harp graphic.
THE HIGH COURT
[2025] IEHC 331
Record No: 2016/707P
BETWEEN:
AMS
PLAINTIFF
AND
LORCAN BIRTHISTLE
DEFENDANT
JUDGMENT of Ms. Justice Emily Egan delivered on the 9th day of April 2025
INDEX
HIV - Opportunistic infections. 1
Epidemiological association between HIV and VL. 3
Association between HLH and VL. 3
The position of the parties. 3
Chronology of the plaintiff's care. 5
Period 1: 19th February - 28th February 2014. 6
Period 2: 1st March 2014 – 18th March 2014. 7
Period 3: 19th March 2014 – 1st April 2014. 9
Legal principles relating to the standard of care. 11
The plaintiff's factual evidence. 13
SJH Haematology consultants. 15
General observations regarding the evidence of the treating clinicians. 17
Was Dr Sheehan's evidence sufficiently independent?. 18
Was Prof. Mehta's evidence sufficiently independent?. 19
Dr. Ellis's specialism in tropical diseases. 19
Review of the expert evidence. 20
Plaintiff's ID expert: Dr. Ellis. 20
Plaintiff's haematology expert: Prof. Mehta. 24
SJH's ID expert: Dr. Sheehan. 26
SJH's Haematology expert: Dr. O'Keefe. 29
Standard of approach- identify the appropriate standard of approach. 31
Is it standard of approach to re-consider a diagnosis in light of developments?. 39
1. On 19.02.14, the plaintiff, a seriously ill young man, newly diagnosed with human immunodeficiency virus ("HIV"), was admitted to St James's Hospital ("SJH"). The plaintiff claims damages for medical negligence on foot of SJH's failure to diagnose visceral leishmaniasis ("VL") during his ensuing 42-day admission. Whilst in SJH, the plaintiff was diagnosed with hemophagocytic lympho-histiocytosis ("HLH"), triggered by herpes virus type 8 ("HHV-8"), [1] in the context of HIV. He was ultimately transferred from SJH to Hospital de la Fe in Valencia, Spain on 01.04.14, where VL was diagnosed 3 days later.
2. It is common case that the plaintiff had HIV, HLH and HHV-8. It is also common case that he had VL and that this was an important trigger of his HLH. SJH also accepts that none of the five Consultants, who managed, investigated and cared for the plaintiff during his admission considered the possibility of a diagnosis of VL at any stage of his admission. The crux of the case is whether SJH's failure to diagnose VL was in breach of the standard of care.
3. It is first necessary to provide some context on the diseases of relevance to this case: HIV, HLH, HHV-8 and VL.
4. HIV severely compromises the immune system leading to a risk that the patient will develop opportunistic infections, in a manner that would not occur outside of this context. There are, in principle, a vast number of opportunistic infections that a person with HIV could develop, many of which can occur simultaneously.
5. HLH is a rare, severe, life-threatening clinical syndrome characterised by an uncontrolled hyperinflammation of body tissues due to excessive activation of the immune system. Lymphocytes and macrophages, both of which are types of white blood cells, combine to phagocytose (or in layman's terms, consume) and thereby eliminate offending material, but also healthy cells. There are a number of other rheumatological, haematological, infectious and medically induced conditions that may cause features similar to HLH.
6. HLH can be genetically acquired ("primary HLH"). There is a body of paediatric literature on the diagnosis and treatment (the "HLH Protocol") of primary HLH. The HLH Protocol involves the use of chemotherapy drugs and dexamethasone to kill white blood cells and reduce phagocytic activity.
7. HLH may also be triggered by a variety of infections, by malignancies, and less commonly by other conditions ("secondary HLH"). Viral infections (such as HIV and HHV-8) are particularly common triggers for secondary HLH. Whilst less common, parasitic infections (such as VL) may also drive HLH. Less than 20% of HLH cases have no detectable trigger.
8. In primary HLH, an inherited abnormality controls the harmful phagocytic activity. However, in secondary HLH, infection (or malignancy), whilst not directly causing the pathological abnormalities characteristic of HLH, drive this mechanism. This means that in cases of acute HLH, infectious triggers (and malignancy) should be diagnosed rapidly in order to commence appropriate therapy, which aims to both target the trigger and to "switch off" the HLH. There are dangers associated with treating HLH without identifying its triggers. This is partly because merely "switching off" the HLH leaves the underlying infection (or malignancy) behind. Chemotherapy is also associated with side effects; it kills normal white blood cells, which fight infection. This becomes more significant in an immunosuppressed patient, such as an HIV patient, leading to low white blood cell count, worsening infection, anaemia and increased the risk of bleeding. There is some controversy between the parties in this case as to whether the chemotherapy administered to the plaintiff for the treatment of his HLH was necessary. As it is crucial to identify the trigger for the HLH, clinicians must administer a wide range of diagnostic tests to cover infections (and malignancies) known to be associated with HLH, which the plaintiff contends includes VL.
9. Diagnosis of HLH requires the presence of 5 of 8 findings. The plaintiff met the following 5 findings: (i) fever >38.5C; (ii) (cytopenia (low levels of (a) red blood cells/ anaemia, (b) white blood cells and (c) platelets/thrombocytopenia); (iii) hemophagocytosis visible as changes in the bone marrow; (iv) high levels of ferritin (a blood protein that contains iron) and (v) splenomegaly (enlarged spleen).
10. HHV-8 infection is a well-known opportunistic infection in patients with HIV/AIDS (initially associated with Kaposi's sarcoma). The mainstay of management is the administration of antiretroviral therapy which has been found to reduce HHV-8 viral shedding and viral load. Antiviral drugs are also used in patients with active HHV-8 disease.
11. There are 3 main forms of the disease leishmaniasis. VL is caused by the flagellate protozoan leishmania infantum. According to the World Health Organisation ("WHO"), "[l]eishmania parasites are transmitted through the bites of infected female phlebotomine sandflies, which feed on blood to produce eggs. Some 70 animal species including humans can be the source of Leishmania parasites." ('Leishmaniasis' (12 January 2023)).
12. VL is fatal if left untreated in 95% of cases. It presents with a classic picture of prolonged, irregular bouts of fever, weight loss, pancytopenia (in which all blood levels are low), hypergammaglobulinemia (an increase in serum proteins other than albumin) and persistent significant splenomegaly (occasionally hepatosplenomegaly, where both the liver and spleen are enlarged). The plaintiff presented with several clinical features which are shared between HLH and VL, such as fever, cytopenia and splenomegaly.
13. There is dispute between the parties as to whether the degree of splenomegaly is a critical diagnostic factor. The plaintiff maintains that whilst splenomegaly is a feature of both HLH and VL, "massive splenomegaly" [2] (with which it is contended he presented), is associated with the former but not the latter. SJH's position is that whilst splenomegaly is associated with both HLH and VL; it is a non-specific sign and is a not a particular marker for VL.
14. Treatment for VL is by way of AmBisome, which is an anti-fungal medication.
15. It is common case that there is an epidemiological association between HIV and VL. Furthermore, although VL is generally a tropical infection, cases of leishmania/HIV coinfection have been reported in the Mediterranean region, mainly in France, Italy, Portugal, and Spain.
16. The literature indicates that at least 10% of HIV positive individuals in southern France and Spain, had asymptomatic leishmania infection on serology. The plaintiff therefore maintains that SJH should have known of this association and tested for VL in his case.
17. SJH's position is that while an Infectious Disease ("ID") physician in Dublin might be expected to know of this epidemiological association, VL remains incredibly rare, even in Spain.
18. There is now a known overlap between the clinical features of HLH on the one hand, and VL on the other. Reaching a diagnosis of HLH triggered by VL in a HIV patient requires both theoretical knowledge of the association between HIV and VL and consideration of that association in a given case. In addition, such a diagnosis would be aided by knowledge and consideration of an association between HLH and VL. In other words, if one is treating an HIV patient in whom one has diagnosed HLH, one is more likely to consider VL as a trigger if one knows both that HIV is associated with VL and that VL is one of the infections that can cause HLH.
19. Whether there was a known association between HLH and VL in 2014, is a matter of controversy between the parties. SJH's defence pleads that this association only emerged in the adult literature in 2019, whereas the plaintiff maintains that this association was well known in 2014.
20. At a high level of generality, the plaintiff claims that:
(i) Two features in particular ought to have alerted the ID and haematology clinicians in SJH to the diagnosis of VL:
· First, the epidemiological association between HIV, VL and Spain, combined with the fact that the plaintiff was HIV positive and from Spain;
· Second, the plaintiff's "massive splenomegaly."
(ii) SJH should have considered and diagnosed VL within four days, i.e. between 19.02.14 and 22.02.14.
(iii) On foot of this diagnosis, SJH should have commenced AmBisome during the same period.
(iv) Alternatively, a reasonable suspicion of VL would have prompted the commencement of empirical AmBisome during the same period.
(v) If AmBisome had been administered, the plaintiff would have recovered within approximately 5 days of admission and would have left SJH within 2-weeks at the latest.
(vi) Instead, he remained in hospital for 6 weeks, received toxic chemotherapy, became an infection risk, acquired infections requiring further heavy treatment, received 14 units of blood transfusions, had restricted mobility, required transfer to intensive care in the Burkitt's Ward and suffered ongoing pain and suffering.
(vii) When the plaintiff arrived in Hospital de La Fe in Valencia, Spain, VL was diagnosed within 3 days and the plaintiff was commenced on AmBisome. The plaintiff recovered sufficiently to be discharged within a week.
21. At a high level of generality, SJH 's response to the case is as follows:
(i) The plaintiff's condition on admission posed a significant risk to his life and required urgent diagnosis and treatment.
(ii) Along with his HIV diagnosis, the clinicians made a timely diagnosis of a rare and life- threatening condition, HLH. The clinicians further correctly identified rare and credible triggers for HLH in the form of HIV and HHV-8. All of these diagnoses were correct and provided a reasonable working hypothesis on foot of which appropriate life-saving treatment was administered.
(iii) Whilst the plaintiff also had VL, it was not a breach of the standard of care not to consider this extraordinarily rare diagnosis. Prior to this case, the five experienced consultants who cared for the plaintiff had never seen or treated a case of VL. Nor had a case of VL ever been encountered in Ireland prior to 2014.
(iv) Vis a vis the two features identified by the plaintiff as potentially alerting the clinicians to VL:
· In an ID clinical setting in Ireland in 2014, VL was understood to be a tropical disease, with the vast majority of cases worldwide in various tropical countries, of which Spain is not one; although there was an epidemiological association between HIV and VL in Spain in 2014, the case numbers were particularly low, at approximately 200 cases per year.
· The SJH clinicians were aware that the plaintiff had significant splenomegaly. However, splenomegaly, even massive splenomegaly, can be caused by a range of other, more common presentations. It would only lead one to consider VL in the absence of other credible diagnoses for a massive spleen, such as HLH.
(v) Having commenced a treatment programme for HLH triggered by HIV and HHV-8, it was reasonable to allow an appropriate period of time for it to work; and by mid-March, it showed signs that it was working.
(vi) Throughout his admission, the plaintiff expressed a desire to return to Spain for treatment as soon as possible, which SJH facilitated when the plaintiff was well enough to travel on 01.04.14. Although SJH did not consider VL during the period of his admission, the plaintiff was not discharged from medical care without this diagnosis having been made. Rather he was transferred to Hospital de la Fe. Had the plaintiff remained in SJH, it is likely that, over time, as other credible triggers fell away, the diagnosis of VL would have emerged.
(vii) The relative speed of diagnosis of VL in Spain is not significant. The Spanish clinicians had the benefit of all of the tests and investigations already carried out in SJH. By then, treatment for the identified triggers had also been given time to work effectively. In addition, whilst VL was unknown in Ireland, this was not the position in Spain.
22. The following issues fall to be determined:
(i) Should SJH have diagnosed VL within four days of the plaintiff's admission?
(ii) Alternatively, should SJH have diagnosed VL at a later point in time during the plaintiff's 42-day admission, and if so, when?
(iii) If the answer to either of the above is affirmative; then what would have followed from the diagnosis of VL in terms of treatment and recovery?
(iv) What is the differential between (a) what would have occurred in terms of treatment and recovery on the counter-factual scenarios at (iii) above and (b) what did in fact occur in this case?
(v) What is the appropriate compensation for such differential?
23. The plaintiff who was born on 07.06.1982 is a Spanish national who had lived his entire life in Alicante, in the southwest of Spain. In 2013, he migrated to Ireland in the hope of getting a job. He lived with his friend, MSF - a pharmacist by profession.
24. In late 2013, the plaintiff became generally unwell and experienced weight loss, high fever, sweats and shivering. He attended a GP in Dublin and after being diagnosed with HIV attended the SJH Department of Genito Urinary Medicine and Infectious Diseases ("the GUIDE Clinic").
25. The plaintiff presented to the GUIDE Clinic with a 6–8 week history of feeling unwell, fevers, sweating, weight loss (7Kg), passage of loose yellow stools, lower abdominal and suprapubic cramping pain and left testicular pain.
26. The plaintiff was admitted to SJH on 19.02.14. He underwent assessment by the GUIDE Senior House Officer who recorded the above history and noted that the plaintiff was Spanish. Although the plaintiff testified that his spleen was swollen, abdominal examination did not reveal splenomegaly. The impression was of a disease of unknown origin in a man with HIV, and seroconversion.
27. Counsel for SJH has sensibly suggested that the plaintiff's 42-day admission is broken up into the following three periods: The first period, 19.02.14 to 28.02.14 is critical as the plaintiff's case is that the diagnosis of VL ought to have been made in the first four to five days of his admission. However, as the complaint is of a continuing failure to make the diagnosis throughout the admission, the entire admission must be examined. In the second period, 01.03.14 to 18.03.14, two important events occur over a very short window: on 13.03.14, the plaintiff was moved to a transplant ward, Burkitt's Ward, because he was in extremis and required intensive care; and on 14.03.14, the plaintiff tested negative for the principal presumed trigger for his HLH, HHV-8. Whilst the plaintiff contends that the diagnosis of VL ought to have been made much earlier than 14.03.14, he states that, by this point, all conceivable justifications argued by SJH fell away. In light of the focus on the potential inflection point in and around 14.03.14, the plaintiff's condition over the second period also requires close examination on causation grounds. The plaintiff argues that he was still very unwell and indeed remained on Burkitt's Ward, whereas SJH argues that his condition improved such that he could be transferred. The third period is 19.03.14 to 01.04.14, when the plaintiff was transferred to Spain. SJH argues that for much of the third period the emphasis was on "containment" to facilitate the plaintiff's transfer to Spain. As such, there was a reticence to carry out risky and invasive diagnostic procedures (such as a splenic biopsy) which might have inhibited that transfer.
28. I will now examine this chronology more closely, highlighting important developments. In so doing, I will incorporate relevant aspects of the oral evidence from the plaintiff, Mr. MSF and the SJH treating clinicians.
(i) The plaintiff was admitted into the GUIDE clinic on 19.02.14. In light of his HIV status, there was a clear potential for dozens of different opportunistic infections to be involved.
(ii) On day 2 (20.02.14), combination anti-retroviral therapy ("HAART") was commenced for HIV.
(iii) Although initially admitted under ID, there was consultation and collaboration between the respective ID, Genito Urinary ("GU") and Haematology departments about the plaintiff's condition. Blood investigations revealed pancytopenia.
(iv) A haematology review took place on day 3 (21.02.14). A bone marrow biopsy was collected and reported on 26.02.14 as revealing prominent macrophage activity believed to be consistent with HLH. In addition, HHV-8 was suggested as a possible source of infection.
(v) The plaintiff started to receive blood transfusions due to anaemia on 22.02.14. These continued on a regular basis throughout his admission.
(vi) The plaintiff underwent a CT scan of the thorax-abdomen-pelvis on 22.02.14, reported on 23.02.14 ("the first CT") which revealed that the "spleen was grossly enlarged measuring over 22cm in maximal dimensions." The haematology team noted, on 23.02.14, that there was "+ splenomegaly 22cm." It was described by the GUIDE Registrar on 25.02.14 as "significant splenomegaly." It appears to have been confirmed at this stage that the plaintiff met the criteria for HLH.
(vii) On 24.02.14, microbiological investigations revealed active HHV-8 infection and so a diagnosis was made of HLH triggered by HIV and HHV-8 infections. The plaintiff's treatment was HAART together with anti-viral prophylaxis for HHV-8. The clinical impression was of "Nil Improvement." SJH summarises the above as demonstrating, that within one week of admission, it had achieved a reasonable working diagnosis of HLH, identified two credible triggers (HIV and HHV-8) and initiated treatment directed at HLH and at the underlying triggers, which needed time to work.
