Qureshi v Royal Brompton & Harefield NHS Trust

This case concerns the Claimant’s case for damages for personal injury arising out of medical care at the Royal Brompton Hospital (RBH) in 1989. The Claimant (Aisha Qureshi) was born on 20^th June 1985. She proceeds in this action by way of her mother and litigation friend, Zahida Qureshi.

Aisha was born with a serious heart condition, a congenital defect called Tetralogy of Fallot (TF). At the age of three weeks, she underwent a palliative operation, a left modified Blalock-Taussig shunt. On 2^nd May 1989, her defect was repaired. Pleural effusions developed post-operatively which were treated. She was discharged from hospital on 14^th May. She had to be re-admitted on 20^th May to Princess Alexandra Hospital (PAH) in Harlow and was transferred the following day to RBH. Cardiography showed a large pericardial effusion (PCE). This was drained on 21st May. 400mls of pericardial effusion was drained. An echocardiogram on 22^nd May following drainage, showed no re-accumulation of fluid and an echocardiogram on 24^th May was reported as showing only a small amount of residual fluid. The Claimant was discharged. She was seen by Dr Redington (a senior registrar in paediatric cardiology) on 31^st May by way of review and was found to be well. He reduced her diuretic medication and arranged for a further review in a months time. She was seen by a Dr Bate on 6^th June at her local hospital, who also found her to be looking well. On 10^th June she was admitted to the PAH as a result of problems which had developed and was transferred to the RBH where on arrival, she suffered cardiac failure. Cardiac massage was started following intubation. 400mls of pericardial effusion was drained. She has suffered severe brain damage as a result of that second incident.

The issue is liability. The claim is that the decisions taken by Dr Redington at the Royal Brompton Hospital on 31^st May 1989 were negligent and that this negligence was the cause of the injuries.

The essence of the Claimant’s grounds are that:

The Defendant’s case is that:

Mr Pozzi is a Consultant Paediatric Cardiac surgeon at Alder Hey Children’s hospital and, inter alia, Clinical lecturer at the University of Liverpool. He has significant experience in TF. His report is dated 23^rd August 2005. Dealing with the events of 31^st May 1989 in relation to the reduced dosage of diuretics, he indicates that whilst such a topic would be left to a paediatric cardiologist, in his view one week was the maximum that would have been acceptable between such a reduction in diuretics and the next follow up with echo control. Since the Claimant had a pleural effusion soon after surgery and a PCE within a couple of weeks from surgery, there was a possibility if not a probability of developing further effusions. The use of diuretics in some cases can reduce the chances of developing further effusions. To reduce the diuretics significantly and then to leave the child for a month without any control was in his view below acceptable standard. This in his opinion allowed the re-development of a very large PCE, which then produced the Tamponade responsible for the cardiac arrest suffered by Aisha on 10^th June 1989.

In evidence Mr Pozzi explained that the although he was a surgeon, he would be involved in the post operative management of the patient where there were implications from a surgical point of view. In his view the history of the patient’s post operative period showed that she had a tendency to accumulate fluid and was sensitive to the use of diuretics in controlling the collection of effusion. The left side of the lung was not drained and it showed loculated fluid on x ray, something he considered was significant. This might affect the capacity of the child to oxygenate. It was not standard to be oxygen dependent until day nine although it can be expected in some patients. This too was a significant complication of post - operative surgery.

Dealing with the events of 20th May, in his view, it was likely that the patient had a certain amount of heart failure, but it would be difficult at this moment in time to give a precise assessment given the overlapping clinical condition produced by the presence of tamponade overwhelming the clinical situation. However he felt that mild heart failure was a possible underlying condition, which was partly responsible for the build up of fluids. Tamponade is very rare. Once a state of Tamponade is reached, diuretics are an inappropriate form of treatment; draining the effusion was the only appropriate form. He saw a connection between the reduction in diuretics on two occasions, namely 14^th and 31^st May and the condition of the patient on 20^th May and 10^th June.

Cross examined he said that the majority of children operated on for TF would be discharged from hospital with a certain dose of Frusemide. At follow up if there was a small amount of fluid in the pericardium the treatment with the diuretic would continue and the child would be reviewed again soon after. If the fluid around the heart had increased, but not large enough to justify drainage, then the diuretic dose might be increased and the child would be reviewed quite soon thereafter. Diuretics are a form of treatment for PCE. He pointed to an extract from an American text book by Mavroudis and Baker called “Pediatric Cardiac Surgery” 3^rd edition 2003, which indicated as much.

The entry on 22^nd May where it showed that the venous pressure was still raised, means that the heart was to a certain degree still in a state of failure and thus the patient would benefit to some extent from diuretics. Heart failure would produce an accumulation of fluids and you would want to prevent this. Diuretics are standard treatment for post operation on TF as an anticipatory measure on the basis that the heart will not function perfectly after the operation. The diuretics will prevent or contain the effect of the failure or lack of efficiency of the heart. It is not a regime in anticipation of an inflammatory reaction to surgery (PCS).

