was normal Doppler velocity through the aortic valve at 1.1M/sec.  The right heart is structurally normal including the tricuspid valve, which opens freely and closes without TR.  There is normal Doppler velocity through the main pulmonary artery at 0.8M/sec and the interarterial septum is intact”

The carotid artery ultrasound scan of 18 June 03 showed  “mild/moderate carotid lesions but none so severe that they would require revascularization.  There was no significant stenosis of either common, internal or external carotid artery.  Anterograde flow was present in both vertebral arteries”

Carotids scans were classified as normal.  Pressures in my left internal carotid (LICA) were reported as systole(78cm/sec) and diastole ( 28 cm/sec. The RICA  was systole 95 diastole 43.   Pressures in the LECA were recorded as systole 77  and diastole (9.)  .  RECA pressures were systole (57) and diastole 14

A report from Coosa Valleys Technical College advises that “Normal velocities of the carotid arteries have not been established . The reported mean peak systolic value (PSV) of the ICA is from 54 to 88 cm/sec and not viewed as abnormal until PSV exceeds 100 cm/sec The mean PSV  of the ECA( External carotid artery) is 77cm/sec with the maximum velocity not exceeding 115cm/sec” 

In 2005  Cardiologist Dr Clarke’ s report  stated “ that blood pressure prior to  exercise testing was 150/90.  After 3 minutes of walking on the treadmill it dropped to 140/70 and then went up to 180/80.  Five minutes after the exercise test was completed her blood pressure was 146/90 at a heart rate of 85/bpm.  She had chest discomfort before during and after the test and it didn’t really change.  Her effort tolerance was 7 minutes of the Bruce protocol.  There was minor ST segment changes which were certainly no worse than on the test done in  2003.  Dr Ellis investigated her in 2003 and found her to have an occluded left circumflex and minor coronary disease in the LAD  and right coronary with normal left ventricular function A repeat angiogram was ruled out in favour of a possible stress echocardiogram test in the future. I have no evidence that there has been progression of her coronary disease.”

 An ECG was undertaken at public hospital in September 2008.  I was advised that the ECG report was not available to the patient.  In his letter dated 8 April 2009 the Chief Medical Officer Dr Sage he  “that the ECG was not normally reported on but was used by doctors to exclude any significant cardiac abnormalities-this ECG is definitely no cause for your concern”       I  provided copies of relevant previous cardiology  reports to public hospital but despite my query the only acknowledgment has been a reference to “numerous enclosures a-r” contained in a letter from the Chief Medical Officer.

Blood pressure readings have ranged from  170/90 in October 2007 , 158/90/ in May 2009, 180/100 in February 2010 and 170/90 in July 2010. They have reduced to more normal levels in 2011 and 2012-2018.

There was a a further consultation with senior cardiologist Dr Ted Clarke  on 28 January 2011.  As with the respiratory physician an x ray monitor was not available the plates being viewed instead on the window pane. ! I pointed out what appeared to be an apparent expansion in the area of the heart in comparison with the x ray of  1989- chest x ray  is generally regarded as being a reasonably accurate indicator of cardiomegaly.

 A resting ECG was undertaken and Clarkes report stated “ appeared to be within the normal limits.  One might argue about the ST segments being a little bit saggy- she didn’t have any heart murmurs no evidence of pulmonary arterial hypertension and I could find no abnormal sounds on listening to her lungs even after coughing.  She has a little bit of pitting oedema of both ankles. The JVP is not elevated.  She has a concern too about the fact that her most recent chest x rays when compared with those of  1989 show a definite enlargement of the cardiac silhouette and I would have to agree with her –certainly no sign on the most recent x rays of any left ventricular failure”

Subsequent to the consultation there were comments overheard from the cardiologist to a visiting young man to the effect that either myself or a woman with the same Christian name had apparently been cited by a former minister of police in connection with behavioural aspects.  A female  hospital staff member wearing a blue uniform was later overheard standing outside in the car park using her phone. She also reiterated the same comment. Police cars together with the fire brigade and a helicopter in the near distance passed by on the road outside the practice after two consultations.

 A stress echocardiogram was performed at Ultravision Cardiac Imaging Mercy Hospital Auckland on 11 February 2011.  “ At peak heart rate and in particular in recovery there was 1.5mm downsloping inferolateral ST segment depression associated with T wave inversion –Baseline: normal left ventricular size with hypokinesis of the mid to distal inferolateral and anterolateral segments.  Overall LVEF is lower limit normal.  Normal left ventricular wall thickness and mild left ventricular diastolic dysfunction. No significant valvular abnormalities.  Normal right ventricular size and function.

At Peak heart rate: there was evidence of a large territory of ischaemia in LAD territory with severe hypoinesis of the mid to distal anterior septum, mid to distal inferior septum, distal anterior wall extending to the entire apex and distal inferior and inferolateral walls. There appears to be minor augmentation of the inferolateral wall.  The left ventricular ejection fraction reduced.

Conclusion: exercise induced chest discomfort at a low workload associated with ischemia in the LAD territory resting wall motion abnormality consistent with known circumflex occlusion

The Mayo Clinic advises “the left ventricle is the heart’s main pumping chamber, so ejection fraction is usually measured only in the left ventricle (LV). An LV ejection fraction of 55 percent or higher is considered normal. An LV ejection fraction of 50 percent or lower is considered reduced. Experts vary in their opinion about an ejection fraction between 50 and 55 percent, and some would consider this a “borderline” range

The ejection fraction may decrease if:

• You have weakness of your heart muscle, such as dilated cardiomyopathy
• A heart attack has damaged your heart
• You have problems with your heart’s valves
• You have had long-standing, uncontrolled high blood pressure

 A  Diagnostic Medlab report dated 24 February 2011 indicated a total cholesterol measure of  6.0* together with an LDL level of 3.7* and Triglyceride of 2.4*). Total cholesterol in October 2012 measured 4.8. In December 2015 the CHOL/HDL ratio was 5.9* ( norm <4.5)

At the subsequent consultation with the cardiologist It was never entirely clear whether the cd/dvd of the procedure was available but it was never produced at the consultation.  The specialist also queried the fact that I would want copy of the film considering that his report should suffice.  

“Preliminary findings: Triple vessel disease : 60 distal left main.  Severe proximal LAD.        Moderate diagonal ostium Severe proximal intermediate LCx=Proximal occlusion .  RCA mild disease. Collaterised to LCx.  Good LV function.   Quadruple coronary artery by-pass recommended”.

An Angiogram was performed at Auckland Hospital on 30 March 2011 The procedure was somewhat marred by the removal of my footwear from beside my bed. I had to resort to travelling home in bare feet. There were the usual background comments from the staff some pertaining to “ property” and others referring to the derogatory comments of an Australian psychiatrist concerning mental health.! :

Although a quadruple bypass was initially recommended the cardiologists agreed with my request and triple stenting  procedure of the LAD was subsequently performed at ADHB  on 15 November 2011. by Drs Webster and Glenie

There were no initial complications.  I attended a follow up consultation with the Dr Webster  on 16 January 2012. He first checked my chest with a stethoscope.  His report referred  to “percutaneous coronary interventional procedure to the  left main and proximal left anterior descending disease.  She is still getting some chest pain requiring nitroglycerine 2-3 times per week.  She has also been troubled by recurrent chest and sinus infections .  She has some discomfort in her lower legs associated with  mild ankle swelling.  She has no other symptoms of note and is not getting claudication in her legs.  Her medications are unchanged.  Examination of  her cardioivascular system was unremarkable apart from a slight reduction in the right dorsalis pedis pulse compared with the left.  Clinically this woman is doing reasonably well from a cardiac viewpoint.  Her ongong angina may relate to the chronic left circumflex occlusion.  At present I suggested that we continue with a conservative approach with a planned review in four months time.  If she has ongoing symptoms repeat angiography with view to a possible attempt at opening the circumflex could be considered.”

 I have experienced discomfort in legs previously most often associated with infection but it has generally responded to antibiotics.  Peripheral arterial disease in the legs is a common problem and is often assessed by an ultrasound, arterial-brachial index or an arteriogram. The use of high levels of atorvastatin can also cause generalised pain. The level of discomfort remains unchanged in April 2012.

No investigative procedures were recommended at this time and he said he would arrange another consultation in about 4 months time.  My blood pressure height and weight were assessed as 132/65, 161cms and 62.9 kgs respectively.) The CRP  was reported as 5 mg/L on 17 January 2012 (<5) H-and my blood pressure was again elevated at  170/94 in February 2012.

My blood tests dated 16 January 2012 indicated a much higher than normal level of creatine kinase at 358 U/L H  ( norm 30-180) .  The additional comments from labtests  stated “ that unexpected elevations of CK are usually due to exercise or muscle trauma.  Other relatively common causes  are medication ( eg statins) hypothyroidism, alcoholic myopathy and myocardial infarction though the latter is is seldom an unexpected finding. Rarer but important causes are diseases of skeletal muscle ,CNS and a wide range of metabolic disorders.”

 A medical website states that “the enzyme creatine kinase (CK) and one of its forms called CK-MB present a similar situation. CK is released into the bloodstream by damaged muscles; CK-MB is released into the bloodstream when the heart muscle is damaged. Therefore, a high level of CK-MB indicates damage to the heart muscle, so this enzyme is one of the indicators used to diagnose heart attacks. Because of their greater muscle mass, men tend to have higher CK levels and the level of CK-MB that indicates a heart attack in men is higher than for women. When the test first came into use, the reference range was based on the higher levels. Many elderly women being tested for a heart attack demonstrated considerably lower levels of CK-MB (because of their smaller muscle mass) and, thus, did not pass the threshold level believed to indicate a heart attack; so heart attacks were often missed in these women.”

In his report dated 20 January 2012 specialist advised: that “ her creatine kinase level to be elevated at 358 which is about twice the upper limit of normal.  This may be due to atorvastatin ( Lipitor). I would be loath to discontinue the medication but that might need to be considered should her symptoms worsen. Alternatively simvastatin could be tried , although this is less potent and also associated with myalgias, particularly at higher dosages

Centre for Adverse Reactions of Dunedin reports as follows:Myopathy known to occur with statins

.Statin treatment should be discontinued immediately if an elevated CK level is found (i.e. CK >10 x upper limit of normal), or where myopathy is suspected or diagnosed. If there is a moderate rise in the CK level (i.e. 3-10 x upper limit of normal) then monitor CK levels weekly and seek specialist advice. It is worth noting that measuring CK levels when statin therapy is initiated will provide a reference baseline; however, undertaking regular CK levels is probably not useful in the absence of therapy changes or the development of co-morbidity.

 Atorvastatin  can cause

• Insomnia and dizziness^[20]
• Chest pain and peripheral edema^[20]
• Rash^[20]
• Abdominal pain, constipation, diarrhea, dyspepsia, flatulence, nausea^[20]
• Urinary tract infection^[20]
• Arthralgia, myalgia, back pain, arthritis^[20]
• Sinusitis, pharyngitis, bronchitis, rhinitis^[20]Infection, flu-like syndrome, allergic reaction

In November 2013 I received the ECG graphs which were performed on 12 and 13 June  2013 at Auckland Hospital  as a result of the haematemesis .  The graph of  12 June  clearly indicated  “ “sinus tachycardia –septal infarct” A subsequent ECG on the same day reported “sinus tachycardia with short PR ST and T wave abnormality consider anterolateral ischemia

Tachycardia  refers to an abnormally fast resting heart rate.

The health website ASK advises that “ A septal infarct is a condition in which the septum of the heart has a patch of dead or dying tissue. This typically results after a heart attack. The prognosis for a septal infarct is a 69 percent chance of survival for living past six years. Survival rate can increase or decrease depending on a person’s general health and their age. A younger person has a higher rate of survival compared to an elderly person.”

“Anterolateral ischemia is a medical term that refers to a condition that is characterised by very little amount of blood flowing to the back side of the heart. This is usually as a result of blockage in an artery responsible for the blood flow” The original diagnosis of occluded proximal circumflex ( which extends around the back of the heart) has yet to be dealt with.

A Basic haemostasis screen was provided by Labplus at Auckland Hospital on 12 June 2013.  APTT test was 25 ( norm 25-37) .   APTT (Activated Partial Thromboplastin Time) is a measure of one part of the clotting system known as the “intrinsic pathway”. This pathway involves a number of coagulation factors, which are proteins involved in the normal clotting process. The APTT is used to measure the effects of treatment with intravenous (IV) Heparin therapy, to ensure that the blood is not thinned too much or too little. Conditions which may be treated with IV Heparin include:

• Deep Vein Thrombosis (DVT)
• Pulmonary Embolism (PE)
• unstable angina – now more commonly known as Acute Coronary Syndrome (ACS)
• Atrial Fibrillation (AF)

The tests also included PR and Fibrinogen Assay . PR measure 1.0  (norm 0.8-1.2)  The fibrinogen Assay result measured 3.0 ( norm 1.5-4.0) .

A Labtest for lipids on 16 september 2013 indicated generally high readings. Cholesterol 7.1* (< 5.0) Triglycerides 2.3* (<2.0)  HD 1.28 ( > 1.28) LDL cholesterol  4.8*  ( <3.4)  Chol/ HDl  ration  5.6 (<4.5)

Blood pressure in September 2013 measured 115/71

I requested an angiogram and a leg ultrasound and he advised that he would arrange both of those procedures.  My blood pressure was 176/83.   I provided Webster with a photo of the haematemesis which occurred a few months earlier.  Apart from saying “ it was quite impressive” he made no  other comment. Neither the details concerning the septal infarct and ischemia detailed in the ECG nor any reference to heart valves  were reported  in any of Webster’s reports.  Regardless he proceeded with further stenting in November.

An angiogram was performed on 26 November 2013 The clinical summary dated 26 November 2013 reported: “ Preliminary results : left main stem proximal LAD, mid LAD stents patent. Severe ostial posterior descending arterydisease L) circumflex occluded.  Severe stenosis at the distal edge of mid/distal LAD stent.  Deployment of 2.25 mm x 12mm x Xience drug-eluting stent with an excellent result. 6 months of clopidogrel prescribed.”  A stress echogcardiogram of February 2011 reported “that the left ventricular ejection fraction was reduced”-a notation on the coronary diagram of November 2013 noted that “ the LVEF was not done”

There was a further consultation with Dr Webster on 17 February 2014. “ she has been reasonably well?-she has had ongoing troubles  with chest infections and notes an occasional twinge in the chest with coughing…..legs ..an ultrasound has been arranged in the past but does not appear to have happened…she has longstanding dull headaches and generalised lethargy.  She saw Dr Ernest Willoughby in December 2013 following an episode of grey patches coming down over both eyes for 15 minutes.  This was associated with light headedness and her heart was not racing at the time.  She has had nothing since .On examination  she was  not distressed. Her pulse was 80 and regular .Her blood pressure was 114/58.  He jugular venous pressure was not elevated.  I could not hear a carotid bruit. Heart sounds were dual.   I  have re-booked a leg ultrasound .  Willoughby felt that her visual symptoms might be related to ischaemia in the posterior circulation .   I would like to review he in nine months.” Webster still considered that nothing further needed to be done in respect of the occluded circumflex artery. Although in 2012 he advised that  “If she has ongoing symptoms repeat angiography with view to a possible attempt at opening the circumflex could be considered.”

Dr Diana Holdright a consultant cardiologist from Harley Street in London advises that “ Narrowing in the carotid arteries increases the risk of stroke and TIA (mini-stroke), and narrowings in other arteries, such as the coronary arteries, frequently co-exist. More recently it has been appreciated that subtle and early changes in the inner lining of the arteries, such as an increased thickness of the “intima and media”, are associated with an increased risk of stroke and  heart attack” ( see also carotid ultrasound of 2003)

An ECG which was performed at Whangarei Hospital on 13 March 2015 at the instigation of Dr Kennedy indicated “ a possible inferior infarct- abnormal ECG” . This was not discussed during the consultation however Kennedy did refer to it in his report: “ A resting 12- lead ECG today showed sinus rhythm 70/min normal QRS axi, small Q waves in the inferior leads , not reaching levels of significance no left ventricular hypertrophy or strain minor T wave flattening in the anterosepetal leads.” “A chronically occluded left circumflex” which was also referred in his initial summation, is still outstanding from an initial diagnosis by Dr Ellis of Auckland in 2003.

A stress echo was performed at whangarei Hospital under the auspices of Dr Nandra.  His report dated 14 July 2015 is as follows:”  Vicki managed 3 minutes 36 seconds of the Bruce protocol today. The test was stopped secondary to chest discomfort.  Resting ECG showed normal sinus rhythm mild inferior lateral ST depressions…..Heart rate rose from 83 beats per minute to 127 beats per minute ( 82% of maximum age predicted heart rate) target heart rate not achieved.  Resting blood pressure was 163/75 mmHg which rose to 190/108 mmHg. Peak exercise ECG did show ST depressions but not significant enough to call it positive. Resting echo showed multiregional wall motion abnormality with mild to moderate LV systolic disfunction. Multiple segments including apical septal/anterior/inferior/and posterior wall akinesia. During exercise LV dilated and showed dyskinetic changes mainly to the anterior wall which correlated with her symptoms and hence the test was deemed positive.

An angiogram was performed at Auckland Hospital on 12 August 2015 by Professor Peter Ruygrok . The preliminary report in the clinical summary dated 12 August stated” Severe triple vessel disease. Normal left ventricular function on left ventriculogram. Plan: out patient coronary artery by-pass surgery”  Spirometry chest x –ray and check of varicose veins done prior  to discharge” (The vein check was not done). However the report did not refer to the stress echo performed at Northland DHB on 14 July 2015.

Dr Ruygrok didn’t consider that occluded proximal circumflex which has been outstanding since 2003 was a candidate for stenting as the hardened  plaque would be a preventative!.  (similar  case histories on the internet have resulted in success for some patients effected by a change of surgeon, balloon angioplasty and/or the rotorblade technique)

In his report dated January 2012 Dr Webster stated that “ her ongoing angina may relate to the chronic left circumflex occlusion. If she has ongoing symptoms repeat angiography with view to a possible attempt at opening the circumflex could be considered.” 

An ECG at ADHB   of 12 June 2013 reported : “Sinus tachycardia with short PR ST and T wave abnormality consider anterolateral ischemia” This was subsequent to an episode of haematemesis. Another ECG on the same day specified “ Septal infarct”   Subsequent ECGs 13 March 2013  and 22 April 2015 at Northland DHB stated: normal sinus rhythm possible inferior infarct ////Sinus rhythm with short PR – possible inferior infarct”

In their emails dated 18 and 19 August 2015 Professor Ruygrok and Dr Mark Webster advised that “ there were complete blockages involving all 3 main coronary arteries and a significant narrowing in one of the other important branch vessels.  Coronary bypass graft surgery with grafts to the downstream vessels is the best option”  I have elected not to have coronary bypass surgery as my preference is angioplasty/stenting.

Lipid tests( non-fasting:) Northland Pathology

Date: 16 December 2015                                  25 September 2017               11 May 2018

  Cholesterol(mmol/L) as 5.7*(< 5.0)               4.3 ( Range <5.0)                    4.0 

 Triglycerides 3.1* (<2.0                                  1.7 ( Range  <2.0)                   1.5

 HDL Cholesterol  0.97* (>1.00)                     1.13 (Range>1.00)                 1.05

 LDL Cholesterol 3.3( <3.4)                            2.4  (Range <3.4)                   2.3            

CHOL/HDL ratio 5.9* (<4.5)                         3.8 (Range <4.5)                    3.8

Diabetic Profile

Date: 25 September 2017

HbAlc           mmo1/mo1                              34 ( Range < 41)                      34

Troponin

Date 28 August 2017                                    < 5 ng/L  ( Range < 14)

 I met Cardiologist Dr Leigh Nairn at Whangarei hospital on 30 December 2015.  His report is as follows: “ she  has a history of ischaemic heart disease with an occlude LAD stent and occlusion of the circumflex and  mid RCA arteries.. PCI is not technically possible and she has been recommended to continue with medical therapy or CABG if she has restricting angina symptoms”  Examination, weight 67 Kgs, BP 124/76, Pulse 74/minute regular. CVP not elevated.  Chest clear.  Quiet systolic murmur at the LSE-apex.  ECG showed sinus rhythm with Q waves inferiorly mild ST slurring in 1, AVL, V4-6. (Only “RCA mild disease” was reported in 2011”

 Dr Nairn stated that while  the left descending artery was often stented the procedure was rarely implemented in respect of the left main.!.  He made no reference to the latter in his report.  Stenting procedures are commonplace in both of these arteries which are commonly known as “ the widow makers”!  

ADHB’s clinical summary dated 26 November 2013 referred to  “stenting of t he distal left main and the left anterior descending artery which  was performed in 2012 Severe proximal intermediate proximal occlusion of the left circumflex artery and mild right coronary disease. In 2013 there was “ severe stenosis at the distal edge of the mid/distal LAD stent . A further stent was deployed”.

The cardiologist seemed to have difficulty locating the previous stress echo performed earlier this year. His report concluded: “ she had a mildly positive stress echo July 2015. The stress echo report stated “ multiregional wall motion abnormality  Multiple segments including apical/septal/anterior /inferior and posterior wall akinesia.  During exercise LV dilated and showed diskinetic changes mainly in the anterior wall”.  “Prognostically she probably would benefit from CABG but in the absence of significant symptoms at the present time Vicki is releuctant to have  CABG. She is not specifically on any anti-anginal medication at the present time and  if she develops deteriorating angina then she should be reviewed in the cardiology OPD, and also have a trial of ISM or CCB.  She is probably unlikely to tolerate beta-blockers because of a history of chronic fatigue fibromyalgia”

There has been no contact with cardiology since 2015. 

An ECG was performed at Onerahi Medical Whangarei on 16 June 2018.   Details are as follows: “ Warning: artefact in ( part of )recording-use  interpretation with caution -sinus rhythm slight inferior repolarisation disturbance, consider ischemia , LV overload or a specific change. Borderline ECG. Unconfirmed report”. Changes are evident V4 and V3 in the latest graph in comparison with the graph of 2015.

An ECG was performed at the Cardiology Clinic at Whangarei Hospital on 27 August 2018 prior to an appointment with cardiologist Dr Lee. There appeared to be no significant changes from earlier ECGs apart from an improvement in V3 and V4 segments. Lee advised “ I have not made any changes to Vickis medications. She does get a bit tight around the chest but this is only severe exertion but she has otherwise been stable without any deterioration in her symptoms  There are no new ischaemic changes. The reality is that she would require bypass surgery but her symptoms have not been particularly progressive suggesting that she has a fair amount of collateralisation….Vicki only requires follow up every three years to see how she is getting on”  He  did not consider that  a further stress echo was necessary nor a further check of  stenting at ADHB.

The American College of Cardiology advises: “You might need an imaging test if your symptoms come back or get worse. This includes symptoms such as chest pain, shortness of breath, feeling tired, or having trouble climbing stairs..  If you don’t have symptoms, you may still need an imaging test if:

• It has been more than five years since your bypass surgery.
• It has been more than two years since your stent procedure.
• You have blockages that weren’t treated during your first heart procedure.
• You have diabetes or aggressive heart disease.”