(viii) On 25.02.14, the plaintiff was reviewed by Haematology. Splenic biopsy was considered.
(ix) By day 8, 26.02.14, HIV was being actively treated. SJH considered Multicentric Castleman's Disease ("Castleman's") secondary to HHV-8 as within the differential diagnosis. However, it appears that Castleman's was ruled out by a PET scan on 26.02.14, demonstrating no lymphadenopathy. EBV and parvovirus were also ruled out. SJH contends that, once these conditions were eliminated, this still left HHV-8 as a credible trigger.
(x) Although the precise date is unknown, I accept that contact was made during this period by SJH with a well-known Consultant Medical Oncologist at Chelsea and Westminster Hospital, the biggest treatment centre in the UK for malignancies associated with HIV. This communication was also noted in the letter dated 31.03.14 from SJH to Hospital de La Fe, Valencia. However, there is no contemporaneous record of these discussions and the SJH clinicians have no specific memory of what information was conveyed, or of what advice was received. It is also unclear whether the conversation was solely about treatment or also included potential diagnoses.
(xi) The plaintiff was commenced on chemotherapy for HLH on 27.02.14 (day 9). It is common case that, as a significant side effect, this reduces white blood cells and causes neutropenia, rendering the patient more susceptible to infection.
(xii) On 28.02.14 it is recorded that the plaintiff "feels much better."
(xiii) Mr. MSF recalls that during this phase, the plaintiff deteriorated. Due to concerns about his survival, Mr. MSF had to inform the plaintiff's family of his sexual orientation and his diagnosis with HIV. On learning of his dire condition, the plaintiff's family came to Ireland. Mr. MSF recalled that the plaintiff continued to have fevers and that, on occasion, he could not recognise him and needed assistance to go to the toilet.
(xiv) The SJH clinicians were extremely concerned about the plaintiff over this period. His blood counts were low, placing him at risk of life-threatening infection; he had high temperatures, problems with his coagulation markers and elevated LDHs, which suggest tissue damage due to diseases or infection. All of this was indicative of an extremely unwell man.
(i) On 01.03.14 it was noted that the plaintiff was apyrexial since receiving chemotherapy. However, this improvement did not persist and by the next day, the plaintiff had a high fever again. He remained pancytopenic. The plaintiff's liver function tests were now also abnormal. Empirical antibiotics were commenced.
(ii) Some improvement was noted on 03.03.14.
(iii) On 05.03.14 (day 16), the plaintiff's viral load for HHV-8 had diminished (from 50,000 to 4,000 c/ml). His condition remained largely unchanged with continuing spiking temperatures, splenomegaly, and disrupted blood and liver function tests. On 09.03.14 the plaintiff's neutrophil count remained very abnormal, and his overall picture was one of concern.
(iv) On 10.03.14, (Day 21), one of the plaintiff's treating clinicians noted that there had been "no response yet to treatment."
(v) On 12.03.14, concern regarding spiking temperature and severe neutropenia led the team to order a repeat CT scan ("the second CT") with a note stating "...? source of infection."
(vi) The second CT confirmed that the spleen was stable relative to the first CT scan, meaning it remained approximately 22 cm in its maximal dimension. There was slight enlargement of the liver. The SJH clinicians prescribed anti-fungal prophylaxis in the form of AmBisome (which coincidentally is also the treatment of choice for VL). The plaintiff had an infusion reaction to AmBisome in the form of back pain. AmBisome was therefore switched to another anti-fungal, caspofungin.
(vii) On 12.03.14 the plaintiff demonstrated profound neutropenia and rising ferritin. Both splenomegaly and hepatomegaly were identified clinically and the notes record "no focus of infection identified."
(viii) On 13.03.14, the plaintiff was still febrile up to 40.1°C and had continuing diarrhoea. Overnight on 13.03.14, following a decision made between the Haematology and ID teams, the plaintiff was moved to Burkitt's Ward because he required intensive care. This ward, which is normally reserved for transplant patients, is staffed by nurses with expertise in the management of very unwell, immunosuppressed patients and is considered state of the art in terms of reducing the likelihood of infection
(ix) The plaintiff's viral load for HHV-8 was noted to be negative by 14.03.14. Despite the clearance of HHV-8, the plaintiff remained unwell with fever, neutropenia, anaemia, and splenomegaly. There was no substantive change in treatment as the view was taken that once chemotherapy is commenced, it should be pursued for a full cycle.
(x) Mr. MSF visited the plaintiff in Burkitt's Ward and recalls that on occasion the plaintiff did not recognise him and was "very confused."
(xi) The plaintiff was commenced on further empirical antibiotics due to febrile neutropenia.
(xii) A bone marrow biopsy of 14.03.14 showed that the HLH was not as active as previously which was viewed as reassuring. On the same date, it was noted that the plaintiff could require a spleen biopsy. This was the second time that a spleen biopsy had been considered, in each case to rule out an underlying lymphoma.
(xiii) It is common case that the decision as to whether to carry out a splenic biopsy is a clinical judgement call. It involves a careful risk-benefit analysis. Splenic biopsy carries a general risk of life threatening haemorrhage of approximately 1/1000; but in a patient with coagulation problems such as the plaintiff, that risk is substantially increased. Even a less serious haemorrhage might require transfusion and ongoing monitoring for a number of weeks. The SJH clinicians considered the fact that the plaintiff wanted to go home to Spain, as relevant to this risk-benefit analysis. If complications ensued, this could delay his transfer to Spain by anything from a few days to a couple of weeks.
(xiv) On 15.03.14 the plaintiff continued to have spiking fevers but was noted to be not unwell.
(xv) On the 16.03.14 the plaintiff was noted to be stable with continuing fevers.
(xvi) On 17.03.14 the plaintiff had a fever of 39°C and pain in his arm at insertion of a drip.
(xvii) On 18.03.14 the plaintiff continued to experience temperature spikes up to 39.2°C.
(i) On 19.03.14 the plaintiff experienced high temperatures and diarrhoea. The plaintiff remained pyrexial on 20.03.14 and 21.03.14.
(ii) The clinical notes record a partial improvement in the plaintiff's symptoms in the last week of March. On 22.03.14 the plaintiff was recorded as "clinically well," "mood better, bright and chatty," with improving blood counts. On 23.03.14, the plaintiff was noted to be "clinically well" but with ongoing diarrhoea. The plaintiff remained febrile on 24.03.14 and 25.03.14 and continued to experience persistent loose stools. However, he was sitting out of bed for long periods and ambulating around the ward. On 26.03.14 the plaintiff was recorded as "well" but with spiking temperatures and his HLH was noted to be "better but still active." On 27.03.14, the plaintiff was noted to be afebrile, " much better" and "in good form no complaints." On 28.03.14 the plaintiff was noted to be "flushed and cold ++" with temperature spikes. On 29.03.14 the plaintiff looked "much better" and on 30.03.14 he was recorded to be "asymptomatic." On 31.03.14 he was recorded as "mobilizing... feels well." On 30.03.14 and 31.03.14 all temperature readings were normal and the plaintiff was afebrile. Finally, on 01.04.14, the day on which he was discharged to Spain, the plaintiff was noted to be "well and apyrexial." From a haematological perspective, it was felt that the plaintiff's low ferritin, a marker for HLH, had improved substantially. In addition, it was felt that the plaintiff's neutrophil count, a marker for immunosuppression and infection risk, was normalising.
(iii) Nursing records tell a similar story of partial improvement. The plaintiff was noted to be "sitting out of bed for long periods," and "ambulating short distances around the ward." On 24.03.14, he was "in good form no complaints"; on 27.03.14, he was "sitting out having lunch"; on 28.03.14, the plaintiff "mobilised around the ward with family members. Appears comfortable. No new issues"; and on 31.03.14, he was "mobilising on ward. Feels well. Looking forward to going home tomorrow."
(iv) It appears to be common case that this limited improvement whilst partially attributable to treatment of HLH with chemotherapy and dexamethasone (which had been started comparatively late in management on 27.03.14), was also due to the coincidental administration of a low dose of AmBisome and caspofungin. The plaintiff's final blood transfusions due to anaemia occurred on 31.03.14.
(v) In the final week of March, the emphasis was on transferring the plaintiff to Spain. The ID and Haematology teams were all in agreement that, whilst the plaintiff was certainly not fit for discharge, he was sufficiently stable to allow for his safe transfer to Spain. On 26.03.14, the plaintiff's treating clinicians met with him, his family and an interpreter to discuss the feasibility and practicality of his return to Spain. The plaintiff's flight was booked on 26.03.14.
(vi) However, it is common case that this improvement in the last week in March was partial only. Neutrophil count, platelet count and fibrinogen had not normalised.
(vii) Overall, the plaintiff recalls constant high temperatures accompanied by strong attacks of shivering on every single day throughout his stay in SJH. When his parents were visiting him, his father had to lie on top of him to stop him from shaking. During fever attacks he would just curl into a ball in the bed and was not able to do anything, even speak. He perceived that his fevers would subside when he took paracetamol or had a blood transfusion. The plaintiff also experienced constant abdominal pain and yellow stools. His spleen was extremely swollen and painful, to the extent that he was unable to move around in the bed. The plaintiff outlined that, during much of his stay the nurses or his parents had to help him to the bathroom as he was not able to move. He lost a very significant amount of weight. Although during his stay in SJH, the plaintiff's parents always told him that they thought he would get better, afterwards they admitted that they had thought he was going to die. The plaintiff's recollection is that a couple of days after he arrived in Spain, the doctors made the correct diagnosis and started treating him. The very next day, his fever was gone. For the first time, he was able rest and sleep without "cycles of fever." Once the fever disappeared, the plaintiff started to eat and to gain some weight. The plaintiff's own view is that he left SJH in a far worse condition than he arrived. Indeed, even when he finally left hospital in Spain on 11.04.14, he was still "very skinny and swollen" and "couldn't have a normal life" for a considerable period of time.
(viii) For his return to Spain, the plaintiff needed assistance to mobilise, a wheelchair, and was hoisted onto and off the plane.
(ix) On 01.04.14, the plaintiff was admitted to the Hospital de la Fe in Valencia, Spain. Leishmania infantum DNA and leishmania antibodies were detected on splenic biopsy on 04.04.14 and a diagnosis of VL was made. Chemotherapy was discontinued and dexamethasone was reduced. Treatment with AmBisome was immediately commenced.
(x) The plaintiff made a substantial clinical improvement (although his spleen took several months to settle back to its normal size). On 11.04.14, the plaintiff was well enough to be discharged on a continuing course of Ambisome for follow up at the General University Hospital of Alicante. On 14.04.14, the plaintiff's tolerance of Ambisome was noted to be "good." The notes record that he been afebrile and asymptomatic since the commencement of this treatment.
(xi) Finally, at review in the General University Hospital of Alicante on the 16.11.15, the plaintiff was recorded as stable with no indication of VL recurrence and good immunological control of HIV. He had, by that stage, completed treatment with Ambisome with good improvement, albeit with some persistence of moderate splenomegaly.
(xii) The plaintiff's treating clinicians at SJH, one of whom knew of an association between HIV, Spain and VL in 2014, stated in evidence that, had the plaintiff remained their responsibility and had they pursued the splenic biopsy this would have led to a diagnosis of VL.
(xiii) A few weeks after the plaintiff was transferred to Spain, SJH emailed the Spanish hospital to enquire about his condition. The reply advised that he had been diagnosed with VL, had started a course of treatment, and was doing well. Two of the plaintiff's treating haematologists then examined the plaintiff's first bone marrow aspirate taken on 21.02.14 and did not find VL.
29. The standard of care is to be determined on the basis of the principles (the "Dunne principles") established in Dunne v. National Maternity Hospital [1989] IR 91 ("Dunne") (per Finlay C.J., p.109).
1. The true test for establishing negligence in diagnosis or treatment on the part of a medical practitioner is whether he has been proved to be guilty of such failure as no medical practitioner of equal specialist or general status and skill would be guilty of if acting with ordinary care.
2. If the allegation of negligence against a medical practitioner is based on proof that he deviated from a general and approved practice, that will not establish negligence unless it is also proved that the course he did take was one which no medical practitioner of like specialisation and skill would have followed had he been taking the ordinary care required from a person of his qualifications.
3. If a medical practitioner charged with negligence defends his conduct by establishing that he followed a practice which was general, and which was approved of by his colleagues of similar specialisation and skill, he cannot escape liability if in reply the plaintiff establishes that such practice has inherent defects which ought to be obvious to any person giving the matter due consideration.
4. An honest difference of opinion between doctors as to which is the better of two ways of treating a patient does not provide any ground for leaving a question to the jury as to whether a person who has followed one course rather than the other has been negligent.
5. It is not for a jury (or for a judge) to decide which of two alternative courses of treatment is in their (or his) opinion preferable, but their (or his) function is merely to decide whether the course of treatment followed, on the evidence, complied with the careful conduct of a medical practitioner of like specialisation and skill to that professed by the defendant.
6. If there is an issue of fact, the determination of which is necessary for the decision as to whether a particular medical practice is or is not general and approved within the meaning of these principles, that issue must in a trial held with a jury be left to the determination of the jury.
30. Clarke C.J. in Morrissey v. HSE [2020] IESC 6, on behalf of the Supreme Court ("Morrisey"), endorsed the Dunne principles and summarised the legal standard of care in a clinical negligence claim, as requiring "the court to assess whether no reasonable professional of the type concerned could have carried out their task in the manner which occurred in the case in question. That overall test requires a court to determine what standard a reasonable professional would apply." He observed that the test in Dunne remains the basis for identifying the legal standard of care by reference to which a claim in clinical negligence is to be assessed.
31. The parties are in dispute as to whether this is truly a "misdiagnosis" case.
32. While SJH accepts that its clinicians did not consider or diagnose VL, it contends that this does not equate to a "misdiagnosis", which requires either an incorrect diagnosis or a failure to make any diagnosis at all. SJH argues that it made a credible working diagnosis which it was working through over the course of the plaintiff's admission.
33. The plaintiff argues that the "misdiagnosis" label is apposite for two reasons: first, because there was an erroneous failure to diagnose VL and second, because there was an incorrect identification of HHV-8 as driving the plaintiff's HLH. The latter point relies upon the concession by SJH's ID expert, Dr. Sheehan that, with the value of hindsight, HHV-8 was an epiphenomenon. [3]
34. Although I appreciate that personal sensibilities may be engaged on both sides, from a legal perspective it does not hugely matter whether or not the label of "misdiagnosis" formally applies. Either way, this was clearly a case of incomplete diagnosis.
35. Crucially, both parties accept that the Dunne principles apply to diagnosis cases as much as treatment cases. In practical terms, the Dunne principles may apply somewhat differently to diagnosis cases, where, for example, there are not two schools of thought about how to go about a particular diagnosis (Morrissey v. HSE at para. 6.11; McCormack v. Timlin [2021] IECA 96, per Collins J. at para. 64). Such is the case here, as there was no evidence of an honest difference of opinion as to the better of two ways of diagnosing a patient such as the plaintiff. In other words, the fourth Dunne principle is not engaged.
36. Equally, the debate did not turn on the second Dunne principle. The case was not advanced on the grounds that SJH deviated from a specific general and approved practice.
37. Likewise, the parties did not focus on the third Dunne principle. This is not a case in which a general and approved practice in diagnosis is said to have inherent defects which ought to be obvious to any person giving the matter due consideration.
38. Here both parties are agreed that this case turns on the first Dunne principle: the question is whether the plaintiff has proved the clinicians in SJH have been "guilty of such failure as no medical practitioner of equal specialist or general status and skill would be guilty of if acting with ordinary care."
39. It is common case that the mere existence of a misdiagnosis, non-diagnosis or incomplete diagnosis does not per se establish a breach of the standard of care; it is necessary to establish the absence of ordinary care (McCormack v.Timlin at para.70).
40. As will be seen, the crux of this case is whether and when SJH ought to have diagnosed VL. If the court considers the failure to do so fell below the ordinary standard of care, then I will have to determine, as a matter of causation, how the diagnosis of VL would have impacted the plaintiff's treatment and outcome.