Dealing with the decisions taken on 31^st May, he agreed that the clinical signs of the patient were good and that she was well controlled pharmacologically. He did not disagree with the principle about reducing the diuretics but in the light of the history of the patient he thought a less dramatic reduction would have been more appropriate, i.e reducing from three to two times a day. His real criticism is that review was set for a month rather than for a week, this was in the light of the whole history of the patient and also making such a significant reduction in the diuretic regime. In his opinion if the dose had been maintained, on the balance of probabilities, the Claimant would not have developed such a significant effusion. In relation to his use of the word “chance” (page 118) he indicated that this word may not have been the appropriate word to use but his opinion remained the same.

PCS could have been partly responsible for the situation but he could not say that it was wholly responsible as the Claimant showed none of the symptoms described for PCS in the text book. He would not exclude the possibility of tamponade from heart failure alone, but it would have to be very severe heart failure, to have caused the accumulation of fluids which took place. To have reached that size and stage, it could have been PCS or PCE and a degree of heart failure.

Whilst he accepted that there were no symptoms suggestive of continuing heart failure. In his view, the patient was not in perfect condition; there was a residual ventricular septum, there was pulmonary regurgitation and in the light of the intrusive surgery these additional problems had to be taken into account. The decision regarding the review should have been taken, bearing in mind both the history and the clinical findings.

He said that the large majority of competent doctors would consider a month review too long and only a minority of competent doctors would have allowed for a week’s review. In re-examination, he finally said, he could not imagine any reason for anyone rationally to want to leave such a long gap with such a significant reduction in the treatment having taken into account both the clinical findings and the history.

Dr Arnold is a consultant paediatric cardiologist also at Alder Hey. He is an honorary lecturer in child life and health at the University of Liverpool. He deals with the different factors contributing to post operative PCE - elevated venous pressure, excessive bleeding, viral infection and PCS. Cardiac Tamponade (which simply put is a squeezing of the heart so it cannot pump blood properly) develops in about 1% of patients with PCE. It is usual for echocardiography to be undertaken a day or two prior to discharge and again at the first post operative visit. Medical treatment of PCE is with anti inflammatory agents and diuretics. He points to a number of complications in the patient’s post operative period - closure of the ventricular septal defect (VSD) was incomplete; bilateral pleural effusions and the need for the patient to be admitted to intensive care on day three. Dealing with the appointment of 31^st May 1989, apart from reference in a letter written by Dr Redington on 31^st May 1989, he can find no evidence in the medical notes to show that an echocardiogram was done on that day. In his view the reference in the letter to an echocardiogram referred to the one that was done on 24^th May. Not to repeat the echocardiogram on 31^st May, would be a serious omission as recurrence of pericardial effusions is not uncommon. To reduce the dose of diuretics without confirming the resolution of the effusion was inappropriate. To arrange a follow up a month later was also inappropriate.

In evidence, he indicated that the post-operative problems encountered by the patient are seen not infrequently and that the Tamponade was the unusual part. PCE could be caused by heart failure or PCS. The fluid is essentially the same, although if examined microscopically or chemically there might be slight differences. He had seen some cases of PCS not amounting to Tamponade where diuretics had been given and the fluid had diminished. They would see 10 cases of PCS a year and would treat some with diuretics and some with anti- inflammatories. They would probably give both diuretics and anti- inflammatories if the patient got PCS following an operation for FT. Using an anti-inflammatory would presume that there was an inflammation present.

Cross examined, he accepted that as a general rule you do not have Tamponade resulting from heart failure. It is very rare. There are particular heart problems that may cause it, but not in this case. As a general principle, fluid overloads were treated with diuretics not with anti- inflammatories; PCE would be treated with anti-inflammatories. However in the context of post FT surgery, the treatment would include diuretics. The standard post-operative response to FT surgery is to put the patient on diuretics straight away, unconnected with PCE.

With PCS leading to isolated PCE, if it were mild you would leave it and watch and hope it would resolve spontaneously. If it were large, it would be drained. If it were in between, you would follow the effusion with daily echocardiograms. If there was evidence of inflammation, fever and high white count you would put them on anti-inflammatories.

He had been mistaken in his assumptions that the reference to an echocardiogram in Dr Redington’s letter of 31^st May related to the echocardiogram done on 24^th May.

He was not sure that a body of responsible cardiologists would have seen no problem in the reduction from three times daily to once daily, as there was also a reduction of the Spironolactone, which apart from potentiating the action of the Frusemide also maintains the potassium level lost as a result of the Frusemide. To keep the patient on the existing dose, but with a careful follow up, did not present a very great risk, as she had been on the treatment for several weeks without any problem.

On 31^st May there were residual symptoms that you would expect to see for any patient who had gone through the TF procedure. There were no adverse clinical findings. Had she stayed on the same high dose, it is impossible to say what would have happened. It is hypothesis. He was not sure that you could predict what would have happened. The Tamponade may still have happened; the effusion may still have happened but more gradually. It is very difficult to extrapolate and very difficult to say what might have happened. He also could not say what would have been the consequences if she had been kept on two doses a day.

By 31^st May, there may still have been impaired right heart function although there was no evidence in front of the court to support this supposition. It would have been helpful to have the echocardiological report of 31^st May to establish that. However, assuming that the doctor was a competent one, he would not expect him to reduce the diuretic unless the defect (the hole) were anything other than tiny. He accepted that there was no evidence that the residual defects caused any symptoms on 31^st May. If the parents had mentioned any symptoms or the doctor had noticed any, then this would have been recorded, as it would have been a cause for concern.

