Estate of White v Accident Compensation Corporation (Treatment Injury)

IN THE DISTRICT COURT AT WELLINGTON ITE KOTI-A-ROHE KI TE WHANGANUI-A-TARA [2019] NZACC 58 ACR 414/17 UNDER THE ACCIDENT COMPENSATION ACT 2001 IN THE MATTER OF AN APPEAL UNDER SECTION 149 OF THE ACT BETWEEN ESTATE OF DOROTHY WHITE Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent Hearing: 9 May 2019 Appearances: Mr T M White on behalf of the appellant Ms C E J Deans for the respondent Judgment: 4 June 2019 RESERVED JUDGMENT OF JUDGE C J MCGUIRE Section 32 - Treatment Injury - Accident Compensation Act 2001 [1] The question at issue in this appeal is whether the death of the deceased in Wellington Hospital on 4 May 2017 was caused by a treatment injury for the purposes of s 32 of the Accident Compensation Act. Background [2] The deceased, Mrs White was diagnosed with Sezary syndrome ("T cell lymphoma") in early 2016. [3] To treat this her doctors administered a course of medication with an anti- cancer agent known as Alemtuzumab (also known as Campath). This was administered in what is described as a low dose three times weekly over six weeks. [4] The course was completed on 23 February 2016 with good results. 5] It was recognised by her doctors that with the damage caused to her immune system by the Alemtuzumab there was a risk of viral or bacterial infection and in fact in the course of her treatment she contracted a cytomegalovirus infection. To deal with this and any other infections she was administered Valganciclovir, an antiviral medication, Acyclovir, an antiviral medication and Cotrimoxazole, an antibiotic. [6] Her medical notes for 29 March 2016 record that there was no circulating viral DNA found and accordingly the Valganciclovir medication was stopped but the Acyclovir and the Cotrimoxazole was to be continued for another month. [7] As mentioned the treatment was largely successful for a period of months. [8] However, her medical notes for 11 August 2016 record that there was a relapse of the underlying T cell lymphoma. A treatment plan was formulated, again to treat the lymphoma with a low dose Alemtuzumab. [9] Significantly, the medical note of 11 August 2016 recorded: The one concerning feature in this regard would be further reactivation of CMV cytomegalovirus), if she embarks on treatment she will be on up front therapy with Valganciclovir. [10] On 1 February 2017 prior to the commencement of her second course of Alemtuzumab the consultant haematologist wrote: As in the past, we will start with a test dose and escalate to 10mg Monday, Wednesday, Friday for at least six weeks. Given the fact that she had CMV (cytomegalovirus) reactivation in the past, we will keep a close watch on her CMV titres. If there is any clinical suggestion we will definitely start her on Valganciclovir. She will also be on Acyclovir in the interim and on PCP prophylaxis with Cotrimoxazole. We will also start her on Fluconazole as an antifungal prophylaxis.. [11] From this point on until her final acute admission into hospital on 5 April 2017 there appeared to be no contemporary clinical records amongst the almost 300 pages of medical records in the Agreed Bundle of Documents. We do know that she commenced her second course of Alemtuzumab on 8 February 2017. It appears common ground that she did not respond to the treatment and that it was stopped early in March 2017. [12] On 18 March 2017 she attended the Emergency Department with pains in her legs. She was however discharged the same day. [13] On 5 April 2017 she was admitted to Wellington Hospital with a history of nausea and vomiting, increasing pain in her legs and erythema of her legs. She also complained of severe itching of her legs which disturbed her sleep. There is also a history of cognitive decline and weight loss. Blood tests showed that she was hyponatremia, that is having dangerously low levels of sodium. [14] The clinical records from 5 April 2017 the date of her admission note her medications as Levothyroxine, Omeprazole, Allopurinol, Gabapentine, Loratadine and Paracodeine. [15] Under the heading "Impression" the admission note says: Impression: 1. Hyponatremia? Cause. Euvolaemic although Hx of vomiting. Potential delayed side effect of Campath. although note ED has discussed with haematology reg (Florence) re Campath in relation to hyponatremia - thought likely to be out of the system by now given treatment discontinued > one month ago). ? possible infection unclear source although afebrile. 2. Cognitive impairment. ? Confusion secondary to hyponatremia. However Hx suggests more chronic/long standing - ? element of undiagnosed dementia acute on chronic leg pain. ? Secondary to Sezary Syndrome. Peripheral neuropathy. 