41. The law in this jurisdiction in respect of professional negligence has been recently restated by the Supreme Court in Morrissey. The starting point is the identification by the court of the standard of approach that would have been applied by a professional of the appropriate standing or skill as the person against whom the allegation of negligence is made. Or, as restated at para. 6.12 of the judgment of the Chief Justice: "what would an ordinary competent professional of the type and skill of the individual concerned have done, and did the professional who is sued meet that standard?" The correct standard of approach is one of fact in each case as identified at para. 6.13 of Morrissey. It is not for the court to determine the standard of approach or impose its own views as to the requisite standard of approach. Rather, it is the standards of the profession itself as demonstrated, by the evidence, that impose the standard required. Expert evidence is required as to how professionals of the relevant type would generally go about their work and the way in which they would have dealt with the case in question. In this case, the court must apply the 2014 standard of approach of an ID consultant on the one hand and a haematology consultant on the other, who held themselves out as an expert in the treatment of HIV.
42. I have summarised the principal aspects of the factual evidence given by the plaintiff and Mr. MSF above.
43. All five of the plaintiff's treating consultants, who managed, investigated and cared for the plaintiff during his admission gave evidence. I will not repeat here aspects of the factual evidence already set out in the chronology. The following additional evidence of relevance was elicited.
44. The GUIDE clinic was set up at SJH in 1987. As this was prior to the introduction of antiretroviral therapy, Prof. A gained experience of a vast range of opportunistic infections that might now be less prevalent in the HIV population. She has looked after approximately 4,500 HIV patients since the start of her time in SJH. As the GUIDE Clinic serves a multi-cultural cohort of people, by 2014, Prof. A was extremely experienced in treating HIV patients from locations all over the world, including countries where VL is endemic.
45. Whilst, Prof. A had never encountered a case in a clinical setting prior to 2014, she had some academic knowledge of VL. She knew that it was spread by sandflies, and that it was associated with mortality. Her understanding was that VL was common in India, Africa and South America and "not in Ireland and not particularly in Europe." In 2014, Prof. A was unaware of any association between HLH and VL.
46. In the five years prior to 2014, Prof. A had treated approximately four/five cases of HLH with HHV-8 being the trigger, in all cases, bar perhaps one. Prof. A's evidence was that in each such case, the patient had a big spleen. Prof. A described the plaintiff's spleen as "moderate" and "typical" having regard to her experience of splenomegaly in her prior four/five HLH cases. She did accept in cross examination that the literature tendered by the plaintiff's experts shows that a massive spleen narrows the diagnostic possibilities to a shorter list of diseases, which include VL.
47. Prof. A's experience of HLH patients was that they required ICU care and had a very high mortality rate. In the plaintiff's case, she was therefore conscious that he needed to be treated very quickly. In her experience, HLH is rare in HIV and HHV-8 causing HLH is extremely rare. It was a "perfect storm."
48. Prof. B qualified in 1994 and worked as an SHO in SJH in GU. Between 2001-2003, she did a fellowship in ID at Boston University Medical Centre. This was a busy clinical-based fellowship with exposure to both HIV and non-HIV patients, which involved the diagnosis and treatment of significantly immunocompromised patients with opportunistic infections. Prof. B spent a year in North Manchester General Hospital as an ID Consultant where she saw a cohort of approximately 3,500 patients, predominantly patients with HIV from Africa, other parts of Europe and South America. In 2005, she returned to take up an ID Consultant post, where she has practiced since.
49. Prof. B's evidence was that in 2014, the cohort of patients with HIV presenting to SJH was predominantly from South America, with a few from Spain. Her experience of HLH was that in the vast majority of cases, the trigger was malignancy, usually lymphoma, or viral infection. In the latter instance, the viral trigger had, in her experience, been HHV-8
50. Prof. B had never encountered a case of VL in a clinical setting, either in Ireland or abroad, prior to 2014. She knew that VL was spread by sandflies and that the vast "majority of cases occur in the South Americas, Eastern Africa, some parts of Asia, and in some cases in the Mediterranean region as well." Although Prof. B was aware that there was "some leishmania" in the Mediterranean, she attributed it primarily to drug users. Although therefore Prof. B was aware in 2014 that people with HIV from the Mediterranean basin were at risk of VL she stated "everything has to be taken relatively... if you have a patient with a fever from the Mediterranean, leishmaniasis is not top of your differential. There is about 250 other things at the top of your differential... It is still not a commonly seen infection, even in those countries..."
51. Prof. B's evidence was that she had seen lots of patients with moderate splenomegaly. She described the plaintiff's spleen as a "moderately sized spleen." Prof. B's only encounter with massive splenomegaly was in the context of her final membership examinations in the setting of Leukaemia.
52. In explaining why the diagnosis of VL was not made in this case, Prof. B stated:
"...So I think in the back of our minds, based on certainly my experience and I'm sure the haematologists experience of what causes HLH, and my knowledge of HLH was it's caused by malignancies, primarily blood malignancies, lymphomas, leukaemias and viruses, my main concern was to make sure that there was nothing else going on there. So I certainly remember having a conversation with Prof. C about doing a splenic biopsy to really make sure that there was no lymphoma or if there was lymphoma, obviously that's a huge thing [that] we need to make sure we're not missing."
"...In order to think of a diagnosis, some associations have to go on in your brain....We were looking at a man who had newly diagnosed HIV, HLH and we were looking for the reasons for that. And that's why we went down the route of looking for the viruses and looking for the lymphomas, because that's where our experience lay and that's what was the cause of HLH. And that's why we weren't thinking of the leishmania route."
53. In this regard, Prof. B stated: "...For someone who has never seen a patient with leishmaniasis before, you're looking at a certain type of presentation. I think if you are living in an endemic area where there's loads of it, you probably cast your net wider and you've probably seen patients who present in slightly atypical or unusual ways. None of us have experienced leishmaniasis before or since. So our perception of what VL is, is a very textbook description. So I think there is kind of lots of reasons why we didn't consider it."
54. In terms of her experience of the HLH Protocol, Prof. B stated that once you start treatment i.e. chemotherapy, you pursue it for a full cycle and that patients often require a second or third cycle of treatment. If chemotherapy is stopped too quickly, HLH can become active again. That is not to say, however, that one simply continues the treatment without taking into account what is happening on a daily basis with the patient. In Prof. B's experience, she would have hoped that an immunocompromised patient like the plaintiff, would start improving within four to six weeks of commencing treatment; i.e. by 27.03.14 - 10.04.14.
55. Prof. B gave evidence that the reduction in HHV-8 levels after one cycle of chemotherapy showed that the treatment was working. Accordingly, they continued the treatment regimen.
56. Prof. B stated that she was conscious of the plaintiff's desire to get treatment back in Spain as soon as he was well enough to travel. In the time leading up to the plaintiff's transfer to Spain, his HLH was noted to be "better," his HIV was noted to be "improving" and in Prof. B 's words, "he certainly seemed to have turned a corner and he seemed to be improving." She stated: "We certainly weren't content that we had completed everything with him and we certainly wouldn't have been discharging him, far from it" and at that point in time, "...we felt that we had a diagnosis and we had our triggers and we were controlling everything."
57. With regards to a splenic biopsy, in Prof. B's view, they would not have wanted the plaintiff travelling for a number of days post- splenic biopsy.
58. A few weeks after the plaintiff was transferred to Spain, Prof. B emailed the Spanish hospital to follow up on his condition. When informed of the VL diagnosis, she carried out a literature search for an association between HLH and VL, but she could not find one.
59. Prof. C was appointed a Consultant Haematologist in SJH in 2002, she completed her degree in medicine in 1983. She completed a four-year PHD in mantle cell-lymphoma in Belgium and also worked in teaching Hospitals in the UK. She gave evidence that in the patients she could remember, prior to the plaintiff, she had two previous cases of EBV triggered HLH in a non-HIV patient and one case of HHV-8 triggered HIV with Castleman's. Prof. C had probably seen two or three cases of HLH annually between 2002 to 2019. This was her first case involving HLH, HIV and HHV-8.
60. Prof. C had never encountered VL in a clinical setting. However, she was aware of VL from training and confirmed that leishmaniasis is a classic exam question for haematology senior registrars. She knew that VL was spread by sandflies and understood it was common in South America, particularly Brazil, and in India. Prof. C did not consider VL in this case "because I didn't realise that VL was endemic in Spain." She accepted that, had she realised that VL was endemic in Spain, she would have considered it. However, she did not specify at what point in the plaintiff's management this consideration would have arisen. Like Prof. B, Prof. C's evidence was that the plaintiff predominantly presented with HLH and that they were "looking after [the plaintiff] from a HLH perspective."
61. Prof. C's practice deals predominantly with lymphomas, which she stated are associated with very large spleens. She would therefore see a lot of enlarged spleens. She would regularly see a spleen as big as the plaintiffs, perhaps every three months.
62. Prof. C viewed the bone marrow result of 14.03.14, as indicating that the plaintiff's HLH was not as active, and that chemotherapy was working. This reassured her that they were pursuing the correct course.
63. Prof. C accepted that, in hindsight, once the plaintiff's viral load for HHV-8 was negative, this would "definitely be relevant." Prof. C's evidence was that she weighed up the risks and benefits of performing a splenic biopsy to out rule lymphoma. She considered the fact that the plaintiff wanted to go home to Spain, as part of the risk-benefit analysis, because if he bled, that would have delayed his transfer for a couple of weeks.
64. Prof. C stated that, from 26.03.14 onwards, "his parameters continued to improve," and they had a "stable patient who was now safe to travel, so we continued with the HLH protocol."
65. Dr. D, Consultant Haematologist, was also in SJH from 1986 - 1989 and had considerable experience dealing with opportunistic infections prior to the advent of anti-retroviral therapy. She was an Attending Consultant in the Haematology section of Vancouver General Hospital, specialising predominantly in leukaemia and stem cell transplantation. She has worked as a Consultant Haematologist in SJH since November 2001. Her experience pre-2014 was of approximately one to two HLH cases annually. She remembered one HLH, HIV and lymphoma case. In non-HIV patients, lymphomas, acute leukaemias and occasionally rheumatological disorders drove the HLH.
66. Dr. D knew of VL as a tropical illness, but she had not seen a case in practice. Discussions about VL did not take place because she stated, VL was not "relevant in our practice." Dr. D was also not aware of the prevalence of VL in the HIV population in Spain.
67. Dr. D described a 22cm spleen as "a big spleen," but she would not have described the plaintiff's spleen as a "massive spleen."
68. In terms of recovery from HLH, Dr. D's experience was that "it can take quite a long time... sometimes be a waxing and waning course... generally, you would treat people... with successive courses and then depending on their response, you may add more...."
69. Dr. E, a Consultant Haematologist qualified in 1994, interned in Boston and did a Degree in Genetics in Trinity College Dublin until 1997. He trained as an SHO at the John Radcliffe Hospital, Oxford until 1999. On returning to Dublin, he joined the higher training scheme in haematology in St. Vincent's University Hospital, Tallaght University Hospital, St. James's Hospital and the Mater Hospitals. Dr. E did a year's fellowship in Boston in 2006 focusing on blood malignancy. He was appointed as a Consultant Haematologist in Galway in 2007 and in 2010 as lead clinician in myeloma plasma cell diseases at SJH. He oversaw the plaintiff's management on his transfer to Burkitt's Ward.
70. Dr. E estimated that he had seen one to two cases a year of HLH pre-2014, with EBV and lymphoma being the classical triggers, albeit he acknowledged it can be seen in the context of lots of different triggers.
71. Dr. E had not encountered VL in practice prior to 2014. When asked about his knowledge and experience of VL in 2014, Dr. E responded "[n]one," save that it was transmitted by sandflies and is a tropical disease and "is in the differential for, you know, large hepatosplenomegaly."
72. With regard to his experience of splenomegaly, Dr. E described a 22cm spleen as "a big spleen, bigger than you would normally see in HLH." On the other hand, haematology was a discipline "where we look after a number of patients who have very large spleens. The two classic ones would be newly presenting chronic myeloid leukaemia or a disease called myelofibrosis. So I suppose in haematology because we see that, I would think of massive splenomegaly as being splenomegaly that extends kind of down under the left costal margin, beyond the umbilicus, where it's actually palpable on the right side of the abdomen. I don't believe that that was the case in this case, but it was a large spleen, certainly at 22cm."
73. Dr. E agreed with the other treating clinicians that a period of four to six weeks would often be required for a response to HLH treatment. Dr. E also gave evidence that "...the fact that it [HHV-8] had come down [on 15 March] and on this subsequent reading is no longer detectible, that is encouraging. Generally, ... that means that obviously the level has come down, and he is clinically improving, but he still has fevers, so it is good to know, but it wouldn't necessarily -- I don't recall it leading to any change in the treatment."
74. I have set out above the main features of the evidence given by the five clinicians who treated the plaintiff. As will be no doubt be apparent, aspects of their testimony under both direct and cross examination, blended factual and opinion evidence, perhaps unavoidably. I accept the plaintiff's submission that his treating clinicians cannot give independent opinion evidence. In any event, as witnesses of fact, the clinician's evidence may only be considered insofar as it amounts to evidence of fact viz "their clinical findings, observations, and actions and the reasons for them in respect of the act or omission the subject matter of proceedings" (Freeney v. HSE [2020] IEHC 115, Hyland J. at para. 15).
75. Therefore, I have not been influenced by any opinions expressed by the plaintiff's treating clinicians on issues such as, for example, anticipated recovery periods for HLH or whether the plaintiff's spleen was unusually large for their cohort of previous HLH patients. The same is the case as regards the clinician's re-examination of the plaintiff's first bone marrow aspirate taken on 21.02.14 to search for signs of VL. This was only carried out after their treatment had concluded and its interpretation is a matter of opinion, not fact.
76. The parties are ad idem that the duties of an expert include:
(i) To present evidence to the court that is and should be seen to be, the independent product of the expert "uninfluenced in form or content by the exigencies of litigation" (National Justice Compania Naviera SA v. Prudential Assurance Company Limited [1993] 2 Lloyd's Rep 68);
(ii) To be impartial and independent, discharging their duty to the court over that owed to the litigant;
(iii) To communicate any change in view as soon as possible;
(iv) To properly research and explain specialised knowledge with the aid of scientific materials;
(v) To present academic materials in a complete and informative manner.
77. Both parties question the impartiality of the opposing party's expert witnesses. The plaintiff contends that SJH's ID expert, Dr. Sheehan lacked objectivity and SJH contends that the plaintiff's haematology expert, Prof . Mehta lacked objectivity. Separately, SJH also contends that the plaintiff's ID expert, Dr. Ellis, was overly influenced by the fact that he spent much of his career in the tropics or in areas where VL is endemic.
78. The parties are agreed that ultimately, it is a matter for the court to consider the weight to be attached to the relevant witnesses' evidence on all issues, including the crux issue as to whether SJH should have considered VL.
79. The parties are also agreed that, where an issue of impartiality arises, the weight to be given to expert evidence, is always a matter for the court (Duffy v.McGee [2022] IECA 254, per Collins J. para.18; Kenneally v.De Puy [2016] IEHC 728;[2017] 2 IR 487, per Barton J. at paras 47-48).
80. Dr. Sheehan has co-authored articles with both Prof. A and Prof. B. He agreed that when co-authoring articles with colleagues, he was involved broadly in a professional engagement in which he effectively shared his reputation with his co-authors.
81. Dr. Sheehan has attended the events of the "HIV Club," a pan-city collegiate collaboration between ID practitioners, regularly from the late 1990s until 2022. Prof. A and Prof. B also attended these events. These functions were primarily educational, but they were also social events. Dr. Sheehan attended these events regularly during the period over which he prepared his report between 13.06.19 and 06.03.20.
82. Dr. Sheehan was also a regular attendee at the ID Society of Ireland ("IDSI"), presenting papers and abstracts. Prof. B was "an attendee and sometimes an officer" of the IDSI. Dr. Sheehan included no reference to the IDSI in his CV, but accepted it ought to have been mentioned.
83. Dr. Sheehan accepted that a long collegiate professional relationship with the treating clinicians involved in the plaintiff's care could potentially impact an expert's objectivity but says that he "tried to look at the case as objectively as [he] possibly could."
84. Although the plaintiff contends that concerns regarding conflicts of interest do arise in relation to Dr. Sheehan, he does not argue for the exclusion of evidence on this ground. Rather, he contends that the court should attach less weight to his evidence.
85. I accept that the above pre-existing professional relationship should have been referred to either in Dr. Sheehan's report or in more detail in his direct evidence. However, such a pre-existing professional relationship is in no way surprising. There were approximately 12-15 ID physicians practicing in Ireland in 2014, and I surmise that most, if not all, have co-published with each other and met each other regularly.
86. I am not satisfied that this pre-existing professional relationship means that Dr. Sheehan is incapable of giving objective evidence or indeed that he failed to do so. Indeed, I do not understand the plaintiff to make such a submission.