He could not remember the details and how many cases of PCE he had seen before with no Tamponade where he administered diuretics and had some response. He gave anti-inflammatories as well. He could not say that the reduction in effusion was due to the diuretics on their own, as it is difficult to assess. “You treat with the drugs and hope that they will have an effect”. He thought diuretics might remove fluid from the pericardial space but he agreed that they take fluid from the body altogether. If there was a localised pericardial effusion, the last thing one would want to do is to take fluid from the rest of the body. He would not say that those who do not treat PCS with diuretics are incompetent.

In response to the court he said had he been treating this patient he would have made no or a small reduction in the diuretics dosage given the history. One had to be cautious in reducing the dose. Usually after surgery for FT the dose is reduced stepwise with careful follow up. If PCE were experienced soon after surgery (4-5 days) he would often prescribe anti-inflammatories. If there is general evidence of fluid retention, he would increase the diuretic dose, but if there was not, then they would probably be put on anti-inflamatories. The reason for giving anti-inflamatories is that they hope to reduce the risk of increasing accumulation of fluid in the pericardium in the hope of avoiding Tamponade.

In his view although on 31^st May Aisha appeared well, there was uncertainty about her heart. He would have expected the registrar to make more notes commenting whether there was good or impaired ventricular function. He would have liked more information about the echo findings and measurements. However he agreed that the note by the lab technician for the echo of 24^th May also did not contain any measurements of the effusion and referred merely to small residual effusion. 0.5cm to 1cm was not a severe PCE.

In the light of the difficulties experienced historically, he would have expected there to be some concerns about the overall function of the heart. If the heart were not functioning properly, the diuretics dose would have been maintained, although he did not necessarily accept that one could infer that it was functioning properly because the dose had been reduced.

Professor Redington as he now is titled, is Head of Paediatric Cardiology for sick children in Toronto, Canada. In 1989 he was Senior Registrar in Paediatric Cardiology at the RBH, London. In his first statement dated 12^th June 2004, he indicates that he had been involved in the treatment of the Claimant prior to 31^st May 1989.

On the 24^th May 1989 an echocardiogram was performed which showed a limited amount of pericardial effusion, localized mostly lateral to the posterior wall of the left ventricle measuring less than 1cm. On review of the patient on 31^st May, he found her to be very well - much improved from previously and her echocardiogram showed that the effusion had all but resolved. There was no evidence at the time or previously that her pericardial effusion was related to cardiovascular compromise, so her diuretics were reduced in accordance with usual practice at that time.

The patient was due to be seen at her local hospital so he arranged to see her at the RBH hospital in one month, prior to handing over her care to the PAH. Although not documented, advice would have been given to contact the local hospital if new symptoms develop or if there is any clinical deterioration. He noted that in fact the claimant’s parents clearly were given the appropriate advice.

In his second statement dated 26^th October 2005, he explains that an echocardiogram was performed on the 31^st May and his findings that effusion had all but resolved implied that any remaining fluid was much less than the 0.1-1cm rim of fluid found on the echocardiogram a week earlier. All people have a degree of fluid in the pericardial space and thus it is not possible to say that no effusion is present.

Dealing with the dosage of diuretics, he indicates that the dose was high and it would have been inappropriate to continue it without good reason. As there was no cardiac compromise by 31^st May, he elected to reduce the dose. This was in accordance with standard practice at the Trust at the time where they would try to wean cardiac patients off diuretics within 2-4 weeks of surgery.

He was aware of the follow up appointment at PAH, but would not have expected them to carry out an echocardiogram. If he had felt such an echocardiogram was warranted, he would have arranged for the Claimant to attend RBH earlier. He considered one month was appropriate. This was in accordance with practice at the Trust at the time.

Professor Redington gave evidence. He was the first witness to do so, this course being agreed by both parties and approved by the court. He was asked some supplementary questions having adopted his two statements. He produced his cv. By the time he was senior registrar, he already held a doctorate in medicine – the specialism being “right ventricular function”. He was an experienced senior registrar. By 1989 he had published quite widely.

Dealing with the case in question, he first became involved with the management of the patient on 7^th May. He had no further involvement until 31^st May 1989. He explained how all cases of TF repair would be put on diuretics post-operation for a period of about 2-4 weeks, and then the dose would be reduced. In relation to this particular case, it was crucial to understand that this was the reason for the prescribing of the diuretics.

He went through the notes of the patient dealing with the history of events. Dealing with the admission of 21^st May, it was the Tamponade which begat the heart failure. This was a reaction to the trauma of heart surgery, an inflammation of the lining of the heart, which is an unusual but well recognised condition. It is called post-cardiotomy syndrome (PCS) and is quite different to the pericardial effusions one sees a day or two after heart surgery. Diuretics are not the treatment for this reaction.

He described his usual working practices when seeing a patient. He would read the notes whilst the patient was being brought in and make some notes of the history himself. He would examine the patient and then carry out the echocardiogram. He would make notes as the patient was leaving and dictate any necessary letter at the same time.