Fibrinogen Assay test dated 2 August 2018 provided a reading of 4.7 g/L   H   (1.5-4.0) (Fibrinogen is  one of 13 coagulation factors responsible for blood clotting)

ESR  and CRP  are both inflammatory indicators- ESRs  have ranged from 26 in July 2009, 34 in November 2009 , and July 2010, 21 in August 2011 and  17 in October  2012  (norm: 1-30). A CRP ( C-Reactive Protein  norm : < 5)  test dated 17 January 2012 was reported as- 6*,   7* mg/L on  7 November 2014, 26 February 2015, and 16 December 2015. These tests have not been repeated.  A CRP reading of 46 mg/L   H  0-5 was reported on 2 August 2018, C-Reactive protein dated 15/2/2019,  6/5/2019 and 5/9/2019 measured 2 2mg/L and 3 mg/L  and  were within the normal range(<5)

  Patient .co.uk states :

C- Reactive Protein (CRP) concentrations characteristically return to normal after seven days of appropriate treatment for bacterial meningitis if no complications develop. Serial monitoring of serum and CSF-CRP concentrations may be useful clinically.

• CRP is nonspecific and its clinical usefulness is therefore limited, especially in diagnosis. CRP is useful in monitoring disease activity in certain conditions (eg, rheumatoid arthritis, infections or malignancy) and as a prognostic marker for conditions such as acute pancreatitis.
•  
• An increased CRP may be due to:
  • Inflammatory disorders – eg, inflammatory arthritis, vasculitis, Crohn’s disease.
  • Tissue injury or necrosis – eg, burns, necrosis, myocardial infarction, pulmonary embolus.

Erythrocyte sedimentation rate ( ESR) and is a sensitive but nonspecific index of plasma protein changes which result from inflammation or tissue damage. Low ESR: polycythaemia, hypofibrinogenaemia, congestive cardiac failure, spherocytosis, sickle cells .

 ALBUMIN/CREATININE RATIO (Random Urine Sample)Date: 05/07/2019

Ref. Range

Ur.Albumin mg/L     < 3       (< 30)

Ur.Creatinine mmol/L   4.1

Alb/Creat ratio mg/mmol < 1.0    (< 3.5)

Lipid tests ( non-fasting)  dated 5 July 2019 from Northland Pathology were within the normal range.

Fasting Status Not stated

Cholesterol mmol/L 3.8     (< 5.0)

Triglycerides mmol/L 1.6  (< 2.0)

HDL Cholesterol mmol/L 1.11  (> 1.00)

LDL Cholesterol mmol/L 2.0  (< 3.4)

Chol/HDL ratio 3.4  (< 4.5)

For established CVD risk (including diabetes) NZGG optimal

levels are Cholesterol < 4.0, LDL < 2.0 and Chol/HDL ratio < 4.0.

I attended the ED clinic at North Shore Hospital on 6 May 2020 as I was afflicted with a chest complaint.  “ Examination on presentation: BP: 128/45 mmHg///HR: 59 bpm////Temp: 35.9C  Heart sounds dual///JVP normal////CRP: <3mg/L (0.5 mg/L)  N

I met Cardiologist Dr Glenie on 12 November 2020.  No heart checks were performed including a blood pressure reading. He did not consider that a subsequent consultation was necessary unless I experienced serious pain when heart surgery would be the only option. “Routine imaging of the left main stents is not indicated particularly in light of the recent ischaemia trial.” Website Seconds Count states: “Even when a stent is implanted, restenosis can develop inside the stent. But sometimes scar tissue forms under the healthy tissue. If that scar tissue grows thick enough, it can cause restenosis.  With drug-eluting stents, the restenosis rate can be under 10 percent. If you have had an angioplasty procedure (with or without stenting), it is very important to have regular follow-up visits with your doctor.

 Your doctor will monitor your health to make sure that you don’t have problems or complications.. This could include angina, shortness of breath, or chest pain with or without physical activity. If you do have symptoms your doctor may recommend tests, such as a stress test  or an angiogram, to determine if you might have restenosis or a new blockage that may require further treatment. Healthline advises “ In the event that scar tissue forms after stenting your doctor may need to repeat the procedure. I have not had significant contact with the specialist who performed the stenting procedures since 2013. 

Resting echo of 2015 at Whangarei Hospital showed:  “multiregional wall motion abnormality with mild to moderate LV systolic disfunction. Multiple segments including apical septal/anterior/inferior/and posterior wall akinesia. During exercise LV dilated and showed dyskinetic changes mainly to the anterior wall which correlated with her symptoms and hence the test was deemed positive”.

Glenie considered that “there is no good percutaneous option for either of the LAD or circumflex occlusions.  She also has a known mid right coronary artery occlusion…again there are no good intervention options from a percutaneous perspective.” In 2012 Dr Webster advised “that an attempted opening of the circumflex might be considered if there were ongoing angina symptoms”. Glenie further advised  “She does have other significant medical history….she comes today for routine review-she gets minimal anginal symptoms-she does not get resting anginal symptoms… has chronic chest infections. Clinically she has dual sounds with no added murmurs. Her venous pressure is not elevated. There are no carotid bruits. She has  occasional crepitation at the left base but otherwise the chest was clear????/  She has stable coronary heart disease the  indication for a repeat angiogram would be for the consideration of coronary artery bypass surgery”. Although a blood pressure reading of 180/90 was referred to by respiratory physician Dr Chapman BP  was not recorded by Dr Glenie.

Abnormalities in the lipid tests from 2014 until are detailed below:

 Cholestorol*=H     16/12/2014*= 5.6*(fasting) 16/12/2015 5.7* 14/9/2016  5.2* //     

Triglyceride 2.8  *=H 16/12/2014   *////////26/2/2015  2.5*  16/12/2015  3.1*////14/9/2016 2.5*

Fibrinogen Assay *=H (1.5-4.0) 2/8/ 2018  4.7g/L  H 

Labtests online advises:  A fibrinogen antigen test measures the amount of fibrinogen in the blood. Fibrinogen is produced by the liver and released into the blood along with several other clotting factors (also called coagulation factors).

Lipid tests are as follows:

Date:                         16/12/15      4/9/2016   11/12/2020   18/2/2021        

Cholesterol               5.7*              5.2*            3.1                4.1                          ( Range <5.0)

Triglycerides            3.1                2.5*           1.1                 1.4                            (Range <2.0 )      

HDL Cholesterol     0.97              1.16           0.97*              1.24                         (Range >1.0) 

LDL Cholesterol      3.3                2.9             1.6                  2.2                            (Range < 3.4)

Chol/HDL ratio       5.9*              4.5*            3.2                  3.3                           (Range <4.5)                         

My recent blood pressure readings are 142/74  on 14 January 2021- 151/85 on 18 March 2021 -116/61 28 March 2021-128/83 15 April 2021

 

DERMATOLOGY

In November 2001 I was afflicted with a bad attack of shingles on the back and extending arought chest wall. I was also diagnosed with bacterial infection Pseudomonas Aeruginosa that sameear.  Zovirax treatment was prescribed.  On 17 January 2008 I attended Dr Baker at  Molecheck for a consultation. Their report advised  “  that dermoscopy of all pigmented lesions was normal apart from a lesion on her left mid abdomen slightly raised 6 x 3 mm in size suspicious of a BCC. She also has a large 1 cm  raised round pink lesion on her right forearm tha she is convinced is a BCC and although it has a wobble sign and is diffusely pink with no real features it does have some slightly arborizing vessels and should also be excised.  Digital dermoscopic imaging was not required.  I treated a large number of seborrhoeic keratoses with cryosurgery. I have asked her to arrange for the excision of the 2 lesions. I have circled the abd lesion”.

On February 13 February 2009.I attended Auckland Dermatology clinic. I explained that in 2002 a clinical Professor of Surgery and Dermatology James Shaw had diagnosed the condition as a basal cell carcinoma  “ BCC on the forearm proximally”.( I have a long history of sun exposure and two incidents of severe sunburn)  The registrar Dr Wong claimed not to be familiar with the professor.   He assessed  the growth  as a “soft fluctuant nodule that was fairly mobile…clincally it did not look like a carcinoma as it was too soft…BCC is normally solid.” The Consultant Dermatologist Dr F Oliver agreed  that  “this was not a basal cell carcinoma and was more likely to be a benign neurofibroma.  The differential diagnosis was a dermal naevus. We have reassured her that no further intervention is necessary for this benign lesion”

 In February 2011 Molemap diagnosed a significant number of kerastoses including black keratoses as “benign lesions”   In July 2011 the ADHB  Registrar Dr Simpkin  in conjunction with a consultant dermatologist Dr Lamb examined the numerous keratoses-their report is as follows:   “On  examination today I performed a full skin check.  She has multiple sebhorreic keratoses and one of concern to her was a large dark sebhorreic keratoses that under dermoscopy had typical appearances including milia –like cysts, crypts with keratin and only one uniform colour and is stuck on appearance with multiple other sebhorrreic keratsoses which appeared similar.  She also had a sebhorreic keratosis behind the right ear.  She had a soft 1.5 pink nodule on the right forearm which under dermoscopy has no concerning feature.  She has also been reviewed by the dermatologist  who agrees the nodule on the right forearm is a neurofibroma and the lesion on the back is a sebhorreic keratoses.  Both of these  lesions and benign and do not require excision but if the patient is wanting them to be excised she could approach a general practitioner . We have not made further arrangements to see this patient again”

My own observation of the dark kerastosis from a dermascopic photo was that it measured approximately 10 mm was slightly irregular with color ranging from dark brown tinged with dark yellow near the edge with a pink pigmentation extending out from the extremities.

I again visited  Molemap in January 2012 for the cryosurgical removal of a large number of lesions.  Dr Langford reported that “ dermoscopy of all pigmented lesions was normal.  Digital deromscopic imaging was not required.  I treated multiple serorrhoeic keratoses with cryosurgery. …will require further treatments to totally eliminate the seborrhoeic keratoses.”

There seemed to be difference of opinion between Molecheck and ADHB’S Dermatology concerning the removal of the two lesions.  Although a lesion on the abdomen “ suspicious of a bcc”  was specified by Molecheck it was not reported on by the dermatology clinic. Likewise while the dark keratosis was assessed by Dermatology and photographed by both Molemap and Molecheck identifying characteristics were not specified by either of the latter .It is of some concern that no follow-up consultations were recommended for the future particularly by public hospital.

A large number of kerastoses were removed by cryosurgery performed by  Dr Cottee of Whangarei in September 2014. In lieu of a consultative report I received a basic summary of Dr Cottee’s consultation notes as provided by his secretary:

“Hi Vicki,As per our conversation today I include Dr. Cottees consult notes for 1 Sept 2014 as requested by you.  EnidTown Basin Specialist Centre

“ BJC – full general skin check done///Lots of Seb Keratoses on back and abdo and arms and legs Cryo done AK R leg cryo done x3 AK L leg  cryo. done x  4  AK R arm cryo done x3  AK abdom  cryo done x  16  AK back cryo  done x 40        

Lesion on R forearm  – a 3 cm dia lesion that has ben present a long time and ? growing  – ? cong nevus  ? to remove”.

A request for a consultation at the Dermatology Clinic was sent by GP Dr Thorpe on 25 September 2020. She had photographed images of lesions on my back and hand which she advised would also be onforwarded to the Clinic.  I contacted a scheduler  at the clinic who advised that the request for a consultation had been denied and a letter had been sent to my general practitioner.  However I have not received any such advice from the clinic.  In the interim I emailed further images and reports to Dr Wood of the clinic however I did not receive an acknowledgment of a receipt of the email and subsequently received a referral from Waitemata DHB to the  dermatology practice of Dr Coe of Devonport on 30 November 2020.    Coe photographed my bamber of moles and a few kerastoses. One kerastosis in particular has been removed on three previous occasions but since returned There were no additional dermoscopic photos taken.  A diagnosis of kerastoses was made on the basis of the one photo.  Removal of the lesions was not provided as a free service by the practice to patients referred by public health.  The duration of the consultation was about 10 minutes and there was no further advice from Coe.

GENERAL PRACTITIONERS

Subsequent to the departure of Dr Harries from Maheke Medical Centre circa 1999 I have found the standard of medical care to be cursory and non-investigative.  Dr Harries successsor was Dr Crombie .  I left the Maheke practice and since then I had been receiving most of  my treatment from  either Eastridge Clinic.  As a result of sputum tests undertaken by Bay care a diagnoses of gram negative  Pseudomonas aeruginosa  and gram positive cocci were made in March and  December 2003 respectively. I have also attended  at  the White Cross Clinic Remuera  and City Med Clinics.

In 2002 I attended Dr Jane Buckley at  Remuera  Rd.    She was quite helpful in some respects and provided me with a spacer for my inhaler.  However, with regard to heart matters she advised that my BP was normal  and that  any further heart checks were not  necessary regardless of the fact that there is a history of heart disease in the family -my father died at Greenlane Hospital in 1997  after his second bypass operation. I smoked for 20 years and have a long history of  chest and sinus infections.   A cholesterol test indicated a total  level of 5.9- ( ratio 3.5) Ms Buckley highlighted the  test with a notation “lots of good cholesterol”.  A level between 5 and 6.5 is normally considered borderline and certainly not good. 

I subsequently selected Dr Tom Marshall OBE and Chairman of  Procare .  He spent about a half hour taking details of my medical history.  He was blatantly sceptical of my complaint  of any ongoing bacterial infection( pseudomonas)  advising that 6 months hence I would be unlikely to be still infected. He suggested that I might need to see the pain clinic . He refused to prescribe and  suggested that I would be  better off consulting a GP  in St Heliers.  He then aborted the consultation.  An Encarta Website which details the investigation of a bacteriologist from Wisconsin  describes Pseudomonas Aueriginosa as a  “fearful antibiotic resistant gram negative  bacteria “ with many side effects including brain lesions, meningitis, septiceamia , damage to heart valves and eyes”

On 12 December 2003 I visited GP  Dr Lyn Graham at White Cross Remuera. I showed her copies of my thermography report , the results of  the lab sputum tests  and I also provided samples of  my recent  yellow coloured sputum on tissues.Ms Graham referred to the laboratory report which advised that only a small number of cocci  were evident and on that basis declined to prescribe.  She felt that I should once again visit my specialist for any further treatment.

On Saturday 13 December 2003 I visited Dr Stoyanoff at Baycare Eastridge.  Stoyanoff expressed little interest in the thermography  and Pseudomonas reports ( the latter was copied from an Encarta website).    He prescribed Erothromycin at my request , but was unable to oblige with regard to medication for the discomfort in the upper abdomen.  No explanation given.

In the intervening year I have consulted 2-3 different GPs at CityMed in the city.On one occasion Dr Knill flatly refused to prescribe antibiotics-he subsequently telephoned me the same afternoon and advised that he had changed his mind and would be sending a prescription in the mail.   On another occasion the attitude of  Dr Megan Corbett left a lot to be desired.  When discussing the merits of an antibiotic prescription  she rather spitefully stated  “that if her daughter was coughing up green stuff she wouldn’t prescribe antibiotics”  However, on  a previous occasion she advised that she had noticed “crackles” in the left side of  my  chest    Dr Ian McDonald at Eastridge thought that he detected a “dullness “on the left side of the chest as opposed to the right. . 

On 28 October 2004 I was prescribed additional antibiotics namely Augmentin and Cotrimoxazole by Dr Hancock of Citimed. I have only recently completed a course of Augmentin and doxycyclin and as at 31 October I am still producing small amounts of gold coloured sputum from the chest.  In the past Dr Hancock has seen fit to take my blood pressure however this was omitted on the two  previous visits –likewise a stethoscope /chest check has never been attempted by her .

As at 25 November 2004  later I am still experiencing discomfort in the left side of the chest and still producing  coloured sputum from lungs and  to a lesser extent also nasal sputum reports. In December 2004 sputum samples have ranged from rust-coloured (possibly symptomatic of bleeding)to yellow coloured. There is also continuing discomfort in the left side of the chest including occasional minor sharp pains together with severe inflammation in the sinuses and head /neck area.

I re-visited Dr Hancock on 16 December 2004-she could find nothing significantly wrong after checking my chest and my blood pressure was reasonably normal.  A peak flow  test  was also undertaken and 10 Romicin tabs prescribed.  ( I had previously been prescribed large number of  Co-Trimoxazole and Augmentin tabs)    When I mentioned that RBCs had not been reported by the laboratory since 1999 Dr Hancock advised that “it was probably due to a different style of reporting”! A spirometry test undertaken by Dr Hancock on 16 December 2004 indicated a level  350  while a check of the chest indicated no significant abnormality. . I was prescribed a further 10 Romicin tabs – As at 21 December I am experiencing severe discomfort particularly  in the lower left chest extending into the back and also afflicting the sinuses head and neck. The chest discomfort is more  pronounced after coughing, 

  On 22 December 2004 Dr Bhai of Glen Innes claimed that he was unable to detect any significant abnormalities in the chest apart from impaired breathing.  While he appeared interested in the fact that I had been infected with Pseudomonas Aeruginosa in the past he expressed a lack of concern when I mentioned that I had also experienced discomfort in the glands in the neck.  He prescribed augmentin and  lora tabs for allergy.

On 26 January 2005 I attended  Dr Crozier at Baycare Eastridge .  He was quite happy to prescribe Romicin tabs ( 300 mg) for an extended period.  He undertook a stethoscope check of the chest and a finger check of oxygen levels which was apparently recorded at 98%.  When I suggested a spirometry test he declined as he felt that the latter test was the better option. I have never been given an oxygen test involving the finger at any other medical practice including specialists –all tests have have either spirometry or stethoscope. A spirometry test instigated by another Baycare doctor some years ago ( recorded a level of 340 ) resulted in my being prescribed an inhaler . More recently it was 350. For somebody of my height the normal level would be approximately 450.

In March 2005 I attended Dr McDonald of Eastridge.  He provided a prescription of  Augmentin tabs.  He said that a check with the stethoscope revealed nothing untoward however as at 15 March I am producing some faintly yellow coloured sputum  and have quite noticeable discomfort in the centre of the chest and sinuses /head. He also provided a prescription for anti-fungal sporanox tabs for thrush. A new prescription for augmentin was provided on 4 april 2005 I was once again prescribed augmentin tabs for on-going chest infection. Dr McDonald checked the chest with the stethoscope and found nothing significant –he seemed a little confused as to my previous history of chest infections ( I have also complained of severe inflammation in the sinuses and head generally)

 The spriometry test was much higher than usual in the 400 range. A follow-up consultation in early May resulted in a prescription for Romicin .  A sputum was also provided for onforwarding to Southern Community Labs.( See Respiratory notes)

A sputum test of 4 April reported a small number of white cells –moderate number of epithelial cells –mixed bacterial flora and the usual oropharyngeal flora.    Culture showed a heavy growth of serratia marcescens which is apparently sensitive to cotrimoxazole and ciprofloxacin. Dr Hancock has prescribed cotrimoxazole

 “Cephalosporins, gentamicin, amikacin are also recommended.   Tests have shown marcescens to be dominant over the B cereus, subtillus, E coli, S lutea and B megaterium. This bacteria is a gram negative.-a human pathogen of the family enterobacteriaceae. It is involved in noscomial infections particularly urinary tract infections and wound infections.   Most strains are resistant to several antibiotics because of the presence of R-factors on plasmids. It occurs naturally in soil and water as well as the intestines.  Its often associated with endocarditis, osteomyelitis, septicemia, wound infections, eye infections and meningitis”.

 (In an experiment conducted by the US Army in the 1950s balloons were filled with Serratia marcescens and burst over the  city of San Francisco Shortly thereafter doctors noted a drastic increase in pneumonia and urinary tract infections.) 

 In 2 subsequent May 2005 consultations with Dr McDonald I have been prescribed ciprofloxacin and Co-trimoxazole and augmentin.  Dr McDonald was initially very reluctant to prescribe any alternative antibiotics until the results of the latest sputum test became available. This was despite the fact that my sputum sample was much the same as previous specimens and 2 of the drugs recommended for treatment by Medlab were Co-Trimoxazole and /or Cipro. My experience is that Cipro is the least effective of all the drugs.  McDonald suggested  “ that I was coming in with bits of paper and asking for this that and the other drug-and that it was negligent for him to keep prescribing”  An illogical statement. As I explained I have a history of 20s+ years of chest and sinus infections-the bacteria are a combination of dangerous gram negative and gram positive-and notorious for their drug resistance.  I suggested a combination of existing drugs or even a larger dosage-while the drugs no longer totally eliminate the infection they can ameliorate many of the symptoms.  McDonald still felt that I should consult a specialist and possibly have a chest x-ray or Ct scan of the chest.  He is aware that I have already consulted 3 respiratory physicians with no result.

A sputum sample sent by Dr McDonald in early May to Southern Commnity Laboratories reported the presence of : “a small number of polymorphs,moderate numbers of epithelial cells large numbers lf gram negative bacilli and large numbers of gram positive cocci”. I requested and was prescribed Romicin antibiotics.  Some wheezing was detected in the left lung .  I have been prescribed co-trimoxazole , augmentiin  Romicin and Ciprofloxacin.   As at 24 May I am still badly affected in the lungs  and with accompanying serious inflammation in the sinuses and head.

Diagnostic Laboratory’s sputum report dated 24 May  reported a “ small number of white cells and mixed bacterial flora”    As  at  10 June 2005 I am still experiencing quite severe symptoms including pains in the lower chest soreness in the centre of the chest and inflammation which is particularly severe in the legs and feet making walking difficult.  I have almost completed a course of augmentin and co-trimoxazole.

During a visit to Dr Julie Hancock at Citymed on 16 June 2005 she refused to prescribe any further antibiotics –and claimed that the 2 most recent sputum tests indicated nothing of significance. We had a difference of opinion on the subject . ( Medlab test of April 05 diagnosed Serratia Marcescens and the lab test of 3 May reported large numbers of gram negative bacilli and gram positive cocci)  I mentioned that Serratia Marcescens had been used for experimental purposes by the US Army in the 1950s over San Francisco-  there was no response from Hancock !  She did however prescribe a nasal spray Butacort  a Pulmicort inhaler.and paradex tablets as a substitute for antibiotics/panadol.  ‘She also requested a blood test –ESR.    ( Note: Shortly after I left Hancock’s room there was a loud comment called out –possibly from Hancocks room –her door was closed –namely  “ she won’t be back here again”)

I subsequently received a copy of a Pelvic scan report undertaken at Green Lane on 22 February 2005.which was sent to me in the mail at my request by one of Citymed’s  nurses.  Although I had a consultation with Dr Hancock the previous week the scan was never mentioned by her.   Dr Hancock has a Dip Obs. Qualification.

On 14 July 2005 I consulted Dr Kala at East Tamaki Healthcare.  She was unfortunately initially very resistant to prescribing antibiotics –citing the most recent sputum test  in which no pathogen was specified.  I showed her excerpts from my respiratory file including the diagnosis of serratia marcescens in April of this year  -I mentioned that the bacteria was implicated in the contamination of  the US 2004 flu vaccine however she chose to ignore that aspect .  She did specify that my breathing was a little laboured and was recommending only cough syrup and possibly losec.  She finally requested a second opinion from Dr Yee and he suggested that antibiotics might be in order and I was given a prescription for co-trimoxazole.  Dr Kala was citing the fact that I was only a casual patient and as such they didn’t have access to Ct scans etc and recommended  that  if I was experiencing discomfort in the chest I should attempt to do something about it other than simply requesting antibiotics.  I explained that I had already consulted 3 chest physicians and had undergone a bronchoscopy.