87. The reality is that Dr. Sheehan and Dr. Ellis agree on many of the issues in the case. Even the plaintiff contends that the difference between them on the issue of whether and when VL ought to have been diagnosed is "paper thin." Dr. Sheehan accepted, albeit under cross examination, that the SJH clinicians ought to have known of the epidemiological association between HIV and VL in a HIV patient from Spain. He did not however, accept that VL should have been top of the list of diagnoses or that, in the presence of other credible triggers for the plaintiff's HLH, it should have been considered in this particular case. The plaintiff argues that, in this, Dr. Sheehan failed to follow his own logic which in itself demonstrates lack of impartiality. Whether or not I accept Dr. Sheehan's opinion on this key issue, I cannot accept that his continued belief that the care provided by the SJH ID consultants was of a professional standard can be fairly labelled as partisan.
88. SJH submits that the evidence of Prof. Mehta lost the necessary character of objectivity which ought to affect the weight of his evidence.
89. It is fair to say that after 6.5 hours total in the witness box, some of Prof. Mehta's observations were rather offhand, and perhaps ill-judged. He was somewhat tetchy in his replies to cross examination-particularly after lunch on day 6. However, I did not interpret this as partisan, but as exasperated. Ideally of course, exasperation would not enter a courtroom. But a courtroom is unfortunately not a tranquil place and at times impatience, however unjustified, will win out. Having observed these exchanges, I can genuinely read nothing into them.
90. SJH suggests that Dr. Ellis's experience in tropical medicine subconsciously influenced his approach to the standard of care of the SJH clinicians who did not possess that specialism. Dr. Sheehan was asked if he would go so far as to state that Dr. Ellis's specialism in tropical diseases might impact his objectivity and replied: "I would. I can't imagine how it would not affect his view on things."
91. I do not accept this criticism. Dr. Ellis worked half his life in European hospitals and at the time of the plaintiff's admission had also worked in Derriford Hospital in Plymouth. His evidence that he would expect a properly trained ID physician working in Europe to have been aware of VL on the basis of their training was ultimately accepted by Dr. Sheehan.
92. Dr. Sheehan also suggested that Dr. Ellis lacked expertise to comment upon an HIV unit in an Irish hospital.
93. However, as the plaintiff points out, if SJH wished to attack Dr. Ellis as inexperienced in the field of HIV, this should have been put to him so that he could respond. In any event, it was clear that Dr. Ellis was well versed in HIV.
94. It was put to both Dr. Ellis and Prof. Mehta that, as they knew that VL had been diagnosed in Spain, it subconsciously influenced their objectivity. However, this criticism could apply to any expert giving evidence for the plaintiff in a medical negligence case. All any such expert can do is to properly acknowledge the dangers of hindsight and to recognise that their pre-eminent duty is owed to the court. I am satisfied that both Dr. Ellis and Prof. Mehta complied with their obligations in this regard.
95. Dr. Ellis prepared a very thorough and clear report. This states that the diagnosis of HLH at SJH was prompt and appropriate and that two of its triggers- HHV-8 and HIV- were correctly identified and appropriately treated with antiretroviral therapy. In his oral evidence, Dr. Ellis conceded that even after HHV-8 levels dropped, it was still reasonable to consider that it had been a potential trigger and to persist with the current course of management. In Dr. Ellis's view, however, none of this could excuse a failure to keep searching for other triggers of HLH, specifically VL.
96. Dr. Ellis's report states that the plaintiff's response to treatment for HLH was "slow." His report gives a number of examples of this such as:
· that by 09.03.14 the plaintiff was so profoundly neutropenic that he required growth factors (GCSF) to stimulate white cell production and function;
· the clinical note of 10.03.14 recording "no response to treatment;"
· the plaintiff's abnormal ferritin levels, which had peaked on 28.02.14, improved by 04.03.14 and rose again by 12.03.14; and
· the clinical note of 14.03.14 recording "needs splenic biopsy to out rule underlying lymphoma."
97. Dr. Ellis's report argues that factors such as these ought to have prompted concern and intensified investigations for an undiagnosed contributing factor.
98. Under the heading, "Failure to consider the diagnosis of [VL]," Dr. Ellis's report states that after two weeks of treatment for HLH (which I assume would be around 12.03.14), there was no "response to treatment." In light of the concern that another pathological process was underway (such as lymphoma, malignancy or infection), a splenic biopsy was considered. Despite this, no such investigation or additional diagnostic tests were performed, and the established treatment was continued for a further three weeks until the transfer to Spain.
99. For reasons I will shortly explain, it is important to note that Dr. Ellis's report accepts that there were no clinical clues that would have pointed unequivocally to a specific diagnosis of VL. He states that there were however sufficient epidemiological clues that should have led to consideration of VL as an explanation for the plaintiff's continued high fever and for the persistence of physical signs and laboratory abnormalities in the face of adequate treatment for HLH, HIV and HHV-8. His report states that whilst it was good clinical practice to have identified HIV and HHV-8 as two triggers for HLH, it was unreasonable not to have considered further possibilities including VL, given the apparent lack of a satisfactory response to treatment (emphasis added).
100. Dr Ellis's report states that the following epidemiological factors were of importance in this case:
· Since the mid-1980s, VL is a known opportunistic infection among immuno-compromised patients.
· It was known since the late 1990s that VL coexists with HIV infection in individuals living in southern Europe and the Mediterranean region.
· By 1999, 1000 cases of HIV/VL co-infection had been reported, the vast majority in Spain, Italy and France.
· By 2014, Spain was among the top 4 southern European countries reporting the majority of cases.
· Reports had emerged by the early 2010's that VL was re-emerging in Spain.
· VL has been proposed since 1995 and recognised since 2014 as an AIDS defining condition in most countries where VL is present.
· Approximately 10% of all HIV infected patients in southern Europe harbor VL organisms. I note that, if anything, the correct figure is slightly higher than that: between 10% and 17% of those with HIV in France and Spain respectively have leishmania antibodies on serology (i.e. they have antibodies demonstrating prior exposure; Begona Monge-Maillo, et al., 'Visceral leishmaniasis and HIV coinfection in the Mediterranean region' (2014) 8 PLOS 1).
· Up to 9% of all HIV infected patients in southern Europe will develop clinical signs of VL. I note that the correct figure is potentially lower at between 2% and 9% (Pintado, et al., "HIV- associated visceral leishmaniasis" (2001) 7 Clinical Microbiology and Infection 291 ("Pintado") and World Health Organisation, 'Leishmania/HIV co-infection in south-western Europe 1990-1998: Retrospective analysis of 956 cases' (1999) 44 Weekly Epidemiology
Reports 365 ("the 1999 WHO paper").
101. In Dr. Ellis's view, the significance of the plaintiff living in Spain for the majority of his life should have been recognised and documented as an important epidemiological factor assisting in the diagnostic workup.
102. Dr. Ellis's report criticises the failure to consider the possibility of an additional diagnosis in a patient who had shown a minimal response to treatment (emphasis added). He states that one would have expected that a specialised ID team would have recognised that VL infection was a strong possibility given the plaintiff's epidemiological background. In his opinion, a representative body of ID specialists, given the particular clinical scenario, would have considered the possibility of VL and performed appropriate investigations. Instead, the plaintiff continued to experience symptoms of his untreated infection, was exposed to potential toxic chemotherapy and had a substantial delay in achieving the correct diagnosis. The report states that this management does not meet the expected standard of clinical care.
103. Dr. Ellis's report concludes by stating that the diagnosis of HLH triggered by HIV and HHV-8 was "an appropriate INITIAL diagnosis." He then states that despite treatment for HLH, HHV-8 and HIV, the plaintiff remained unwell for the duration of his 42 day stay. Dr. Ellis's report concludes that there was a negligent failure by the ID team at SJH to investigate the reason for the plaintiff's ongoing symptoms and persistent associated blood and marrow abnormalities, in the face of the treatment being administered (emphasis added).
104. Thus, Dr. Ellis's report strongly suggests that his criticism of SJH is not focused upon the first few days of treatment but rather upon the plaintiff's management, in the period after definitive improvement would have been expected. By definition, this must post-date (by some time) the commencement of chemotherapy on 27.02.14.
105. In oral evidence, Dr. Ellis hardened his position considerably on this point. The primary reason for this change in emphasis was because he placed far greater importance than previously on the plaintiff's "massive splenomegaly" (a clinical term which I explain at para. 210 below), which he stated was an important clinical clue narrowing the differential diagnosis.
106. Dr. Ellis's oral evidence was that although HLH is associated with splenomegaly, "it doesn't occur to the extent that it produces a 22cm sized spleen." Whilst it was reasonable in such circumstances for SJH to explore the possibility of lymphoma, it was unreasonable to have failed to consider VL because one of the clinical features of leishmania "is the finding that the spleen is usually massively enlarged." Dr. Ellis stated that VL is something that all ID physicians should know about and that, when faced with a patient with a massive spleen, infective causes should be top of the list of potential diagnoses. VL is "one of the textbook causes of massive splenomegaly." Dr. Ellis went so far as to contend massive splenomegaly was a "barn door" physical sign for VL. He stated that if a registrar is taking a Tropical Medicine exam, then they would fail if they did not note that a massive spleen is indicative of VL. In his oral evidence Dr. Ellis stated: "if you get a patient ... with massive splenomegaly, who has been living in a leishmania prone area, then leishmania is your... diagnosis until proved otherwise." Dr. Ellis further opined that "the fact that [the plaintiff] had lived in Spain and knowing that Spain, for an HIV-positive individual was a risk factor for acquiring several opportunistic infections, including VL... then they should have synthesised that with the fact that he had a massive splenomegaly and then that really narrows the differential diagnosis down."
107. Therefore, according to Dr. Ellis, the diagnosis of VL should have been made around the time of admission or very soon afterwards.
108. I have a significant reservation about this aspect of Dr. Ellis's evidence. It is inconsistent with the statement in his report that there were no clinical clues pointing unequivocally to VL. If as he says the plaintiff's massive splenomegaly was a "barn door" indicator of VL, why did he not so state in his report? Whilst his report recites that the plaintiff's spleen was measured at 22cm on the CT, no comment is made upon the degree of the plaintiff's splenomegaly as indicative of VL. If an expert examining medical notes and preparing a clinical negligence liability report with the benefit of the ultimate diagnosis of VL does not think that massive splenomegaly is even worthy of mention as a factor, then how can it be said that it is standard of approach to immediately attribute a massive spleen to VL?
109. I am therefore not convinced by this aspect of the opinion.
110. I am however fully convinced by Dr. Ellis's evidence that, in 2014, an ID specialist holding themselves out as an expert in HIV should have known about its epidemiological association with VL and that it would be unacceptable not to know. The link between HIV and VL in Spain is long- established. It is referred to in the 1999 WHO paper as far back as the turn of the century. The WHO states that HIV/VL co-infection has emerged as a result of the increasing overlap between AIDS and VL. This is stated to have important clinical diagnostic, chemotherapeutic and epidemiological implications. At the time of this publication, cases of co-infection had been reported in 33 countries worldwide most of which had been notified in south western Europe- France, Italy, Portugal and Spain. Patients in reported non endemic areas seemed to be mainly those who had previously lived or travelled in endemic areas such as southern Europe. The highest number of cases was found in Spain, which the WHO states, may be related to the higher proportion of HIV/ AIDS cases among intravenous drug users in Spain compared to France and Portugal, and to the greater overlap between AIDS and VL in Spain compared to Italy or France. The WHO observes that in south western Europe there is a clear predominance of intravenous drug use among the co-infected cases. In discussing opportunistic infections, the WHO states that AIDS increases the risk of VL by 100 to 1000 times in endemic areas. It observes that clinical diagnosis of VL in VL/ HIV co infected patients is particularly difficult as the usual clinical features of VL, such as fever, weight loss and swelling of the liver, spleen and lymph nodes are not always present, or may be hidden by other opportunistic infections.
111. Dr. Ellis disagreed with the proposition that in order to diagnose a particular presentation one must have previously encountered it in practice. It was, he stated, very important to keep up to date with world literature. I accept, that one would expect ordinary ID physicians to have been aware of this literature.
112. Dr. Ellis testified that "the travel history is vitally important in any patient that presents with a fever of uncertain origin. You have to get the travel history, you have to see what diseases are endemic in that country, you have to be aware of the current ID profile for that country." The WHO recommends that "patients infected with HIV and who have fever, swelling of the spleen, liver or lymph nodes, and anaemia, should have their travel history checked for any visits to areas where leishmaniasis is endemic." I accept that VL is at least hypo-endemic in Spain and is substantially more prevalent in the HIV population. I also accept as the contemporary literature demonstrates, that 10% of HIV patients in Spain had antibodies for leishmania in the 2010's, thus the numbers are not tiny as SJH contends.
113. Dr. Ellis's testimony on the importance of epidemiology was highly compelling. Indeed, Dr. Sheehan, SJH's ID expert ultimately accepted that an ordinary ID consultant ought to know of the association between HIV, VL and Spain.
114. What is in dispute, however, is what flows from this knowledge in the diagnosis of patients generally, and the plaintiff in particular. Thus, the main issue that now separates Dr. Ellis and Dr. Sheehan is whether knowledge of the epidemiological association between HIV, VL, and Spain necessarily means that VL should have been actively considered by SJH in the differential diagnosis and if so, when.
115. Turning to treatment options, Dr. Ellis states that approximately two-thirds of patients with HLH due to VL respond to specific treatment for VL (by way of AmBisome), obviating the need for toxicity associated with chemotherapy. However, I did not understand Dr. Ellis to state that earlier diagnosis could definitively have avoided the need for chemotherapy in the plaintiff's case.
116. As with the other witnesses (both factual and expert), much of Dr. Ellis's testimony was concerned with lead times for the diagnosis of VL, which varies according to which testing modality is employed. However, Dr. Sheehan conceded that if one were faced with a lengthy turn-around time for testing, one would consider empirical treatment where there is at least a "considerable suspicion" of VL. Dr. O'Keeffe, SJH's haematology expert, agrees that Ambisome can be administered empirically, albeit concurrently with chemotherapy. It is therefore not necessary to further discuss testing modalities.
117. Dr. Ellis accepted that the plaintiff may have made a limited improvement due to treatment of his HLH with chemotherapy and dexamethasone. However, he compared this to a surgeon removing a collection of pus secondary to a foreign body, but not the foreign body itself. Indeed, his view was that chemotherapy can make the situation worse by killing white blood cells further predisposing the patient to infection.
118. Dr. Ellis (and Prof. Mehta) agreed that the decision to carry out a splenic biopsy is a clinical judgement call. It involves a careful benefit risk analysis. Dr. Ellis accepted that the risk of haemorrhage "is approximately 1/1000 cases. But in a patient with a coagulopathy," such as the plaintiff, the risk is "substantially increased."
119. Prof. Mehta's report is short and primarily considers whether the failure of the SJH haematologists to diagnose VL on a biopsy was negligent. He states that he "would be in a better position to judge whether a competent haematologist should or should not have made that diagnosis [VL]" on viewing the slides. Ultimately, this particular issue has fallen away.
120. Prof. Mehta's report states that HLH is a difficult diagnosis to make. Most haematologists will only see one or two cases of HLH per year and diagnosis on a morphologic basis alone, is difficult. Most haematologists will only see one or two cases of VL per decade. However, he states that "many" will be aware that this condition is common among HIV positive patients, particularly in Spain, as such patients are typically managed jointly with a specialist in ID. I infer from this that knowledge of the epidemiological significance of the factors presenting in this case, is in general, more likely to fall within the bailiwick of an ID consultant than a haematologist.
121. Prof. Mehta's report states that it is a failure of care to administer chemotherapy to an individual suffering from an undiagnosed infection. He states that in this case, the failure to make the correct diagnosis led to the administration of chemotherapy and the unnecessary detention in hospital for six weeks.
122. Prof. Mehta's report makes no mention whatsoever of massive splenomegaly.
123. Despite his very short report, Prof. Mehta gave lengthy direct evidence, much of which was valuable to the court's understanding of HLH and VL. Prof. Mehta, who had authored a chapter entitled 'Tropical Diseases for the Haematologist' contained in the textbook, Postgraduate Haematology (6th ed, 2011), explained (i) the association between HLH and parasitic infections such as VL (ii) the need to identify the trigger in a patient with HLH and (iii) the inappropriateness of treating HLH without rigorously looking for the trigger and treating it. In each respect, he presented literature supporting his position.
