[2022] UKPC 15
Privy Council Appeal No 0105 of 2018
JUDGMENT
Dr Kong Sheik Achong Low (Appellant)
v
Brian Lezama (Administrator of the Estate of Karen Lezama, Deceased) (Respondent) (Trinidad and Tobago)
From the Court of Appeal of the Republic of Trinidad and Tobago
before
Lord Hodge
Lord Kitchin
Lord Leggatt
Lord Burrows
Dame Nicola Davies
JUDGMENT GIVEN ON
9 May 2022
Heard on 25 and 26 January 2022
Ian L Benjamin SC
Pierre Rudder
(Instructed by Charles Russell Speechlys LLP (London))
Respondent
Theresa Hadad
Patricia Dindyal
(Instructed by Nera Narine (Trinidad))
The facts
The action and pleadings
“The defendants who treated and attended to the deceased at all material times and who knew or ought reasonably to have known that the deceased was a ‘gestational diabetic’ and/or a ‘known bleeder’, were guilty of negligence and failed to use reasonable care, skill and diligence in or about the said treatment, attendance and advice which they gave to the deceased and as a result of which she suffered much pain and distress and ultimately died.
PARTICULARS OF NEGLIGENCE
(1) Failed to heed that the deceased was a ‘known bleeder’ and to request, consult or to have due and/or any regard for the medical record of the deceased;
(2) Failed to do or to have done any blood investigations;
(3) Failed to have any or any sufficient quantity of blood on hand in the event of any need for such blood and particularly so in the instant care as the deceased was a ‘known bleeder’;
(4) Failed to administer any or any sufficient medication to stop the bleeding;
(5) Failed to take urgent and immediate or any reasonable steps to stop the haemorrhage once it had started;
(6) Generally, failed to exercise all due care and diligence in the treatment of the deceased in all circumstances of the case.”
The judgment of Rahim J
(i) the cause of Mrs Lezama’s death was PPH; the judge made no determination as to the possible cause of PPH;
(ii) there was no causal link between Mrs Lezama’s status as a gestational diabetic and the risk of haemorrhaging post-delivery;
(iii) Mrs Lezama was not a “known bleeder”;
(iv) the appellant was neither unreasonable nor negligent in not having blood on hand in anticipation of Mrs Lezama’s delivery;
(v) the appellant ought to have taken on board the representation of Dr Manning-Alleyne that the deceased suffered from PPH and acted consistently with the accepted practice in those cases and as a result, the appellant ought to have requested blood at an earlier stage than he did;
(vi) the appellant was negligent in failing to take urgent or reasonable steps to stop the haemorrhage once it started;
(vii) the appellant was negligent in failing to administer sufficient medication (Syntocinon) to stop the bleeding;
(viii) the appellant ought to have enlisted assistance earlier than when Dr Chang was called;
(ix) the appellant was negligent by failing to ensure better intravenous access and thus, failed to exercise due care and diligence in the treatment of Mrs Lezama;
(x) it was more likely than not that the omission to administer more blood and blood products in a timely fashion resulted in the death of the deceased from PPH.
The judgment of the Court of Appeal
(i) failing to decide whether the appellant did diagnose AFE and whether such a diagnosis was reasonable thereby failing to consider a major part of the appellant’s case;
(ii) holding that Dr Manning-Alleyne’s statement that the deceased was a “known bleeder” should have caused the appellant to act upon it; and
(iii) concluding that the appellant had administered insufficient dosages of Syntocinon which conclusion was not supported by the evidence.
(i) the appellant failed to take urgent and immediate steps to stop the haemorrhage once it started;
(ii) the appellant failed to administer sufficient medication to stop the bleeding; and
(iii) the appellant failed to exercise all due care and diligence in the treatment of Mrs Lezama in all the circumstances of the case.
The Court of Appeal’s review of the evidence
The appellant
“6 April 2003 - Postpartum Note
Patient demised @ 10.10 pm after delivery occurred @ 4.53 pm.
Almost immediately upon delivery of a peeling SB (stillbirth) XY (boy), there was significant bleeding which after repair of a median laceration at the post (posterior) fourchette, the PPH (postpartum haemorrhage) was controlled by IV (intravenous) Syntocinon drip and fundal massage ([about] 500 cc).
However the BP (blood pressure) was shocking (systolic 40-70) and the PR (pulse rate) ↑ (increasing) and thready.
Whole blood obtained and hung, but VS (vital signs) began to deteriorate rapidly.
Dr H Chang was called and when the pulse stopped, EX (external) cardiac massage commenced and bag X ambu (ambu bag).