On 7 August 2005. I was further prescribed a 2 week course of augmentin, and at my request, a prescription for lipex from Dr Muller of East Tamaki Medical.  Dr Muller checked my chest with a stethoscope and claimed he couldn’t find anything untoward apart from a “rasping?” sound.  . He was unable to locate any previous details about previous infections even though I had  shown Dr Kala copies of my previous recent lab /sputum tests.  When I mentioned that I had been recently afflicted with serratia marcescens Dr Muller appeared to be confused concerning this particular medical condition and did not comment on specifics pertaining to the serratia strains although he seemed to take note of the fact that pseudomonas had also been diagnosed in the past.

A consultation with Dr David Chee at East Tamaki Healthcare on 7 September 05 resulted in a prescription for 20 Romicin tablets.  The nurse had previously taken my blood pressure -140/90  which only received a brief mention by Chee after I brought it to his attention..   A stethoscope examination of my chest revealed “ nothing of significance” .  Although I requested a peak flow test  this was not done.

I attended the Southern Cross clinic on 23 September 2005. I had already been waiting for approx 1-1 ½ hours, and another ½ hr to ¾ hr period elapsed subsequent to the apparent departure of the last patient. I enquired from the receptionist as to the next appointment –she advised that the doctor was taking out stitches.  The duty doctor was a young Indian woman.  I walked past her office and she was busy using her word processor.   She advised “ that she didn’t know when the next appointment might eventuate as she had a patient to attend to”.   I departed soon afterwards without a consultation. . 

Antibiotics were denied by Dr Crozier at at consultation on 25 September at Eastridge.   He felt he was unable to assist-he would need to see evidence of infection – and  it was a matter for either a GP or a specialist.   I explained that I did not have a GP at the present time and had been to the Eastridge Clinic many times over the years and that the clinic retained all my particulars and details of chest infections.  Also Dr Crozier had no such reservations when he prescribed antibiotics in January of this year.  When  I mentioned that my recent BP tests were 140/150 /90 he suggested that he might “ get the nurse to check”  –however that did not eventuate. The consultation ended after about 10 minutes.

There was a consultation with Dr Coral Fonseca of East Tamaki Healthcare  in Glen Innes on 5 November 2005.   I had been experiencing fairly severe pain in both the sinuses and neck area.  I produced some nasal sputum which although predominantly white in colour did contain significant flecks of yellowish/green sputum. Dr Fonseca claimed that  checks of my chest and glands revealed nothing untoward and she contended that that I was afflicted with nothing more than routine hayfever..  I disagreed and reiterated that after 30 years of experiencing severe chest and sinus infections I should be able to tell the difference between allergy and the onset of  infection.  Fonseca then made a rather extraordinary statement “that if you have been taking antibiotics for 30 years without any significant improvement what then is the point of taking any more”   When I advised that my history included having been afflicted with assorted gram negative infections and having almost been hospitalized on one occasion a few years ago she claimed that there was no evidence of those details on the computer .  I advised that doctors had been advised of those details during previous consultations and they should most certainly be on the computer.   I told Dr Fonseca that I was dissatisfied with her prescription of allergy medication only and ended the consultation.

A Sputum/gram stain  test of 16 November 2005 indicated a large number of white cells , no epithelial cells and mixed bacterial flora together with a moderated growth of normal respiratory flora.   I was prescribed a course of Augmentin . Dr Thomson enquired as to whether my sputum was fairly typical ( frothy?) and whether I had ever had TB.  I explained that I had been tested for Tb at my request a few years ago and it was negative.  I explained that I thought there was a slight muscular weakness in the left lower arm –however Dr Thomson made no comment after testing.

 A prescription for  Augmentin and Co-Trimoxazole were prescribed by Specialist Dr Orr-Walker on 21 March 06.

A consultation with Dr Martin Thomson of Eastbay Medical Centre on 17 November 2005 resulted in a prescription of augmentin together with eye drops and inhalers.   I provided a sputum sample and Thompson commented on the of the latter and enquired as to whether this was the norm . ( My sputum was also very frothy which can be indicative of Pneumonia or  Pleurisy ) I advised that this virtually the case. Apart from that he made no other comment.  He also asked whether I had ever visited Africa ( presumably in response to my advice that I had been afflicted with Pseudomonas Aeruginosa in the past)  and whether I had ever been afflicted with Tb.  I advised that I had a skin test for Tb some years ago and there was no indication of the disease.   He checked my chest and made no comment. He declined to look at my file suggesting that it might be more appropriate next time.  ( He is a locum –standing in for Dr Lyn Henrys on Wednesday of every week). Medlab results indicated large number of white cells , no epithelial cells and mixed bacterial flora. The culture specified a moderate growth of normal respiratory flora.

I attended Dr Henrys at Eastbay Medical on 22 December 2005.  I once again complained of severe inflammation in the sinuses head and neck area co-inciding with the increasing respiratory discomfort and sputum.  She took my temperature  and checked my chest without further comment and agreed that if I was experiencing pain then an antibiotic prescription would be in order.  I suggested a change to erythromycin and she agreed.   She did not check my blood pressure.  With my regard to my broken toe she advised that the break would probably take about 3 months to heal and advised me to strap both toes together with cotton wool between.   She did not physically check the toe nor  she did recommend an x-ray.  She had a brief glance at the details on my personal respiratory file and the thermography reports but otherwise made no comment.  The consultation did not really lend itself to any further in-depth discussion about any of my other medical concerns.  I made only moderate progress on the eryrothmycin and by the end of the course was worsening with significant inflammation in the sinuses frontal lobes and neck together with increasing inflammation in the legs and feet.

I again visited Dr Thomson again on 13 January 2006.   He checked my chest by claimed to have detected nothing of significance.  I advised that the pain in the sinuses/head and neck was seriously debilitating and at times necessitated use of an ice pack on the head…I advised that I had coughed up a small amount of yellow coloured sputum a couple of days earlier. The mucous is viscous and often hard to dislodge.   I explained that I had experienced pains in the lower parts and centre of the chest.   When I referred to my previous frothy sputum sample and suggested that it might be suggestive of pleurisy pneumonia or Tb Dr Thomson feigned ignorance of any such diagnosis.  (Pleurisy had once been diagnosed by a Wellington GP in the early 1980s)

 I advised that I had attended 2 ENT specialists  and that I felt that their findings were at variance with the thermography report.     I also advised that I wasn’t satisfied with the assessments of the 3 Respiratory Physicians that I had attended either however Thomson queried my scepticism. I suggested a referral to another Chest Physician however this request was not followed up.

With regard to my apparently broken toe Thomson asked me to flex the latter and then provided a referral to radiology.   Thomson then provided  (inadvertently )  some  rather extraordinary data on a referral to Medlab including  my BP, weight,usual drug regime-   “recent # 6 weeks ago of the 3^rd R toe///chest clear sl tender sinusis all over and T 36.6/////prone to recurrent bronchitis cond///and feels need for antibiotic and names it///has control over her own health and carries own file around///ME and a number of ailments and very firm in her ideas”     The reference to recurrent bronchitis is erroneous as was a similar reference in a previous  report from respiratory physician Dr Garrett subsequent to a bronchoscopy. Once again Thomson declined to look at my file on the grounds that he did not have enough time.  If he had done so he would have have found evidence of previous infections such as Pseudomonas aeruginosa and serratia marcescens and reference to a thirty year history of chest and sinus infections coupled with  a history of childhood asthma and a 20 year history of smoking. Irrespective that I experience discomfort in the neck he claimed that he could not find anything significantly wrong with the glands. My BP was 138/72.  A prescription of  Romicin was ultimately prescribed.

On 2 January 2006 I attempted to get an appointment with yet another GP. The receptionist at the practice of Dr Twigg and White at Orakei advised that they were not taking on any new patients.  A further attempt at the Auckland Family Practice of Dr S James on 94 Remuera Road resulted in ten minute conversation with the young receptionist as she took down all my personal particulars – she was obviously taking instructions from another female staff member in the background –she  then advised me that the initial consultation would cost $116.00 .   I concluded the conversation at that point.

I visited Dr Dan Anderson at Baycare White Cross Eastridge on 27 January 2006.    He was a young man aged in his 30s.  I advised him of my symptoms ie pain in the sinuses head back of the neck and in the centre and lower chest. He duly checked my chest with the stethoscope but could not find anything amiss.  He also commented that “ I looked so well”.  I showed him some sputum which was mainly white and frothy with some yellowish discolouration.  I advised him that a sputum sample had been sent to Medlab earlier in the week and I was awaiting details.   He didn’t consider that the sample which he described as a “ yellow productive cough –clammy with aches and pains and photophobia  warranted a prescription and advised me to to another sputum test and provided a receptacle.    The fact that I have a 30+ year history of chest and sinus infections fell on deaf ears .  As I departed the office Anderson passed a remark “ doesn’t like f…king “ .  He charged me $40.00 I advised him that his inaction and comment  might be regarded as negligence and  might ultimately be a matter for either the police or lawyers.   He agreed that might be the case but was apparently unconcerned.

On 3 February 2006 I visited Dr Jane Henrys in West Tamaki:  I requested antibiotics as treatment for stenotrophomonas maltophilia .   Henrys checked by chest and advised that she could not find anything amiss .She also checked my temperature and advised that it was normal. This does rather contradict with the findings of a GP Dr Anderson at Eastridge the previous Sunday who reported “ yellow productive cough feels hot and clammy/pains in the back of the head and neck”   Dr Henrys felt that although this particular bacteria was diagnosed it was not necessarily an abnormal bacteria and I would not necessarily be affected by it.  She was initially reluctant to prescribe any medication on the grounds “ it might harm me”  I replied that this was the third  gram negative bacteria that I had been afflicted with over the past few years and if the bacteria was so innocuous why then was there a recommendation by the laboratory for treatment with specific drugs including gentamicin which is normally administered intraveneously in severe cases.  …I further advised that in my experience of drugs Augmentin was the most effective drug –that I had found the recommended drug cotrimoxazole ( a generic) to be not especially effective.  Dr Henrys reluctantly provided a prescription for Augmentin .

She requested a blood test /CRP and had initially suggested that I should wait for the result before starting on the prescription.   I didn’t feel that was necessary as the proof had already been provided in the sputum test and I was also experiencing quite significant pain particularly in the sinuses and neck.

Dr Butterfield of  White Cross Ascot  provided further prescriptions for Lipek, Diclofenac and Combivent inhalers on 26 May 2006.  I advised that I was near the end of a previous antibiotic  prescription –he prescribed 14 Romicin tablets. He checked my chest but not my BP.  I requested a peak flow meter test and levels of 250 and 300 were indicated.   Butterfield made no comment other than to ask me what I thought the levels should be.   I had complained of pain and discomfort in both the sinuses and chest however his only recommendation was to see yet another ENT specialist.  I reiterated as I do at most consultations that I have been afflicted with various gram-negative strains over the last few years and as stated on the medlab form they are considered to be multi-drug resistant.    Dr Orr-Walker had no hesitation in providing me with 3 months supply of antibiotic.  Latterly GPs have been either reluctant to prescribe any antibiotics or they prescribe a minimal amount.

As I had been experiencing a very stuffy nose and painful sinuses with the development of a chest infection and severe cough I received a prescription from Dr  Retford for ciprofloxacin and Romicin on 19 August 2006

My mother had also been similarly affected. Yellowish coloured sputum was sent for analysis –both  tests dated 19 & August reported small numbers of epithelial cells , mixed bacterial flora and heavy growth of normal respiratory flora. Both tests were done 2 days apart however the first test reported no white cells while the second reported  large numbers of the same.  Dr Retford checked my chest and found evidence of “ crackles” on the left side .  She did not however check my blood pressure.

A prescription for Romicin and Co-Trimoxazole Tabs were provided by Dr Chebbi on 12 October 2006..  Dr Chebbi did an oxygen saturation test on the finger- it indicated 97%. At my request a further test was undertaken with a peak flow meter –it registered 300. ( the normal  reading for somebody of my height is 450- previous specialist spirometry tests have been classified as low but within the normal range at 340-370).

When I asked Chebbi about the disparity between the 2 different tests he shrugged his shoulders and said he didn’t know. 

A consultation with Dr Talbot of White Cross Eastridge resulted in a prescription for augmentin.  Bp appeared to relatively normal.  Subsequent to a sputum test in Jan 07 which reported Serratia liquefaciens Dr Retford provided a prescription for a combination of Co-trimoxazole and Ciprofloxacin.

I visited Dr Francis at White Cross Eastridge on 2 May 2007.  An “assault “ comment was heard from the doctor outside the consulting room.  The door remained open for the almost the duration of the consultation.  The practice nurse was also overheard commenting as to “ why psychiatrist committed her”.  The consultation was unnecessarily protracted-Francis seemed to be little confused as to which cholesterol  medication I had been prescribed –he insisted that I had been prescribed Lipitor in the past and I insisted that I had been prescribe the generic Lipex.  He finally acknowledged that I had been prescribed Lipex/Simvastatin tabs.   He checked my chest and throat and could not find anything significantly amiss   He did not check my neck or glands   I had been experiencing quite significant soreness and stiffness in the neck. . Regardless he prescribed augmentin tabs together with renewed prescriptions of Lipex and diclofenac.  A peak flow meter test indicated a level of 300 which Dr Francis considered to relatively normal.

On 20 July 2007 I  again consulted with Dr Suresh Francis an Indian doctor at Eastridge. I also produced a small amount of slightly yellowish coloured sputum. Francis was very resistant to prescribing antibiotics described the sputum sample as “colourless” and insisted I was probably afflicted with a virus. I advised that I had been attending the clinic for about 20 years, had a history of gram negative infections, and had generally been prescribed antibiotics. I have a history of gram negative infections. He reluctantly prescribed augmentin . He also pointed to a notation on the screen that may have indicated that I had contact with Dr Crozier in April.  My last consultation with Dr On Crozier was  in 2005.

On 3 September 2007 I met Dr Carol Lawton of St Heliers Health Centre in Polygon Road St Heliers.  Lawton was quite obliging and prescribed antibiotics and checked my blood pressure. She gave me referrals to a respiratory physician Dr Rea of Manukau. and Dr Bartlett of Epsom. Unfortunately Dr Rea is no longer taking any private patients and the consultation with Dr Bartlett was not a success as he terminated the consultation because he erroneousely considered that I was not prepared to accept his opinion.

There was a consultation with English general practitioner Dr Angela Jacobsen of Selwyn Medical Centre on 8 January 2008.  I had brought a number of CT chest scans for discussion however she stated that she was unable to read them and suggested that perhaps I could take the matter up with the radiographers next door.  I had expressed concern about a mole on my back which had changed colour and was now black-also a small round pink lump on the right arm.  She doubted that the mole was a melanoma but rather a keratosis and referred to the pink lump as a  “squigy thing” .  In fact the pink lump was diagnosed by Professor J Shaw a few years ago as basal cell carcinoma who advised  that the BCC does not normally penetrate beneath the skin and simply increases in size. Jacobsen  seemed very reluctant to refer me onto the public health system as she considered that there would be serious delays.  I said that obviously if a melanoma was suspected then some priority would be given by the hospital. In  2001 Dermatology Greenlane advised that a melanoma or query melanoma was assessed as a Lesion A+ category.  BCC’s on the trunk or limbs were assessed as Lesion A- and were not seen.  Dr Jacobsen did however recommend Mole Check on Remuera Road and I  made an appointment with them.      I had also requested a referral to neurologist Dr Elizabeth Walker . I made the appointment however no referral has as yet been received by the staff at Adventist Hospital.  I have twice spoken to the staff at Selwyn Medical- on one occasion Dr Jacobsen was absent and the receptionist put a note in Jacobsen’s  diary.  On Friday 11 January 2008 Dr Jacobsen had briefly visited  the practice however the referral had still not been dealt with. 

On 19 March 2008 I consulted Dr Sunil at Eastridge White Cross.  He checked the chest with stethoscope ( although not the areas where I experience discomfort namely the centre and left side ). He did not check my throat nor did he take my blood pressure. He made no comment concerning the result of his stethoscope check.  He didn’t think I had a temperature and although was prepared to prescribe antibiotics would provide a week’s dosage of augmentin and 30 diclofenac anti-inflammatory tabs. ( I normally receive a prescription for 2 weeks of antibiotics and three months supply of anti-inflammatory tabs).

I met Dr James Dryden on 29 July 2008 as I was once again experiencing flu symptoms.  He duly checked my chest with his stethoscope but not the centre of  the chest nor the left side where I experience most of my discomfort.  I suggested that he undertake a BP test but this request was ignored.  ( I have a heart condition)   At my request I undertook a peak flow meter reading which indicated a level of 300 .  I tried to discuss this with the doctor but was told “ not to worry about it”.  ( several years ago another GP from Eastridge initiated a peak flow meter reading and advised that for somebody of my height the norm should be around 450).  Spirometry testing by a respiratory physician has indicated a maximum of 370 assessed as “ low but within the normal range”. He prescribed a combination of Romicin and Co-Trimoxazole antibiotics-somewhat less than the usual number prescribed by female general practitioners.

At a consultation with Dr Retford on 15 August 2008. She prescribed antibiotics and a referral to the gastroenterologist of my choice.

Two “ committed” comments were overheard from a local general practitioner namely Dr Van Roekel a few years ago while I was waiting in the practice’s reception area. He provided an effusive written reply/apology as a result of my complaint via The Health and Disabilty Commissioner/Advocacy Service in 2008.

Two replies from Wellington general practitioners namely Doctors Delaney and Dr Waite were unsatisfactory –the former was somewhat incoherent whilst the latter reply contained erroneous biographical detail and recall.

On 22 October 2008 with Retford she again prescribed antibiotics namely cipflox and co trimoxazole  also anti inflammatory tablets and lipex.  She checked my chest with the stethoscope and advised that she detected some “crackles” in the left lower lobe.  Although she didn’t examine the nostrils/sinuses she did take a swab from the right nostril . She also sent a referral to Greenlane Dermatology the probable basal cell carcinoma –nodule- on the right arm.  She didn’t know whether the hospital policy had changed –several years ago Greenlane would remove only the more serious lesions –anything less serious, particularly a lesion on the limbs was normally attended to in private practice.  She did not take my blood pressure on this occasion.Dr Retford  prescribed ciprofloxacin co-trimoxazole and lipex .  On 24 December 2008 she prescribed Metronidazole prior to a tooth extraction.

 On 15 May 2009  I had as usual been experiencing discomfort in the chest particularly the left lung  associated with some morning chest sputum and  discharge from the nose.  Dr Retford did not check my chest but prescribed a course of amoxicillin and ciprofloxacillin.   Her nurse tested my blood pressure and it was somewhat higher than normal at 158/90. Retford also seemed a little concerned about the higher diastole reading.

On 13 August 2009 I attended Dr Gates at the Meadowbank Medical Practice.   Prior to the consultation there were  “ assassinated and committed” asides from Dr Gates. He was unable to prescribe ciprofloxacillen  as he  considered he was unable to do so without specialist approval and felt that I should take the matter up with Dr Wilsher. He seemed to have scant regard for the seriousness of the gram negative infections suggesting that even though the bacteria was specified I wasn’t necessarily being affected by it – he also cited the lack of reporting of white cells in this regard He did however renew some prescriptions of carbimazole diclofenac and lipex.  

Dr Retford has set up a new practice on Remuera Road in conjunction with 3 other doctors .As I had been experiencing the usual set of flu symptoms Dr Retford prescribed a combination of erythromycin and Romicin on 19 November.  A few days later I was afflicted with severe pain in the legs and the appearance of copious amounts of thick green sputum from the chest accompanied by severe coughing fits most often in the wee small hours. The prescribed antibiotics were virtually ineffectual and subsequent to a sputum test undertaken by Labplus on 24 November  there was a diagnosis of Haemophilus Influenzae -. Recommended drug treatment is amoxicillin, cefaclor ,cotrimixazole and tetracycline. I also received a referral to radiology for a breast ultrasound. I obtained a script for Augmentin from Dr Dryden at  Eastridge medical on 30 November however I subsequently discovered that I had been provided with  a generic substitute namely Synermox 625mg which had replaced Augmentin .

Since the onset I have developed severe discomfort in the right lower lumbar area and also the right knee-possibly a type of septic arthritis resulting from the infection. On 8 December the worst of the infection has significantly diminished although there has not been much change in the pain. I visited Dr K Aweidah on 10 December 2009 and received a prescription of  Amoxycillin.  He undertook a brief check of my chest with the stethoscope and claimed to find nothing of significance.  He did not check my blood pressure.

A further consultation with Dr Nicki Retford on 17 December 2009 resulted in a prescription of both synermox and doxine tablets.  The blood test performed by Labplus on 19 November indicated a higher than usual neutrophil count of 7.84 ( norm 1.90-7.50) and monocyte count of 1.10 ( norm 0.20-1.00).  The lymphocytes remain a constant 1.63 (norm 0.90-4.00) which might be considered borderline low. The ESR ( an inflammatory indicator) was also high at 34 ( norm: 0-30.  She did not undertake a blood pressure check nor did she refer to the blood test results.   ).  

In the absence of Dr Retford I consulted with Dr A Twhigg at One Dental on 19 February 2010. I requested another round of antibiotics as I was still afflicted with a chest infection and inflammation. She seemed to be intent on prescribing a combination of antibiotics namely Romicin and synermox ( a generic substitute for Augmentin) as she felt Romicin would assist with the inflammation.  I pointed out that in respect of Haemophilus influenzae with which I was possibly still afflicted a specific drug regime was recommended by Labplus and it did not include Romicin. I had taken a course of erythromycin during the early stages of  influenzae and the drug was ineffective. The likelihood of Romicin being any more effective is probably also remote. Medsafe drug sheets advise that Romicin has intermediate sensitivity to Haemophilus but is not the first drug of choice. I was prescribed courses of Synermox and Co-Trimoxazole.  A check of my blood pressure showed a reading of 180/?.  Dr Twigg suggested that I contact the nurse and continue to have the pressure checked.   

On 15 April 2010 Dr Retford  prescribed synermox , romicin and simvastatin tabs. My Bp was 160/???.  I had emailed her a number of files prior to the consultation however she claimed not to have received them.  The files were emailed a second time with a request for her to acknowledge receipt of same however there was no reply.

I consulted Dr Govind at One Health Remuera on 22 May.  He prescribed Romicin and Co –Trimoxazole for continuing infection.  My blood pressure reading at this time was 160/88 .

On 25 January 2011  a blood pressure check indicated a reading of 150/90?.  I advised that my symptoms including the bouts of  severe discomfort in the centre of the chest had not changed since last July. Retford did not attempt to stethoscope the chest or check the throat for inflammation and simply prescribed another round of alternative antibiotics namely ceclor and doxycycline.

A consultation with Dr Aweidah on 7 April 2011 resulted in a prescription for amoxycillen clavulate.  I advised that doctor that I had been afflicted with a nagging cough for several months –he apparently considered that most cough medications wre a waste of time.  Mr Aweidah is invariably a “minimalist” in terms of medical advice.