2 and 3 exacerbated by hypertronia. [16] Under the heading "Plan" the admission note records: 1. Complete slow IV saline - aim increase of Na of 0.5 mmol/hr as per ED. 2. Blood cultures plus cxr. 3. Add LFTS, CRP. CMV PCR if LFTs deranged. A . Repeat bloods mane (form out). Delirium screen: 4 AT score: 1-3: possible cognitive impairment. [17] The hospital treated Mrs White for hyponatremia and her other conditions but were unable to make any significant progress. On 13 April 2017 she was transferred to ICU. Her discharge summary from the general ward includes the following: Primary Diagnosis: Hyponatremia - likely secondary to Alemtuzumab. [18] The discharge summary includes a diagnosis of syndrome of inappropriate antidiuretic hormone (SIADH) the notes also record that she required transfer to ICU due to type II respiratory failure. [19] Her intensive care admission report of the same day, 13 April 2017 includes reference to her being admitted to hospital on 5 April 2017 with confusion and acute hyponatremia. The report then says: Thought to be SIADH - ? secondary to medication: Alemtuzumab. [20] Before the intensive care admission report concludes it notes these issues: Type II respiratory failure, hyponatremia, global weakness, confusion. [21] On 18 April 2017 Mrs White underwent a nerve conduction study. Neurologist Dr Rosemergy reported: Mrs White was reviewed in the Intensive Care Unit today for her progressive weakness and neuromuscular failure resulting in intubation and ventilation. Our understanding is that she had a short and quickly progressive weakness which resulted in difficulty breathing. The history only spans 7-10 days. She has a background of cutaneous T cell lymphoma for which has been given Alemtuzumab. We are not aware of any history of other chemotherapy agents. ... this is an abnormal study. ... these findings are most in keeping with an Acute Motor Axonal Neuropathy. ... there is a case report of AMAN following Alemtuzumab treatment for MS. Our understanding is that Mrs White was treated many months ago. [22] On the same day, 18 April 2017, Dr Shawn Sturland completed an ACC claim form on behalf of Mrs White. In a separate treatment injury claim Dr Sturland listed the injury as "Guillain-Barre syndrome (acute motor axonal neuropathy)" and described the signs and symptoms of injury as "total paralysis (ICU dependent), autonomic instability - STEMI". Under the heading "what treatment gave rise to the injury" Dr Sturland wrote: Alemtuzumab Rx for T 4 cell lymphoma". [23] Mrs White required a tracheostomy and ventilation during a 21 day stay in the Intensive Care Unit, where she received treatment for Guillain-Barre syndrome. Sadly, there was a poor response to treatment and she died on 4 May 2017. Evidence [24] To investigate the claim ACC obtained copies of relevant clinical records and sought expert advice from a clinical pharmacologist an emeritus professor of medicine Carl Burgess. In a report dated 30 June 2017 he advised: Before considering whether Alemtuzumab was responsible for the Acute Motor Axonal Neuropathy (AMAN) in this case I think one has to ask whether Alemtuzumab was responsible for the acute syndrome of inappropriate antidiuretic hormone (SIADH) that caused this patient's admission because the two may be related. There is evidence that the serum sodium was normal in March 2017, I think this was after the Alemtuzumab had been stopped. It was below the normal range one day prior to admission and then suddenly decreased by the day of admission and may have been responsible for Mrs White's confusion and later hallucinations. By this time the drug would have been stopped for about a month. In a publication ... SIADH occurred during the use of the drug. In this case there is no documentation that Mrs White had hyponatremia while she was taking Alemtuzumab so it seems unlikely that Alemtuzumab was responsible for the SIADH. SIADH can occur with Guillain-Barre syndrome ... however there was no sign of weakness on clinical examination when Mrs White was admitted (25] As to AMAN Professor Burgess stated: Alemtuzumab has a half life in blood (15-21 days), but the effects on B- lymphocytes last 180 days or longer. ... so it is possible that this illness could be due to Alemtuzumab. Although it is possible that the GBS was due to Alemtuzumab I think it more likely because her immune system was depressed because of her disease and the Alemtuzumab I think that the probable cause for her final illness related to a viral cause for her GBS. [26] In a further report obtained after the review hearing Professor Burgess advised: The late Mrs White was diagnosed with cytomegalovirus during her first