7.30 pm Upon Dr Chang’s arrival - Defib (defibrillation) applied and meds given. Fluids and hemacel pushed. o/e (on examination) then, pupils fixed and dilated. Heart rate obtained 132, SR tachy and O2 sat 97. Decision to transfer to ICU (Intensive Care Unit) for further management. But patient began to bleed again x̄PV(extremely per vagina) and from all venipuncture sites and orifices.
… HR (heart rate) ↓ (decreasing) and irregular. Unable to restore SR by … attempts to resus (resuscitate) halted @ 9:4 …”
“12. Almost immediately post delivery of the peeling still birth there was significant per vagina bleeding, which I estimated to be approximately 500 cc. The blood was pale, pink, and watery, not bright red, and was not clotting. The fact that the blood was not clotting in my experience usually is an ominous sign indicating a possible intravascular coagulopathy.
13. During delivery one will try to limit the amount of blood loss. The expected average volume of blood loss during delivery is about 200 to 300 cc. When there is about 500 cc or more of blood loss there is the need for even greater care. The definition of post partum hemorrhage is loss of 500 cc or more.
14. As I stated above, the delivery occurred quickly at 4.53 pm and the placenta was delivered immediately after and was complete and spontaneous. Upon realizing that there was this amount of blood loss I began to take steps to arrest it. Syntocinon was already administered at the delivery of the baby in order to achieve contraction of the uterus and therefore to diminish blood loss. On my instructions the nurse administered an additional dose of ten units of Syntocinon intravenously in an attempt to curtail blood loss …
15. At 5.00 pm 20 units of Syntocinon were added to the 300 mls of IV infusion. At 5.15 pm another litre of fluid, ringers lactate, was placed and another 20 units of Syntocinon were placed as well. The reason ringers lactate was being administered was to attempt to expand the intravascular volume of the patient, in other words the volume in the patient’s circulatory system.
16. At 5.15 pm the patient had lost less than an additional 300 cc of blood. At about that time the patient’s blood pressure fell to 41 over 32 which indicated that she was in shock. Any patient going into shock after the loss of 800 cc of blood within 22 minutes is highly atypical, unless there is some other underlying factor. As I said above, the blood was not clotting and when I saw the blood was not clotting, due to my experience, I presumed that I had to be dealing with some sort of consumptive coagulopathy which is something that occurs in the presence of amniotic fluid embolism.
17. Karen Lezama’s blood pressure loss/drop, as outlined above, could not be explained by blood loss. I diagnosed her as having an amniotic fluid embolus. An amniotic fluid embolus occurs when during labour, amniotic fluid, because of the contraction of the uterus, gets squeezed into the vessels of the uterus which then goes into the lungs and creates a significant reaction in the individual. This reaction takes the form of a combination of acute respiratory distress, acute cardiovascular collapse and usually a coagulation defect, which means that the patient has difficulty clotting and is at much greater risk of bleeding. Her blood pressure drop, loss of blood, blood not clotting etc was pathogonomic, which means it is absolutely typical of ‘amniotic fluid embolism’ and its attendant sequelae, or complications that come thereafter. The patient had presented no symptoms prior to delivery to indicate that an amniotic fluid embolus may have occurred. The occurrence of such an event may occur at the actual delivery process itself.
18. An amniotic fluid embolus is devastating with more than 50% mortality. It is a statistical occurrence, it cannot be prevented. I personally have attended at least five cases of this nature of which I am happy to say that all, except, one person, survived. The person who died after delivering did not have any significant bleeding at delivery and after delivery she went back into her bed, sat up, spoke to the nurse and then fell dead.
19. Because of the blood loss I instructed that the patient be also administered a blood substitute. At 5.15 pm the first unit of blood substitute, haemacel, was hung in the IV …
20. The normal and accepted things that one would do to control ‘post partum hemorrhage’ would be to use oxytocics, to massage the uterine fundus, to ensure there are no vaginal lacerations actively bleeding, and to replace blood loss and to give a volume expander. All of which were done.
21. After delivery, the patient’s fundus was being massaged continuously by the nurse. We did succeed in getting the blood pressure back up. At 6.15 pm her blood pressure was recorded as 103/67 and her pulse was 90 bpm. That was reasonable and we were observing the patient still because at this stage, the bleeding was not significant.
22. I also obtained two units of blood for her. The first unit was started at 7.36 pm. This blood was only obtained because of my intervention otherwise we would not be able to get blood at Stanley’s. Stanley’s did not carry any blood units. I was able to obtain these units because I demanded it from St Clair Medical an institution in which I have a relationship.