I saw Dr Retford again on 11 June 2011.  She prescribed synermox ,ciprofloxacillen and 2 inhalers –my chest and sinus infections together with the irritating cough have continued for almost 12 months. In respect of gastroenterology  Retford had discussed the matter with her colleagues and she did not think that barium investigations would serve much purpose and that perhaps any further scans generally might not be appropriate if not perhaps harmful.  A CT scan was not mentioned. I had explained that I had suggested barium scans as an alternative as no film of either the endoscopy or colonoscopy were retained at public hospital in 2003.  I had been experiencing a few problems with delays in bowel evacuation.   Melanosis coli was diagnosed –attributed to overuse of laxatives.   Retford advised that the non-retention of film was standard procedure at public hospital.  Nothing untoward was diagnosed in the recent thoracic spinal x ray –I had suggested a whole spine/neck as I have problems in that area as well as the lumbar area.  She has requested a follow up pelvic ultrasound. Retford did check my throat which she considered to be inflamed and proceeded with a throat swab. 

I spoke to a receptionist at One health on 22 June and she advised that there was nothing untoward in the lab result  and that I would have been contacted by the nurses if that was the case.  It is now nearly 12 months and the symptoms of quite severe discomfort /inflammation  in the centre of the chest and throat accompanied by a persistent night time cough have resulted in no diagnosis despite a  sputum test  and throat swab.   An article contained in  Greypowers magazine of June 2011 reported that an increasing number of adults had been afflicted with pertussis ( whooping cough) in the Waikato area over the last ten years. Waikato DHBs programme Manager of Comunications Kathy Jenkin had a severe bout of whooping cough for almost six months in 2009/10. She complained of being “ “unable to breathe in…and would nearly pass out-the worst illness I  had ever experienced” The recommended drug regime is either erythromycin or co-trimoxazole.

 On 22 September 2011 Dr  Retford She gave me the results of recent blood tests performed on 31 August 2011.  A probable streptococcus pyogenes infection was diagnosed ( 600 U/mL (<200?H) – 200-680 Equivocal. I wasn’t contacted about this diagnosis and only became aware of  it at the consultation of 22 September 2011. Possible complications arising from S Pyogenes include pharyngitis, impetigo,necrotizing fasciitis,rheumatic and scarlet fevers.  The CRP ( C-reactive protein) was elevated -5mg/L ( <5) H. CRP is an inflammatory indicator. CRP level is an independent risk factor for atherosclerotic disease. Patients with high CRP concentrations are more likely to develop stroke, myocardial infarction, and severe peripheral vascular disease. Elevated CRP values of Streptococcus pyogenes or Streptococcus pneumoniae in etiology, if left untreated, may also  lead to sinus empyema.( abscess) I received a prescription for co-trimoxazole and ciprofloxacin

The CRP  level  was not referred to  by Retford neither were a high GGT 54 U/L ( <50)H and a low eGFR .  – The ESTIMATED GLOMERULAR FILTRATION  68 mL/min/1.73m2 (>90)L is an indicator of kidney health. In adults, the normal GFR number is 90 or higher.  Laboratory tests performed for Cardiologist  Dr Webster/Dr Retford on 17 January 2012 were almost identical  i.e. eGFR 70Ml raised or high GGT  mma-glytamyl transpeptidase is an enzyme which is found in hepatocytes and biliary epithelial cells. GGT may be high in liver disease. In particular it is a feature of biliary outflow obstruction rather than hepatocellular damage.

GGT (in men) = 11 – 50 i.u./l

 GGT (in women) = 7 – 32 i.u./l

 Note reference ranges may vary between laboratories.

“ GGT serum measurement provides a very sensitive indicator of the presence or absence of hepatobiliary disease. However the usefulness of measurement of serum GGT is limited by its lack of specificity. Raised GGT levels have been reported in a variety of clinical conditions including (1):  pancreatic disease, myocardial infarction, chronic obstructive pulmonary disease. renal failure, diabetes, obesity, alcoholism

GGT levels may be elevated in heart failure. Some studies have shown that people with increased GGT levels have an elevated risk of dying from heart disease, but the reason for this association is not known.

Drugs that may cause an elevated GGT level include phenytoin, carbamazepine, and barbiturates such as phenobarbital. Use of many other prescription and non-prescription drugs, including nonsteroidal anti-inflammatory drugs (NSAIDs), lipid-lowering drugs, antibiotics, histamine receptor blockers (used to treat excess stomach acid production), antifungal agents, antidepressants, and hormones such as testosterone, can increase GGT levels. Clofibrate and oral contraceptives can decrease GGT levels.”

On 5  December 2011 I discussed with Dr Retford  the recent stenting of the LAD undertaken at ADHB by Dr Webster.  I explained that I had been experiencing fairly generalized pain including quite severe pain in the spine legs and feet which was most probably attributable to the continuing infections that I  have been afflicted with particularly in the last 12 months with a lingering cough and severe irritation in the throat.  I expressed my concern about the attitude of Dr Christmas toward the most recent Streptococcus Pyogones infection and the lack of any reference to this detail in his report.  Retford agreed but didn’t discuss the matter further.  I had accidentally banged the upper part of my arm in the area near the elbow used in the stenting procedure resulting in some additional bruising and a possible haematoma.  Retford provided a stretch bandage and considered that the antibiotics would prevent any infection.  She also took a throat swab however she did not request an antibody test as she had done previously. The previous swab had ruled out streptoccus pyogenes.  Antibiotics Synermox and Romicin were prescribed .

In consultations with Dr Retford in 2012 I have mentioned the attitude of the two most recent respiratory physicians that I have attended and also queried the additional detail( opacities)  on the most recent thoracic x ray.There was little in the way of significant response from Retford .

On 8 June 2012 I emailed Dr Retford with an x ray image of the thoracic spine. Retford authorised  the scan  in May 2011 .   I also queried the houseman unit details pertaining to a nodule in the basis of the right lung and which were specified in the report of the chest CT dated  14 November 2011 from Greenlane.

Retford replied that “ I think that you need to raise these concerns with the respiratory doctors at the hospital, as I have limited experience with reading CT scans and also no access to those done at the hospital. What you are talking about is really in the realm of the specialist. Have you any follow-up booked with the hospital as that is really the place to discuss it? Retford had presumably forgotten?that she had initiated the thoracic x ray and no doubt considered that  as a result of the report further specialist consultation was not warranted. .I had nevertheless  mentioned my concern about the scan in a  consultation with Retford.    I find it difficult to believe that her experience with scans is so limited that she doesn’t have an opinion and no doubt she could easily request a copy of the scan as required.  She would also presumably be mindful of my dissatisfaction with the attitude of some of the respiratory specialists

On 16 August 2012 I suffered a fall down some concrete steps and banged my head on the adjacent  brick wall .  There was extensive bruising at the base of the spine and on the right buttock with accompanying swelling and haematoma .

I attended Dr Anna Twhigg at One Health Remuera on 24 August 2012 . There was a cursory check of the buttock and head area with no general examination. If there is no reduction in swelling syringing of the area can sometimes be a consideration however  Twhigg didn’t seem to be in favour of this course of action. There were subsequently a few generalised aches and pains including the neck and shoulder coupled with a mild headache and soreness on the right side of the head. Haemorraging from the gluteal artery can very occasionally be a concern .  This was mentioned but not further discussed.  There is also a smaller haematoma on my head.

She considered that the haematoma on the head would be better left alone and did not consider that a CT scan would be necessarily appropriate at this time based on my lack of significant symptoms since the accident a week earlier.  She considered that both the ACC and a specialist might be of the same opinion. She concurred with the skull x ray diagnosis. “ no fracture is seen”

Despite the fact that I was afflicted with severe pain in the lumbo/sacral area  in the spine there was no recommendation from the general practitioner as to topical treatment nor a referral for a spinal scan. An ultrasound of the right buttock was performed  at Auckland Radiology on 24 August 2012 reported and  the haematoma was syringed by orthopaedic surgeon  Dr Hucker on 12 September 2012.

Dr Retford on the 2^nd of November 2012:  Retford had a brief glance at the small bump on the right side of my head but otherwise made no comment and only briefly alluded to the haematoma on the right buttock  which  had been drained by Dr Hucker .  I explained I had also been experiencing some disc pain in left lumbar-I suggested that I might require physiotherapy and she agreed.  A lumbar x ray was not discussed.

I referred to the continuing problems in the sinuses i.e blood spotting , occasional severe nose bleeds coupled with stiff necks mild headaches and memory problems. I suggested that empyema/or meningitis  might be the reason however Retford doubted that would be the case considering that I would exhibit more serious symptoms if that were the case.

Dr Retford on 8 April 2013: We briefly discussed the result of the metanephrine urine test which generally normal.  ( Metanephrine is aka catechcolemine).  I am still afflicted with a sinus and chest infection ( last diagnosed by labtests in late January) and I am still experiencing serious discomfort in the legs . She prescribed Cipro and doxycyclin . She did not repeat roxythromycin as she considered that there might be an interaction between the latter and statin medication.  She is awaiting the result of another CK test.

Dr Nicki Retford – 4 July 2013:  We discusssed the recent blood test which showed an improvement in Hb and RBC’s but an increase in platelets. Retford didn’t consider this to be of any consequence pending another blood test in a week. ( excessive platelets can cause dangerous clotting)  The blood test of 4 July 2013 indicates normal results .  With regard to the scan of my legs Retford advised she  might pursue the matter via Dr Webster –although I might still have the scan done privately. Unfortunately I had transport problems and had to take a taxi from Glen Innes . I was perhaps 10 minutes late for the consultation. A receptionist a large woman with glasses aged 50s was initially very insistent that I could not see Retford as she was very busy etc.  She suggested that I see the duty doctor.  I said that as I was only 5 -10 minutes late It was surely only a matter of taking another patient ahead of me. After about 10 minutes she had a chat to Retford and we proceeded with the consultation.

Dr Retford -3 september 2013:  She advised that she would do a referral to Mr Webster with regard to a possible follow-up angiogram and ultrasound of the legs. She prescribed ciprofloxacillin for the recent diagnosis by Labtests of Pseudomonas and also Trisul.  She did not check my blood pressure .

 Dr Govind- 22 September 2013- Dr Govind of One Health prescribed Trisul and Cipro ( one weeks supply).

Dr Retford- 18  December 2013. Retford checked my throat chest and carotids –she advised there were no bruits .  I recently experienced another episode of sudden  collapse precipitated by some discomfort in the forehead area coupled with vision problems namely dark patches in front of the eyes.  I recovered after resting for about 15 minutes.  Retford suggested a mini stroke was a possiblilty and referred me for a consultation with a neurologist at Auckland Hospital.  She did not take my blood pressure . Antibiotics were again prescribed with Curam Duo ( penicillin ) re- introduced.  A prescription for cipro was also provided if required.  Further sputum tests were requested.”  Cardiologist Dr Webster was somewhat vague in his last report concerning my request for a leg ultrasound. Retford suggested that I take the matter up with him at the next onsultation.

On  29 January 2014 I advised Retford  that my chest condition had worsened in the last ten days and I was again experiencing quite severe discomfort in the centre of the chest extending around to the spine. She took my blood pressure which was 130/?. She did  not check my chest .  She re-prescribed roxythromycin only together with codeine and paracetamol for pain relief. She did not consider that additional antibiotics would be necessary until a further sputum test was provided. I emailed Retford images of my chest CT , a carotid report  a chest x ray of my mother’s dated 2001, a some earlier spinal reports of mine.  She was unable to proffer an opinion concerning either the scans or the reports.   This was my final consultation with Dr Retford prior to shifting to Whangarei.

 Dr M Gavin of the Medical practice in Onerahi in July 2014:  I provided her copies of relevant reports.  She did not check my chest although she did provide a prescription for romicin and penicillin –curam duo.  A blood pressure check was also omitted Ms Gavin initially suggested that I might be better off attending a more senior doctor and I would agree with her on that. There was a lot to discuss and further referrals will have to be dealt with in subsequent consultations.  To date I  have received notification from Whangarei hospital concerning a forthcoming chest CT.

 Dr Adrienne Henderson at Onerahi Clinic on 21 August 2014:   She efficiently proceeded through a number of issues including setting up hospital appointments.  With regard to a selection of a neurologist she didn’t think a local neurologist was available and suggested Dr Mark Kennedy.    A neurologist is however advertised as being on the staff of Whangarei Hospital. She provided me with a script for Romicin, blood pressure, cholesterol and gastric medication. pending the results of blood and sputum tests.  The Blood and thyroid tests have been returned from Northland Pathology on 8 September –still waiting on the sputum test.  My blood pressure was 160/?.  Henderson did not check my chest or sinuses.  She was present when I presented for the blood and sputum tests on 4 September.

During a visit to the laboratory  reception at Onerahi medical I briefly visited Dr Henderson to acquire a referral for a continuous sputum tests . She declined advising  that I would need to further consult her – suggesting  that  “ I had been around the ring” and that in fact I was Dr Gavins patient.

I then consulted Dr Roblin of the same practice on …….. He stood behind  his desk and computer –the discussion was brief and lasted about 15 minutes when Roblin stated that he had other patients to see.

 Dr Russell of white Cross Clinic whangarei ? 2014.  My blood pressure was recorded at . 182/118.  I showed Russell the result from Northland Pathology –a diagnosis of  “Pseudomonas species” and she prescribed both ciprofloxacin and curam duo ( penicillin).

 Dr Arkinstall  of Primecare Kensington  on 16 December 2014:   She advised that she felt she was  unable to assist me as my case “ was too complicated” Dr Arkinstall is a senior GP. When  I suggested that her attitude was discriminatory she consulted with the practice manager to see whether I could see an alternative practitioner in the future.   I was then advised that Arkinstall had a full practice and she was not taking on any new patients although this was not specified at the beginning of the consultation nor previously  at the reception desk.   I asked to look at the x ray of the skull dated 2012 and she concurred with the radiologists assessment of “ no fracture evident” I advised that I was concerned about what was probably a lineal fracture and a possible injury in the area of the crown . A BP test was 134/?. There was a quick aside from the practitioner namely a reference to “ its POP” ( i.e my email outwards)

Arkinstall did provide a referral for a sputum and blood test together with prescriptions for antibiotics and repeats on other drugs.  I advised that I had been having monthly thyroid and lipid tests however she  considered that the tests only needed to be performed once a year! Dr Arkinstall rang at 5.20 pm to advise that she had received the results of both the blood and lipid tests-the blood test was normal and the cholesterol was 5.3.  

Dr Vujcich on 7 January 2015 at the Accident and Medical Clinic on Bank St:  He refused to provide any treatment stating that it was inappropriate medically as I didn’t have a temperature  (the nurse did record my temperature- only my blood pressure) and that the reason for my being  virtual permanently afflicted with pseudomonas aeruginosa was the  overuse of antibiotics. I suggested to him that this was spurious reasoning.  I have 30-40 year history of lung infections with a variety of pathogens diagnosed since 2003.

 I stated that if a diagnosis of a  “heavy growth of pseudomonas species” with an accompanying recommendation for antibiotic treatment is made by the laboratory then  the general practitioner is surely expected to comply and provide the appropriate  treatment.    I explained that I frequently experienced severe pain in the centre of the chest, the base of the lungs, the thoracic spine  together ith significant inflammation elsewhere including  discomfort in the head and neck. – I was also frequently  experience a sporadic nagging cough. I explained that I had previously been diagnosed with a lung nodule which has been monitored since 1999 and there now seems to be a disparity concerning the status and treatment of the nodule  . I have most recently diagnosed with fibrosis and scarring in the lungs   All of these symptoms fell on deaf ears. Vujcich also disregarded the latest CRP ( an inflammatory  indicator) result which was recorded as just above the maximum. suggested that meningitis might be an issue however Vujcich considered penicillin inappropriate. Meningitis and even abscesses are often diagnosed in conjunction with  Pseudomonas Aeruginosa. I had copies of the laboratory test results for the last 12 months which indicated continuous pseudomonas infections however Vujcich stated that he did not have time to consult the reports.

He insisted that my case was not a matter for a clinic and should be dealt with by a general practice and to that end he made an appointment at the Primecare Clinic with Dr Ryan for later in the afternoon. . I changed the  appointment to another date. He also stated that I shouldn’t return to the A & E  clinic.   I explained that I had previously been to see Dr Arkinstall at Primecare  and she had refused to handle my case initially claiming that it was too complex and subsequently that she was no  longer taking on any new patients.

The form that is completed by any patient attending any accident and emergency clinic clearly advises the patients that they have the option of having their notes onforwarded to their general practitioner- in other words there is nothing to preclude A & E  medical practitioners from substituting for the patient’s own  doctors in  general practice . Blood pressure was taken by a middle aged blond nurse ( nz/Russian?) 139/75.In addition there was a comment from one of the doctors in the hallway i.e “ that Lou Bone was going to get rid of  her!”

I consider Dr Vujcich’s attitude to be nothing more than a callous disregard and unacceptable. By contrast I had  a normal consultation with Dr Russell at your clinic a few months ago. I have also attended at clinics in Auckland for many years . The Code of Rights of the Health and Disability Commissioner state:

RIGHT 2

Right to Freedom from Discrimination, Coercion, Harassment, and Exploitation

Every consumer has the right to be free from discrimination, coercion, harassment, and   sexual, financial or other exploitation.

            RIGHT 3       
Right to Dignity and Independence

Every consumer has the right to have services provided in a manner that respects the dignity and independence of the individual.

RIGHT 4
Right to Services of an Appropriate Standard

1) Every consumer has the right to have services provided with reasonable care and skill.

2) Every consumer has the right to have services provided that comply with legal, professional, ethical, and other relevant standards.

3) Every consumer has the right to have services provided in a manner consistent with his or her needs.

4) Every consumer has the right to have services provided in a manner that minimises the potential harm to, and optimises the quality of life of, that consumer.

5) Every consumer has the right to co-operation among providers to ensure quality and continuity of services.

I lodged a complaint about Dr Vujcich’s attitude with the Medical Director of the Clinic Dr Prinsloo. Extracts from his reply dated 13 January 2015  are as follows: “It is  not in our field of practice to treat longstanding problems and it certainly is not the best place to attend for these chronic conditions. Even though the GP gets a copy of the consultation notes it impedes the continuation of care and is not good clinical practice or best for the patient..I agree with Dr Vujcich that there did not seem to be enough evidence at the time of your presesntation to suggest an acute incident or any clinical evidence of an acute lung infection.  Unless the culture of “ heavy growth of pseudomonas” is a new one ( within the last few days) and there is clinical evidence of an acute lung infection it is definitely contraindicated to prescribe antibiotics .  Dr Vujcich did not refuse you treatment but certainly went out of his way to provide you with the best possible care by making sure you had an appointment at your GP practice within a few house on t he same day you presented here for assessment and treatment”

 Dr Sophie Hicks at the practice in the Paramount Plaza Tipunga on 20 January 2015:  She provided a general neurological check as I had advised that I was concerned about the areas of discomfort including areas of the skull and accompanying short term memory loss.  A lack of response in the left knee ( recently diagnosed with osteo arthritis) was evident during the reflex test.  Hicks made no comment other than to suggest that although I might have a consultation with a neurologist I wouldn’t necessarily be provided with a scan .   She checked my lungs  with a stethescope but made no comment.  She agreed to prescribe a prescription for 2 weeks of ciprofloxacillin but was not prepared to provide an additional prescription for augmentin. I advised that meningitis was a concern as I exhibited repeated episodes of stiff necks, sleepiness and extensive inflammation and Dr Retford had no qualms about prescribing same.

 I pointed out that a recent CRP test an inflammatory indicator was just in excess of the maximum however she seemed to downplay the significance of the test.   In respect of my respiratory concerns I advised that I had not been provided with a follow-up consultation at the chest clinic subsequent to a recent chest .I discussed the CT diagnoses of the past few years and my concern about the disparity between the recent recommendation of the radiologist and that of the two senior respiratory physicians in respect of a lung nodule.  Hicks demurred and seemed to try to rationalise the disparity.  I emailed her film from the thoracic x ray of december 2013 . I had been concerned about one frame namely the T lateral breathing and requested that she onforward the frame/frames to the respiratory clinic and she agreed to this request.  .Hicks also  agreed to request referrals to both the respiratory and neurology clinics.

I subsequently received a letter from Hicks dated 20 January “ at our appointment you requested a referral to a neurologist to discuss scalp tenderness and memory problems. I can see that you have had a number of opinions and tests regarding these symptoms and I am unsure there is anything more to be gained from a further opinion. I can reasssure you that I do not feel there is a neurological cause to your symptoms”

In fact I received two recent neurological opinions namely those of neurologist Dr Willoughby of Auckland and Dr Kennedy of Whangari a general physician. Kennedy referred to Willoughby’s comments namely that “ he felt the symptoms in late 2013 were likely syncopal in nature with no typical features of posterior circulation TIA or evidence of anterior circulatory disease and did  not believe neuroimaging or carotid Doppler would be helpful”

In his report dated January 2014 Willoughby advised:  “The recent episode of symptoms were of uncertain cause but sound most like a pre-syncopal episode. There were no typical features of a posterior circulation TIA although it is difficult to exclude that – we can reasonably exclude a carotid territory TIA and I do not think there is an indication to repeat a carotid ultrasound although Ms Wilson has wondered about that. A carotid ultrasound in 2003 showed minor plaque in both common carotids with no stenosis. I do not think repeat brain imaging is indicated but we should re-consider that if her course is unsatisfactory.

Dr Hicks’s assessment would seem to be at odds with that of Willoughby”s

In her email dated 28 January 2015 Hicks advised  “I apologise that I did not confirm the referral I made to the respiratory clinic in my letter and that I did not acknowledge your email last week.  This was indeed completed on the 20^th January and has been accepted by Whangarei Hospital, you should receive an appointment in the post.  I am struggling to attach all the images that you requested though.  The referrals are electronic and have a limit on data quantity that can be sent. I have attached what I am able and the most relevant that I felt”.

 A spokesperson at the respiratory outpatients clinic at Northland DHB  initally advised that the referral hadn’t been received then after a  further search advised that only the referral had been received but not the  images.

On 2 February 2015 Hicks further advised:  “I am not sure why that is.  It has definitely been received as the practice receives confirmation from the physicians.  I suspect it is to do with processing through to appointments and we need to wait a little longer”.

In the event I emailed one image of the T lateral breathing to the clinic.

I visited Dr Kim Rapson of Paramount Medical on 25 February 2015.  We discussed cardio neurology and respiratory matters.  She was reluctant to refer me to cardiology  outpatients until I provided a copy of the latest report from Dr Webster dated February 2014 in which he referred to a follow –up consultation. I emailed her a copy of the report. 

 I expressed my concern concerning the notation concerning a “ septal infarct” ( heart attack)reported  in the ECG of June 2013 subsequent to a gastric hemorrhage. This detail  was not referred to in the Cardiologist Webster’s  reports.  Rapson’s could only comment was “ what would you expect them to do about it?”  . !”  She did however  provide a referral to cardiology.

In respect of my neurological concerns she was not prepared to make a referral to the clinic. There is no resident neurologist at Whangarei Hospital . Rapson  was in possession of the latest CT chest scan report from October 2014. I expressed my concern about the disparities concerning the nodule in the right lower lobe-she merely nodded and made no other comment.   She provided a prescription Ciprofloxacin but was not prepared to provide an additional prescription for Augmentin. Her concluding comment after about 20 minutes  was “ I think you are just about done here

I visited Dr L Harvey who occasionally assists at Paramount Medical in Tipunga.  Initially Harvey advised that they were not liberty to prescribe Ciprofloxacin as it had to be initiated by a microbiologist. I stated that would obviously be the case. She then referred to the recommendation from Physician Dr Kennedy that the  prescribing of Cipro should cease and a similar  earlier recommendation in 2009 from Dr Wilsher. (which was actually  ignored by the general practitioners).