He went through his clinical findings of 31^st May and the result of the echocardiogram. This appointment was the post-discharge, one week review. He reduced the diuretics dose, as there was no evidence of fluid retention or re-accumulation. If there had been significant fluid around the heart, the feeling of the heartbeat on examination would have been lost and it was not. If the patient had had a larger effusion or the same size as on 24^th May then he would have arranged to see her in a week for a further echocardiogram. In his view at the time, the risk of re-occurrence of the events of 21^st May was extremely small. In the many hundreds of patients they had at the time, he had never come across an incident of reoccurrence of PCE. The risk of Tamponade as a result of PCE is 1%. Diuretics were not indicated. They carry adverse effects, so he reduced the dose and in accordance with normal practice fixed a follow up for a month’s time.

Cross examined, Professor Redington accepted that an echocardiogram on 7^th June would have revealed the effusion. He was taken through the history of the patient’s post-operative recovery. He would have expected the varying doses of diuretics as occurred in this case. PCE could be caused by heart failure but Tamponade is not. His echocardiogram on 31^st May showed that fluid was less than existed on 24^th May. The important issue was that the PCE had resolved or as he put it in his letter “all but resolved”. Even if there had been an increase of fluid between 23^rd and 24^th May it would not have made any difference to his approach, as the important issue was that his findings showed it had got smaller in the intervening week.

He accepted that there was a slight distinction between the word “resolved” and the phrase “all but resolved” but they meant the same thing. Everyone has a small amount of fluid around the heart. If there had been a significant amount, he would have said so. In terms of her post- operative course the patient was standard, but the development of Tamponade was unusual. In terms of diuretic treatment, there was nothing in the history to indicate that the dose should not be reduced.

He knew that she would not be receiving an echocardiogram at PAH the following week, as being a regular visitor there, he knew they did not have the facilities and indeed did not have the expertise. He denied that paragraph 12 of his first statement was an attempt to justify the lack of weekly follow up by indicating that he knew she was to be seen in PAH the following week. Whilst he accepted that it could be interpreted as such, it is not what he meant. He could not possibly have thought that as there was no equipment there.

If he had thought that there was a significant risk of re-accumulation he would have seen the patient a week later. The complication of Tamponade was not caused by the reduction of diuretics. Diuretics are not for the treatment of Tamponade or PCS.

Aisha had a terrible series of consequences unrelated to her dose of diuretics. The diuretics were independent to the risk of PCE. She had not developed gross fluid retention and thus the reduction of diuretics was appropriate. The risk of developing PCE was incredibly small.

Mr Stark is an honorary senior lecturer at the Institute of Child Health. He was consultant paediatric cardiac surgeon at Great Ormond St Hospital since 1971 but retired some eight years ago from practice. He notes that Aisha had a stormy postoperative course, not unusual in some patients after the repair of TF. In his view the reduction of diuretics on 31^st May was not negligent; there is no evidence that a higher dose of diuretics would have prevented the re-accumulation of the effusion. According to the practices at the time, there was no indication to schedule a follow up echocardiogram for one week after 31^st May. Some clinicians might have done a follow up for two weeks but one month was and is standard practice. She was seen on 6^th June just three days before her sudden deterioration. If there had been any concern felt by the consultant on that date, she would have been referred to the RBH, as there were no echocardiogram facilities at PAH. The echocardiogram performed on 31^st May 1989 showed that the effusion had all but resolved, so all appropriate investigations were done on that date. The management of her post- operative management was not in his opinion negligent.

In evidence, he explained that PCE is caused by an accumulation of fluid, blood or fatty tissue around the pericardium and also around both lungs which is called pleural effusion. Heart failure can cause PCE, generally, immediately after surgery. The other cause of PCE, PCS usually occurs weeks or even months after the operation and is not usually associated with heart failure. It is an isolated reaction of the lining of the heart.

In his opinion, Aisha suffered PCS leading to PCE and tamponade. His reason for so saying, is that on discharge on 14^th May, Aisha was on a reasonable dose of diuretics, yet developed the tamponade. When she was seen by Dr Redington on 31^st May, there was no evidence of heart failure. On 6^th June, Aisha was seen by the consultant paediatrician, and she was well. A paediatrician would have observed an enlarged liver or raised jugular pressure had she been suffering from heart failure. The fact she developed the large effusion so quickly, militates against heart failure being the cause.

The decision taken by Dr Redington to reduce the diuretics in the circumstances was reasonable. In his opinion, it would have made no difference to the second incident had she been kept on Frusemide three times a day because the patient had suffered from PCS. Diuretics are not the treatment for PCS. Diuretics would be the treatment for heart failure. With heart failure, the danger of developing Tamponade would be non- existent, as effusion from heart failure does not produce Tamponade. With heart failure, the fluid accumulates more slowly, and the pericardium can dilate to accommodate the fluid.

If the doctor thought that the cause was not heart failure and was PCS as the evidence suggests, then the decision to review in one month was fully acceptable practice then as it would be today. PCE very rarely occurs in the same patient twice with some interval of time in between.