124. Prof. Mehta drew specific attention to guidelines authored by a group of international experts- Paul La Rosée, 'Recommendations for the management of hemophagocytic lymphohistiocytosis in adults' (2019) 133 Blood 2465. Although dated 06.06.19 , this publication was based on studies pre- dating the plaintiff's admission. It states that a meticulous search for HLH triggers should be carried out and continued, despite HLH treatment. In contrast to certain other papers, infections are said to be the most prevalent HLH trigger. Infections are defined as mainly viruses such as EBV, HIV and CMV but also bacterium, parasites and fungi. HLH induced by inter alia, VL does not need to be treated with chemotherapy. Indeed, the HLH Protocol should be avoided in patients with inter alia leishmaniasis, as antimicrobial treatment and Ambisome cure leishmania
125. Clinically, Prof. Mehta had "only limited experience of HIV patients," and had "not got a lot of experience of treating leishmaniasis." He had never come across HHV-8 as a trigger of HLH and had seen only one case of HLH, HIV and VL co-infection.
126. Prof. Mehta, who appears to have had a particular teaching role in relation to spleens, placed a very significant emphasis on the plaintiff's massive splenomegaly. VL is associated with a massive spleen because the spleen is an important focus of parasitic infection and becomes "engorged with the parasite."
127. Whereas modest and intermediate splenomegaly is not specific, massive splenomegaly "should highlight certain specific conditions." Haematologists find that "massive splenomegaly...is a useful term which points us to certain conditions that can cause massive splenomegaly." In Prof. Mehta's opinion, massive splenic enlargement ought classically cause a haematologist to consider the following five differential diagnoses: (i) blood cancer such as leukaemia (ii) myofibrosis (iii) Gaucher's disease;(iv) malaria; and (v) leishmaniasis. Here he stated, one could exclude all potential causes save perhaps leukaemia and most pertinently VL.
128. Prof. Mehta's evidence was that a normal spleen would weigh about 100 to 150 grams. In size and in shape it would be like a crushed cricket ball. It will be 11 to 13 cm long at its largest diameter and will not be palpable if normal. Prof. Mehta's uncontested estimate was that a 22 cm spleen is approximately the size of a rugby ball, and that the plaintiff's spleen is likely to have weighed 2 kilograms. It was, he stated, 20-25 times the size of a normal spleen.
129. According to Prof. Mehta the significance of a massively enlarged spleen in a patient from Spain with HIV and pancytopenia is that it "... immediately means leishmaniasis" and "if somebody had asked me in 2014 to comment on this presentation, I would take into account that the individual is immunosuppressed, he is HIV positive. He comes from Spain. That's an endemic area, I know that that is an endemic area for leishmaniasis. He has a fever. He has phagocytosis. He has increased activity of the macrophages in the marrow, an abnormal appearance in the marrow with cellular debris and possibly other debris is being ingested by macrophages."
130. Prof. Mehta's opinion was therefore that the epidemiological features of the plaintiff's presentation, his massive splenomegaly and his other clinical features which, albeit nonspecific were nonetheless compatible with VL, strongly suggested VL. The diagnosis should have been VL until proven otherwise.
131. I fully accept that the epidemiological features were crucial here. However, the same reservation applies in relation to the significance of splenomegaly. Prof. Mehta contended in oral evidence that massive splenomegaly was a highly significant indicator of VL, which no reasonable clinician would overlook. If so, why did he overlook this issue in the preparation of an expert report? This is not simply a matter of an expert report placing minor emphasis on a factor later contended to be of greater relevance. There can be many explanations for this. Here, the expert report is entirely silent on a factor said in evidence to be virtually determinative. This clear inconsistency in approach was never explained in evidence or in written or oral legal submissions. I have formed the view that, in their late reliance on the degree of splenomegaly in this case, the plaintiff's experts were impacted by confirmation bias, which is one's tendency to process material by looking for, or interpreting, information consistent with one's existing beliefs.
132. As such, I can place little weight upon the degree of splenomegaly as demonstrating that no reasonable haematologist (or ID consultant) if acting with reasonable care would fail to diagnose VL.
133. Prof. Mehta did not dispute that lymphoma, a type of blood cancer, was a common driver of HLH. He accepted that 60% of HLH is caused by lymphoma and that this was considered as a possible trigger of the HLH in this case. Although he was critical of SJH's failure to perform a splenic biopsy to investigate this, he did not however, go so far as to state that this was a "failure [such]as no medical practitioner of equal specialist or general status and skill would be guilty of if acting with ordinary care."
134. It was put to Prof. Mehta that the five vastly experienced consultants in SJH who treated the plaintiff across both ID and haematology had never come across or treated a case of VL in Ireland before. Prof. Mehta conceded that one's personal experience is a factor of importance but maintained, correctly in my view, that other factors must feed in too, such as literature and conference materials.
135. In terms of causation, Prof. Mehta's view is that the failure to diagnosis VL resulted in the suppression of the plaintiff's immune system, his exposure to various infections and his leaving the hospital in no better condition than he came in. The plaintiff left in a wheelchair with significant muscle wasting and weight loss. In Prof. Mehta's opinion, a patient's response to treatment should be determined by clinical and laboratory evidence of resolution. His view is that the plaintiff showed no marked improvement.
136. AmBisome should have been commenced from the moment the plaintiff met a haematologist in SJH because it was at this time that a high index of suspicion for VL ought to have arisen. Prof. Mehta would have expected substantial improvement within three to five days and the plaintiff would have avoided chemotherapy. It was put to Prof. Mehta that once the chemotherapy treatment programme started, it would not be unusual to see patients take six to eight weeks to substantially improve. This was not Prof. Mehta's experience.
137. VL transmission does not occur in Ireland and imported cases have been almost nonexistent. Since commencing his ID practice in Ireland in 1993, Dr. Sheehan has not diagnosed a case of VL and is unaware of any colleague who has done so in an adult patient.
138. The complete list of potential diagnostic infections in an immunosuppressed HIV patient is vast, some with unique geographic links. Differential diagnoses for the plaintiff's presentation included: lymphoma, leukemia, HLH, endocarditis, sarcoidosis, disseminated histoplasmosis and specific tropical infections in those with a travel history.
139. GU and ID consultants in Ireland will have prior experience of most opportunistic infections, especially those who practiced pre-1996, when almost all patients with HIV advanced to severe immunosuppression and repeated opportunistic infections. However, there are extremely rare conditions such as VL where there will be no prior experience, which creates a difficulty in considering the diagnosis in the first instance. It is often necessary to see a particular presentation to readily recognise it again. Diagnostic acumen very much depends on direct experience with at least one prior case, and in circumstances such as the present, delay in diagnosis will often arise.
140. Because of this, delay in the diagnosis of VL is common outside of highly endemic countries. This is also true in lower risk countries such as Spain and Italy, even when local outbreaks are underway. In countries such as Ireland, with no experience of cases of VL, greater delay is inevitable.
141. In Dr. Sheehan's opinion, it is not surprising that the possibility of VL was not entertained by the SJH ID or GU physicians, or haematologists, given its extreme rarity in Ireland. By contrast, the clinicians in Spain likely had experience of patients with HIV/VL co-infection overlapping with HLH, which would have presented a familiar constellation of clinical and laboratory findings, facilitating diagnosis.
142. Dr. Sheehan's report contends that, had the plaintiff remained at SJH into April/May 2014, his failure to improve with therapy for HLH would most likely have led to a revision of the diagnosis and to a diagnosis of VL.
143. Dr. Sheehan accepts that HHV-8 was an epiphenomenon in this case and was not the cause of the plaintiff's disease. Notwithstanding this, he states that the initial assessment that HIV and HHV-8 were driving HLH was reasonable.
144. Dr Sheehan's report contends that awareness of the association between HLH and VL only crystallised very recently. As of 2014, almost all publications concerning VL/HLH were pediatric single case reports in endemic countries. Although there had been some discussion in the pediatric literature, that VL could mimic HLH in children, the first significant adult publication was only in 2019, i.e. Horrillo, et al., 'Clinical aspects of visceral leishmaniasis caused by L.infantum in adults. Ten years of experience of the largest outbreak in Europe: what have we learned?' (2019) 12 Parasites and Vectors 359 ("Horrillo"). Horrillo, an observational study of a cohort of 111 adult patients with VL in Spain, examines the overlap in the clinical features of HLH and VL in adults. Horrillo states that fever, splenomegaly and pancytopenia are the main clinical criteria of VL but does not suggest that massive splenomegaly is a specific indicator of VL. Horrillo, concerns the largest outbreak of VL in Europe to date, which occurred in south western Spain in June 2009. It observes that in areas where VL is little expected, diagnosis can be difficult. SJH empahsises the high median diagnostic delay of 30 days in the initial stages of the outbreak. However, Horrillo defines diagnostic delay as running, not from the date of admission to the hospital, but from the date of symptom onset. I therefore agree with the plaintiff's submission that this 30 day delay cannot be directly translated across to the present case in which the plaintiff's symptoms started many weeks prior to his presentation at SJH.
145. Under cross examination, Dr. Sheehan conceded that, in 2014, an ID consultant who held themselves out as an expert in the treatment of HIV should have known of the epidemiological association between HIV and VL in Spain. They should know that HIV is a risk factor for VL in Spain and that having HIV increases the chances of getting VL considerably. Indeed, Dr Sheehan's report notes that HIV increases the risk of clinically overt VL by 100-fold to 2,320-fold.
146. Dr. Sheehan accepted that the British HIV Association and the British Infection Association Guidelines for the Treatment of Opportunistic Infection in HIV Sero-Positive Individuals 2011 (the "British HIV Guidelines"), reflected standard practice for the GUIDE Clinic in 2014. These Guidelines consider the most common opportunistic infections such as respiratory, gastrointestinal and neurological disease. Specific organisms, such as herpes simplex ( e.g., HHV-8) are then examined. The British HIV Guidelines then discuss "special circumstances" such as, the background, epidemiology, presentation, treatment and prophylaxis of imported and travel related opportunistic infections, including VL.VL is said to be transmitted by sandflies and rarely by injecting drug use. In the UK, most imported cases of VL come from the Mediterranean, East Africa or India. VL usually presents with systemic features of fever and weight loss, along with hepatosplenomegaly (with splenic enlargement most prominent) with or without bone marrow involvement. The systemic features may be mistaken for other opportunistic infections. Where VL is strongly suspected but standard tests are negative, discussion with tropical medical specialists is recommended. The treatment of choice for VL is AmBisome.
147. When asked whether it was acceptable that the ID clinicians in SJH seemed unaware of the significance of the above epidemiological factors discussed in the British HIV Guidelines, Dr. Sheehan responded by stating "it either clicks with them or it doesn't click that a rare, uncommon, possibility such as VL is possible and if they think of it, then they do, but I do not fault them for not thinking of it."
148. Dr. Sheehan stated that even with knowledge of the association between HIV, VL and Spain, VL would have remained an extremely rare possibility He stated that it "is an excessive expectation that they should be able to get this right on the first case coming into the country." In Dr. Sheehan's view Dr. Ellis's practice was not informed by a northern European context because he had practised most of his consultant career in the Middle East, the United Arab Emirates and Saudi Arabia, where he saw VL on a regular basis. By contrast, people working in a northern European country such as Ireland in 2014, "would find the idea of VL emerging to be ...an extraordinary rarity." VL was understood as a tropical disease associated with countries, such as India, Africa, or South America.
149. In Dr. Sheehan's opinion, when faced with the plaintiff's clinical constellation, it was quite rational to diagnose HLH. When EBV, parvovirus and Castleman's were ruled out, this left HHV-8 as a credible trigger and it was reasonable to proceed on that basis, whilst continuing to search for lymphoma with the CT and PET scans. Dr. Sheehan noted that "...it is very important that you have a credible explanation with HHV-8, that the main drivers of HLH will be lymphoma or infection, within infections it's mainly one of three viruses, EBV, CMV and HHV- 8 and you have the HHV-8. And so it is not surprising then that they failed to think of the alternative of visceral leishmaniasis."
150. When asked by the court whether the SJH clinicians should have considered the plaintiff's Spanish origin, Dr. Sheehan stated: "I don't think that the James's doctors spotted the fact that his Spanish origin meant that VL was a consideration. And in some ways, this is the nub of the case, in a way." Whilst being Spanish would put the plaintiff at a slightly higher risk of VL, which needed to be considered, this did not dictate treatment, and Dr. Sheehan did not criticise the clinicians for failing to make this diagnosis immediately.
151. Dr. Sheehan opined that while epidemiology is important, it must be balanced with all of the other prevailing circumstances and "to be saying it's extremely important imagines that you can sort out most clinical problems based on epidemiology, you clearly can't...." Returning to the theme of diagnostic acumen outlined in his report, Dr. Sheehan stated that where an individual practices and what their usual practice of medicine consists of, would influence them. The past personal experience of the treating clinician is highly relevant in terms of their knowledge base.
152. In Dr. Sheehan's view the plaintiff was assessed to a high standard. Against an HIV diagnosis exposing him to a vast number of opportunistic infections, HLH triggered by HHV- 8 was diagnosed. A rational plan for treatment was devised and it was important to give it a chance to work. The clinicians could be forgiven for not thinking of VL because they had a good working diagnosis.
153. In Dr. Sheehan's opinion:
"it is intrinsically difficult, next to impossible, to include all of the illnesses of the globe in your set of possibilities when you're dealing with a case making a diagnosis. And more especially when you make a reasonable conclusion and you had a reasonable working hypothesis as to what was causing everything. If you are expected to seriously think of VL in this context, then the same applies to most or all of the infections that might arise in all the various other countries that might be there as well."
154. Dr. Sheehan further opined that:
"...the assessment that was made in James's initially was of a high standard and the pattern of things that they saw very much pointed towards underlying HIV causing HLH triggered by HHV-8 and they put in plan a sensible rational plan to deal with that and they had to see what happened and give it a chance."
155. In Dr. Sheehan's view the size of the plaintiff's spleen was not of central importance from a diagnostic perspective. He stated that "a large spleen" has a substantial number of differential diagnoses including HLH and lymphoma. In his view, it does not particularly point towards VL.
156. Dr. Sheehan agreed that epidemiological factors narrowed the diagnostic possibilities and brought VL into focus. However, the expectation that an ID clinician should know of an association between HIV, Spain and VL would only come into play sometime in April or May 2014, if the plaintiff had remained ill at a time when the working diagnosis would no longer remain credible.
157. VL is an extremely rare diagnosis in Ireland. In his career as a consultant haematologist working in the United Kingdom, Ireland and New Zealand, Dr. O'Keefe has not made a diagnosis of VL. It is a condition which is common in tropical countries. Dr. O'Keefe notes that VL does occur in Spain, but with an incidence of about 1 in 100,000 in the general population. This of course overlooks the more crucial statistic issue, which is the far higher prevalence of VL in the Spanish HIV positive population.
158. Dr. O'Keefe believes that the treatment given for HLH probably had a secondary benefit in reducing the impact of VL. However, to completely resolve VL, the treatment given in Spain, in the form of AmBisome, was required.
159. When asked about the significance of the plaintiff's enlarged spleen, Dr. O'Keefe agreed the spleen was probably 20 to 25 times its usual size. Whilst the plaintiff's spleen was certainly very large, which was somewhat unusual, it was still not particularly unheard of or surprising. Dr. O'Keefe stressed that in medicine unusual things happen all the time. He stated that "medicine is never that black and white, that inevitably, you have what is probable and then inevitably you have what occurs rarely, and so when you have a patient who has multiple abnormal parameters, the fact that one is unusual, you know, is just one factor."
160. A spleen of 22 cm, whilst an outlier, was not of the significance contended by the plaintiff's experts. It would not alter the diagnosis of the triggers, as splenomegaly is firmly a feature in the diagnosis of HLH. Critically, spleen size would not be to the forefront of his mind because it does not impact treatment of HLH and its two credible triggers
161. Considering how rarely the diagnosis is made in Ireland and the unusual mechanism by which it presented, with features overlapping with HLH, Dr. O'Keefe did not criticise the SJH clinicians for not considering VL. He stated:
"It's not simply the fact that they have never seen it before, it's the fact that they have alternative diagnoses, reasonable alternative diagnoses in a patient who is in a life threatening situation, they know HLH syndrome can kill you, they know it is an abnormal reaction of the immune system. So they have got to act and they have got reasonable drivers. So, in my opinion, I think I would have done exactly the same as they did. I would not have considered VL because to me, the only time I have heard of it is as a tropical condition in the Tropics. I would not have considered it because he's from Spain and I think if you asked my colleagues... across Northern Europe, we would not have considered it because of that fact. The only awareness we would have had of leishmaniasis would have been a tropical disease and, rightly or wrongly, we would have thought of ... tropical countries."