course of treatment with Alemtuzumab despite treatment. She was at further risk of developing infection with the second course. A cytomegalovirus infection is one of the major predisposing illnesses for GBS. Her immune system would have been depressed allowing for recrudescence of megalavirus infection and GBS. ... There are two potential causes of the terminal illness that being GBS. The most likely cause is that there was a recrudescence of a cytomegalovirus infection; one needs to remember that the late Mrs White was admitted with an illness characterised by nausea, vomiting, anorexia (two days), weight loss (one month), painful legs and memory and concentration problems (months). Her serum sodium was low and she had decreased lymphocytes. She also had a myocardial infarction to the GBS, thus the late Mrs White would have been under physical stress and it is likely that her resistance would have been low. The second cause would be GBS from Alemtuzumab, this would be due to an autoimmune phenomenon. The late Mrs White had a goitre that may have been due to autoimmune thyroid disease. As far as I am aware there have been only two cases of GBS following the use of Alemtuzumab reported in the literature, one similar to this claim and one with sensory changes as well. This could reflect the rarity of GBS (3.3/100,000 patients/year), but it has been used more extensively in patients with multiple sclerosis, so one might expect more cases to have been reported. On balance, I think it is more likely that the GBS is due to recrudescence of cytomegalovirus infection. The Law [27] Treatment injury is defined in s 32 of the Act. The relevant parts of s 32 provide: 32 Treatment injury (1) Treatment injury means personal injury that is- (a) suffered by a person- seeking treatment from 1 or more registered health professionals; or (ii) receiving treatment from, or at the direction of, 1 or more registered health professionals; or (ifi) referred to in subsection (7); and (b) caused by treatment; and (c) not a necessary part, or ordinary consequence, of the treatment, taking into account all the circumstances of the treatment, including- (i) the person's underlying health condition at the time of the treatment; and (ii) the clinical knowledge at the time of the treatment. (2) Treatment injury does not include the following kinds of personal injury: (a) personal injury that is wholly or substantially caused by a person's underlying health condition: (b) personal injury that is solely attributable to a resource allocation decision: personal injury that is a result of a person unreasonably withholding or delaying their consent to undergo treatment. (3) The fact that the treatment did not achieve a desired result does not, of itself, constitute treatment injury. Submissions [28] Mr White, who represented his late wife's estate referred to the notes of a meeting on 21 April 2017 where the ICU SMO was present and told Mrs White and other family members: We believe that the drug treatment for her lymphoma was the cause. I also told her we had registered an ACC claim (for a treatment injury) because of this. [29] In a letter dated 4 August 2017 Mr White said: But the second course was stopped after 14 of the 18 injections as there was no change at all since the first injection and the immune system still attacked the periphery nerve system which gave her the pains in her legs which was the G-B syndrome ... And why would they [the doctors] write an ACC form off their own bat before I knew anything about it when I was asked to sign it they were blaming the Campath. Dorothy probably would not have had the heart attack if the immune system hadn't gone haywire being caused by the second course of Campath and bringing on the GBS. [30] And in a follow up letter of 7 August 2017 referring to the virus theory, Mr White said: .. how did it come about? You should be asking yourself. The immune system let it in and why or how did it do that? - because it was weak or depressed ... caused by the Campath! There's no getting away from that! "The immune system". [31] In handwritten submissions filed on 19 January 2018 Mr White said: But the second course was stopped after 14 injections as there was no change at all since the second course started. But the immune system still attacked the peripheral nerve system which gave her the leg pains which was the Guillain-Barre syndrome, and the G-B gave her the heart attack, I'm thinking? No hard problems before this. ... the Prof has shot himself in the foot by his virus "theory". How come she got a virus? Her immune system had been weakened by the Campath! Sound familiar?! We're going around in circles here if nobody wants to