Harvey advised  that she would first  have to examine me .    She doubted that there would be enough time remaining in the consultation to discuss other issues.  I considered this scenario to be unsatisfactory and aborted the consultation.

 Dr Halaghi- Mccarthy of Whangarei city  on 4 August 2015:  The receptionist provided me with a form to complete as a casual patient but at the same time advising that if I enrolled as a patient it would obviously be cheaper than the $80.00 casual charge . McCarthy checked my lungs with her stethescope and claimed she could find nothing significantly amiss.  My blood pressure was 120/80 and my oxygen saturation level normal. I explained that I was experiencing pain in the lungs, the neck ( glands) sinuses and head. Despite these symptoms  Dr Mccarthy adopted much the same stance as Dr Harvey advising that she was unable to provide antibiotics without a further sputum test and further advice from specialist Dr Kennedy.  I explained that I was dissatisfied with Kennedy particularly his disregard for the recommendation of his radiologist in respect of ending CT lung scans.  I showed her the previous sputum tests the most recent being in March of this year and empty packets of previous ciprofloxacin prescriptions including those provided by Whangarei doctors.

 She also alluded to Kennedys report which suggested that the sputum samples might have been merely   “a mouth contaminant”.   Although Kennedys report if 13 March 2013 stated  “Ciprofloxacin 500 mg about to cease” he did not necessarily preclude further prescriptions with his subsequent statement “ I  have not recommended a further course of antibiotics at this time” McCarthy  was not prepared to provide any alternative antibiotic treatment but provided repeat prescriptions of various other medications and advised that I should re-visit my previous GP as she was no longer taking on new patients.  I mentioned this to the receptionist after the consultation-she advised that she thought I was an enrolled patient which was obviously untrue as she was well aware that I was a casual patient. Another example of discrimination.

I had twice attempted to contact Dr Retford of One Health Remuera in July 2015 with regard to re-joining the practice. I received no reply from her however I did receive a reply from senior nursing staff Jean Richards  on 21 July 2015:  “Dr Retford is aware of your request, but her patient register is closed.  Nikki is accepting no new patients and this includes re-enrolment of previous patients, as she is over-registered for the number of appointments she has available.  Therefore, as patients transfer out, they are not being replaced. 

Dr Retford is unable to be seen on a casual basis, as the General Practice service is only available to enrolled patients.  However, as Sharon advised, you are welcome to enrol with Dr Letica who is accepting new patients.” I recall a derogatory comment from Letica in reception. I had been a patient of Retford’s for approximately 10 years.

I have attended Dr Nikki Retford for several years and while she has been generally overtly helpful she seems to be reliant on the opinion of specialist and radiologists and reluctant to proffer an opinion on radiological scans. She is now a practitioner in a Beachlands.

As I had experienced difficulty obtaining a referral to a neurologist ( there  is no resident neurologist in whangarei) I received a referral from Dr Catalina Wong of Auckland to neurologist Dr David McCauley who requested a brain MRI. As I received no further advice from McCauley subsequent to the scan  and due to the fact that I also  had queries concerning two areas of non-diagnosis I contacted Dr Wong detailing my concern however  in her email dated 21 December 2015 she advised “ you are a casual patient..  living in Whangarei……you will be better served if you enrolled in a practice closer to you.  I therefore urge to take your MRI report together with your history to a local clinic of your choice to help you”

 A consultation with Dr Bornholdt on 9 December 2015:   I explained that I had a combination of problems including symptoms  detailed in  the recent MRI brain scan in combination with ongoing Pseudomonas Aeruginosa sinus and chest infections and also a  probable cases of maelena precipitated by an anti-inflammatory tablet.   I had copies of two images from the brain MRI however Bornholdt claimed he was unable to interpret scans and doubted that I would be likely to either.   He checked my chest with the stethoscope and could find no evidence of anything amiss and a similar assessment after  a manipulation of the sinuses. I had explained that I get pains in the chest and suffer from inflammatory discomfort  in the head and have a long history of gram negative infections.    He reluctantly prescribed a minimal dosage of Ciprofloxacin namely 500 mg per day for a week ( normal prescription 1000 mgs per day for 2 weeks.) supplemented by a weeks supply of augmentin.  As he considered we were of differing opinions he advised against registering with him. As of 3 January I have a severe croup like cough particularly in the morning.

 Dr Henderson at Onerahi Medical centre on 11 March 2016.:   I attended as a casual patient.  She provided referrals to both a respiratory and neurologist in private practice. I showed her 2 images copied from the recent  MRI brain scan, one indicating leptomeningeal enhancement  and the other probable thrombus/thrombi? In the superior sagittal sinus.   I expressed my concern that neither of these 2 conditions had been diagnosed at Mercy radiology however Henderson seemed to disregard this aspect as somewhat insignificant . While she prescribed a 10 day prescription for  ciprofloxacin she would not prescribe any penicillin .  She considered that the Cipro would be sufficient treatment for the meningitis as I wasn’t afflicted with the full range of symptoms. Medscape “:Ceftazidime or cefepime are the recommended antibiotics for treatment of meningitis arising from a pseudomonas aeruginosa infection. Ciprofloxacin is an alternative treatment.”

  Dr Henderson  September 2016:  She checked my blood pressure at my request which was recorded at 135/80.   She agreed to onforward requests for consultations at endocrinology ,  CT radiology, mammography. She also provided a form for a blood test a referral to the laboratory for a stool specimen ( no abnormality was subsequently indicated in the laboratory report) In respect of my neurology concerns she seemed doubtful that she could make any further progess in this regard suggesting that alternative neurologists might be of the same mind as McCauley and Charlesworth.! 

On 15  August 2016 I received emailed advice from Practice Manager Ian Watkins of the West end practice in Maunu Whangarei : “ I am sorry I cannot meet your request as our books are currently closed and we are not taking on new patients”.

4 April 2017:  I was once again afflicted with a chest and sinus infection and was duly prescribed ciprofloxacin together with repeats for my regular medications by Dr Henderson.. A stethoscope investigation of the chest revealed some “ crackles” in the left lung. As I had complained of occasional small sharp pains in the stomach and occasionally in the right groin augmentin was also prescribed.

Wikepedia advises   “ Crackles are often associated with inflammation or infection of the small bronchi, bronchioles, and alveoli. Crackles that do not clear after a cough may indicate pulmonary edema or fluid in the alveoli due to heart failure, pulmonary fibrosis, or acute respiratory distress syndrome.”

On 22 June 2017 I emailed Dr Henderson a copy of a recent mammogram which also depicted an area of the chest which when magnified showed an area of dense opacities.  In her reply Henderson advised :

Hi Vicki

Thank you for the films.  I am not a radiologist but from my training I cannot see any features on your imaging that would raise alarm bells for me.  The patchy changes in your screen shot are normal findings on many x-rays – particularly when looking through dense tissue due to the variable uptake of the x-ray radiation.  Dr Kim Shepherd is a very skilled radiologist who reads the vast majority of breast imaging and I have faith that she would have reported any changes of concern.  Regards Dr Henderson

Ciprofloxacin continued to be prescribed in August and 25 September 2017.  Prior to the consultation on 25 September an unfortunate comment was overheard from  Dr Henderson namely “ committed nut case”.  She has since left the practice.

In December 2017 Dr Sophie Cruse at onerahi medical:  my request for a prescription of ciprofloxacin was declined by Dr Sophie Cruse  as  while a “ heavy growth of gram negative bacilli” had been reported a culture had not been specified in the laboratory test.

Although I pointed out to both doctors that  laboratory microscopy details which  specify “ large numbers of  gram negative bacilli” are the equivalent of a diagnosis of pseudomonas aeruginosa which I have been almost exclusively afflicted with for almost 20 years and almost exclusively for the past  the last few years. However the logic of this argument fell on deaf ears.

Consultation with Dr Deijten of Onerahi Health on 6 January 2018.   She checked my heart and lung function but made no comment.  She also checked my throat which she advised was a little inflamed on one side and took a swab for the laboratory.  I advised that I regularly experience severe discomfort in the centre of the chest and lower lobes of the lungs in conjunction with occasional pains in the head and sinuses and memory problems. Dr Deijten did not consider that a prescription for cipro was appropriate as the two most recent sputum tests specified “ large numbers of gram negative bacilli” but not a pseudomonas aeruginosa culture.  She provided a form for a chest x ray at public hospital.   In respect of my head injury on 20 December 2018  Detjen conducted some visual tests and lightly touched my head.  She completed  an ACC form but did not  but failed to hand it to me . I visited ED at Whangarei Hospital on 8 January 2017 where the reception staff subsequently obtained the ACC number from the practice.

A reply received from Dr Tan in February 2018 a respiratory physician at Whangarei Hospital recommending a cessation of antibiotics was in response to an apparent identical request from a medical practitioner assumed to be Dr Detjen of the Onerahi medical centre. In addition the practitioner had requested a “block” at Labtests concerning any future lung sputum tests.    This would appear to be seriously obstructive tactic as the practitioner  could easily have checked sputum tests over the last 15 years which clearly indicate a chronic long term sufferer  Recent CT lung scans indicate  scarring, fibrosis and a possible malignant lung nodule. ( see also RESPIRATORY)      Any coughing is related to my chronic long term chest infections and not ACE induced.

A prescription  was eventually provided by Dr Barnes at Onerahi Medical on 21 February 2018  subsequent to a culture diagnosis of “ heavy growth of pseudomonas aeruginosa” on 19 February 2018. Although photographs of the sputum tests of 19 February and 7 March 2018 were virtually identical pseudomonas was only specified in February with  -“  small numbers of gram negative bacilli” reported in  March.

 The diagnosis of a “heavy growth of gram negative bacilli” is the equivalent of a culture “heavy growth of pseudomonas aeruginosa” . Although the miscroscopy details are the same the culture is not always specified. As a result  I had been without appropriate antibiotic treatment from September 2017 until February 2018. The medical practitioners seem to be unnecessarily obtuse in this regard. I queried this disparity with Labtests however I was advised that the query should be initiated by my medical practitioner. On 12 June Dr Sprague seemed a little reluctant to pursue the matter .

23 March 2018:  Subsequent to checking my chest with his stethoscope Dr Barton of Onerahi medical claimed evidence of any infection wasn’t readily apparent although I had been producing significant somewhat viscous sputum for the last month. A photographic  enlargement of  sputum specimen clearly illustrated large bubbles however Barton made no comment. He did not consider a further referral to the heart clinic was necessary but was amenable to an ECG performed at the practice. Neither did he consider that a referral to gastroenterology was necessary at this stage.  Dr Barton did provide a prescription for ciprofloxacillin and Romicin and a form for further sputum tests at pathology. 

During a visit to reception at the Onerahi practice Dr Roblin appeared, uttered a “ nutter” comment,  laughed,  and returned to his office.

Although Dr Bloedon of  Onerahi medical had provided a prescription of Ciprofloxacillin on 7 July 2018 he was reluctant to repeat the prescription on 31 July . He seemed to have misinterpreted the advice of  Respiratory Physician Dr Bradley who although she had sounded  a note of caution in respect of antibiotic treatment she did not preclude treatment when there was “ a marked increase  in sputum with colour change plus or minus fever and true infection is indicated. (I have provided photographic evidence of the yellowish sputum over the years.) She added the proviso “  I would stop culturing unless she was clearly not responding ” 

On 9 August 2018 Dr Sprague provided a prescription for Doxycycline and Ciprofloxacin . I provided him with photographic evidence of two areas of concern namely the dense opacities evident in a mammography frame and the probable skull fracture.  Dr Sprague was not prepared to provide an opinion and suggested that I should consult a lawyer who specialises in  medico-legal matters. He didn’t provide a referral to the gastroenterology clinic or a possible endoscopy procedure.

On 10 October English general practitioner Dr Prenton provided a prescription for Ciprofloxacillin and doxycycline. She also provided a referral for a thyroid lab test.   I had requested an extended consultation time which was taken up with my advice concerning my medical concerns.  Prenton advised that in the interim she would prefer to investigate my medical history and suggested that I make a subsequent appointment.  I had previously emailed medical images to administration at Onerahi Medical which I was advised were retained in a folder however it isn’t clear as to whether either practitioner have seen them.

I attended Dr Grace Couper at Bush medical Kamo on 8 January 2019.  She provided me with a script for my regular medications as well as Ciprofloxacillin for Pseudomonas infection.  I had sent her an email complete with images which detailed my concerns however these were not discussed .  Dr Couper is now on maternity leave.

Chest sputum tests of December 2018 and February 2019 indicated a recurrence of “Pseudomonas Aeruginosa and predominantly gram negative bacillus Unfortunately on 6 March 2019 Bush Road practitioner Dr Hedlund did not see fit to prescribe antibiotics but rather considered that the only medical requirement was a nasal spray. I had also emailed copies of medical images together with my queries to Bush Road Administration. Dr Hedlund appeared to have the images in a file. As I abbreviated the consultation these matters were not discussed.

On 16 April 2019 Dr Zender of Bush Road Medical provided a script for my usual medications as well as Ciprofloxacillin and Romicin. I had sent Dr Zender an email on the previous day advising that she could retrieve the file of images from Dr Hedlund however she claimed that she hadn’t receive the email so I  provided her with a copy of it.  Gastroenterology matters were discussed and Dr Zender indicated she might progess further investigations.  She suggested that I return for another ½ hour appointment to discuss respiratory, neurology , haematology and other matters.

At a subsequent consultation with Dr Zender on 4 June 2019 she provided me with a script for ciprofloxacillin and doxycycline for treatment of the endlessly recurring pseudomonas aeruginosa. Approximately 10 minutes of the 15 minute consultation was taken up with a protracted explanation as to why she hadn’t progressed a request for further investigations at the gastroenterology clinic. On this occasion Zender seemed to agree to progress a request for an endoscopy and ultrasound however she considered there were limited resources at the hospital clinics and a repeat endoscopy and colonoscopy might not be likely.

The previous endoscopy/colonoscopy was performed at ADHB in 2003. Melanosis Coli was diagnosed. I had requested that a panel dated August 2018 be repeated at the laboratory at Whangarei Hospital . High immature granulocytes, High fibrinogen Assay, High anion gap and abnormal leucocytes were diagnosed . However Dr Zender only provided a referral to Northland pathology for lipid and ACR urine tests. The test for lipids had been omitted from a recent blood test. She examined my stomach, and my chest with a stethoscope and also took my blood pressure but otherwise made no comment! I have since received notification that a gastroscopy procedure has been scheduled. The previously emailed abbreviated complaint which also contained medical images had still not been retrieved for discussion at the consultation.

Heavy growth of Pseudomonas species was reported by Labtests Auckland on 29 July 2019.  In August 2019 I requested a script from Dr Zender for Ciprofloxacillin and Trisul. A text reply from a member of the nursing staff advised that Dr Zender was only prepared to provide a script for a limited number of Trisul tablets. I decided to seek an alternative opinion and visited Dr Limby of the same practice on 8 August 2019. Limbys attitude to prescribing Cipro was identical to that of Dr Zender. 

She claimed that there was a restriction and prescribing Cipro was bad practice.  A script for 2 weeks supply of Trisul was provided.  (Although Trisul is prescribed for some gram negative infections  pseudomonas is considered to be somewhat resistant to this drug). Dr Limby also queried the need for sputum tests.   The last specialist seen in April 2016 was Dr Cornere of Waitemata DHB . She prescribed Ciprofloxacillin and suggested “If pseudomonas remains a concern we could consider 3 months treatment with nebulised aminoglycosides as she has had multiple courses of ciprofloxacin in the past”.

 I requested a referral to Norpaths hospital laboratory.  In respect of a high immature granulocytes reading provided by Norpath  in 2018 Limby was rather dismissive of the test seemed to ignore the fact that granulocytes are an important sub-group involving the bone marrow. She alluded to a recent normal  neutrophil count as indicative and sufficient.  Norpath advises “Causes of a raised Immature Granulocyte Count include sepsis, inflammation, haematological or other malignancies, and conditions where there is a leucoerythroblastic picture.”  I undertook a colonoscopy at ADHB in 2004 and Melanosis Coli was diagnosed  . I requested a referral to NDHB for a sigmoidoscopy however Dr Limby advised that she could only refer me for the procedure as a private patient.  I had brought copies of the medical images about which I was concerned however once again they were not discussed.  Limby did not consider that a further attempt to resurrect specialist consulations and scans at NDHB was her responsibility.

On 2 September 2019 Bush Road practitioner Dr Miller provided prescriptions for two weeks each  of Ciprofloxacin and Doxycycline as treatment for Pseudomonas Aeruginosa and a blood test at Labtests. He also provided a referral for a CT colonography which is scheduled for October.   I provided him with copies of medical images about which I was concerned however there was no response from Miller.  I subsequently onforwarded the images to Dr Miller via email.  He did not check either my blood pressure or my chest.

On 25 September I endeavoured to obtain a further prescription for Cipro and was advised by the nurse/receptionist that a script would be available the following day.  On 26 September I received a text from Staff member Ronda to advise that Dr Miller would not be prescribing a script and she enquired as to my symptoms and in particular whether I had temperature.  I advised that was not usually the case but that I was afflicted with the usual symptoms in the chest and sinuses.  It does seem rather unusual that a doctor would request a staff member to diagnose over the phone.  Ronda  also advised that Dr Miller would not be available to see me again as he already had too many patients and that the previously scheduled appointment on 9 October 2019 would be cancelled. This was confirmed by Dr Miller by way of an email “Hi Vicki. I’m only working part _me and was job sharing with another doctor who has just left so I’m swamped with my own registered patients and hers. My admin staff have been asked to make appointments with me for only my patients. That is the reason Rhonda advised you I wasn’t available.”  I had seen Dr Miller previously on 2 September however I was not provided with that advice on that occasion.

On 30 September I received a statement of account requesting payment of $20.00 to Dr Noda for a prescription.  I telephoned the practice and was advised  by another staff member that there was a prescription for 2 week of ciprofloxacillin provided by Dr Noda which had been onforwarded to Orrs chemist.  A subsequent check with Orrs revealed that there was no trace of a prescription. During  a follow up phone/con with Ronda she became rather belligerent insisting that I had been told “that I was not clinically unwell and thus no prescription” and it was her opinion” that ciprofloxacillin was not an appropriate medication for pseudomonas.”.

She couldn’t seem to explain the account from Dr Noda. I emailed a query to Dr Noda on 2 October 2019 but received no reply. An email was received from Sandra Hawkins the practice manager who advised “you can leave your account balance in credit by $20 which will pay towards any visits or prescription charges in the future.Dr Noda asked me to reply to your email as she had not completed a prescription for you and has not seen you previously.”  !!  I agreed that the account could be left in credit.

During a consultation with Dr Noda on 24 October 2019 she advised that she had not previously prescribed ciprofloxacillin which didnt explain the   $20.00 prescription attributed to her. She  provided me with scripts for my usual medications and eventually after much persuading and reluctance an additional prescription for ciprofloxacillin. I provided Dr Noda  with evidence of 16 years of primarily gram negative chest infections She was not prepared to make any comment about the image from a mammogram  depicting dense opacities apparently involving the chest wall.   Dr Noda then erroneously advised Northland Pathology “ sputums are no longer required for this patient .

 A subsequent consultation with Dr Geoff Cunningham of Bush Road medical on  17  December 2019 resulted in a protracted discussion with Cunningham about the lack of reporting of a sputum culture despite the microscopy details in tests being identical in some of the tests. Dr Cunningham would not accept that there was a disparity and was not prepared to prescribe medication even though  “predominantly gram negative bacilli” had been indicated in the test dated  7 December 2019. The identical details were reported in July 2019 with a specified  culture of “ heavy growth of pseudomonas aeruginosa” . I presented my list of chest infections diagnosed since 2003 however this evoked no response. 

In addition I had advised that I had been experiencing head and chest pain and a very sore throat. Dr Cunningham took a swabs from both the throat and tongue but otherwise made no comment.  He also  requested another sputum test which has now been undertaken as I subsequently developed a severe chest and sinus infection.  I managed to reduce the severity of the symptoms with natural emedies. 

I showed Dr Cunningham  an image indicating dense opacities apparently involving the chest /breast areas however he dismissed that as “ that’s nothing”. He was likewise dismissive concerning Dr Corneres’ suggestion of a 3 month trial of aminoglycocides as treatment for chronic long term sufferers. Dr Cornere is the clinical Director of Waitemata Respiratory medicine.

I consulted with Dr Audrey Thorpe at North Harbour Medical on 1 July 2020.  There were assorted comments from both Dr Audrey and  her male counterparts/incarceration( “why committing/JB and CD .)  Dr Thorpe was helpful and provided a referral to the breast clinic. Referrals to the Cardiology, Neurology, ENT ,Dermatology and Orthopaedic clinics have yet to be arranged. She also provided a prescription for all my medications

At our consultation on 24 November 2020 Dr Thorpe and I further discussed the unsatisfactory aspects of the breast ultrasound performed  in July 2020.  Dr Thorpe seemed reluctant to progress the enquiry beyond once again requesting another review of the scan. She also did not consider it necessary for her to obtain a copy of the breast ultrasound dvd. She agreed to request a further consultation at the neurology clinic.  The antibiotic Levofloxacillin was discussed as an alternative to ciprofloxacillin and Thorpe advised that she would need to seek advice from a microbiologist. ILevofloxacillin  was available but at considerable cost as the drug was not on the approved list. In the interim she provided a prescription for co-trimoxazole to treat a recent diagnosis of serratia liquefaciens. A blood test has also been requested

PATRICIA WILSON.

.In 2003  Patricia suffered  a fracture in the sternum,  probable fractures in her pubic bones and deafness in a car accident. She recuperated at home after spending 2 days in hospital.   In February 2009 she had a serious fall which result in deep cut in her forehead –she had also banged her head on the concrete floor 

Although  there was excellent wound care at public hospital neither an x-ray nor a cranial CT was undertaken. Many international medical websites advise that in respect of the elderly a cranial CT is mandatory primarily because of the likelihood of submatomas in people of that age group. The CT would also indicate any skull fractures and highlight problems with the hearing nerve. Medline Plus a service of the American Institute of Health advises  “that a skull x-ray is rarely used to evaluate head injuries or brain disorders” A skull x-ray ordered by mother’s General Practitioner Dr Crombie was essentially normal.

In early June 2009 my elderly mother  fell against the wooden stair rail  inside our home.  An x ray of 4 June 2009 specified  “approximately 10mm of anterolistheisis of L5 on S1.  This is thought  to be on the basis of severe degenerative facet joint change at this level………..there is moderate generalised loss of the veterbral height at the L1 level consistent with a compression injury…..lumbar films from 2005 report preserved vertebral body heights and therefore this is an interval finding”

  We consulted with spinal surgeon Mr Hadlow on 19 June 2009 . His diagnosis was “ a compression fracture of the superior endplate at L1” He recommended “panadol medication” and advised  “that it would take 2 to 3 months for the pain in her back to settle”. Patricia has received pain medication from her general practitioners  Dr Crombie and Dr Ivori including codeine phosphate codeine  oxycodone amtryptiline and tramadol  supplemented with panadol and panadeine

In the interim we attempted to have an assessment at Auckland public hospital.  The young ambulance officer queried the necessity for an ambulance and suggested that confinement to public hospital was a decision for the the general practitioner.  We received much the same advice from the male head of triage when we arrived at the hospital. Mother had been admitted there in February of 2009 with a head injury.  There were perhaps 6 people in the Emergency  waiting room 2 of the more serious cases appeared to have been attended to. The gentleman from triage sat in his office for about an hour then consulted with mother and I –he advised that if we wanted to see the supervising specialist we would probably have another hour’s wait.  Apparently no priority was to be given to an elderly eighty year old with severe back pain.  Mother chose not to wait and returned home.