162. Dr. O'Keeffe disagrees with Prof. Mehta's proposition that it was unacceptable that VL was missed as soon as the plaintiff came into contact with haematologists on 21.02.14. By this time, the team had a reasonable working diagnosis for this gravely ill patient. If he had been managing the plaintiff, Dr. O'Keeffe would have been extremely worried about his condition. Having made the diagnosis of HLH, one starts the relatively standard chemotherapy combination followed here, which continues until one had switched off the abnormal response of the immune system. Dr. O'Keeffe observed: "therefore, you know, he's very sick, this syndrome [HLH] could kill him, I'm going to move on and treat him."
163. In Dr. O'Keeffe's view, the plaintiff should have been moved into the intensive Burkitt's Ward, on 09.03.14 due to his low neutrophil count.
164. In Dr. O'Keeffe's opinion, the records demonstrate that the clinicians were "quite rightly... always thinking" and "still worried about this guy." This is evident from the clinical note of 14.03.14, "needs splenic biopsy next week to outrule underlying lymphoma" which demonstrates that if the plaintiff "is not improving, we have got to start thinking about other possibilities." Once the plaintiff's coagulation and platelet count normalised, splenic biopsy would have been advisable as "the risk of a splenic biopsy now is hugely changed." This would have been advisable had the plaintiff remained unwell in SJH into April.
165. Notwithstanding both the findings of the bone marrow biopsy showing reduced levels of HLH activity and negative HHV-8 levels, one would certainly complete the course of treatment because it takes time for a patient to respond to HLH treatment. It was reasonable to expect that treatment would continue for eight weeks, with a hope of "some evidence of improvement" by the four-week mark. Often it will be up to eight weeks for a more complete response, with no guarantee that it will happen.
166. In this regard, Dr. O'Keeffe relied upon Jae-Ho Yoon, et al,. 'Treatment outcomes and prognostic factors in adult patients with secondary hemophagocytic lymphohistiocytosis not associated with malignancy' (2019) 104 Haematologica 269 ("Yoon"). This concerned a retrospective study of 126 adult cases of non-cancer associated HLH adult patients (like the plaintiff) between 2001 and 2017. In that study, of the 64.3% of patients who achieved a complete response after treatment, 43 did so within four weeks and 38 by eight weeks or longer.
167. SJH appears to rely upon Yoon in two ways: first, to demonstrate that it was reasonable to wait 6 to 8 weeks for definitive response to chemotherapy (which is relevant to the duty of care) and second to demonstrate that, even if VL had been diagnosed and treated early in the plaintiff's admission, he might have taken many weeks to recover in any event (which is relevant to causation). However, the plaintiff's treatment regimen was different to that examined in Yoon in certain respects which it is unnecessary to detail here. One cannot therefore apply Yoon to the plaintiff's progress during his admission. In any event, as Yoon was only published in 2019 (albeit of course that it cites earlier papers) SJH could not have drawn comfort from it in assessing the plaintiff's progress in 2014. Yoon is also of no great assistance as regards causation, because it concerns recovery times from HLH generally and not recovery times from HLH triggered by VL. HLH triggered by VL appears to be highly responsive to AmBisome and one cannot reasonably superimpose the 6–8-week recovery period.
168. In accordance, with Morrissey, the starting point is: "what would an ordinary competent professional of the type and skill of the individual concerned have done, and did the professional who is sued meet that standard?"
169. Here, there is a dispute between the parties as to the correct standard of approach in 2014 for both an ID consultant in a clinic such as the GUIDE Clinic and a consultant haematologist. It is therefore necessary to identify the appropriate standard of approach of an ID consultant who held themselves out as an expert in the diagnosis, treatment and management of HIV positive patients and also of a consultant haematologist in relation to the potential diagnosis of VL in an HIV patient. It must then be considered whether SJH met that standard.
170. Both parties have tendered evidence from an expert ID consultant and an expert consultant haematologist. The oral evidence of the plaintiff's experts identified the standard of approach as following a particular diagnostic pathway. The diagnostic pathway connects:
(a) the epidemiological factors comprising first, the known epidemiological association between VL and HIV in Spain, second, the fact that the plaintiff was within that cohort and third, the alleged known association between HLH and VL with;
(b) the plaintiff's massive splenomegaly.
171. Combined, these factors are said to draw an arrow pointed straight at VL. The plaintiff's experts contend that this diagnostic process of enquiry, analysis, elimination and identification is the standard of approach.
172. SJH's experts argue that the key task in a presentation as complex and challenging as this is to identify and treat the life-threatening syndrome with which the plaintiff presented, which was HLH, and to identify and treat the most credible triggers of it.
173. In the circumstances of this case, my analysis and findings of the relevant standard of approach is as follows:
174. Epidemiology is a branch of medical science that studies the incidence, distribution and control of diseases in a population. At its simplest, epidemiology is the study of how often diseases occur in different groups of people and why. It explores the 5W's of any scenario: what, who, where when and why/ how. These factors are translated into case definition, person, place, time and causes/risk factors/ modes of transmission. Epidemiology identifies areas or groups within the population that have a higher-than-normal incidence of a particular disease which provides important clues as to the causes of disease, and the diagnosis thereof. I accept, and indeed it is common case, that epidemiological information is part and parcel of the standard of approach to diagnosis and treatment for an ID consultant. Although perhaps epidemiology is more likely to arise in the ID specialism than in haematology, I also accept that the epidemiological approach informs the practice of haematology.
175. Dr. Ellis strongly contends that the SJH ID clinicians should have known of the link between HIV and VL, in a HIV positive patient from Spain. Dr. Sheehan accepted this too.
176. I am therefore satisfied that, in 2014, an ID consultant who was a specialist in HIV should have had knowledge of the epidemiological association between HIV and VL in a patient from Spain.
177. As it is common case that this was the first diagnosis of VL in Ireland, I am also satisfied that an ID consultant's knowledge of this association, and of VL generally, would have been though the corpus of knowledge and literature in their field, rather than by way of direct clinical experience.
178. Prof. Mehta and Dr. O'Keeffe give diametrically opposing answers to this question. Prof. Mehta appears to take the view that it would be standard of approach for a consultant haematologist to analyse the epidemiological factors presenting here as highly indicative of VL, at least when combined with massive splenomegaly. Dr. O'Keefe would expect a consultant haematologist to view VL as a tropical disease only and to be unaware of the epidemiological association between HIV, VL and Spain and thus be unaware that HIV was a risk factor for VL. Dr. O'Keeffe did not expect the haematologists working with the GUIDE Clinic in SJH to have considered VL in this case.
179. The plaintiff submits that the evidence of Prof. Mehta should be favoured over that of Dr. O'Keeffe. It is argued that Dr. O'Keeffe has limited experience with HIV patients relative to the haematologists in SJH, because there has not been a consistent specialist ID service at University Hospital Limerick ("UHL") for many years. I accept that haematologists in UHL would not have the same exposure to HIV patients as those in Dublin. The same however could be said of Prof. Mehta who had "only limited experience of HIV patients," had "read a little bit about VL" and had "not got a lot of experience of treating leishmaniasis."
180. It is hard to choose between these competing views. If I had to do so, I would be inclined towards an affirmative answer to the question above, provided that the relevant consultant haematologist had a specialism in the treatment of an international cohort of HIV patients. However, on the facts of this case, it is not necessary to decide this issue. This case is concerned with the plaintiff's management by SJH as a whole, rather than with his management by clinicians of specific specialties or by named individual clinicians. At all stages of the plaintiff's management, there was clear consultation and collaboration between the ID, GU and haematology departments. If, as I accept, it was standard of approach for an ID consultant who held themselves out as an expert in the management of HIV positive patients, to know of this association, then little turns on whether or not the consultant haematologists working closely with ID as part of a clinical team, ought to have been separately so aware. On the facts of this case, my finding that the ID consultants in the GUIDE Clinic should have had knowledge of this association means that the plaintiff's clinical team as a whole ("the SJH clinicians") should have had this knowledge. This permits me to adjudicate upon the liability of SJH as a whole.
181. It is first necessary to emphasise two matters. First, it is common case that in the case of secondary HLH, it is necessary to treat both the triggering disease and the exuberant immune response. Second, knowledge of the association between HLH and VL in the adult population was not necessarily a pre-condition to at least suspecting VL in this particular case, as knowledge of the epidemiological association between HIV and VL in Spain is an entirely separate matter (which I am satisfied was within the standard of approach).
182. Having said that, if one is unaware of the association between VL and HLH, then one will not be alerted to the potential that HLH may be attributable to a trigger other than those more usually encountered, such as HIV/HHV-8. Conversely, if one does know of the overlapping associations between all of the variables present here (i.e. the connection between HIV, VL and Spain and the connection between HLH and VL) this would undoubtedly increase the likelihood of diagnosing VL.
183. The SJH Defence pleads that "... the overlap in the clinical features of VL and Hemophagocytic Lympho-histiocytosis only emerged in the adult medical literature in 2019." This is a reference to the Horrillo paper briefly discussed above. Dr. Sheehan later qualified this plea by stating that the association "was not well known or widely recognised" in 2014.
184. The plaintiff contends to the contrary. Dr. Ellis testified that the association between VL and HLH emerged as far back as 1979. He presented the following literature available in 2014, which he states documents the association between VL and HLH:
· Henter, et al., 'HLH-2004: Diagnostic and Therapeutic guidelines for hemophagocytic lympohistiocytosis' (2007) 48 Paediatric Blood Cancer 124 notes that many conditions can lead to the clinical picture of HLH including malignancies (leukemia, lymphoma and other solid tumors), infections (viral, bacterial or parasitic) and rheumatoid disorders. I cannot accept that the mere reference to parasitic infections as potentially leading to HLH is sufficient to require knowledge of an association between HLH and VL as part of the standard of care.
· Badreddine Kilani, et al., 'Hemophagocytic Syndrome Associated with Visceral Leishmaniasis' (2006) 10 International Journal of Infectious Diseases 2005 85 presents the first report of HLH associated with VL in adults in Tunisia. The paper states that the association between HLH and VL is only rarely found in adults. When VL and HLH present together in patients, diagnosis of the disease may be difficult as the clinical signs are similar in both VL and HLH. Because of this difficulty, the paper recommends that VL should be considered when discussing the cause of HLH in countries where the disease is endemic, such as Tunisia. This single case report from Tunisia, does not bring matters any further in dictating standard of care in Ireland.
· Srinivas Rajagopala, et al., 'Visceral Leishmaniasis Associated Hemophagocytic Lympho- histiocytosis - case report and systematic review' (2008) 56 Journal of Infection 381 ("Rajagopala") is a wider study published in the Journal of British Infection. It records an overlap in the symptoms of HLH and VL and recommends a diligent search for VL in all HLH cases. However, the papers also states that VL associated HLH is rare, with 56 cases reported in the English literature, of which only 16% were adults (a total of 8 reported cases by 2008). Whilst Dr. Sheehan confirmed that the journal in which Rajagopala features is reputable, he did not view it as a significant publication in general ID medicine. It is hard to disagree with this. It is therefore difficult to contend that this represents the standard of care in an adult population.
· Antonio Cascio, et. al., 'Secondary Hemophagocytic Lymphohistiocytosis in zoonoses: A systematic review' (2012) ("Cascio") appears in the European Review for Medical and Pharmacological Science, which Dr. Ellis described as a prominent publication; but which Dr. Sheehan stated would not be well known in Ireland. Cascio concludes that zoonotic diseases are an important cause of HLH and explores different kinds of agents of zoonosis, such as bacteria, viruses, protozoa and funguses. The article notes that VL can cause HLH and can mimic the syndrome. Because of this, secondary HLH can delay the correct diagnosis of the zoonotic disease and contribute to an adverse outcome. Far from suggesting that the association between VL and HLH is widely known, this paper suggests that delay in diagnosis is understandable.
· Neelam Varma, et al., 'Hematologic changes in visceral leishmaniasis' (2010) 26 Indian Journal of Hematology and Blood Transfusions 78 ("Varma") notes that haematological abnormalities in VL are common and recommends that a high degree of suspicion for VL needs to be maintained by the haematologist. VL should be included in the differential diagnosis of patients presenting with fever, hepatosplenomegaly, anaemia, leukopenia, thrombocytopenia, pancytopenia or histiocytosis, and DIC, particularly in geographical areas where it is endemic. There is a dispute between the parties as to whether VL can be described as endemic or merely hypo endemic in the Mediterranean region. Varma states that VL is endemic in more than 60 countries worldwide including north Africa, the Middle East, Central and South America, the Indian subcontinent and southern Europe. This reference to southern Europe is not further elucidated and there was no specific reference to Spain. No case numbers are provided. Dr. Sheehan's evidence was that the journal in which this article was published would not be widely read in Ireland.
185. The above represents the totality of the literature referred to by the plaintiff as demonstrating that it would be standard of approach to know of the association between VL and HLH in 2014. One cannot, in my view, describe these publications as "significant" in the adult literature. Further, these papers note that HLH and VL can mimic each other, especially in the presence of pancytopenia, which was present here. This literature describes the association between HLH and VL, as "rarely known" and whilst a high degree of suspicion for VL is recommended, there is every suggestion that this association can be easily missed. I am therefore not satisfied that this literature is sufficiently significant, relevant or compelling to dictate the standard of approach.
186. Furthermore, bearing in mind that one is considering the standard of approach in relation to an HIV positive patient admitted through the GUIDE clinic, it is worth noting that none of this literature discusses the association between HLH and VL in the context of HIV patients. There is no particular reason therefore to expect these papers would have come to the attention of the SJH clinicians.
187. No clinician can be expected to be in touch with every single piece of literature and every publication or Guideline. Rather they would be expected to follow those most relevant to their own practice. For example, Dr. D gave evidence that she would follow three such publications closely. I accept SJH's submission that it is not "real medicine" to expect a clinician to carry an encyclopedia in their head to check off against every individual patient. As Prof. A stated: "...Clinically... a patient isn't just all of these lists of things; they are what you examine and see [in] the patient on a regular basis."
188. I find that in light of the paucity of adult literature on the subject in 2014, knowledge of the association between HLH and VL is not required by the standard of approach.
189. I have found that it was standard of approach in Ireland in 2014 for the SJH clinicians to have known of the epidemiological association between HIV, VL and Spain. The plaintiff presents the case as fairly cut and dried: either the SJH clinicians should have known of this association and did not in, which case they failed to meet the standard of approach or, alternatively the clinicians did know of the association and failed to consider VL in the differential diagnosis, thereby also failing to meet the standard of approach.
190. However, the issue is not that simple. The ultimate terminus of the court's inquiry is not to determine, as I have, that the standard of approach requires the SJH clinicians to know of this association. I must also determine how that knowledge informs the standard of approach in relation to diagnosis and treatment. In other words, what would the knowledge of this association have led "an ordinary competent professional of the type and skill of these clinicians to have done?"
191. Dr. Sheehan acknowledged that from an epidemiological point of view, the SJH clinicians should have known of the association between HIV and VL, in a HIV positive patient from Spain. He was then asked to confirm that, if the clinicians had known of this association, they would have considered it in the plaintiff's case. Although Dr. Sheehan responded in the affirmative to this question, it is critical to note that this exchange did not specify when precisely in the plaintiff's management this epidemiological association ought to have been specifically considered.
192. On further questioning, Dr. Sheehan's consistent position was that it would be excessive to expect that this epidemiological association would have come to mind in this case.
193. This issue was returned to on re-examination. Dr. Sheehan was asked where and when the expectation that clinicians would know of the epidemiological association fits "into the context of this case." Dr. Sheehan's answer was that this expectation would only have arisen in the present case some time in April or May 2014. By this time, had the plaintiff remained sick, the previously credible explanation for his condition - HLH triggered by HIV/HHV-8 - would no longer be credible. This would in turn have implicated some other undiagnosed process of disease.
194. Dr. Ellis and Prof. Mehta, on the other hand, were clearly of the view that VL ought to have been specifically considered and the diagnosis made within a matter of days of the plaintiff's admission.
195. I prefer Dr. Sheehan's view that knowledge of the epidemiological association between HIV, VL and Spain, does not necessarily mean that the standard of approach requires that this association must suggest itself in respect of a patient within the relevant cohort, particularly at an early point in management. I find that knowledge of the epidemiological association does not mean that the standard of approach requires that VL is automatically included in the differential diagnosis of every HIV positive patient from Spain. Nor does it require that the association is expressly evaluated and discounted in every such case. How strong this association is in a given case will depend upon the plaintiff's clinical presentation and the evaluation of a wide range of possible causes, risk factors or modes of transmission, of which "place" or geographic origin (i.e. Spain) is only one- albeit an important one.