He did not accept the connection between the reduction in dose of diuretics on discharge on 14^th May and the first incident of Tamponade. The reduction was a relatively minor reduction. The increase in diuretics following the first incident was what he would expect, as the Tamponade had caused a temporary impairment of the heart function and it would be appropriate to increase the dose to deal with the general fluid build up which was likely to result. Regarding the second Tamponade, she would not have developed such a huge effusion in such a short period of time if it were due to heart failure and the reduced diuretics. He had never seen such a massive effusion in such a short period of time before.

Cross examined, he said that the Claimant’s post-operative history was a fairly common history after the repair of TF save for the Tamponade. He did not accept the coincidence of the correlation between the reduction in diuretics and the onset of Tamponade. The evidence pointed clearly to PCS in the light of the fact that the patient had suffered Tamponade. He accepted that there was nothing in the notes to indicate that the cause was thought to be PCS, but he said he would not be surprised, as it was the symptoms and treatment you would expect to see in the notes.

In relation to the reduction of the diuretics on 31^st May, in his view the dose was a very small one and not a very effective dose, but that reductions would be made rather than immediate cessation. This was so as not to disturb the patient’s metabolism. It was a matter of clinical opinion as to whether they should have been reduced to once or twice a day.

Even if there had been an accumulation of fluid between the two echo findings on 23^rd and 24^th May, in his view it made no difference as Dr Redington on 31^st May had found that the effusionhad all but resolved.

There was no evidence to suggest any problems with regard to the VSD and the PR. VSD by itself does not indicate that the heart is not working to full capacity. It does not indicate anything about the heart function. There are other means to determine the significance of VSD and whether it is affecting the heart. PR is not connected to VSD. If the registrar had found anything of significance with the VSD and PR, he would have discussed it with the surgeon, because the first question is – does it need a re-operation? There is no evidence of such problems/concerns.

On 31^st May, the patient had two potential problems. These are present in the majority of patients after an operation involving TF. Her history did not take her out of the majority. She had the operation on 2^nd May. She was extubated on 3^rd May which is very early. Most patients in 1989 would be on ventricular support for 2-3 days. She developed heart failure and was treated with diuretics, which is common. The only unusual feature was the PCE with Tamponade, the rest was very straight forward. Tamponade is very rare and reoccurrence is very, very rare indeed. The fact that she suffered one episode of Tamponade, although unusual, did not take the patient out of the usual practice.

The fact that the symptoms for PCS as set out in the text book were not apparent, was not of significance, as the symptoms recorded are those exhibited by mainly by adults and adolescents, and rarely in small children whose symptoms are very different to adults.

He accepted that he did not mention PCS by name in his report nor that it was the cause of the Tamponade. He should have done. He did mention in his report the use of anti-inflammatory agents for PCE and you would not use those for heart failure. Despite not having mentioned PCS in the report, he had taken the view from the very beginning that it was PCS and he is not the only person to think so.

Looking at Dr Redington’s position on 31^st May, knowing that the patient had suffered one Tamponade and given the clinical findings, knowing that a repetition was highly unlikely, sending the patient away with instructions to the parents with review in a month was appropriate.

He repeated his opinion that both incidents of Tamponade were due to PCS. Given the speed of the build-up of the effusions they could not have been due to heart failure. There are only two causes of PCE – heart failure and PCS. If the process had started immediately after 31^st May he would have expected an enlarged liver and raised VP to have been picked up by the paediatrician on 6^th June – it was not. The patient was well. In any event if it were heart failure, it would not develop into Tamponade.

In answer to questions from the court, he said that a combination of heart failure and PCS could exist, but if it had been a combination in this case you would expect to see more signs of heart failure on 6^th June, when she was seen by the consultant. Moreover the rapidity with which it developed militates against heart failure being involved.

The first incidence of Tamponade would have adversely affected the heart but it would be gone in 3-4 days. When she was seen on 31^st May, the reasoning would have been that she had been on diuretics since the operation; a month had passed since the operation; she was not in heart failure and therefore it was time to start reducing the diuretics. The appointment on 31^st May was in fact the standard weekly review post discharge. So far as review was concerned, one doctor may set the review for two weeks, another may set it for one month. There were appropriate instructions given to the family and therefore what he did was appropriate.

It was not uncommon to have a patient in this situation on oxygen for nine days. As they had decided not to evacuate the left side effusion, this fact would have contributed to the decision to give the oxygen.

With PCS, there is isolated fluid in the pericardium and diuretics work on overall fluid in the body and reduce circulating plasma in the body. They would have little effect on the fluid in the pericardium.

Dr Dickinson is a consultant paediatric cardiologist at Leeds General Infirmary. His statement is dated 13^th October 2005. He like others indicates that pleural and pericardial effusions are not uncommon complications of the surgery undergone by the Claimant. PCE was not a problem during the initial admission for surgery between 1^st and 13^th May. At the time of discharge, Aisha was on regular diuretics as one would expect following surgery for TF, irrespective of the presence or absence of pleural or pericardial effusions. The timing of the outpatient review on 31^st May 1989 following discharge on 25^th May was entirely appropriate. His interpretation of the evidence is that the fluid present on 31^st May was substantially less than that present on 24^th May on the Claimants discharge from hospital and not very different to the minimal amount of fluid present in the pericardial space in normal healthy individuals. The risk of recurrence of PCE was low. As there was no clinical evidence of cardiac failure, it was entirely appropriate to reduce the dose of diuretics. Aisha was receiving a high dose for an infant weighing 11 kg. Continuation of the higher dose would carry a significant risk of causing dehydration and electrolyte loss in a patient who was not in cardiac failure. Post-operative PCE in these circumstances are more likely to be the result of PCS rather than cardiac failure. It is likely that the effusion would have developed even with the higher dose of diuretics. It could not have been foreseen as a likely event at 31.5.1989. Dr Dickinson would have made the same follow up arrangements as those made by Dr Redington. They were appropriate and reasonable.