On 29 July 2009 mother attended spinal surgeon Mr Greg Finch .There were a couple of  “committed” asides at the door prior to the start of the consultation. After checking the recent lumbar x –ray he appeared to dispute the previous diagnosis of Mr Hadlow in respect of the compression fracture and otherwise would not commit himself to a diagnosis pending an MRI scan.  He doubted that a surgical procedure would be necessary.  He did not check her earlier scans .  A CT scan from 1994 reported “anterolisthesis with disc bulge and a possible compromise of the nerve”………  He did not discuss pain relief and when I asked him outside the consulting room he referred me to the general practitioner.  His website quite clearly recommends alternative pain killers including Panadeine forte amongst others. I provided Mr Finch with some previous hospital and accident reports however he did not consult them.

 Mr Finch’s report dated 29 July 2009 stated  “ a little bit of weakness in the right S1 right nerve root and a little bit of dorsiflexion on the left …certainly has pain localised into the lower part of the lumbar spine….a little bit of wedging of L1… spondylolistheis based on the wear and tear in her lumbar at 5/1 level”

The MRI report dated 4 August 2009 reported “moderate to severe compression fracture of L1 with a loss of approximately 50% of height of the vertebral body…..moderate oedema within the vertebral body…..prominent narrowing of the T11/12 foramen on the left and compression of the left nerve root cannot be excluded…narrowing of the right foramen  due to disc and nerve root compression is also difficult to exclude….grade 1 spondylosisthesis of L4 on L5…..The L5/S1m disc shows marked loss of height and signal intensity there is grade 1 spondylosisthesis of L5 on S1…..There is a compression fracture of T12 with prominent associated bone marrow oedema suggesting that it may be fairly recent. There is marked narrowing of the T11/12 foramina and nerve root compression is difficult to exclude.

On 1 September 2009 Patricia consulted Mr Gordon. In his report dated 1 September 2009  specialist Mr Gordon stated that mother “ had sustained a fracture of the L1..but the pain is lower down her lumbar spine than the site of the fracture might suggest.  On evaluation she had a thoracic kyphosis and a list to the left-she was imbalanced in the coronal and saggital planes.  Power was normal in all muscle groups of the lower extremities-sensation was normal in all dermatome areas and the straight leg raise test was negative. There was no percussion tenderness at the thoracolumbar junction….there is evidence of a compression fracture of L1 with this compressed approximately 50% and there is some retropulsion but this not causing any significant canal compromise.

 I am somewhat mystified as to why the pain is in the lower lumbar spine when her fracture was at the thoracolumbar junction. Her daughter is somewhat convinced that her pain is coming from the lumbrosacral area and in particular the facet joints…I think it is reasonable to inject the facet joints at L5.S1…It is possible that the pain is  coming from the L1 fracture and a vertebroplasty may be necessary but the pain is in an  unusual location for this. I have referred her to pain specialist Keith Laubscher for evaluation and treatment and hopefully he may be better able to localise where the pain is coming from.”

 An email dated from 21 September 2009 from Ms Good Mr Gordon’s Practice Manager stated “  Mr Gordon stated that the results from the steroid facet injection performed on Mrs Wilson indicate that her pain is not localised to the area that was injected. The little pain relief that she did experience was from the steroid component of the injection which would have acted all around her body and provided her with some relief.”

We had an interim consultation with Gordon on 25 September 2009. A  brief aside from Gordon to his receptionist concerning “ lunacy” was overheard before the consultation.  He has virtually discounted proceeding with further injections in the lumbar area at this time and has instead referred Mother for a selective root block procedure in T12 . The procedure was  undertaken on 27 October but resulted in no alleviation of the pain.

In his report dated 30 September 2009 pain specialist K Laubscher stated in respect of the bilateral facet joint injection at L5/S1 “ she reports that her pain was abolished for about two days following that procedure-it is the lumbar pain that is her main complaint-she is tender to firm  palpitation particularly over the right paralumbar region L4-S1 and extending into the sacrociliac area and around to the right iliac crest-it is possible that she has both an upper and lower lumbar focus.   In relation to her lumbosacral  pain it might be reasonable to try medial branch blocks for L4/5 and L5/S1 facet joints –if positive radiofrequency denervation might be an option”  In his email dated 9 October 2009 Laubscher advised  “that I have had a chance to look at the block sheet that recorded the response to local anaesthetic and cortisone to the joint.   I had understood that the injection had abolished the pain for two days. This is not reflected in the “ block sheet .”

 In his emails dated 13 and 14 October 2009 Mr Laubscher stated “ that the record sheet indicates that the level of pain was 7/10 following the procedure which means it did not numb the source of the pain. This is the most important time frame from my perspective. I had understood that the joint blocks had abolished the pain but it appears that they did not and that is the reason for the reconsideration of the options.”   The pain level was recorded at 7 on a scale of 1-10 during the hours immediately after the procedure and then reduced to 4/6 for the 2 subsequent days. The only significant discomfort during those 2 days emanated from the injection site . Presumably that indicated that the steroid component of the injection was having some beneficial effect.

We again met with pain specialist (Mr Laubscher) on 26 January 2010.  He maintained his previous negative stance toward performing medial branch blocks .  Mother advised that she still has early morning  pain which is most often very severe.  Laubscher advised that the pain had to be of sufficient severity on the day of the procedure for the medial branch blocks to be effective and that Patricia might not qualify in this regard.   At my request (and not of Mr Laubscher’s own violition) he examined mother’s lower lumbar region and it was fairly obvious that there is still severe pain when pressure is applied . She assessed  the pain as 8 on a scale of 1-10. Upon departure Laubscher advised that the ACC approval for the medial branch blocks was valid for 6 months and could be renewed if the procedure should need to be undertaken at a later date. It is perhaps a matter of opinion as to whether Patricia has simply been the victim of a discriminatory denial of appropriate treatment.   

 A selective nerve root block for T12/L1 was performed by SRG Radiology on 27 October 2009. There was no reduction in the pain as a result of the procedure. In his report dated 16 November 2009   Mr Gordon stated that “ this lady still has pain over the pelvic rim on the left hand side ..she remains neurologically intact but she has a kyphotic flexed posture with a list to the left and her rib cage is inside the pelvis on the left hand side . She is quite tender in this area but palpating in this area does not exacerbate the pain that she normally feels. The latest injections exacerbated the pain but did not alleviate the pain in any way. if the root block at T12/L1 was not effective then medial branch blocks might be necessary. …a vertebroplasty would not improve her posture or improve her posture or improve her pain …the procedure would involve a major realignment of her spine to correct her kyphosis” 

NCBI PMC: the US Library of Medicine NIH  published an article by Professor Professor Huilin Yang and associates dated 17 January 2018:   “Very severe osteoporotic vertebral compression fractures (vsOVCFs) are osteoporotic vertebral compression fractures with vertebral body collapse to less than one third of their original height. PKP (percutaneous kyphoplasty) is a safe and effective procedure for the treatment of vsOVCFs with spinal canal compromise, achieving significant vertebral height restoration and kyphotic angle reduction and leading to a significant pain relief and improvement in function. However, in vsOVCFs with spinal compromise, many authors considered these two procedures to be relatively or even absolutely contraindicated because of technical difficulty, high risk of cement leakage and further spinal canal compromise . Nevertheless, the literature and our own experience demonstrate this assertion to be unfounded.”

 Some studies reported good results with PVP owing to its analgesic and stabilising effects in the treatment of osteoporotic vertebral fractures with spinal canal compromise In our study, to avoid perforating the endplate, a low lateral transpedicular approach was adopted and bilateral double balloon inflation was performed to achieve en masse reduction [23] in all cases. PKP is a safe and effective procedure for the treatment of vsOVCFs with spinal canal compromise, achieving significant vertebral height restoration and kyphotic angle reduction and leading to a significant pain relief and improvement in function”.

My mother attended at Kepa Radiology for a left wrist ultrasound. The sonographer, a Scottish woman who had performed by breast ultrasound also undertook this procedure.  A brief aside namely “getting rid” was overheard from the woman as she returned to her room along the hallway. .  ( The former owners of our property and subsequent neighbours in St Heliers were the  Scottish Vicars family).

Subsequent to a further MRI scan Patricia visited Hand and Upper Limb Surgeon (Mr Tim Tasman Jones). H is report dated 26 November 2009 advised  “ advance osteoarthritis of the radiocarpal joint lst CMC triscaphoid and DRUJ joints with almost complete loss of the articular cartilage and an associated synovitis involving the radiocarpal joints and long flexor tendons of the carpal tunnel. Importantly there are no signs of soft tissue tumour.  I would recommend continuing to treat the wrist symptomatically  with avoidance of loading intermittent use of a wrist brace and occasional use of ant-inflammatories.  If her symptoms persist then I would consider a cortisone injection into the carpal tunnel.’

We again consulted specialist (Mr Tasman Jones) on 31 March 2010.     Unfortunately On 31 March 2010 Patricia advised that she had decided against receiving a cortisone injection.  . Tasman Jones made a rather unusual comment namely “ in the past people with carpal tunnel syndrome were place into a mental institution as nobody knew what was wrong with them”  There seemed to be a measure of indifference about his attitude  -he greeted  mother when we arrived at his office –I was ignored and nor was there a free  chair available – I had to remove an object from a chair nearby prior to  moving  it closer to the desk.  We were not farewelled at the end of the consultation.

 On 8 December 2009 we consulted with Orthopaedic specialist (Mr Barnes). He consulted only the plates of the MRI lumbar scan but not the accompanying CD.  L1.  His physical examination was confined to a light tapping in the upper part of the back. In his report dated 8 December 2008 he erroneously  reported  “ that Keith Laubscher  initially performed medial branch blocks in the lower lumbar region”  His report continued “ for the last six months she has had pain in the left upper gluteal region related to weight bearing and walking. This does not radiate. It seemed to develop after a fall.   She has a severe kyphosis which is fixed and cephaled to the L1 vertebral body fracture with some loss of body height .  There is no particular tenderness over the spine and she does not have lower extremity symptoms. I do not think she would benefit from either kyphoplasty or vertebroplasty procedures-there is no surgery which can benefit her in my opinion… she has also lost significant weight and has appetite loss….. she could possibly have an insufficiency fracture to account for her symptoms-it might be worth therefore ordering a bone scan to be sure there is no increased uptake around the sacroiliac joint-other than that I do not think I can be of further help”

When discussing the loss of weight and appetite (Mr Barnes) purported to be puzzled as to how kyphosis  would impact on her food intake.  He was unaware of anyone performing vertebroplasty in Auckland –there was no response when I mentioned that according to an internet site the first vertebroplasty was performed at Middlemore Hospital in 2004.  He jokingly referred to the fact that “ ACC paid me a lot of money to see you” There was a “nut case”   comment from his blond English receptionist as we departed.

We consulted with orthopaedic specialist Geoffrey Coldham and his report dated 16 February 2010 refers. Coldham advised “ she walks comfortably-she is kyphotic through the thoracic spine. There are approximately six inches anterior translation of her sagittal axis. On forward flexion fingers reach the mid tibia but she cannot extend to a neutral position.  There is tenderness in the midline of the lower lumbar spine at L4/5 and L5/S1. Comfortable hip motion. Normal lower extremity power, sensation and reflexes . Distal pulses intact. Plantars are down going..  …asked me to discuss medial branch blocks. I advised that I have no experience in that area and cannot advise her with respect to that.  There is no place for surgery in this lady….whether compression fracture is symptomatic and whether or not vertebroplasty should be contemplated… I will organise a bone scan . If the scan indicates isolated uptake around the L1 level I may refer her to Professor Doyle for consideration of vertebroplasty. If it shows diffuse uptake through the lumbar spine there is nothing I would recommend. I reviewed the repeat x-rays today.  They confirm multi level degenerative changes in her lower lumbar spine.  There is almost complete loss of height in the L1 vertebral body with 100% loss of height anteriorly and 60%-70% posteriorly with wedging through this area and focal kyphosis.

There was no discussion of either her weight loss or  loss of appetite in respect of her kyphosis as has been the case with all previous specialists.   Mr Coldham advised that he it was many years since he had undertaken a vertebroplasty procedure –he referred to kyphoplasty as being performed “ with balloons – and more expensive.”. He didn’t consider that any remedial physical therapy would serve much purpose. Dr Coldham is also a consultant with the Back Institute .

 He did initiate another lumbar x ray which clearly indicated a worsening of the situation in L1.   A previous MRI scan had reported a 50% loss of height which  Coldham estimated  had now  increased to approximately 75%.  Mr Coldham was apparently au fait with all our previous specialist  consultations and occasionally  seemed to reiterate details from their reports.  In particular he repeated the recommendation of Mr Barnes that in view of the possibility of an insufficiency fracture a bone scan might be a possiblility.  Coldham qualified this comment by suggesting that the scan would probably only be appropriate if mother was considering vertebroplasty.!   

 On 11 March we met with  geriatrician Dr Scott.at the Greenlane Clinical Centre.   Although we had provided x rays and scans she chose not to consult them. .She undertook an examination of Patricia’s leg movements and an examination of a section of her spine and stomach.  She referred to Patricia’s early morning pain as “ a left upper quadrant ache particularly noticeable when she gets up in the morning worse on standing and overall much better than initially”  She reiterated the findings contained in the MRI report pertaining to the compression /loss of height in L1 and the anterolisthesis in the lumbar/sacral area.  “On examination she was kyphotic from about L1 but neurological examination normal in the legs, apart from absent vibration sense. She has allodynia ( pain to mild palpitation ) and hyperalgesia to pin prick over the T11 dermotome ( lower abdomen on the left just below umbilicus extending posteriorly over her lower ribs to mid line not tender over T11-12 vertebrae. T 11 nerve root irritation seems to best explain her pain”  Scott disregarded kyphosis as being the likely culprit for her weight loss attributing it to stress.  There was no recommendation for further investigation in this area.

She noted that a public hospital recorded Patricia’s weight as 68 kilos( nearly 11 stone)  in 2004. She now weighs 57 kgs.     Patricia  is afflicted with hypothyroidism so any previous attempts at weight loss have proved fruitless. The matter of her spondylolisthesis and severe facet joint chondral loss and hypertrophy involving L4/L5 and L5 on Sl were not discussed.-Scott being more concerned with the compression and 100% loss  of height in L1.    Dr Scott was quite happy with Patricia’s treatment thus far and felt that there was nothing further that she could contribute.

In his report dated  10 May 2010 Pain specialist   Mr Quin reported that Patricia had a  “noticeable thoracic  kyphoscoliosis”.  He identified  “the source of the pain as the point over the lower third of the left sacroiliac joint and this is tender to palpitation. She is also tender to the lumbosacral junction but has no spontaneous pain from that site at this time. There appears to be no neurocompressive disease or radiculopathy.”  Mr Quin considered that Patricia “ was suffering from nociception from the left sacroiliac joint origin.’  He offered Patricia dec“ an office injection of triamcinolone and xylocaine into the subligamentous region below the long dorsal ilosacral ligament…or an x-ray guided sacroiliac joint injection at SRG” Patricia declined to proceed with injections at this time due to her concern about the side effects of cortisone injections.  She was afflicted with a mild allergic reaction with flushing of the skin after a previous joint injection.  Mr Quin also did not consider that a vertebroplasty was appropriate however he had recommended other patients to SRG for this procedure.

Patricia’s had a  consultation with ENT specialist Dr Colin Brown on 14 April 2010 Subsequent to hearing tests Patricia was assessed as suffering from bilateral moderate to severe hearing loss. A recent CT of the brain and temporal bones reported “ mild to moderate age related changes in the cerebral white matter .No intracranial haematoma or other manifestation of head injury is shown.  …the temporal bones show no sign of bony injury. The right middle ear and mastoid are normally aerated…..a small amount of fluid in the inferior aspect of the left mastoid but no sign of a fracture of the temporal bones on either side”  Patricia was provided with hearing aids.

 Patricia consulted with Dr M Butler an orthopaedic specialist assocated with the Pain Clinic at the Greenlane clinical centre in June 2010.  In his report dated  24 January 2011 Butler advised “when seen 15 15/6/10 Mrs Wilson commented that on waking in the morning she had sharp pain in the left iliac crest region Grade 8-9/10 severity , after walking for 15 to 30 minutes ,Grade 6/10 severity, with slight tenderness and sometimes “almost numb” sensation in the iliac crest region, a long walk tending to increase pain. But no change with weather.  She  has had no L buttock or diffuse leg pain and has  no present knee pain.

 Management of musculoskeletal pain in association with spinal  and peripheral joint osteroarthritis discussed, likely additional pathophysiology  of a fluctuating postulated central neural sensistization disorder with elements of neurogenic inflammation ( such as flexor tenosynovitis at the left wrist) option acupuncture ( used as nerve stimulation technique)  to the lower back and L leg used once weekly in a prone position with needles to the low back and L leg with 20-30 minutes minimal stimulation, occurring without break weekly for 10-12 weeks but with no guarantees as to outcome”    

 Patricia had earlier received acupuncture treatment in the lower lumbar area at Pilates.  Unfortunately the procedure caused severe pain and was not repeated.   Dr Butler did not consult any of the scans which we had brought to the consultation .

Subsequent to Patricia’s fall virtually nothing was achieved  due to a combination of underlying attitudes, some variation in and the occasionally inconsistent opinions of specialists coupled with the latent reluctance of Patricia to proceed with steroid injections.

Patricia had another fall at home on 9 August 2010.  She sustained injury to the upper part  chest and the left knee.(a  knee replacement was performed on this knee several years ago)  As she was experiencing pain in the upper part of her chest when either breathing deeply or coughing her general practitioner  Dr Crombie  assessed it as a probable rib fracture .  While she requested an x-ray of the knee she did not consider a x-ray of the ribs was necessary and it might constitute an over-exposure to x-rays even though this is about the third or fourth incidence of rib fracture.

In his  report dated 16 April 2013 Dr Quin further  advised “ on examination she has a severe kyphoscoliosis of the spine and she tends to be somewhat flexed habitus.  She is tender over both sacroiliac joints but more on the left than on the right, but does not acknowledge any significant pain arising spontaneously from the joints.  It was questionable whether bilateral office injections of subligamentous triamcinolone and bupivicaine would be of  great use….suggested however that she should try taking Acupan 30 mg tablets three times a day for about 10 days ….if she feels that sacroiliac joints are contributing to pain , her daughter could bring her back and I would be more comfortable about treating her by injection”

Patricia had another severe fall in her bedroom on 2 april 2013.  She was hospitalised for about 5-6 hours at the bequest of the St Johns ambulance officers.   She was in severe pain with her shoulder and wrist . Unfortunately the lone female ambulance officer was also unable to lift Patricia off the floor and so had to wait for the assistance of two alternative officers including a female officer..  Subsequent  to x- ray at the Emergency clinic in Auckland city hospital her clinical summary prepared by Dr Shyam sankaran reported  “bruising around the right shoulder and wrist.  Limitation of abduction to 50 degrees and limited flexion and extension.  Limited wrist flexion and extension and lateral movement. Neurovascularly intact.  X –rays showed no fractures.  Given analgesia in AED .  Discharged when able to mobilise and comfortable.”

As a result of subsequent severe pain and bruising an x ray was performed by Horizon radiology at White Cross Clinic Lunn avenue on 3 April  and a splint provided . Patricia was attended by nursing staff , Dr Ekdahl and specialist Dr Rawlinson. A fracture was suspected and a cast was applied.  The Horizon  radiology report dated 17 april advised :  “advanced osteoarthritis is present involving the distal scaphoid, 1^st CMCJ, small joints of the thumb and DIPJ’S  of the fingers.  There is also degenerative calcification at the triangular fibrocartilage.  In retrospect there was an undisplaced fracture across the base of the ulnar styloid and this is now clearly evident with mild bone resorption here. In addition there now appears to be a subtle undisplaced fracture distal radial metaphysis.”

 On 24 February 2011 Patricia underwent  a labplus test for Troponin. The test  which is normally  used as an indicator of acute cardiac ischaemia was reported as 60 ng/L * (norm (< 40).  Higher troponin values are associated with increasing degrees of tissue injury and a worse prognosis. The test is normally repeated however that action was not undertaken in this case.   Lab Tests Online state that “ Troponins are the preferred tests for a suspected heart attack because they are more specific for heart injury than other tests . Some people who have a heart attack will have normal troponin concentrations and some people with increased troponin concentrations have no apparent heart injury. Troponin levels may also be elevated with acute or chronic conditions such as mycoarditis ( heart inflammation) congestive heart failure severe infections, kidney disease and certain chronic inflammatory conditions of muscle and skin” It is unclear whether this test, which was requested by the General practitioner was onforwarded to the  Cardiologist-it was not referred to in his report and apparently ignored.

An Echocardiograph was performed at Ultravison Cardiac Imaging on 3 March 2011.   Extracts from the report indicated “ the left ventricle is of normal (small ) size with SVEDD 3.8m and the LVESD 2. 3 cm……..there is a mildly prominent subaortic septal knuckle.  There is good LV systolic function.  There is a mild LV diastolic dysfunction seen as a relaxation abnormality.  ……normal left atrial filling pressures on the day of the study.  ….the left atrium itself is moderately dilated with a dimension of 4.7cm and  an area of 31cm 2.  The mitral valve is mildly thickened and calcified , there is a prominent calcification of the mitral valve annulus.  The valve opens freely and closes with posterior leaflet mitral valve prolapse and significant probably severe MR .  The aortic valve is trileaflet with the cusps are mildly thickend , calcified with minor restriction, they close without AR. There is normal Doppler velocity through the   aortic valve at 1.2m/sec.   The aortic root is of normal size at 3.6 cm.  The ascending aorta is borderline large at 3.5 cm….the right ventricle is of normal size and systolic function.  ………the right atrium is of normal size at 16cm2 .. there is normal Doppler velocity through the main pulmonary artery at 0.4m/sec and the interatrial septum appears intact. The IVC  is not dilated and collapses  appropriately with a sniff indicating no significant rise in right sided pressures” Comments> Severe mitral regurgitation from mild posterior mitral valve leaflet prolapse/////Normal LV size with good systolic function///////Mild TR with normal right sided pressures and unremarkable right heart.”.

Ellis’s general assessment contained in his report dated 14 March 2011 was “ an incidental finding of mitral regurgitation – I don’t think that Patricia has symptoms from her MR but I will suggest a further review in 6 months …to be sure by repeating the echo that the situation is not requiring a change in medical management such as frusemide.”

A  subsequent report dated 14 March 2011 stated “ previously a prominent carotid pulsation had been noted and …..reviewed Patricia in 1994 and demonstrated a kinked right common carotid artery without any flow limiting stenosis. “Examining her today I found.. a weight of 60.3 kg a blood pressure of 164/86 when lying her venous pressure was not raised. Hearts sounds were dual with a 2/4 systolic murmur at the apex and her chest was clinically clear. Her resting ECG showed sinus rhythm a normal axis 69bpm with a right bundle branch block pattern.  The right bundle branch block pattern has developed from 2001. At this stage I think Patricia has symptoms from her MR but I will suggest a further review in 6 months to reevaluate this and to be sure by repeating the echo that the situation is not requiring a change in medical management such as frusemide ( a diuretic)….what I think is an incidental finding of mitral regurgitation.”