196. It is common case that clinicians treating HIV patients will know of the potential that their patients may be at risk of many dozens of opportunistic infections and other serious diseases. Each such potential opportunistic infection or condition will therefore have an "association" with their patient's HIV status.
197. To be of any value, a differential diagnosis must be focused. Clinical judgement and experience are what focuses the differential, guides the clinicians through the many possible associations and informs which potential diagnoses ought to be pursued at a given time in a patient's management arc. Whilst an association with a given infection or disease based on geographic origin is relevant, its importance and cogency in directing investigations and treatment is always in complex interplay with all other potential associations that might also apply. Inexorably, the cogency of a particular association will wax and wane over time as other potential associations emerge, take pre-eminence and recede. Clinical judgement and experience must guide the analysis and prioritisation of all these associations.
198. Therefore, whilst clinicians treating HIV positive patients may "know" of potential associations with dozens of opportunistic infections and other diseases, the standard of approach requires that they apply discrimination to the task of diagnosis. This permits and requires clinicians to identify signs and symptoms suggestive of the opportunistic infections and diseases that in their knowledge and experience are commonly encountered in such patients. When such signs and symptoms are identified, clinicians may be expected to first carry out investigations targeted at the diagnosis of the opportunistic infections and diseases, which their knowledge and experience tells them are associated with these signs and symptoms. If such investigations identify a particular opportunistic infection, which provides a credible and rational explanation for the patient's condition, then the clinician is entitled to pursue and treat that diagnosis. Of course, clinicians must keep their diagnosis under review. However, they are not compelled, at least at an early stage of management, to explore each and every potentially viable diagnosis that might conceivably apply. Something concrete must alert the clinician to an alternative potential diagnosis. All of this is summed up in the well-worn phrase "common things are common."
199. SJH observes that, although the literature well documents the epidemiological association between HIV, VL and Spain, the number of VL cases in the Mediterranean region, let alone in Spain, are low. For example, Pintado notes that:
"Since the mid-1980s, VL has been increasingly reported as a complication of AIDS. As of 1999, more than 1400 cases of HIV leishmania co-infection had been reported, over 90% of the published cases reported worldwide being observed in Spain, Italy and France."
200. SJH calculates that this means that over 14 years approximately 1,260 (90% of 1,400) cases of HIV-leishmania co-infection were observed in the three countries. After dividing 1,260 cases, between the three countries, over the 14 years, it follows that only approximately 30 cases were reported in Spain. SJH reinforces the rarity by way of a further example drawn from one of the papers relied upon by Dr. Ellis, "Visceral leishmaniasis and HIV coinfection in the Mediterranean Region" by Monge- Maillo et al. [4] Under "Key Learning Points" on page 6, it is stated in the first bullet point:
"VL is endemic [previously referred to as hypo endemic in the same article] in the Mediterranean region; where the causative agent in is the protozoan parasite L infantum. Cases in the region only contribute to 5% - 6% of the global burden of VL, with an estimated annual incidence of 1,200- 2,000."
201. The article also notes that "the introduction of highly active antiretroviral therapy (i.e. HAART) in 1997 contributed to a marked decrease in cases in coinfection (from 1440 cases during the period of 1990 - 1998 to 299 cases during 2001 - 2006)...."
202. This literature supports SJH's submission that notwithstanding the accepted association between VL and HIV in Spain in 2014, VL was not circulating at a level in Spain that obliged the SJH clinicians to consider it as part of a differential diagnosis in the first ever case of VL encountered in Ireland, particularly at the early stages of the plaintiff's admission.
203. Knowledge of an association between HIV, VL and Spain is not axiomatic to the mandatory consideration of that association in the case of a given patient. Nor, for the same reason, does this association need to be discounted in every such case, particularly at the earlier stages of management and when the clinician has identified another credible and rational explanation for the patient's condition. The standard of approach permits and indeed requires a clinician to work through the many potential diagnoses and triggers on a cascading basis. If a rational and credible diagnosis is reached, then a clinician is entitled to pursue it.
204. Recalling once again my finding that the standard of approach does not require knowledge of the association between HLH and VL in the adult population, I find that, in the case of an HIV positive patient from Spain, the standard of approach does not require the SJH clinicians to expressly consider VL as a potential trigger for HLH on epidemiological grounds alone, particularly at the outset of management.
205. Indeed, I do not read the reports of either Dr. Ellis or Prof. Mehta as suggesting that this epidemiological association alone compelled the inclusion of VL in the differential diagnosis at an early stage of the plaintiff's admission. As stated above, Dr. Ellis's report suggests that his criticism of the failure to consider VL emerges later in the time sequence, when the plaintiff's response to therapy for his HLH, HIV and HHV-8 was "slow." Even though Dr. Ellis and Prof. Mehta went further than this in their oral evidence, this was not due to epidemiological factors alone but to a combination of epidemiology and "massive splenomegaly," which the plaintiff submits is "a very important diagnostic clue."
206. It is therefore necessary to examine whether it was standard of approach in 2014 for the SJH ID clinicians to interpret massive splenomegaly as strongly indicative of VL.
207. For the reasons explained at paras. 108 and 131 above, I am not convinced by Dr. Ellis's and Prof. Mehta's opinion that it would be standard of approach to interpret massive splenomegaly as strongly indicative of VL.
208. I have also separately considered whether the literature placed before the court by the plaintiff's experts, offers a sufficiently compelling basis upon which to conclude that it would be standard of approach to interpret massive splenomegaly as strongly indicative of VL.
209. Dr. Ellis and Prof. Mehta relied on one particular article, Liran Levy, et al., 'Prolonged Fever, Hepatosplenomegaly, and Pancytopenia in a 46 year old Woman' 6 (2009) PLOS 1 ("Levy").This is a case study from a group of Israeli doctors of a 46 year old woman who was hospitalised due to a range of symptoms including fever, weakness and weight loss. In such a case, the authors state that "massive splenomegaly narrows down the differential diagnosis, as only a few conditions generally cause this degree of splenic enlargement."
210. Levy defines "massive splenomegaly" as a spleen extended "greater than 8cm below the left costal margin and/or weighing more than 1,000g." Prof. Mehta's uncontradicted evidence is that the plaintiff's spleen in all likelihood exceeded these measurements.
211. Levy sets out a table, "Box 1 Diseases Associated with Massive Splenomegaly" which lists the diagnostic possibilities associated with massive splenomegaly. Prof. Mehta and Dr. Ellis contend that almost all of the diseases listed could have been excluded early in the plaintiff's management, save for blood cancer such as leukaemia and, of course, VL.
212. Dr. Sheehan accepted that Box 1 was a typical list of diseases associated with large splenomegaly that might come up in medical examinations. Dr. O'Keeffe agreed and stated that where one has massive splenomegaly and "you don't know what you are looking for," then "this is what you should be thinking of."
213. Critically however, neither Dr. Sheehan nor Dr. O'Keefe accepted that this logic applied in the present case. This was because, in their view, the plaintiff's splenomegaly was consistent with the diagnosis of HLH. Furthermore, the plaintiff's experts did not dispute that massive splenomegaly may also be associated with lymphoma, also a major cause of HLH, which was still under active consideration by the SJH clinicians up to the time of the plaintiff's transfer to Spain.
214. Ultimately, Levy is just one paper. It cannot be seen as a compendium. I am more influenced by more broadly applicable publications. For example, the plaintiff tenders the British HIV Guidelines as a good reflection of standard practice for the SJH clinicians. These Guidelines do not suggest that the degree of splenomegaly is a discriminating factor in the diagnosis of VL. Nor indeed, does the 1999 WHO paper on which the plaintiff places significant reliance.
215. I fully accept that a doctor is obliged to keep up to date with medical thinking, developments, and literature in their field and must command the corpus of knowledge which forms part of the professional equipment of an ordinary member of their profession: HM v.HSE [2011] IEHC 339, per Charleton J., at para. 25. In the present case, notwithstanding the meticulous research carried out by the plaintiff's experts, only two of the twenty pieces of literature put before the court (one of which was authored by Prof. Mehta himself), speak to an association between massive splenomegaly and VL. This is not sufficient in my view, to demonstrate that knowledge of this association is, as the plaintiff contends, mandatory.
216. I therefore accept the evidence of Dr. Sheehan and Dr. O'Keefe that HLH is itself associated with a significantly enlarged spleen. I am not satisfied that it is standard of approach to place particular significance on the precise degree of splenic enlargement. Because HLH is itself associated with significant splenomegaly, I am not satisfied that it is standard of approach to look beyond a reasonable diagnosis of HLH for which credible triggers have been identified.
217. I am satisfied that the chemotherapy treatment regimen administered to the plaintiff for his HLH accorded with the HLH protocol. I am also satisfied that, once the SJH clinicians, for good reason, chose their treatment programme, they had to give it a reasonable period of time to work.
218. However, I am also satisfied that the standard of approach requires clinicians to keep an open mind and to re-consider diagnoses in light of developments. In practice, this would generally require that in cases of unexplained deterioration or if alternative triggers are excluded, clinicians expressly consider the association between VL and HIV in Spain. Further, I do not accept Dr. Sheehan's view that this point is not reached unless and until the patient remains unwell at the conclusion of the course of treatment initially selected.
219. I am satisfied that once the diagnosis of VL is reasonably suspected, the standard of approach in Ireland in 2014, would have been to confirm same by a range of testing modalities which would have taken between ten days and several weeks to conclude. However, I am equally satisfied that when a reasonable or considerable suspicion of VL arises, the standard of approach requires the administration of empirical AmBisome. Empirical AmBisome is minimally invasive, and in general, reasonably tolerated. I am also satisfied that in such circumstances the standard of approach would be to assist a patient with necessary pain relief to ensure that they can tolerate the required treatment with AmBisome.
220. I found that the standard of approach required an ID consultant (or a consultant haematologist) in SJH, in 2014, who held themselves out as expert in the diagnosis, treatment and management of HIV positive patients, to have knowledge of the association between HIV and VL, in patients from Spain. I have also found that the standard of approach does not require an ID consultant (or a consultant haematologist) in SJH, in 2014, who held themselves out as expert in the diagnosis, treatment and management of HIV positive patients who knows of this association, to consider VL in the differential diagnosis of every HIV positive patient from Spain, particularly in the earlier stages of management. Having established the correct standard of approach, I must then turn to the question of whether SJH complied with the above standard of approach.
221. As appears from what is set out above, in 2014, the SJH clinicians were largely unaware of the association between HIV, VL and Spain.
222. Prof. B who first saw the plaintiff on 03.03.14, had knowledge of this association, albeit that she viewed it as applying predominantly to patients who were intravenous drug users. The plaintiff argues that this degree of knowledge is insufficient to discharge the duty of care as it would exclude from consideration patients who were not intravenous drug users (such as the plaintiff himself).
223. However, that is not how I understand Prof. B's evidence. Although her understanding was that VL was more associated with intravenous drug use, she was also aware that it could be spread by a bite from a sandfly.
224. In any event, I am not convinced that an understanding that this association applied predominantly to intravenous drug users was particularly out of sync with the medical literature in 2014. It is true that some of the papers upon which the plaintiff relies, for example, the British HIV Guidelines state that VL is spread in the Mediterranean basin "only rarely" by intravenous drug use and "usually" by sandflies. On the other hand, three of the articles put forward by the plaintiff's experts- the 1999 WHO paper; Pintado; and Jorge Alvar, et al., 'The Relationship between Leishmaniasis and AIDS: the Second 10 Years' (2008) 21 Clinical Microbiology Review, are broadly consistent with Prof. B 's understanding of an association with intravenous drug use.
225. Overall, I am not satisfied that this point of distinction in Prof. B's knowledge of the epidemiological association could possibly amount to a breach of the standard of care. It follows, therefore that the SJH's clinician's knowledge of the epidemiological association between HIV, VL and Spain was broadly in accordance with the standard of approach from the time of Prof. B 's involvement on 03.03.14, day 13 of the plaintiff's admission.
226. It also follows that, the SJH clinician's knowledge of the epidemiological association was not in accordance with this aspect of the standard of approach prior to that point in time-i.e. the first fortnight of the plaintiff's admission.
227. However, for reasons I will now explain, I also find that even if the SJH clinical team had been aware of the association from the first day of the plaintiff's admission, compliance with the standard of approach does not require that VL was expressly considered in the differential diagnosis of the plaintiff during this early period of his admission between 19.02.14 and 03.03.14, when Prof. B-who I find was sufficiently aware of this association- became involved in the plaintiff's management.
228. In reaching this conclusion, I place some weight upon the broad knowledge base of each of the consultants involved in the care of the plaintiff. They each engaged in continuing medical education to include attendance at national, European and International conferences, reading of publications, involvement in Associations, Societies and Boards, publishing of articles and teaching roles, etc. It would be unreal to ignore the fact that, to the best of their recollection, this continuing medical education had not involved discussion of VL in the context of either Ireland or Europe, prior to 2014. Therefore, whilst I accept that knowledge of the association between VL, HIV and Spain should have been part of the clinician's toolkit, it may not have been at the top of the box, so to speak.
229. Given that the number of Spanish HIV patients infected with VL was still very low in practical terms, it was reasonable, as the starting point, for the SJH clinicians in making a diagnosis to rely on their own prior clinical experience of what was common to them and to consider the potential triggers they most commonly encountered. The prior knowledge and clinical experience guiding the SJH clinicians, was of a multicultural cohort of patients, in whom they had never previously come across a case of VL.
230. I accept that from an early stage in the plaintiff's admission, the clinicians used their experience to reach a reasonable working diagnosis in a very seriously ill man who was at risk of dying. They correctly identified HLH, a rare syndrome in a timely manner, and also identified two credible triggers in HIV and HHV-8, the latter also a rarity. In a case such as the present, there is urgency in commencing treatment for the syndrome identified, HLH and its presumed triggers.
231. The plaintiff argues that it is not sufficient that a working diagnosis is credible, when the correct diagnosis has not even been considered. I am invited to hold that VL ought to have been considered and diagnosed virtually immediately. The plaintiff relies on paras. 4.035 - 4.039 of Michael Jones, 'Medical Negligence' (Sweet & Maxwell, 6th edn 2021) where the author considers a doctor's duty to keep an initial diagnosis under review, revise same as appropriate and to be alive to the possibility of concurrent conditions which may on occasion mask each other. However, it seems to me that the gravamen of the passages cited is that the obligation to consider other causes of a patient's condition and to devise an alternative theory to direct their treatment, arises primarily if the first diagnosis and treatment should fail to produce the improvement expected in their patient's condition.
232. Whilst I am satisfied that it is a standard part of the practice of ID to have appropriate regard to epidemiological factors, the question which remains is when in this particular case specific consideration of the epidemiological association ought to have arisen? The plaintiff has pointed to no case which holds that epidemiology alone is a sufficient basis for a finding of negligent misdiagnosis.
233. The plaintiff relies on Langley v. Campbell [1975] 1 WLUK 312 in which a general practitioner was found liable for failing to diagnose malaria in a patient recently returned from Uganda who presented with non-specific symptoms. Although general practitioners do not generally come across malaria, the court held that it should have entered the defendant's head that the plaintiff might be suffering from a tropical disease of some sort. However, in making this finding the court relied upon medical evidence to the effect that in the absence of complications, a patient with ordinary influenza should begin to feel better after three or four days, and that the patient's continued deterioration should therefore have been a cause of special concern. Equally, the patient's family had told the defendant that he had previously suffered from malaria suggested blood tests. These facts are not comparable to the present case.
234. Aside from academic knowledge of the epidemiological association between HIV, VL and Spain, there were no equivalent clinical clues in the early period of this plaintiff's admission. In particular, I reject the argument that it was standard of approach to regard massive splenomegaly as indicative of VL. Further, whilst I do not accept that it would have been reasonable to wait 6 or 8 weeks for recovery before questioning the working diagnosis (as contended by Drs. Sheehan and O'Keefe), I am satisfied that, having commenced a treatment programme for HLH, HIV and HHV-8, it was reasonable to allow an appropriate period of time for it take effect. I find that in so doing, the SJH clinicians acted in accordance with this aspect of the standard of approach.
235. In these circumstances, I find that the plaintiff has not made out a case that either the epidemiological factors or his constellation of clinical symptoms and signs, including his splenomegaly, were such that in 2014, no reasonable ID or haematology consultant with a specialism in the management of HIV positive patients, could have failed to specifically consider VL within the differential diagnosis during the early period of the plaintiff's admissions. On the contrary, I find that even with knowledge of the epidemiological link between HIV, VL and Spain, many reasonable clinicians would have made an initial diagnosis of HLH triggered by HIV and HHV-8. The plaintiff presented with unusual and non-specific clinical symptoms that can overlap with and mimic HLH, which means that diagnosing VL was an extremely complex task which required time. I find on the balance of probabilities, that in 2014, an ordinary competent ID Consultant or haematologist specialising in the management of HIV positive patients in Ireland would have proceeded in a similar manner to the SJH clinicians.