23. Between 5.15 pm and 9.45 pm the two units of blood were given and seven units of haemacel were given, in addition to volume expanders like ringers lactate and normal saline. There was no shortage of volume expanders and blood substitutes utilized ...”
(Dr Chang in his witness statement recorded that only three units of fluid were given to Mrs Lezama between 5.15pm and 7.30pm.)
“28. The patient was pronounced dead at 10.10 pm, despite my best efforts. On the death certificate I stated the primary cause of death as being disseminated intravascular coagulopathy. I explain this as follows, in the blood stream there are lot of blood factors that are involved in the clotting mechanism. In certain conditions all of these clotting factors are consumed and because you have a depletion in the level of clotting factors, the patient can begin to bleed, be it from, trauma, incisions or spontaneous occurrence. One of the conditions where disseminated intravascular coagulopathy can occur is with an amniotic fluid embolism ... The secondary cause of death was postpartum haemorrhage.”
Mr Brian Lezama (para 24 of Bereaux JA’s judgment)
Dr Manning-Alleyne (paras 25-29 of Bereaux JA’s judgment)
Dr Harold Chang (para 30 of Bereaux JA’s judgment)
“(1) On Sunday 6 April 2003 at around 7.30 pm I received a call from Dr Manning-Alleyne who asked me to come to Stanley’s Nursing Home to assist her friend, a patient, at Stanley’s Nursing Home. Dr Achong Low was the attending obstetrician and had agreed for me to come to assist.
(2) I attended immediately and on my arrival about 15 to 20 minutes later I went into the delivery room. There were a lot of persons in the room and the place and atmosphere was chaotic. There were two drips up but only one was working. The patient who I later found out was Karen Lezama was comatose and had a cardiac arrest. The patient was being resuscitated via external cardiac massage and ventilated manually via Bag/Mask. The patient was also being given blood.
(3) My immediate reaction was to continue to implement the ABC’s of resuscitation ie Airway, Breathing, Circulation. The airway was secured by inserting an endotracheal tube to make ventilation more effective, I also asked for the ECG monitor to be started.
(4) Attention to her Circulation was next. The working diagnosis was post-partum haemorrhage and the aim was to resuscitate her adequately by volume replacement of fluids of nonblood products and blood. Another intravenous access was put up via a central venous catheter and intravenous fluids run in.
(5) She was defibrillated at 8.25 pm and a heart rate of 132/minute and oxygen saturation of 98% was recorded at 8.40 pm.
(6) There were no haemoglobin tests done. The patient had been given three litres of fluid between the hours of 5.15 pm and 7.25 pm and the urine output was only 20 ml. This informs me that the intravenous resuscitation effort was not adequate and the patient was not adequately hydrated. If a patient is adequately hydrated the urine output would be at least 1/2 ml per kilogram per hour ie 35 mls/hour for a 70 kg adult.
(7) After her resuscitation for her cardiac arrest, ventilation and other supportive therapy was continued and a decision was made that the patient had to be taken to an Intensive Care Unit.
(8) Her condition continued to deteriorate and she arrested again and resuscitation efforts were restarted at 9.36 pm by Dr Achong Low. The patient was pronounced dead at 10.10 pm.
(9) I did not make notes of my attendance at Stanley’s Nursing Home but I have refreshed my memory from the notes of the nurse, the doctor and the charts which are in the agreed bundle filed in the Court.”
Dr Singh Bhola (paras 32-40 of Bereaux JA’s judgment)
“33. … Her opinion supported the use of syntocinon or more generally oxytocin as an appropriate drug to manage and stem the haemorrhaging (so did Drs Persad and Jibodh). She deposed that the most common cause of PPH is uterine atony (a soft non-contracted uterus). The use of oxytocic agents such as syntocinon would help to achieve contraction. This too was supported by Drs Persad and Jibodh …
34. … management would involve several steps which had to be undertaken simultaneously. Extra personnel should be called. It would also be necessary to contact the blood bank and the anaesthetist in case surgical intervention was necessary. The patient’s airway and breathing should be assessed. A high concentration of oxygen via a facemask should be administered. The circulation must be evaluated. Intravenous access should also be established to take blood for full blood count, coagulation screen, urea and electrolytes, and crossmatching. It would be necessary to commence infusion of crystalloid solutions such as normal saline or Ringer’s lactate followed by infusion of colloids such as Haemaccel. Where there is a significant amount of blood volume lost, replacement of clotting factors such as fresh frozen plasma, platelet concentrates and cryoprecipitate is necessary. A foley’s catheter should be inserted into the bladder to monitor the urine output. The patient’s condition should be continuously monitored. An assessment of the cause of the bleeding must be made by clinical examination. Management is then directed to the underlying cause. Measures that can be used are simple non-medical interventions such as uterine massage, medical interventions such as use of oxytocic agents and surgical interventions such as hysterectomy. If the source of the bleeding is a coagulation disorder then replacement of the blood and clotting factors is essential.