A New York Times Health Guide advises that in respect of this condition 

“Medications may include:

1.Antibiotics to fight any bacterial infections

2.Antiarrhythmics to control heart rhythms

3.Blood thinners to prevent clot formation if atrial fibrillation is present used for patients with chronic mitral regurgitation .

4.Digitalis to strengthen the heartbeat

5.Diuretics to remove excess fluid in the lungs

6.Vasodilators to dilate blood vessels and reduce the workload of the heart.

If blood pressure cannot be controlled an intro-aortic balloon pump may be used to help move forward into the aorta the main artery from the heart.”

If surgical valve replacement or repair is not an option the Mayo Clinic advises “Doctors are developing less invasive techniques to treat valve disorders, such as repairing or replacing mitral valves using heart catheterization techniques”

Patricia again consulted with Dr Ellis on 24 November 2011.  Ellis reported : “ she was till able to walk down our corridor to come to the clinic room without difficulty certainly no shortness of breath or chest pain” In fact from my observations at home  Patricia has difficulty walking as her balance is quite significantly affected and she appears to have a shortness of breath with a rapid intake. “ Her BP was 166/84 ….in the medium term Patricia might require an ACE  Inhibitor as her BP was a little raised today but would only initially start a very gentle dose if her BP remains raised as I would not wish to cause any symptoms of postural hypotension”  (Hypotension or a sudden drop  in blood pressure  occurs when a person stretches or stands up) Both of  Patricia’s blood pressure readings are indicative of hypertension however her general practitioner Dr Crombie has advised that these readings are not the norm.  ‘Her heart sounds were dual with a 3/4 murmur heard throughout the precordium and her chest was clinically clear –her resting ECG showed sinus rhythm with a normal axix,70 bpm with a right bundle branch block pattern.-….a cholesterol of 5.4 ( norm<4.0 mmol/L))….her troponin was normal at 9 ng/L –her BNP was reassuring at 17 pmol /L.”

BNP is a substance secreted from the ventricles or lower chambers of the heart in response to changes in pressure that occur when heart failure develops and worsens.  Ellis seemed to be of the opinion that I  had suggested mother be prescribed medication for heart failure “I have explained that that Patricia does not have heart failure and therefore the Digoxin anti-coagulants and vasodilators which Vicki has suggested are not currently appropriate”  I had indeed enquired as to why no medication or even minor surgery had been recommended but I had never suggested  heart failure as an alternative diagnosis to  severe mitral regurgitation.” Ellis stated “ that  a slight rise in troponin is  not unexpected for a lady of 89 years with severe MR and does not signify any particular problem”-as opposed to the reading of February 2011 ( 60 ng/L * (norm (< 40).)

The Adult transthoracic Echocardiogram final report dated 24 November 2011  advised  “there is an anteromedially directed jet as expected but there is also an important posteriorly directed jet that raises the possibility  of anterior mitral valve leaflet prolapse too. MR limited to an assessment by color Doppler and LV dimensions” ( MR not fully assessed at this scan)

“Cleveland Clinic surgeons are pioneers in the development of minimally invasive techniques for mitral valve repair. Today, nearly all mitral valve repairs can be performed through a 2-3 inch incision on the right side of the chest. This approach may also include the use of a surgical robot, which allows an even smaller incision. Cleveland Clinic surgeons have been instrumental in the development and application of modern mitral valve repair techniques. Problems with the posterior leaflet are generally corrected by a small resection of the abnormal portion of the valve. Anterior leaflet dysfunction is managed by creation of new chords or chordal transfer. Anterior leaflet repair techniques are technically challenging, requiring a skilled and experienced surgical team to achieve the best result. All repairs include an annuloplasty, which is a complete or partial ring placed around the circumference (rim) of the valve.”

Patricia was admitted to public hospital on 30 July 2012 with diagnosed angina. ADHB report dated  “ retrosternal chest tightness which radiated to the throat and left arm  No SOB palpitation or waterbrush…no rise and fall of troponin-started on asprin and metoprolol. To use GTN spray for chest pain She has been prescribed asprin, metoprolol and nitrolingual spray. Had no more episodes of chest pain in the hospital.” Although her treatment was satisfactory mother was placed in the mens ward in general surgery where there was an elderly gentleman with a very noisy chest condition. Patricia is a light sleeper at the best of times. 

In his report dated  29 November 2012 Dr Ellis stated “ Earlier this year Patricia was admited to the ACH with a prolonged discomfort in the chest. The troponin level did not rise, and the clinical diagnosis from the medical team was of angina although, going through her symptoms once more, I wonder in fact whether she had some bad reflux.  I have started  her on Lansoprozole on a regular basis from today”  

Dr Ellis’s belated report dated 7 January 2013 advised “ the discharge summary of 31 July 2012 also noted  T wave inversion in 3 and AVF new from her previous ECG-the ECG performed today showed sinus rhythm a normal axis, 64 bpm with a right bundle branch block pattern and t-wave inversion in leads 3 and AVF which is a normal finding. Going back through her hospital records I concur that the ECG of 30 July 2012 did also show that she had inversion in leads 3 and and AVF which were not present with the ECG of  24 November 2011 when the T-waves were upright.  However these changes do not particularly imply ischaemia the degree of MR present and some slight LV volume change or other causes may account for these changes.  …I think the addition of metropolol at  a low dose and a statin is of help. Patricia had a height of 143 cm, and a weight of 59 kg and a blood  pressure of 165/82 when taken by our Clinic staff.   Her pulse was regular, venous pressure not raised, heart sounds dual with a ¾ murmur, and her chest was clear

Patricia underwent an echocardiogram on 23 November 2012 the preliminary report has noted a normal LV size with good systolic function posterior mitral valve prolapse as previously seen with severe eccentric anteriorly directed MR, severe LA dilation with an area of 33 cm2, but a normal right size  and a systolic function and  normal right sided pressures estimated form the mild –moderate TR. I think Patricia is currently stable. A review is planned for a year’s time.

DERMATOLOGY

We finally received reports pertaining to Patricia’s previous history from Dermatologists Dr Peter Gould.   Only one report namely that pertaining to an excision in 2008 seemed to be in the possession of patricia’s practitioner  Dr Sue Crombie. Reports were not provided  to cover cryosurgery.  Goulds covering  letter dated 15 February stated  ‘ as for her other consultations , these have all involved simple cryosurgery to numerous lesions on her face trunk and limbs over many years”

A Diagnostic Medlab  report dated October 1991 reported as follows: “ SKIN LESION DORSUM LEFT ANKLE….the sections are of skin including partial thickness of dermis and show a cup shaped squamous proliferation with a keratinous core.  There is some asymmetry.  The base of the lesion shows a moderate inflammatory cell infiltrate which does not include eosinophils.  Neutrophilic intraepithelial abscesses are not demonstrated.  Although the appearances are consistent with an early keratoacanthoma,  the alternative diagnosis of invasive well differentiated squamous cell carcinoma cannot be excluded on histological grounds.   The lesion reaches the deep surgical margin  Summary: consistent with keratoacanthoma.”

A Diagnostic Medlab report of March 2006 reported on a “SKIN LESION L EFT INNER ANKLE-CURETTINGS…..the specimen consists of a keratotic light brown skin nodule 7. x 6x 4 mm. Microscopy:  the sections show a superficial biopsy of papillomatous skin.  There is an irregular epidermal invagination with overlying hyperorthokeratosis and focal  parakeratosis.  The squamous epithelium shows mild hyperplasia and forms horn cysts at the base of the lesion.  The surrounding dermis contains scar tissue and a light chronic inflammatory infiltrate.  The epithelium shows no dysplastic change and there is no invasive malignancy in the sections examined.  SKIN LESION LEFT I NNER ANKLE CURETTINGS: CONSISTENT W ITH VERRUCAL KERATOSIS.”

In November 2007 Medlab reported on a “LESION LEFT CHEEK:  the specimen consists of a skin Ellipse 12 x 4 x 4 mm .  No cyst is seen on section.   MICROSCOPY:  histological assessment reveals dense solar elastosis and mild perivascualar chronic inflammation  in the dermis.  No cystic lesion, significant cytological atypia or malignant changes are seen in the original or  in deeper levels.   LESION LEFT CHEEK DENSE SOLAR ELASTOSIS”

In his letter dated 26 June 2008 Dr Gould advised “ that he had excised the lesion on the left cheek on November 2007 the histology of which was reported as a dense solar elastosis.  I have not seen the lesion recently however it has recurred and I presume it must be a squamous cell carcinoma or similar”   

In his report dated November 2008 Dermatology registrar Dr Raj referred to the previous removal of a skin lesion from Patricias left cheek. He advised  “ she had previous elective removal of a lesion on her left cheek in august 2008.   Histology  had suggested a squamous cell carcinoma with clear excision margins .On examination her cheek was unremarkable  there was a small actinic kerastosis lateral to her left  outer eye which was frozen today with liquid nitrogen there were no other lesions of concern.”

My elderly mother Patricia had 2 lesions on her right leg one of which was considered to be a probable squamous cell carcinoma. A consultation with locum Dr Bailey of St Heliers medical centre in early January 2012 resulted in the prescription of a bacterial cream bactrofan and antibiotics. As the result of a consultation with Dr Sue Crombie over a week later on 23 January 2012 a biopsy was performed by Labtests.

 Their microscopy report dated 25 January 2012 advised “ skin lesion right lower leg – the specimen consists of a piece of skin 2 x 4 mm. Microscopy: sections show skin without subcutaneous tissue. A well differentiated squamous cell carcinoma invades severely sun damaged and scarred upper and mid dermis. Diagnosis: skin lesion right lower leg squamous cell carcinoma. Skin lesion right lower lateral leg : the specimen consists of three fragmented pieces of skin ranging from 2 x 1 mm to 3x 2 mm . Microscopy: sections show parakeratotic scale and unevenly thickened dysplastic epidermis with a small amount of underlying dermal tissue. The appearances are at least those of a solar keratosis. Invasion cannot be excluded.”

Mother had one consultation with a dermatological registrar Dr Lim in March and the excision/graft was performed by Dr Pillai ( consultant Dr Cranshaw) of General surgery on 10 April 2012. Patricia returned to Greenlane Clinical Centre on 19 April 2012 for the removal of the staples and dressing over the graft on the lower right leg. Removal of the staples was quite a painful procedure without anaesthetic and further stitches were removed at St Heliers medical centre on 2 May 2012.

In her report dated 26 April 2012 Dr Pillai reported that “ the graft site looked healthy and the graft has taken 100%”..Patricia was quite pleased with the outcome…Patricia’s daughter asked about reconstructive surgery for her mother…I explained why the excision needs to be taken down to fascia so as to avoid grafting on to subcutaneous fat…that at the age of 90 this reconstructive surgery would be major and unwarranted there will always be a lesser degree of indentation in the area ………Histology shows no residual SCC”

An alternative to grafting is the provision of a keystone  flap A case history involving an 84 year old man with a SCC on the lower leg is de

The Keystone Flap for Lower Extremity Defects:

Mengjunan  Hu BS and  Jeremy S. Bordeaux MD, MPH^2,*

Article first published online: 5 DEC 2011

DOI: 10.1111/j.1524-4725.2011.02236.x

© 2011 by the American Society for Dermatologic Surgery, Inc. Published by Wiley Periodicals, Inc.

Mother is 90 years old and not only was there a waiting time of three months but also a delay of approximately 4 hours on the day of surgery. Contrary to Dr Pillai’s assertion that “Patricia seemed to quite pleased with the outcome” she was quite alarmed at the depth of the excision She has been prescribed antibiotics ( synermox) by her general practitioner Dr Crombie.

The prognosis for grafting contrasts sharply with that of a flap procedure which has quick healing time, reduces pain and importantly also restores contour . At her age one might have considered the latter to be the more humane of the two options.

 Patricia has been attended by district nurses for dressing changes since the surgery.  They normally attend  ( three times a week ) with the exception of weekends.  By early June the wound had still not completely healed there was a small amount of greenish coloured slightly odorous discharge. Although reasonably attentive the nurses seemed reluctant to acknowledge either infection or the presence of 2 small ulcers on the edge of the wound which had been mentioned previously by a male nurse.

Unfortunately the misjudgement of a British nurse named Jan resulted a delay of 5 days before the dressing was changed. She had advised me  by telephone that she considered that this was an appropriate course of action.

She did apply iodine to the wound in early June 2012 by which time the discharge seemed to have significantly improved. Laboratory testing of  the swab on 12 June 2012 reported a “ heavy growth of  corynebacterium species” with a recommended antibiotic treatment.

 I had  emailed a complaint to Donna Deans of the Quality department of ADHB  on 4 May 2012 concerning the type of  surgical procedure, the waiting time of  4 hours on the day of the surgery , the twice rescheduled date of consultation at the general surgical clinic to the end of June 2012  and the delay of 5 days between a change of dressing on the leg wound on one occasion by nurse Jan.  I spoke to Ms Deans in June and she claimed to have no trace of the complaint.

We visited Greenlane clinical centre on 28 June 2012.  Patricia was given a very cursory examination of the healing graft by a young male doctor Dr Toner while she was seated in her chair. He was not interested the laboratory report detailing the bacterial infection nor did he show much regard for the continuing soreness or the small amount of discharge still evident in the wound.. With regard to the lab report  the consultant suggested that the heavy growth might only be indicative of a colonisation rather than a significant infection.    He left Patricia with the option of continuing her care under the auspices of her general practitioner.  She  continued with a prescription of erythromycin .

She visited Dr Toner At Greenlane Clinical centre on 23 August 2012.  Patricia is still experiencing discomfort in a small area adjacent to the  the now generally healed leg graft.

A histology report dated 24 august 2012 stated : Wide excision of 2 lesions in April with grafting. The wound healed with a large crater and patient still has a lot of pain in medial border of wound where there is a tender raised hyperkeratotic looking area-concerning for a scc. On examination wound healed crater and base looks fine. Very tender ( not red) area on medial edge-raised irregular + hyperkeratotic.”

 A punch biopsy was performed on “ a new lesion just at the inferoposterior aspect of the graft site”

Punch Biopsy Right Leg

Macro : a punch of skin 3 x 3 x 3 mm

Micro: sections show a punch biopsy of skin to upper papillary demis.  The section is cross cut which hampers assessment.  There is a well diffferentiated partially cystic squamous lesion in the dermis. In areas the squamous epithelium shows enlarged cells with abundant glassy cytoplasm and spongiosis.  Scattered mitoses are identified. Within the underlying papillary dermis there are thin walled vessels and a scattered inflammatory infiltrate, in keeping with stasis. The lesion is insufficiently well profiled for a definitive diagnosis.  Possibilities include keratoacanthoma, squamous cell carcinoma and epithelian inclusion cyst.

DIAGNOSIS:  PUNCH BIOPSY RIGHT LEG: WELL DIFFERENTIATED SQUAMOUS LESION

Subsequent to biopsy histology report dated 29 October 2012 stated “ a resolving keratoacanthoma surgical margins clear”

At a consultation on 25 March 2013 Sue Crombie took a biopsy from the area of the ankle in Patricia’s left leg. There was some some minor swelling and pain above the area of the graft in the right leg in conjunction with a haematoma caused by a knock to the leg.   Crombie didn’t consider that antibiotics were necessary .

A labtests histology  report dated 25 March 2013 advised :

Specimen 1

“ Punch biopsy skin lesion left mid shin: the specimen consists of two skin punch biopsies each 2 mm in diameter x 2 mm in depth.

Microscopy:  Sections show one fragment of focally ulcerated skin and accompanying fragment of adipoise tissue only showing medial calcification of vessel wall.  Skin shows presence of an early minimally invasive well differentiated squamous cell carcinoma with superficial focal dermal involvement.  Accompanying fragment of adipose tissue shows no tumour.

Diagnosis: Early squamous cell carcinoma.

Specimen 2:

Punch biopsy skin lesion left lower shin

Gross description: the specimen consists of a skin punch biopsy 3 mm in diamenter  x 4 mm in depth

Microscopy: Sections show sun-damaged skin with epidermal features of a proliferative actinic keratosis.  There is no invasive malignancy.

Diagnosis:  Actinic Keratosis”

NEUROLOGY

Geriatrician Dr M Scott conducted a brief general and neurological  examination of Patricia on 14 October 2012. Patricia’s “neurological  examination essentially normal apart from cognition and impaired memory and fluency”  Interestingly her “ visuospatial was 13/16” although she is almost blind in her left eye. “Her pulse was 60 bpm and her blood pressure is 120/60. Her PINP 42 was  the the lower third of post menopausal range. A Ct head scan in May 2010 showed mild to moderate age related cerebral white matter changes as well as a small amount of fluid in the left mastoid- a repeat scan was not considered essential.  It was considered that as Patricia is mildly bradycardiac her condition might be exacerbated by donepezil medication. She can continue driving albeit in a limited capacity. Pat is also seriously deaf and wears a hearing aid.

OPTHAMOLOGY

Patricia was afflicted with a with a probable spider bite on her right hand  in October 2012 with the typical “bullseye” appearance which can be  indicative of  of a more severe bite.   Patricia was concerned that her sight had been affected to some degree and she mentioned this to Dr Toner at Greenlane who didn’t seem unduly concerned as some of the bruising had disappeared. He prescribed her augmentin antibiotics. A tetanus injection and a referral to a local optometrist Mr Hirst were later provided by general practitioner Dr V Ivori.   

An eye examination by Kerry Atkinson of Optometrists Mortimer Hirst on 31 October 2012  reported that “ in the left eye it looks like a central retinal artery occlusion which could be related to her health the recent spider bite or possibly giant cell arteritis” Atkinson onforwarded his report to Patricia’s former eye specialist Mr Donaldson and the eye clinic at Greenlane and Dr Crombie .  I requested that he also onforward the images which he agreed to do. I also emailed both Atkinsons report and image to Crombie via her practice manager Kathy. Unfortunately at her consultation on 7 November Dr Crombie was unable to access the optometrists images and she was a little sceptical about the effect of a spider bite on the eye ( There are many similar complaints on the internet).  Patricia was provided with a vitamin B injection as her levels were lower than usual .

Patricia visited the acute eye clinic at Greenlane on 7 November 2012. Unfortunately nearly 2 hours elapsed and she had still not seen a consultant. At 3pm I queried the delay with the receptionist who apologised and said she would ask the nurse to give Patricia priority. This never occurred.  .

.A number of patients who had arrived later than ourselves had all been attended to and had departed. We decided not to wait and after a blood test  departed at 3.30 pm. A young registrar conducting the clinic was observed making a quiet comment concerning sanity to the nurse.    A British middle aged doctor with dark grey hair made a couple of rather loud comments concerning “ a bad patient” and “ the police as well”

 Shortly after we arrived home I received a phone call from the staff nurse a middle aged woman with dark blond hair  –she claimed to have been calling Pat’s name for triage which was certainly not the case . This is not the first time that Pat had experienced long delays in obtaining treatment including having to wait for approximately 4 hours for graft surgery –hardly the most considerate of treatment for a 90 year old.

In 2009 eye surgeon Mr Donaldson  reported that Patricia’s “ uncorrected visual acuity was 6/20 for both eyes. She has astigmatism in the left eye and when this is corrected the vision in that eye corrects up to 6/6. Introocular pressures this morning 18mmHg right and left. I would recommend that Patricia have right cataract surgery.”  A subsequent report dated September 2010 stated:    “her visual acuity was 6/9 right and left . I have previously done a left cataract operation. She  has nuclear sclerosis on the right side which is reducing her contrast on that side.  Her intraocular pressure is 22mm Hg right and left “.

The optometrist’s diagnosis was refuted. .In his report dated  28 November 2012 specialist Mr Donaldson  advised “ that her visual acuity is currently 6/15 R and hand movements L.  She has previously had left cataract surgery . She has dense nuclear cataract affecting the right eye with a normal macula.  The left eye as intraocular lens and a disciform scar at the macula.  I think she would benefit from having right cataract surgery.” .

Cataract surgery was successfully performed by Dr Gray at the ADHB eye clinic on February 18 2013.

 In his post operative report dated 19 March 2013 opthamology registrar Dr Cunningham advised: 

“Diagnoses:  1.right cataract plus Toric lens insertion 18/2/13

2. left pseudophakia
3. left macular scar

 Visual acuity:  right eye unaided 6/12. 6/9 pinhole

4. Left eye hand movements

Examination today showed the right eye was quiet.  Her lens was well –positioned and on axis at 0 degrees. Her lens measurement was a 22 diopter and power with a 2.25 cylinder correction. ……new spectacle prescription “

GASTROENTEROLOGY

Patricia has been referred to the gastroenterology clinic at Greenlane.  Her general practitioner Dr S Crombie received a reply from the clinical director of Gastroenterology at the ADHB dated 31 January 2013. He advised “ I note that Patricia had a successful fundopliction in 2001 as she was intolerant of PPI.  This was a very successful operation but in recent months she has had reduced appetite and a recurrence of reflux symptoms.  We will indeed place her on the waiting list for an upper GI endoscopy. She had a low risk polyp in 2004 on a colonoscopy performed in the private sector. There are no bowel symptoms other than a tendency to constipation and certainly no evidence of iron deficiency or anaemia.  There is no indication to perform a repeat colonoscopy as there are no bowel symptoms. A single low risk polyp at the age of 81 does not confer a significantly increased lifetime risk of colorectal cancer.”  After a lifetime of chronic constipation one would have thought that a further investigative procedure might be in order.   Medical websites suggest that an alternative would be an MRI of the colon. 

 Patricia Wilson aged 91 years was first admitted to Auckland Hospital at the end of April for small  bowel re-section surgery and again on 12 June 2013.. Unfortunately I was not contacted immediately after surgery by the operating surgeon Dr Jason Wong and eventually received later advice concerning mother’s condition from a clinician-christian name James.  Patricia was shifted to the Awatea ward where apart from the nursing staff  my only contact was Geriatrician Ms McMillan. There was an unfortunate comment concerning a “bastard mental case” overheard from a Maori person outside the ward. In addition a young male asian university student passed a loud comment in a crowded bus concerning “ Pat Wilson’s sacrifice”

The pathology report dated 30 April 2013 advised: “MICRO: The mucosa is atrophy with loss of villi and erosion.  The submucosa is haemorhagic, oedamatous  and acute inflamed..  The inerstitial haemorrhage and inflammation  extends into the mesocolon. Acute inflammatory exudate is present on the mucosa surface.  The resection margins appear viable .  No thrombus is seen in the examnined mesenteric vessels.   Features are consistent with haemorrhagic ischaemic enteritis”

DIAGNOSIS.  SMALL INTESTINE –HAEMORRHAGIC ISCHAEMIC ENTERITIS

The operational report dated 1 May 2013 advised that “ the small bowel was adherent in the pelvis with a loop behind the bladder where the uterus used to be.  There was a slight twist on this causing  a small bowel obstruction. The small bowel  was ischaemic with an area of early necrosis requiring a resection……The small area of  bowel that was stuck in the pelvis with a closed loop of obstruction. …..A lower midline laparotomy was performed…..Features are consistent with haemorrhagic ischaemic enteritis”

 Post-op low urine output

Recent fracture(wrist) fracture sustained following a fall on 2/5/13. The cast was removed and discussed with orthopaedics –she will be seen at the fracture clinic one week following discharge”

ADHB’s report of 28 May seemed to be somewhat contradictory – there was reportedly no sign of infection however the the wound was being treated with oral augmentin!  One nurse advised me that Patricia had a stitch abscess. Another nurse advised me that a swab from the stomach wound assessed by Labplus  indicated gram positive cocci. Large numbers of gram positive cocci were also reported by Labtests on 31 May 2013-  “ large number of polymorphs and large numbers of gram positive cocci”. Culture: moderate growth of skin flora

After discharge from Hospital nursing/medical  care was provided by Patricia’s medical practice and the district nursing staff.