believe the facts and wasting a whole lot of taxpayers' money in the false hope of saving money avoiding the facts. ... and why would the doctor in charge write out an ACC form for a treatment injury off his own bat (I only found out about it when I was asked to sign it) if that's what he calls it that's what it must be surely. ... Finally, I have marked a paragraph on 176 of Dorothy's medical file of a report by one of her doctors, Dr James Taylor, stating his thoughts on the matter, somebody who was working at the coal face. I cannot see how these facts can suggest a "no" answer against the ACC's fairy tale case. .. . The Respondent's Submissions [32] The primary submission is that the specialist medical evidence does not support the contention that Mrs White's GBS was caused by Alemtuzumab rather the evidence establishes that it was more likely than not that there was a viral cause for Mrs White's GBS. Ms Miller makes these points: [a] That when admitted to hospital Mrs White had stopped taking Alemtuzumab more than a month before and that the medication was "likely to be out of her system"; [b] Professor Burgess acknowledged a longer effect of Alemtuzumab because of its long half life in the blood but was only prepared to say that any connection between Alemtuzumab and CBS was "possible"; [c] Suspicion as to a possible link does not form a valid basis for drawing inferences as to causation; [d] Depressed immunity is an "expected outcome of treatment with Alemtuzumab" and the Act is clear that an ordinary consequence of treatment does not attract cover for a treatment injury (s 32(1)(c)). Depressed immunity in itself is not evidence of injury; [e] Mrs Whites' T Cell lymphoma affected her body's ability to ward off infection and that her health was compromised by illness on her admission to hospital in April 2017; [f] Professor Burgess does not directly link Mrs White's state of health at the time of her admission to Alemtuzumab; [g] Mrs White was diagnosed with cytomegalovirus (CMV) during her first course of treatment with Alemtuzumab. Professor Burgess notes that Alemtuzumab is "invariably" given concurrently with antibiotics and antiviral medication and that Mrs White developed CMV "despite treatment"; and [h] CMV is "one of the major predisposing illnesses for GBS" according to Professor Burgess and that the recurrence of CMV is the most likely cause of GBS in Mrs White's case. He reaches this view taking into account the physical stress that she would have been under due to her ill health at, and during, her admission. Decision [33] I have reached the clear view in this case the appeal should be allowed. [34] So far as it is relevant in this case I find that for the purposes of s 32 Mrs White suffered a personal injury while: seeking treatment from one or more registered health professionals; caused by treatment; not a necessary part or ordinary consequence of the treatment, taking into account all the circumstances of treatment including the person's underlying health condition at the time of the treatment; and the clinical knowledge at the time of the treatment. [35] In reaching this view I am mindful of s 32(2) and (3) that a treatment injury does not include personal injury which is wholly or substantially caused by a person's underlying health condition and that a treatment injury does not arise from the fact that a treatment did not achieve a desired result. Reasons (a) When Mrs White received her first course of treatment in 2016 she contracted cytomegalovirus. In his report of 9 March 2018 Professor Burgess says: The late Mrs White was diagnosed with cytomegalovirus during her first course of treatment with Alemtuzumab despite treatment. She was at further risk of developing infection for the second course. Cytomegalovirus infection is one of the major predisposing illnesses for GBS. Her immune system would have been depressed allowing for recrudescence of cytomegalovirus infection and GBS. (b) The Agreed Bundle of Documents is poorly put together. There are plainly documents missing and what is included does not follow a logical or date sequence. (c) The earliest reference I have been able to find to her first course of treatment is dated 27 January 2016 some two weeks after the Campath treatment commenced. The haematologist's report of that date says: Her serology profile does not show any increase in CMV PCR suggestive of CMV reactivation. (d) Included under the heading "problem" list is this: To closely monitor for CMV reactivation with weekly CMV PCR. (e) The next report is dated 11 February 2016. Again under the "problem" list is the same reference to monitoring for CMV reactivation. The report also says this: Her