In evidence, He explained that where PCE is caused by heart failure, the fluid accumulates slowly all over the body in a passive way if diuretics are not given. With PCS, fluid is actively secreted into the pericardial space alone, very rarely the pleural space. In his experience most of the patients he sees will not have all of the features of PCS as set out in the American textbook.

The PCE of 21^st May had all the characteristics of PCS as it was confined to the pericardial space and it accumulated very rapidly from discharge from the hospital. This suggests fluid being actively secreted and not cardiac failure. The patient was not in cardiac failure on discharge from hospital. He was very confident that it was a PCS effusion. A day later there is reference to aspirin which is an NSAID which tells him that whoever was dealing with the effusion considered that he was probably dealing with PCS effusion. The reason that NSAID was not started, is because on the echo of 23^rd May there was no accumulation of fluid. There was no reason therefore to use NSAID.

The echo on 24^th May was what he would have expected after tapping of the effusion. His interpretation of the results of the 31^st May echo was that there was very much less fluid on that day than on 24^th May. This can reasonably mean that the process of active secretion had stopped and PCS had come to an end. He had never had a case of PCE reoccurring.

The notes of 31^st May showed a girl who was very well. It was not a picture of a girl in cardiac failure. Children in cardiac failure are usually miserable and lethargic. The residual VSD was not uncommon. As for PR it is pretty well inevitable in any patient undergoing repair to TF that they will have PR in the short term. It would not have any implications for immediate management. If there were residual VSD, which was causing symptoms, the only way to deal with it would be to have another operation. It would be flagged up prominently in the notes. If the VSD had been significant, then the diuretics would not have been reduced. He had absolutely no doubt that the reduction of diuretics at that stage was entirely appropriate.

The period of the one-month review could not be taken in isolation. You have to look at it in the context of the other evidence, in particular the strategy in place to deal with unexpected events. You cannot deal with such unpredictable matters by fixing a date in advance. You give full advice to the family and provide contact numbers in case of problems. This strategy had worked in the case of the first Tamponade. Dr Redington’s approach was reasonable and acceptable management and he was sure that he (Dr Dickinson) would have done the same then and now.

Cross examined, he said that it would not have been important if the effusion had grown between 22^nd and 24^th May. What was important was that it had decreased and all but resolved between 24^th and 31^st May. 0.5cm to 1cm was a sensible amount of fluid to leave when tapping the effusion. Whilst the registrar would want to know what happened between 22^nd and 24^th May, it was crucial to know what happened between 24^th and 31^st. The two echocardiograms on 21^st and 22^nd May would have no prognostic value from the registrar’s perspective on 31^st May.

The development of a large effusion causing Tamponade is very significant, as it can be life threatening and it is unusual only in the sense that it occurs in 1% of cases but it is not an unfamiliar event. There was an extremely small risk that the effusion might enlarge. He had never seen one re-appear before. He had never described the risk as very small and accepted that he had used the phrase “low risk” in his report, but indicated that he had not qualified and explained how low as it is difficult to quantify.

He said that there was a slight difference in emphasis between his report and oral evidence about his view that the PCE was caused by PCS. He accepted that there was no reference to PCS in the medical notes and there were no symptoms of PCS save the PCE. He had many patients who were considered to have PCS who had no other symptoms apart from PCE, in the absence of heart failure. Most senior doctors would recognise that a rapid build up of fluid in the absence of heart failure would be PCS. The fact that they did not write it down in the notes came as no surprise to him.

The cause of the first PCE could not have been heart failure as the effusion developed very rapidly and this speaks of active effusion into the heart as there was a very large amount. Although the notes are limited, when she was discharged on 14^th May there was no evidence of cardiac failure. For those reasons he is confident it was PCS. If PCE had been present on the chest x ray done on the day of discharge, the heart shadow would be enlarged.

The registrar, given the lack of information, would have been in some difficulties about when the effusion started, but he was faced with a child who once Tamponade was resolved, was not in cardiac failure. If she was not in cardiac failure, the subsequent Tamponade could not have been due to cardiac failure and had to be PCS. All cardiac failure carries some signs, some more subtle than others. The first PCE was a huge one, but was not accompanied by a general accumulation of fluid elsewhere in the body. That is not the picture of cardiac failure.

There was no need for the registrar to give more details of the history as the patient was familiar to him and his colleagues and that sort of detail would not be necessary. The notes would all be together in one file and the history could be ascertained from the earlier entries.