 Patricia was readmitted to Auckland hospital on 12 June and discharged on 14 June. The report of Clinician Nicholas Bryden advised  “On examination: Obs stable, abdomen soft non-tender.  Chest clear, heart sounds dual  At the top of the wound there s a small opening with granulation at the base . No cellulitis.

Investigations:  FBC nad, LFT nad, U +E nad, CRP 4    Swab –growth of staph aureus

Discharge medications: Flucloxacillin 500mg ( 7 days) and Paracetomol

 IMP Slow wound healing

Progress and management : Admitted under general surgery. Wound was reviewed by the team and looked to be healing well.

Plan:D/c home///District nurse for dressings ///Analgesia////Antibiotics

Both Labplus and a Labtests ( 31 May 2013) reported large numbers of gram positive cocci.

Patricia met Dr Crombie on 31 May and 4 June 2013 after observation of the wound she advised  that antibiotics would be required and prescribed augmentin.  Nursing staff concurred that significant pus as a brown exudate was still evident in the wound  . Assistance was also provided by district nursing staff.   

I only became aware that the wound infection had been categorised as being infected with Staphylococcus aureus after reading the discharge summary dated 14 June 2013. Medical and nursing staff are very reluctant to discuss infection and the young male registrar who handed me the summary was non-committal. It is unclear as to when  staphylococcus aureus was first diagnosed by Labplus or whether it could have been  treated earlier  with more potent antibiotics. .Her discharge medication was a 7 day script of Flucloxacillin and this has been extended.

By the end of June and  despite nearly two month courses of augmentin and also  flucloxacillin  progress not unsurprisingly slow. It is particularly stressful for a 91 year old particularly since it only 12 months since she had a leg graft. District nursing staff attend on a daily basis and provide dressing changes excluding any topical anti-bacterial  applications .

Patricia returned to the colo-rectal unit at  Greenlane Clinical centre on 9 July 2013 where she met Janet  a member of the surgical team. She examined Patricia’s stomach wound took a photograph and discussed it with her superior. It was suggested that Patricia return for a follow up in six weeks –she was also given the option of cancelling the consultation if she considered that the wound was sufficiently healed! Once again there was minimal discussion concerning the staphylococcus aureus infection in the wound. It was considered that continuing antibiotic treatment should be the responsibility of the general practitioner.    A wound swab was also taken .

Patricia experienced  nausea sickness and diarrhoea for approximately a week in late August 2013.She met a local general practitioner Dr Hazlewood on 23 August 2013.. A Blood pressure reading was 150/82? She recommended both a urine and faecal test.A mid-stream urine test performed by Labtests on 30 August 2013 showed “ no significant culture” A faecal test was not undertaken.  The prescription was also provided for amoxicillin antibiotics. 

Patricia underwent an upper GI endoscopy with Dr Mark Lane at Auckland Hospital on 6 September 2013.  “findings: the examined oesophagus was normal. A large hiatus hernia was present .  The nissen fundoplication is probably intact. The exam of the stomach was otherwise normal.. The exam of the dusodenum was otherwise normal.  Impression: normal oesophagus fundoplication intact Hiatus Hernia.  These findings account for symptoms however no easy fix…would require a re-operation not do-able given her age”

Lane suggested that the matter be left in the hands of Susan Crombie. He claimed to be unaware that Patricia had a bowel re-section in May and also claimed not to be familiar with the department of gastroenterology  Mr Wong who actually performed Patricia‘s surgery in May. Dr Lane was also responsible for my gastroscopy in June of this year however he did not enquire as to my well being.

Pat visited Dr Sue Crombie on 24 September 2013. A B 12 injection was provided.  We discussed Dr Mark Lane’s assessement of Pat’s recent endoscopy –Crombie didn’t really have an alternative opinion other than to confirm Lane’s status as  a senior gastroenterologist. She didn’t discusss the likelihood of a laparoscopic procedure .

In respect of Pats weight loss (  from 59 kgs ( November 2012) to  47 kgs September 2013) Crombie seemed to be of the opinion that this matter could be dealt with by the geriatrician  However I requested that Pat be re-referred to the colorectal clinic at greenlane and she agreed to send a referral there however as at 18 October no referral to the colo-rectal unit has been received.

The journal of Gastroenterology and Hapatology advises that in the treatment of older patients with hiatal hernia :

“It is reasonable to perform laparoscopic repair for a type 3 paraesophageal hernia in a relatively healthy older individual if the surgical expertise is available. However, close observation can be a reasonable approach in patients without complicated symptoms. As mentioned above, it is very important to recognize the signs of impending strangulation in a patient with paraesophageal hernia to surgically correct it and avert a life-threatening situation” 

The lung  CT dated  17 October 2013 advised “ There is prominence of soft tissue associated with a gastroesophageal junction which appears mass like although it seems more likely this simply represents compressed rugal fold due to the hiatus hernia.”

After experiencing two bouts of giddiness accompanied chest pain and breathing problems. Pat was admitted to Auckland Hospital on  16 October 2013.  Dr Singh requested a chest x ray subsequent to a check by stethescope  in which “ crackles” were evident.   She was subsequently admitted to general medical on the sixth floor of Auckland Hospital.  A female Indian doctor advised that Pat was probably suffering from heart failure and to that end they were attempting to reduce the fluid level around the heart by increasing the amount of frusemide.  Patricia has been afflicted with a severe cough for the last few weeks which I suggested might be attributable to a bacterial  infection as I had been diagnosed  with Pseudomonas in September. The Indian registrar didn’t think that a bacterial infection was necessarily indicated in the chest x ray and that no antibiotics were prescribed at this time. Nor did she consider that a loss of appetite could be caused by a hiatus hernia.

  The North Penn Hernia Institute advises “when intestine becomes trapped within the hernia  the normal flows of food becomes blocked.  This creates a progressive back up within the intestine and may result nausea and vomiting. If the intestine is only partially blocked nausea ( without vomiting) and poor appetite may be the result.”  Likewise “ nausea vomiting or loss of appetite can result from a bowel resection” The following day Patricia’s nurse who had previously also advised that no antibiotics has been prescribed discovered that in fact one rulide tablet per day had been scheduled.   Pat rang me early evening on Saturday 12 October to advise that she had become disorientated while walking . Nursing staff were advised.

 CT of the abdomen and pelvis were performed at ADHB on 21 October 2013.

“CLINICAL INDICATION: Widespread malignancy on HRCT.  Thought to be a possible lung primary.

  Within the abdomen there is a nodule associated with the left adrenal which could represent an adrenal mass or left para aortic lymph node metastasis.  1.5 aortocaval lymph node is present and just below that level and neither of these lesions were seen on the previous CT from April.  Inferiorly there are further enlarged retroperitoneal nodes and lymph nodes within the root of them mesentery .  There is a paucity of an intra- abdominal and pelvic fat but the pelvic appearances are undermarkable with no pelvic or inguinal lymph node enlargement.

Liver parenchyma is  normal with no evidence of hepatic metastasis.  There is a solitary large gallstsone within an otherwise normal looking gallbladder.  No biliary dilation.  Unprepared study but there is no gross bowel lesion identified.  Stapled surgical anastomosis seen within the left iliac fossa.  The is  no ascites.  Pancreas, spleen and kidneys are unremarkable for age.

A wedge compression frature of L1 with degenerative spinal canal narowing ??? . No evidence of destructive bone lesion. 

Opinion:  Appearances remain consistent with metastatic lung cancer.  A lymph node involvement in the upper abdomen and retroperitoneum with ??? easy biopsy targets in the abdomen and pelvis.”

Despite my request that an investigation be undertaken concerning Patricia’s symptoms including significant loss of appetite and weight it appears that nothing was achieved in this regard.  Her hospital meals continued to be provided but were not eaten.  The meals were occasionally supplemented by Fortsip  a high energy nutritionally complete drink.

RESPIRATORY

An ADHB report dated 4 May 2013 advised “Post-op atelectasis and pneuomonia-treated with Augmentin and roxithromycin-chest x ray on 4/5/13. This is compared with previous day’s film. Similar volumes of free gas -demonstrated beneath the diaphragm with very distended loops of bowel still present.  The diaphragms are elevated and there is atelectasis at both bases and small pleural effusions present.  Air bronchogram seen behind the heart on the left indicating some degree of consolidation.  The patient probably has a hiatus hernia as well.”–

Patricia had been experiencing bouts of vomiting mild chest pain and a prolonged cough and streaming nose. She attended Dr Govind of One Health on 22 September 2013 . An ECG was performed, which  aside from a right branch block pattern was assessed as  comparatively normal . A stethescope of the chest revealed some “ crackles “ in the lower lung and amoxicillin prescribed. Her BP was 110/? Patricia has been afflicted with severe coughing bouts in the past –however Dr Crombie has not been prepared to prescribe on at least two occasions .

After experiencing two bouts of giddiness accompanied chest pain and breathing problems. Pat was admitted to Auckland Hospital on 10 October 2013. A chest x ray was requested and  Dr Singh advised that  “crackles” were evident during his stethescope examination.  Patricia  was subsequently admitted to the  general medical ward.  A female Indian registrar  advised that Pat was probably suffering from heart failure and to that end they were attempting to reduce the fluid level around the heart by increasing the amount of frusemide.  Patricia has been afflicted with a severe cough for the last few weeks which I suggested might be attributable to a bacterial  infection as I had been diagnosed  with Pseudomonas in September and cross-infection would be a probability. The Indian registrar didn’t think that a bacterial infection was necessarily indicated in the chest x ray and that no antibiotics were prescribed at this time. Nor did she consider that a loss of appetite could be caused by a hiatus hernia

Patricia’s  cough seems to be improved however she is still afflicted with a runny nose. It was unclear as to whether a throat swab or chest sputum samples had been taken for analysis. Once again a female African registrar also claimed that Patricia was not receiving antibiotic treatment.  Patricia has been receiving additional oxygen . Her Bp was 100/?.  The initial chest x ray indicated “ interstitial changes” and an HRCT was performed on 17 October 2013 which clearly showed extensive cancer in both lungs. One might have assumed that a CT of the lungs could have been initiated after the lung x ray of 3 April 2013.

 A high resolution CT of the chest dated 17 October 2013 revealed: “extensive reticular nodular shadowing on the chest x ray. Extensive bibasal lung nodularity with nodular interlobular septal thickening consistent with lympangitis carcinomatosis.   Interspersed among the areas of interstitial thickening there  are small nodules which are more predominant in the lung bases.  Peripheral areas of consolidation are present in the lingula, but medially adjacent to the mediastinum in the right upper lobe there is a more spiculated mass like area of consolidation.  Enlarged mediastinal lymph nodes are noted, the largest a subcarinal node measuring at least 2.2 cm short axis  daimeter.  Paratracheal adenopathy is also noted exending to the base of the neck, note it is  measuring up to 1.8 short axis diameter.   A Left supraclavicular node measuring 13mm short axis diameter is also noted. 

There is trace of pleural thickening at the right base but no pleural fluid or pericardial fluid identified. The heart is not particularly enlarged although the cardiac valves are somewhat calcified.

The adrenals are normal.  Small portion of the visualised abdominal organs are unremarkable.   There is a left para-aortic node measuring 16 mm short axis diameter just medial to the left adrenal gland. 

Bones: Gross degenerative change invloves both shoulder joints.  There is sclerosis of the right posterolateral 6^th rib without destruction.  No other discrete bony deposit seen. 

Comment : Overall the conglomeration findings  within the lung also associated with adenopathy favors malignancy;  The lesion in the right upper lobe could represent a lung primary.  Lymphoma is a possibility given the adenopathy.  There is prominence of soft tissue associated with a gastroesophageal junction which appears mass like although it seems more likely this simply represents compressed rugal fold due to the hiatus hernia.

 18 October 2013 I met registrar Louise and consultant Dr Hotu.  They discussed the CT chest scan of the previous day which indicated significant lung cancer.  There was no explanation as to why further investigations were not instigated in May 2013 at the time of Patricia’s last chest x ray. Huton suggested that changes in the lung can occur rapidly in a matter of months.  She suggested that needle biopsy could be attempted although it was optional. She was of the opinion that oncology would first need to be presented with biopsy results before consideration could be given to admission to the oncology ward.  Huton did not recommend a consultation with a respiratory physician but seemed to think that palliative care was the best option.  Patricia had been a smoker  but stopped in the 1960s.   Such extensive  (primary?) cancer seems to be unusual for a long-term non smoker .  A chest  x ray was  performed by Mercy Radiology in February 2001.

 Website Radiopaedia advises that “Lymphangitis carcinomatosis is most commonly seen secondary to adenocarcinomas such as:

• breast cancer – most common ³
• lung cancer (bronchogenic adenocarcinoma)
• colon cancer
• stomach cancer

It can also be seen in numerous other primary cancers, e.g. thyroid cancer, laryngeal cancer, pancreatic cancer, cervical cancer and prostate cancer.

Spread into the lymphatics in most cases (except in bronchogenic adenocarcinoma) usually occurs following haematogeneous seeding of the lungs, with subsequent lymphatic involvement ^1,3. Both the peripheral lymphatics coursing in the interlobular septa and beneath the pleura, and the central lymphatics coursing in the bronchovascular interstitium are involved ².

Histologically tumour is seen both within lymphatics and in the adjacent interstitium, with associated oedema and desmoplasia”^3-4.

ADHB website advises that “ Once lung cancer is diagnosed, a process known as staging determines the extent of the disease. Knowing the type and stage of cancer means the doctor can plan your treatment.

Different treatment options include: surgery.  The type of surgery depends on the size and type of cancer// radiotherapy is a form of high energy radiation (X-ray) that kills cancer cells// chemotherapy is the use of drugs aimed at killing cancer cells.

The aim of treatment is to keep the person as well as possible even if the cancer cannot be cured.

If you have a lung cancer there will be ongoing follow up with specialists and nurses throughout treatment and afterwards

Patricia was discharged from hospital  on 25 October . She was provided with oxygen equipment for use at home however her breathing was generally laboured.  After her return home she had been experiencing giddiness including occasional  problems with her eyesight  (seeing wavy lines) and extreme  general discomfort including  the chest..  She said she felt as if “ she was going to die” She had to be assisted to and from the  the bathroom and lavatory. She was readmitted to hospital. I visited the hospital and ward 21  (planning unit) on Labour Day 28 October 2013 however details from the nursing staff were scant .

 I enquired of Nurse Eleanor? ( a british nurse) as to whether Pat was receiving antibiotics She advised that they had  not been  prescribed as Pat did  not have a temperature!  I was not aware that a lack of a temperature would preclude an antibiotic prescription.  Patricia was formerly prescribed antibiotics in the  general medical ward to where she had once again been returned.   I have been afflicted with severe chest and sinus infections and most often my temperature is classified as normal.

 It appeared that she was only receiving one tablet per day which was probably inadequate.  I collected a pottle of  golden coloured  sputum from Patricia which was  handed over to the ambulance officers and presumably onforwarded  to Labplus .  I spoke to the senior nurse Rowena on 31 October and she advised that the sputum test initially showed the presence of some bacteria  and was awaiting a culture. I also later  spoke to the gerontologist  Dr Spriggs  concerning the sputum test results. He seemed to be singularly unconcerned and considered that providing antibiotics “would be a waste of time.-that Patricia was at the end of her life” The clinical summary dated 25 October “ thought to be heart failure vs atypical chest infection-thus given IV antibiotics”

Pat has been re-admitted to the general medical ward on 29 October 2013.  We again spoke to the female Indian house surgeon who we met  previously in ward 65.  It seems that the status quo is much as it was-Pat has not yet been prescribed antibiotics “ because she doesn’t have a temperature”. !

The question of Pats serious loss of weight and appetite was not addressed during the previous 2 weeks in hospital . I  had hoped that there would have been a further investigation of the bowel re-section in conjunction with the hiatus hernia. 

She was no longer seemed able to walk on her own.  She has also given up reading and listening to the radio .She previously would read the newspaper for 2-3 hours in the morning.

I visited Pat in hospital on 1 November 2013.  According to the nurse Pat had her usual breakfast of porridge earlier in the morning and had put on her makeup. . When I arrived she was in a semi-comatose state unable to open her eyes and sounding distressed and groaning loudly.   She was barely conscious and was shifted to another ward where she was alone.   At one stage she pointed to her left side and again said “ she was going to die”! 

There was no further medical investigation concerning the latest symptoms. She was given morphine by the nurse, a Pacific Islander, which seemed to quieten her down. I provided Patricia with ginger ale on the end of a small sponge . This action elicited some response for a time until she gave two gasps and ceased breathing.  Her head was tilted to the side and her tongue was protruding slightly from the inside of her cheek. It would appear that she may have died from a serious heart attack/and or stroke.   Dr Lm visited her about an hour and and a half later and confirmed her death.   Her death certificate stated  “lung cancer months –cognitive impairment years”. 

In June 2018 I  received a hospital  summary for the period 27 October 2013 until her death on 1 November 2013.  The summary is as follows:

“ A swab growth of Staphylcoccus aureus” was reported  in a discharge summary of 14 June 2013 and a “7 day prescription of Flucloxacillin . Recent admission with small bowel obstruction 30/4/13 complicated by post-op atelectasis and pneumonia and then required a period of rehab.

Laboratory test for P Sexton 27 October 2013.  “Muco-purulent large numbers of gram positive cocci seen-  large numbers of gram negative bacilli seen

Culture: a moderate growth of mixed oropharyngeal flora///gram negative organisms  (mixed species) ////at least three different organisms present” ( Al Anbuky)

‘Patient watch report 28/10/13   “pat said her spinal hurts in pain so as her chest told the nurse about it”//   marked systolic murmur MR: respiratory scattered crackles : fine crepitation throughout lower zone//sputum mucopurulent large numbers of gram positive cocci and gram negative bacilli//Daughter visited very concerned that pat is not on antibiotics..?? explained docs plan”

A Medical internet site advises “Marked variability of systolic heart murmur associated with idiopathic hypertrophic subaortic stenosis. Variation in the severity of left ventricular outflow tract obstruction in response to physiologic and pharmacologic maneuvers is characteristic of idiopathic hypertrophic subaortic stenosis (IHSS), and useful in distinguishing it from other types of cardiac disease.‘,

Medical journal Circle states:  “Idiopathic hypertrophic subaortic stenosis (IHSS) is a disease characterized by marked hypertrophy of the left ventricle, involving in particular the interventricular septum and the left ventricular outflow tract.”

Review of the literature indicates that sudden death occurs in a significant proportion of patients with IHSS and appears to be more frequent in those with the familial than in those with the nonfamilial form of the disease.  It may occur in patients who were previously asymptomtic as well as in patients who had been severely limited prior to death.”

29 October 2013  “Pat woke at 0500 with slightly increase resp rate speaking in short sentences productive cough with greenish sputum given a  hot drink.///Obs within pats usual range before 1300 hrs but RR went up to 40 beats /min while c/o chest pain soon after daughter left. Pat claims she is scared wanting daughter to come back to support her-no one answered home phone”. The greenish sputum would have been characteristic of pseudomonas aeruginosa.

The  US National Institute of Health advises “ in Lung cancer patients are characterized by the frequent presence of Pseudomonas aeruginosa in chronic obstructive pulmonary disease, together with age-related comorbidities, aggressive tumors and rapid clinical

In his report dated 30 October 2013 Gerontologist Dr  Spriggs reported: “ This 91 years old lady went  home just before the long weekend and came back after a couple  of days.  I think because her daughter found her more short of breath.  We had a discussion with Mrs Wilson and  her daughter on several occasions about the cause of the shortness of breath.  It is due to lymphangitis .  We are not going to be able to fix it”.

31 October 2013 Assessment summary: “Mrs Wilson has had a recent admission  (discharged 25 /10/13) and it is felt she returned as her daughter was concerned about her breathlessness.”

In fact I had readmitted Patricia because of her complaint about the pain in her chest.

1/11/2013  Notes from Dr Lim:  “Pat currently deteriorating may pass away in hours/days.  Daughter asking for details of sputum culture. /Vicki would like her mother to be treated with antibiotics -explained that she is unable to swallow in  her recent condition and to put in an intravenous line would be cruel and inappropriate : sputum culture Nil infection”  ??

There is no reference in the nursing or medical notes on the day she died to Patricia’s obvious extreme discomfort in her chest or the fact that she was obviously groaning in pain and complaining that she was going to die.  It might be construed that Patricia died of a heart attack complicated by acute respiratory distress caused by a lack of medication.

CONCLUSION

 Whether this saga of unprecedented victimisation which involves discrimination evasiveness and disregard might also be assessed as involving  serious negligence and criminal intent has yet to be determined. Duplicitous infiltration/substitution might also another significant factor to be considered.

The entrapment of totally sane individuals with diagnoses of insanity in order to use them for experimental purposes, in effect treating them like monkeys in a laboratory, is not only blatantly criminal, if not indicative of fascist eugenics , but also seriously undemocratic. It seems to represent nothing more than a terrible role reversal where in an oppressive society the totally sane but politically unwanted are incarcerated or otherwise disposed of and the socio-psychopaths are left to run the asylum, so to speak. 

Any assistance which could effectively end this long running odious saga and prevent the disposal and dispossession of a suffering pensioner would be welcome. Please contact me @ jazminnex4@gmail.com particularly if you can provide any  financial or  legal assistance. Images and family photos are also available on my Facebook page.

GENEALOGY

Genealogy might also be relevant. My family is descended from Emily Hilda (Wallis) Wilson who in turn was descended from Emily Sarah the  daughter of Captain Thomas Wing. Another relative namely James Wallis helped to establish the Wesleyan Mission in North Island and was a signatory to the Treaty of Waitangi.

 Wing was  a former harbourmaster of Port Phillip in Melbourne and the Manukau of Auckland New Zealand in the late nineteenth century.  Captain Wing handed down lockets to his offspring. Wing also had a daughter Fanny by the sister of Chief Tutu. The little girl was apparently killed in a raiding party by Hone Heke in Russell where she was living with the Tapper family.

 The partial tracing of an almost identical image of the locket which is inset into the wall/ gate of Wingfield Castle Suffolk was made by a relative some years ago. That is the only tentative connection between the Wingfield and Wing families known to us.  Wingfield Castle was the ancestral home of the Dukes of Suffolk –Wingfield is their family name.

 Mr and Mrs B Wingfield and their son and daughter lived in a nearby street in Karori Wellington in the 1950’s and 60’s. We had only very limited contact with the family.  Pippa  (Glanville) Blake, the wife of my cousin  former yachtsman Peter Blake ( deceased) is also descended from the Wingfield line as is the Duchesss of York. 

British Author Laurence Gardner  used his books to propose several theories, including a belief that Jesus and Mary Magdalene had married and had children, whose descendants included King Arthur and the House Of Stuart, British kings, and families including the Wingfield family.