236. In summary, I find that even if the SJH clinicians had been aware of the epidemiological association from the first day of the plaintiff's admission, their working diagnosis was reasonable and remained tenable and credible up to the time of Prof. B's first involvement and also for some time after this. However, I also find that by 14.03.14, at the latest, a combination of factors ought to have suggested to the SJH clinicians that the diagnosis of HLH triggered by HHV-8 was less likely.
237. 14.03.14 is significant for the following reasons. First, testing on that date showed that the plaintiff's HHV-8 levels were negative. Second, by this time the plaintiff was entering his third week of treatment under the HLH protocol. Third, the plaintiff's condition had not substantially or consistently improved. On the contrary, on 13.03.14, the plaintiff needed to be moved to Burkitt's Ward because of the very high level of care he required. These factors in consort, ought to have prompted a full reconsideration of the plaintiff's diagnosis. By this point at the latest, I find that the failure to specifically consider VL was a failure to comply with the standard of approach outlined at para. 218 above.
238. Indeed, I also accept on the balance of probabilities that consideration of VL ought to have arisen some days prior to 14.03.14. Whilst it is difficult to nominate a precise date the following three factors ought to have considerably increased suspicion. First, on 05.03.14 (Day 16), the plaintiff's viral load for HHV-8 had diminished (from 50,000 to 4,000), yet his condition remained largely unchanged. Second, by 09.03.14. the plaintiff was so profoundly neutropenic that Dr. O'Keefe believes that he should have been moved to Burkitt's Ward. Third, I accept the view expressed in Dr. Ellis's report that the plaintiff's slow response to treatment under the HLH protocol, ought to have become evident after more than two weeks of treatment. It is apparent that the clinicians were clearly perplexed by the plaintiff's lack of response to treatment. On 10.03.14. the clinical notes record "no response to treatment." On 12.03.14, there was concern regarding the plaintiff's spiking temperature and severe neutropenia, which led the team to query "...? source of infection" and to consider another diagnosis, specifically lymphoma. By this point, I find that a lack of prior clinical experience of VL, does not excuse failure to specifically consider it in the differential diagnosis.
239. SJH argues that it is unreasonable to expect the clinicians to have processed every possible opportunistic infection in people with HIV, or as Dr. Sheehan put it to apply "a vast ocean of data that is impossible for any individual to keep track of." Although this argument has force in the early stages of the plaintiff's admission, I find as fact that the position changed in the week of 10.03.14 and no later than 14.03.14. By that time, I believe that it ought to have become evident that the "common" was significantly less likely. Other diagnoses, including VL, ought to have been sought out.
240. SJH contends that, in assessing the standard of care throughout the plaintiff's admission, the court must take into account the plaintiff's wish to return to Spain for his treatment which the clinicians ultimately facilitated when it was safe to do so. The suggestion appears to be that, as the plaintiff's condition improved somewhat in the later stages of his admission, it was reasonable for SJH to focus on ensuring that the plaintiff was well enough for the transfer to Spain. This logic informed the clinical risk benefit analysis concerning the advisability of invasive diagnostic tests such as, for example, splenic biopsy. In short, it is said that in the latter stages of the plaintiff's admission it was reasonable to prioritise "containment" and safe transfer to Spain.
241. In truth, this is not a factor of weight. Reaching a definitive diagnosis of VL would have necessitated a variety of investigations, some of which could have been invasive. However, the active consideration of VL in the differential diagnosis and the forming of a suspicion of same would not have required invasive diagnostic tests. In any event, the "containment" argument only applies after the HLH treatment regimen showed some signs of working which was towards the end of March 2014. However, I find that specific consideration ought to have been given to VL well before then, between 10.03.14 and 14.03.14. Events postdating this critical period cannot be taken into account in assessing whether there had been a breach of the standard of care.
242. In short, I find that circumstances were such that in the period 10.03.14 to 14.03.14 a considerable suspicion of VL ought to have arisen, leading to the commencement of empirical AmBisome in that time window.
243. The plaintiff's case is that VL ought to have been diagnosed within 4 or 5 days of his admission and that AmBisome ought then to have been administered empirically. SJH tentatively submits that the plaintiff may not have tolerated AmBisome. However, it is not disputed that, had VL been suspected and AmBisome prescribed, the plaintiff would have been supported with appropriate pain relief to ensure that this treatment could be maintained.
244. Prof. Mehta would have expected a substantial recovery within 3 to 5 days of commencing AmBisome. Dr. Ellis's time frame was substantially longer. He expected improvement within a week or so of commencing AmBisome and a substantial recovery within a couple of weeks. Dr. Sheehan's report states that symptomatic improvement could be expected a week after commencing Ambisome.
245. The plaintiff submits that as a consequence of the defendant's negligence, he remained in hospital for 6 weeks. He received toxic chemotherapy, which could otherwise have been avoided. He became an infection risk which required further heavy treatment. He suffered from hospital acquired infections requiring further treatment. He required transfer to enhanced care in the Burkitt's Ward. He received 14 units of blood transfusions. The plaintiff left hospital in a wheelchair with fever, low blood counts, an enlarged spleen, weight loss and muscle loss.
246. By way of contrast, the clinical notes from Spain record that the plaintiff was afebrile and asymptomatic once Ambisome was commenced and that he was well enough for discharge from hospital a week later. The plaintiff invites me to transpose these time-frames to February 2014.
247. However, I have found that it was not beneath the standard of care to fail to either strongly suspect, or to diagnose VL prior to the week of 10.03.14. There was therefore no indication to commence empirical AmBisome prior to this. By this time, the plaintiff was unfortunately already severely ill. As such, I am satisfied that one cannot infer that the plaintiff's response to AmBisome in the week of 10.03.14 would have mirrored his response in April in Spain. By the time the plaintiff was transferred to Spain, his condition had substantially improved as compared to 10.03.14. Therefore, even if Ambisome had been administered empirically in the week of 10.03.14, it would be unreasonable to expect the same rapid improvement.
248. As it was reasonable not to consider VL prior to the week of 10.03.14 and indeed to pursue the reasonable and credible diagnosis of HLH triggered by HHV-8 and HIV, it was also reasonable to have commenced chemotherapy on 27.02.14. I accept, as Dr. O'Keeffe put it, that the clinicians needed to urgently treat the plaintiff's HLH as "the syndrome could kill him." Therefore, even on the counter- factual scenario, chemotherapy would have been administered for almost three weeks.
249. I find that VL should have been strongly suspected in the week of 10.03.04, mandating treatment with Ambisome empirically. Instead, Ambisome was not commenced until over three weeks later on 04.04.14.
250. I find that if the plaintiff had been commenced on AmBisome in the week of 10.03.14 improvement within a week and substantial recovery within two weeks could reasonably have been anticipated. Because the plaintiff was already severely ill by this time, Prof. Mehta's shorter time estimate of recovery within 3-5 days of commencing AmBisome cannot apply. On the other hand, given that the plaintiff improved somewhat even without AmBisome by 22.03.14, it is reasonable to conclude that, with AmBisome he would have felt substantially better in himself within this time fame.
251. The plaintiff has not submitted a condition and prognosis report. Crucially, he alleges no long- term ill effects either physical or psychological arising from SJH's failure to diagnose VL within 5 days of his admission. Fortunately, the plaintiff has made a full recovery, albeit that his splenomegaly took many months to fully resolve. [5]
252. I will not repeat the details of the plaintiff's course between 10.03.14 and 04.04.14 when AmBisome was commenced in Spain. Suffice to say he initially required intensive management in Burkitt's Ward and that he experienced a waxing and waning course of fever, confusion, fatigue, weakness, diarrhoea, anorexia, and anxiety for the remainder of his admission. Although the plaintiff certainly improved, it appears that even by the end of his SJH admission, he remained clinically unwell and was only able to ambulate for short distances. Furthermore, the plaintiff was administered five blood transfusions between 14.03.14 and 31.03.14.
253. One cannot attribute all of the plaintiff's symptoms during this period to SJH's negligence. I have concluded that, even with AmBisome, recovery would inevitably have taken some time. However, I find on the balance of probabilities that, if AmBisome had been commenced in the week of 10.03.14, the plaintiff would have improved symptomatically towards the end of that week or the beginning of the next, which is approximately three weeks earlier than actually occurred. Substantial recovery would have occurred a week after that. All in all, the plaintiff would have been spared approximately three weeks of painful and debilitating symptoms. He would have been spared approximately three weeks of hospital admission. He would also have been spared anxiety, distress and worry as to his health.
254. SJH submits that I must have regard to equivalent awards in comparable cases and to those indicated in the Book of Quantum. [6]
255. The plaintiff draws the court's attention to Ewing v. North Western Health Board [1998] IEHC 171 ("Ewing") in which the court awarded general damages of £25,000 to date and £10,000 into the future as a consequence of an unnecessary surgery in the form of the removal of an ovary by way of an open procedure. The plaintiff argues that the court ought to update the court's 1998 award in accordance with the consumer price index. He suggests a contemporary figure of €70,000.
256. I accept SJH's submission that this is not a legally valid approach. Although the Personal Injury Guidelines Committee has recently recommended an increase in the figures set out in the Personal Injury Guidelines ("the Guidelines") to take account of inflation, this approach has not been adopted by the courts to historic awards of general damages, save in respect of catastrophic injuries. In any event, I am not convinced that there is any real similarity between the injuries suffered in Ewing and those in issue here. In Ewing, the plaintiff had been subjected to an unnecessary surgery with all its attendant risks and fears. The plaintiff was also left with an abdominal scar which, whilst only visible on very close inspection, was nonetheless a blemish she would carry for the rest of her days. Save that it relates to a case of medical negligence, the plaintiff's experience here is completely different.
257. The plaintiff also refers to O'Driscoll v. Hurley [2015] IECA 158 ("O'Driscoll") in which the plaintiff appealed a judgment of the High Court awarding €50,000 by way of general damages arising from negligence in the course of an appendectomy procedure. The Court of Appeal held that €50,000 was far from an insignificant sum having regard to the "relatively modest sequelae" which could be attributed to the defendant's negligence after the plaintiff was discharged from hospital 8 days after the unfortunate surgery. The plaintiff argues that if an award of €50,000 was deemed appropriate to a patient discharged 8 days after an unnecessary surgery, then a significantly greater reward is merited for his 42 day admission. I cannot agree. The award in O'Driscoll was not related solely to the hospital admission per se but to the fact that the plaintiff continued to experience enuresis, an enlarged bladder and post- traumatic stress disorder. The award also took account of the perforation of the plaintiff's bladder during the appendectomy procedure necessitating bladder repair surgery. The Court of Appeal held that the award of €50,000 was within the range that might reasonably be awarded by the High Court for all of these sequalae, even taking further account of a future risk of adhesions, potentially requiring surgery. I cannot find any equivalence with the present case in which no long-term sequelae or complications are alleged.
258. The plaintiff also draws the courts attention to Jones v. Ministry of Defence [2020] EWHC 1603 (QB), a clinical negligence case concerning the medical consequences of a 10-month delay in the diagnosis of the plaintiff's HIV status, for which the plaintiff was awarded £25,000. Save for noting the relatively modest award of damages in Jones, I cannot discern any real equivalence on the facts.
259. SJH submits that the court ought to have regard to the Book of Quantum and that the category that most closely captures the plaintiff's experience is that for food poisoning requiring hospital admission:
"There are varying degrees of food poisoning and the effects will vary from person to person. Some types of food poisoning will have short term effects whereas other more serious types may have a lasting effect on a person's appetite and daily living.
Minor to Moderate - up to €14,500
Uncomplicated recovery with pain, cramps and diarrhoea continuing, causing significant discomfort, stomach cramps, altered bowel function and fatigue.
Severe and permanent conditions – €23,700 to €40,300
Severe poisoning with diarrhoea and vomiting diminishing over a prolonged period of weeks but with some remaining discomfort and bowel function over a longer period."
260. The plaintiff does not fit neatly into either the "minor to moderate" or the "severe and permanent" categories. Whilst the symptoms listed in the Book of Quantum, i.e. pains, cramps, diarrhoea, and fatigue, all apply in this case, the plaintiff's clinical history and symptoms in SJH could not be described as "an uncomplicated recovery." Equally, the nomenclature "severe and permanent conditions" does not appear to fit with the plaintiff's ultimate recovery in this case. There may be some parallel between a patient suffering "severe poisoning and diarrhoea with vomiting, diminishing over a prolonged period of weeks" and the plaintiff's experience in this case. At the same time, however the plaintiff has not made out a case of "remaining discomfort and bowel function over a longer period," which suggests that an award at the top end of the "severe and permanent" range is not indicated for the three week period implicated here.
261. SJH also urges the court to have a regard to the Guidelines which consider damages for food poisoning causing "moderate" symptoms including vomiting, discomfort, stomach cramps, alteration of bowel function and fatigue, where symptoms are severe enough to warrant hospital admission lasting some days but where there is complete recovery within twelve months. The Guidelines assess such damages at €6,000-€20,000, (albeit that, where hospitalisation is required, an award should be made towards the top of the bracket).
262. It is fair to say that the plaintiff experienced the "moderate" symptoms listed above- vomiting, discomfort, stomach cramps, alteration of bowel function and fatigue. Same were also serious enough to warrant continued hospital admission for well in excess of "some days." In addition, however, the plaintiff was in the ICU and was clearly in extremis. Such severe illness is not captured by the above description in the Guidelines. At the same time, the plaintiff has not made out a case of prolonged recovery of up to 12 months. Again, therefore the plaintiff's injury does not fit neatly into the relevant description. More fundamentally, this case is not governed by the Guidelines.
263. SJH submits that even on the plaintiff's highest case, i.e. assuming full liability for failure to prescribe AmBisome on day 4 or 5, damages would be in the region of €30,000 to €35,000 falling within the remit of the Circuit Court. On the assumption that VL ought to have been diagnosed on or about 14.03.14, only half of the relevant time would be compensable. SJH fairly accepts that, because the plaintiff was genuinely in extremis, he could not be confined to only 50% of the figure just indicated.
264. I am of the view that SJH's full liability estimate is on the low side. Bearing in mind how gravely ill the plaintiff remained and all of the anxiety, stress and fear thus engendered, I would have assessed general damages on a full liability basis at €40,000 - €42,500. I agree that, as a matter of logic, damages somewhat in excess of half of that amount are warranted.
265. I have had regard to the plaintiff's suffering, the requirement that general damages are proportionate to the maximum, to awards for other comparable injuries and to the guidance of the Book of Quantum. General damages in this case for past pain and suffering may fairly be assessed at €26,000. No damages for future pain and suffering arise.
266. Counsel on behalf of the plaintiff made an application that reporting restrictions be imposed in order to ensure his anonymity. SJH confirmed that it supported this application.
267. There is a constitutional imperative that justice be administered in public save in such special and limited cases as may be prescribed by law. However, s.27 of the Civil Law (Miscellaneous Provisions) Act 2008 ("the 2008 Act") allows a court to make an order prohibiting the publication or broadcast of any matter relating to proceedings which would, or would be likely to, identify a party to the proceedings as having a (sensitive) medical condition. Such an order may only be made where the court is satisfied that: (a) the relevant person has a medical condition, (b) his or her identification as a person with that medical condition would be likely to cause undue stress to him or her, and (c) the order would not be prejudicial to the interests of justice.
268. In the present case, I am satisfied that these criteria are fulfilled in this case. It would cause undue stress to the plaintiff were the fact that he is HIV positive to be published or broadcast. It would cause further undue stress to the plaintiff were he to be identified in any reportage of the present proceedings.
269. I have therefore made an order pursuant to s. 27 of the 2008 Act precluding the publication or broadcast of any matter relating to the proceedings which would, or would be likely to, identify the plaintiff. In so far as is necessary to maintain the integrity of this order, I have also redacted from this judgment the personal details of the involved parties. Given that this judgment contains a detailed summary of the evidence, the outcome of the proceedings and the full reasons for same, I am satisfied that the imposition of these limited restrictions is not prejudicial to the interests of justice.
[1] These conditions are all explained below at paras. 5-10.
[2] As defined at para. 210 below.
[3] A secondary phenomenon that occurs alongside or in parallel to a primary phenomenon.
[4] See para. 100 above.
[5] This is not alleged to result from SJH's negligence.
[6] As these proceedings pre-date the commencement of the Personal Injuries Guidelines.