weekly CMV titres have definitely shown recent positivity. I have discussed this issue with her ID consultant and we feel that we need to start her on oral Valgamciclovir to prevent it from causing systemic CMV disease. We will keep a close watch on her CMV titres in the next three weeks. (f) In the next report of 23 February 2016 is this: ... without any significant infections hospitalisation or any renal toxicity. Her weekly CMV PCR did pick up mild increase in the viral titres last week and has been started on Valgamciclovir at 450mg bd for the last fortnight. She reports no new fevers or any symptoms suggestive of an underlying infection. ... she will continue weekly CMV PCR and we will monitor toxicities on Valgamciclovir g) The next report is dated 29 March 2016. It records: She had two CMV serologies which have been found to be negative for any circulating viral DNA and I have stopped Valgamciclovir. h) Several months later when there was a relapse of her underlying Sezary syndrome a second course of treatment with low dose Alemtuzumab was proposed. The consultant haematologist noted in the clinical letter of 11 August 2016: The one concerning feature in this regard would be further reactivation of CMV. If she embarks on treatment she will be on upfront therapy with Valgamciclovir. (i) The next clinical letter that I have been able to find is dated 1 February 2017. This letter indicates that her second course of Alemtuzumab is due to start the following week. The consultant haematologist notes: Given the fact that she had CMV reactivation in the past, we will keep a close watch on her CMV titres. If there is any clinical suggestion, we will definitely start her on Valgamciclovir. Astonishingly, there are no clinical records that I have been able to find in the Bundle of Documents between 1 February 2017 (mentioned above) and her acute admission into hospital on 5 April 2017. The period in question covers the time when she underwent the second unsuccessful treatment with Alemtuzumab. (k) Furthermore, there is no clinical record of her entry into hospital on 18 March 2017 with pains in her legs and her discharge the same day. So we are left to guess whether or not during her second course of treatment with Alemtuzumab there was in fact a CMV reactivation, and if so, whether she was again given Valganciclovir to deal with this issue. (1) What we do know is that when she was admitted to hospital on 5 April 2017 her medications were listed as Levothyroxine; Omeprazole; Allopurinol; Gabapentine; Loratadine and Paracodeine. None of these are antiviral drugs. (m) Therefore, based on the fact that at the commencement of the period 1 February 2017 to 5 April 2017 for which I have been unable to find any clinical records, we know she was not being prescribed Valganciclovir and at the end of that period there is no mention of that medication. I conclude on the balance of probabilities she did not receive it. (n) Assuming, as Ms Miller submits on behalf of the respondent that as Professor Burgess opines, the more likely cause of the terminal illness, GBS, was the recrudescence of cytomegalovirus infection, I find that the criteria for a treatment injury as defined in s 32 is met. Namely, that this injury was suffered by the deceased while receiving treatment from registered health professionals and that it was caused by the treatment she received namely the failure by one or more health professionals to follow through with their own treatment plan to use Valganciclovir to prevent the recrudescence of cytomegalovirus infection which according to Professor Burgess was the cause of her fatal GBS illness. (o) In these circumstances the exceptions in subs (2) of s 32 do not apply namely that on account of the identified need to address the issue of recrudescence of cytomegalovirus infection the injury was not wholly or substantially caused by Mrs White's underlying health condition; nor was this attributable to a resource allocation decision nor was it a result of a person unreasonably withholding or delaying consent to undergo treatment. (p) Finally, I cannot overlook that it was a clinician himself who initiated the treatment injury claim on behalf of Mrs White on 18 April 2017 and that he did so of his own initiative without prompting from the patient or her family. The inescapable inference to be drawn is that the doctor concluded that the Guillain-Barre syndrome could have been avoided. [36] The appeal is accordingly allowed. I reserve leave to both parties to apply to the Court if any issue arises relating to costs. Judge C J McGuire District Court Judge Solicitors: Claro - Wellington, Wellington for the respondent ACR 414-17-Est of D White