The note painted a picture of a standard TF repair. PCE is flagged up as a complication, but that is not that unusual. If the registrar thought there was no valid reason to give the diuretics, then there is no point in running a risk. There is a risk and not a small risk, in giving a patient diuretics, when it is not indicated. A patient not in cardiac failure will respond very very quickly to diuretics and will lose sodium quickly and that can cause problems. If there is no valid reason for giving them, then you should reduce or stop.

15mg of Spironolactone in a 10kg child was a reasonable effective dose for its diuretic effect. Also it would still have had some potassium conserving effect, especially in the light that the Frusemide, which is the potassium loss agent, had been substantially reduced. The combination of the two would still be effective in regulating the fluid balance.

On discharge from the hospital on 14^th May, the patient was on a very adequate therapeutic diuretic dosage. The decision to reduce on the 31^st May should not be judged in the light of the effusion, which developed a few days later. From the registrar’s perspective he could not be expected to predict the re-occurrence or that the arrangements about going to hospital if there was a problem would not work. You cannot bring patients back to the out patient clinic all the time because something unpredictable might happen. The arrangements made by the registrar were appropriate and reasonable.

In response to the court, He said that you expect a stormy post-operative course in this kind of operation. It is common. The fact that she developed pleural effusion is no surprise. PCE is a little more unusual insofar as it was so large and quick and led to Tamponade. The fact of Tamponade did not turn her into a special non-standard case. By 31^st May, the process came to an end and she had returned to the course of recovery that you would expect any other patient with TF to take. He would not have predicted that the effusion would have reoccurred.

The agreed statement of Dr Shinebourne of the Royal Brompton Hospital was read. In 1989 it was standard practice to prescribe diuretics following cardiac surgery and to reduce the dose between 2-4 weeks after discharge. By 21^st May they would normally have been reducing the dose.

An agreed extract from the statement of Dr Natali was read out. He was working at PAH at the material time. He saw the patient on 10^th June and on reviewing her realised that she needed attention. The claimants parents had provided him with a card with contact details of the Rose Ward at the Brompton Hospital. He phoned the number provided and spoke to Dr Birch the registrar in paediatric cardiology.

I have read the three joint statements of the experts and taken them into account. I am not summarising them, as the issues are dealt with in the experts’ reports and their evidence.

Both sides have produced written closing submissions, which have been supplemented by oral submissions. I have taken them all into account. I set out a very brief summary of the thrust of the submissions. There are four main issues: a) whether Dr Redington performed an echocardiogram on 31^st May 1989; b) whether he was negligent to reduce the dose of diuretics on 31^st May 1989; c) causation flowing from the reduction of diuretics; d) that in the light of the reduction of the diuretics he was negligent to set a review for one month instead of seven days.

Before setting out my findings, and in order to put them in context, I deal with my overall assessment of the expert witnesses on whom this case turns. Between them, they were persons of considerable experience; some more than others. They were witnesses who were trying their best to assist the court.

Mr Pozzi is a Paediatric Cardiac Surgeon of some experience. He first trained in paediatric cardiac surgery at Great Ormond St hospital in 1986 -7. At the time of this incident he would have been fairly new to this area. Since he became a consultant paediatric cardiac surgeon in 1992, he has carried out some 300 operations for repair of TF. His post-operative clinical management is limited to discussion and decisions which have surgical implications. Mr Pozzi was an articulate witness. He was quite a good witness generally, but I found his evidence contained certain weaknesses which affect the weight to be attributed it. I set out some of those matters below.

His report is short. It is critical of the decision to delay the correction of TF; the decision not to tap the effusion on the left ventricle; the one month review and the treatment at the RBH on 10^th June. He withdrew his criticism of the last issue during evidence, accepting that he had been too harsh in his criticisms. In this short report, he does not mention or consider Tamponade (even inferentially) at all. He does not go into the possible causes of the Tamponade, the rarity of Tamponade, the fact that Tamponade is almost never caused by heart failure alone, the rarity of recurring PCE. These matters were developed in evidence, cross-examination in particular. His evidence carried a different emphasis to his report and answers in the joint report. For example – he gives the impression in the reports that the cause of the PCE (and it follows as a result the Tamponade) was from heart failure -see in particular answer 17 page 111. In cross examination he said the cause was likely to be PCS together with heart failure. However he was unable to assess the degree in the light of the clinical condition produced by the Tamponade. In the report he says that recurrence of effusions is a possibility and indeed a probability; then in cross examination he said that the occurrence of a large PCE such as in this case is rare. Moreover he went on to concede that multiple PCE was very rare.

I did not find his evidence about the causal effect of diuretics on the PCE in this case to be satisfactory. He says in the joint report (page 118) that there is a “chance” that had the diuretics been maintained, that the Claimant would not have developed such a significant PCE. In another joint report he says that it is more likely than not that if the diuretic dose had been maintained, it could or would have prevented the growth or development of the PCE. In evidence he said that it is probable that it would have prevented the development of the PCE.

I found the alacrity with which he sought refuge in the support of a text book for some of his answers somewhat concerning for someone who is meant to be an expert. On more than one occasion, to justify his evidence that diuretics would have been effective, he cited the textbook as showing that diuretics were used in the treatment of PCE. The textbook does not and nor did he distinguish the situations when it would be more appropriate to use diuretics and/or anti-inflammatories. He was also very keen to rely on the textbook to show that this patient showed none of the signs of PCS as set out in the textbook. In fact neither he nor the textbook distinguished or indicated that in practice, different patients, depending on age for example, may show none or few of the symptoms.