35. … it is ‘the clinical picture’ that should be the main determinant of the need for blood and blood product transfusion. … The sooner blood and blood products are replaced, the greater the reduction in the risk of organ damage and death.
36. She found the following aspects of the care provided to have been substandard:
- The appellant failed to call for help in a timely manner. Despite the fact that an anaesthetist would have been invaluable, for example, in helping with resuscitation, maintaining the patient’s airway and inserting lines, he was not called until two and a half hours after the delivery.
- The resuscitation was inadequate. Only three litres of fluid were given during the first two hours after delivery. The fact that the patient remained cold, clammy, tachycardic, hypotensive and had little urine output would indicate that fluid replacement was inadequate. Even though seven units of colloids (haemaccel) were eventually given, most of this was after the first two hours. By this time the patient’s condition had deteriorated significantly. Further, insufficient blood was given. Volume expanders (haemaccel) and blood were not given in a timely manner.
- No request was made for clotting factors. She said that ‘if the cause of bleeding is due to a coagulation disorder (lack of clotting factors as in DIC) then replacement of blood and clotting factors is essential’. …
37. Dr Singh-Bhola also listed factors which made Dr Achong Low’s diagnosis of AFE questionable:
(i) There was no evidence of cyanosis (bluish discoloration of the skin from lack of oxygen) which is often seen in patients with AFE.
(ii) The appellant stated that the degree of shock was not in keeping with the amount of blood lost and that the profound hypotension was due to AFE, not massive PPH. If this was the case, the patient’s mucous membranes would have been pink and not pale as was stated in the nurses’ notes. The patient’s pallor would have suggested significant blood loss. The patient was cold, clammy, restless, tachycardic and hypotensive. These are all classic features of hypovolemic shock …
(iii) If the PPH was due to DIC secondary to AFE, the uterus would have been bleeding but well contracted. The measures instituted - continuous administration of oxytocin, rubbing the uterus continually for several hours after delivery - would not have been needed if the PPH was due to DIC secondary to AFE. These measures would have suggested uterine atony, which is the most common cause of PPH. This opinion was supported by the appellant in cross-examination when he conceded that DIC could not be controlled by fundal uterine massage.
38. Dr Singh-Bhola concluded that it would not have been possible, without a post-mortem, to say conclusively whether this was a case of AFE. She opined that while AFE was a possibility, the more likely possibility was that of massive PPH leading to DIC and ultimately death. She stated that PPH was not predictable or avoidable in this case. Once it occurred however it was not managed to a standard that was accepted as proper by the body of medical practitioners skilled in the field of obstetrics and gynaecology.”
Dr Persad (paras 46-51 of Bereaux JA’s judgment)
Dr Jibodh (paras 52-56 of Bereaux JA’s judgment)
Determination of the Court of Appeal
(i) if AFE was the appellant’s working diagnosis at the time of the emergency it would have affected his treatment of the patient;
(ii) it would have been reasonable for the appellant to have diagnosed AFE;
(iii) the continued rubbing of Mrs Lezama’s stomach for four hours suggested that the working diagnosis was PPH caused by an atonic uterus rather than AFE, the appellant’s evidence that he was rubbing “prophylactically” was “unpersuasive”;
(iv) if AFE was operative in the appellant’s mind it would have been made known to Dr Chang given his critical role in the emergency;
(v) it would have been reasonable for the appellant to enter AFE as a cause of death on the death registration certificate; the appellant’s explanation for the omission, namely that he had made a presumptive diagnosis of AFE but as the death certificate was an official document he did not think it appropriate to include a presumptive diagnosis, was “unpersuasive”;
(vi) the appellant’s conclusion that the diagnosis was AFE was reached only after “sober reflection”, he did not make the diagnosis at the time Mrs Lezama was haemorrhaging;
(vii) the appellant refused to request an autopsy, a finding which Bereaux JA stated affected his credibility.
(i) There was a need for urgent and immediate infusion of blood. The appellant ought to have made a request for blood at 4:53 pm immediately upon the manifestation of the haemorrhage. The appellant’s relationship with the St Clair Medical Centre was such that he was able to obtain blood from the facility and thus he had no difficulty obtaining blood for Mrs Lezama.