In my judgement, Mr Pozzi’s approach was one very much taken in hindsight. He placed great emphasis on the correlation between the reduction in diuretics on both occasions and the incidents of PCE, seeing a direct relationship between them “ I am convinced there is a connection between the two”. On close analysis this does not stand up; nor is it consistent with the question the court has to ask, which relates to the information in front of Dr Redington on 31^st May 1989 before the second incident of PCE.

In cross examination, Mr Pozzi said this about the test facing the court: “Only a minority of competent doctors would have allowed for a month’s review” In re-examination, Counsel for the Claimant was forced to spell out the test to him, phrase by phrase. In the end he said, “ In my opinion given the history of the child and the degree of diuretic reduction introduced, to leave the review for one month would be unacceptable and I cannot imagine any reason for anyone rationally to want to leave such a long gap with such a significant reduction in the treatment and the next follow on”. The two statements do not sit easily together.

It has been submitted by the Claimant that the evidence of Dr Arnold, although given in a hesitant and uncertain way, making it difficult to get a clear view of his expertise - when analysed, was thoughtful and logical. This is taking a generous approach to his evidence. On the face of it, Dr Arnold is a very experienced man. His report is clear and unlike Mr Pozzi, does deal with the question of Tamponade and its rarity, albeit briefly. However, the report has to be viewed in the light of the approach taken by Dr Arnold at the time, namely that no echocardiogram had been performed by Dr Redington on 31^st May.

His evidence on occasions was muddled and contradictory. He sometimes descended into detail, which in my view, clouded his judgement. His evidence was coloured by his own very cautious “belt and braces” approach, rather than being able to stand back and view the matter dispassionately. Even by the end of his evidence, he was still commenting about his uncertainty that an echocardiogram was done on 31^st May. It could not be the case that Dr Redington was writing in the notes “PCE – resolved” if he had been looking at the echocardiogram of 24^th May, given its findings. This in my view shows an inability of Dr Arnold properly to stand back and evaluate the evidence overall in a commonsense way. Whilst I do not criticise Dr Arnold for having such a cautious approach, his evidence often boiled down to what he personally would do rather than what a body of competent practitioners would or would not do.

In evidence in chief, his view was that the reduction in diuretics did cause the rapid accumulation of PCE. His observations in the joint statement indicated that diuretics “might have” slowed down the growth of the effusion. By the end of cross-examination he was saying that it was impossible to say or predict what effect the diuretics would have had. In the end his evidence boiled down to – I would have, and it wouldn’t have harmed to carry on the diuretics at the higher dose with a review within a week. That is not test.

Mr Stark is a very experienced surgeon in the field of Paediatric Cardiology. He has been a Consultant in that field since 1971. He also has experience of post-operative management as a result of his private practice at his Harley Street Clinic. He is very widely published and has had many other appointments. He has much more experience than Mr Pozzi overall and in particular in relation to the period with which we are concerned. His name informs his approach to this case - stark. Whilst allowing for possibilities, his evidence is very much “black and white”. However, I found that his conclusions were reached with logic and reasoning. There is criticism of him by the Claimant that he never directly referred to PCS in his report. It should be noted that neither did Mr Pozzi and Dr Arnold only mentioned it in passing, although all experts seem to be agreed that PCS played a part in the development of the effusions, the difference between the experts being whether heart failure was also involved. In any event, the inference to be drawn from the content of Mr Stark’s report in the context of this case, was that he was indicating as he did in evidence, that PCS not heart failure was the cause of Tamponade.

Dr Dickinson like Mr Stark is also a man of great experience. He has been a consultant since 1982 and is therefore very familiar with the practices in the period with which we are concerned. I found him to be a very sound witness who gave logical reasons for his opinions. I do not accept the suggestion that he may have been espousing a cause and interpreting the evidence in a way which would fit in with Dr Redington. I do not find the fact that it appeared when cross-examined that his conclusions had become firmer since writing his report, supports the suggestion made. In cross- examination he was being pressed to quantify precisely the assessment of risk, whereas in his report he was taking a broader approach. He was the one expert who in his report explicitly went into the question of PCS in some detail.

I set out my findings below and the witness/es on whose evidence the findings are based. Within my findings, I have attempted to deal with questions set out at the end of the Claimants closing submissions. I will refer to the question number for clarity.

Before setting out the findings, I make the following observations:

I set out the findings below

This was a sad case, with catastrophic consequences for the Claimant. Having said that, the case has to be decided on the evidence and not on sympathy. Overall, I prefer the evidence of the defence experts. The Defence experts are professionals (from two different institutions) with a wealth of experience in this field. The Claimant’s experts have done little to undermine their evidence, let alone cause me to reject it. It follows from what has gone before, that I am not persuaded by the evidence of the Claimant, sufficient to discharge the necessary standard of proof, namely that on the balance of probabilities, the management Dr Redington directed on 31^st May 1989 was management which no responsible body of Senior Registrars in 1989, on those particular facts, would have taken. Judgement is in favour of the defendant.