(ii) The hydration of the patient was inadequate. Only three units of fluid were given during the first two hours after delivery. The clinical signs indicated that fluid replacement was inadequate. Seven units of Haemaccel were eventually given but not as quickly as the condition of Mrs Lezama required. The second litre of Haemaccel was not commenced until 6:40 pm.
(iii) The appellant failed to call for professional assistance in a timely manner. An anaesthetist would have been invaluable in helping with the resuscitation, maintaining the patient’s airway and inserting lines. Dr Chang was not called until two and a half hours after delivery and was requested by Dr Manning-Alleyne rather than the appellant. By the time Dr Chang arrived Mrs Lezama was virtually dead. Further, the appellant refused Dr Kuruvilla’s earlier offer of assistance. An earlier request for professional help would have given Mrs Lezama a greater chance of survival.
(iv) The findings summarised at (i)-(iii) above, belied the appellant’s contention that he diagnosed AFE. The alleged diagnosis of AFE was made quite soon after the commencement of the haemorrhaging, yet no effort was made to obtain blood until 6:40 pm at the earliest. If in fact the appellant had made such a diagnosis, then his failure to move with alacrity to obtain blood and to call for assistance was “even more compelling of negligence”.
(v) If the appellant’s evidence that he had experience of five previous cases of AFE and had been successful in saving four of those patients was true, the appellant ought to have had more than a fair knowledge of how to successfully deal with such a condition.
(vi) In the alternative, even if the appellant did diagnose AFE he was still negligent for the reasons previously stated.
(vii) The insufficient infusion of volume expanders supported the trial judge’s finding of a failure to administer sufficient medication to stop the bleeding and, in any event, was sufficient to support a finding of failure to exercise due care and diligence in the treatment of the deceased in all the circumstances of the case.
(viii) The fact that only one intravenous access was in operation prior to the arrival of Dr Chang contributed to the lack of hydration and was itself evidence of the appellant’s negligence in failing to exercise all due care and diligence in the treatment of the deceased.
“(i) The appellant did not diagnose AFE as the cause of the DIC and PPH at the time of the emergency. His conclusion was more likely arrived at upon reflection after Mrs Lezama’s death …
(ii) The more likely cause of Mrs Lezama’s death was massive PPH brought about by uterine atony leading to DIC and ultimately death. Dr Achong Low’s original endorsement on the death certificate and his continued application of uterine massage for four hours also support this view. His attempts to explain away the death registration entries were unpersuasive. The fact that there was a massive haemorrhage is borne out by Mr Lezama’s account … My own suspicion is that the volume of blood lost by Mrs Lezama is a lot more than the appellant was willing to admit. I accept the evidence of Dr Singh-Bhola set out at paras 37 and 38 above. Further, for the reasons set out at paras 83 to 97, I agree with Dr Singh-Bhola that once PPH occurred, it was not managed to a standard accepted as proper by a body of medical practitioners skilled in the field of obstetrics and gynaecology and it was this that caused Mrs Lezama’s demise.
(iii) But, in the event that I am wrong that Dr Achong Low did not diagnose AFE and he did diagnose AFE, I say that for the same reasons, his treatment of the patient still fell below the Bolam standard. That negligent treatment, on a balance of probabilities, was the cause of the demise of Mrs Lezama and the appellant is liable in damages.”
Grounds of appeal
(a) the appellant ought to have made a request for blood earlier;
(b) the appellant failed to call for help in a timely manner;
(c) the appellant failed to hydrate Mrs Lezama adequately;
(d) the appellant’s negligent treatment was the cause of Mrs Lezama’s death; there is no evidential basis for the finding that the appellant did not diagnose AFE during Mrs Lezama’s haemorrhaging and instead arrived at the conclusion later;
(e) the cause of Mrs Lezama’s death was massive post-partum haemorrhaging brought about by uterine atony leading to disseminated intravascular coagulopathy.
(i) whether the Court of Appeal erred in finding that the appellant’s treatment of Mrs Lezama was below the Bolam standard;
(ii) whether the Court of Appeal erred in finding that the appellant’s treatment of Mrs Lezama caused her death on the application of the test set out in Bolitho v City and Hackney Health Authority [1998] AC 232 (“Bolitho”);
(iii) whether the Court of Appeal erred in finding that the appellant’s treatment of Mrs Lezama caused her death on the application of the Bolitho test;
(iv) whether the Court of Appeal erred in finding that the appellant did not diagnose Mrs Lezama with AFE;
(v) whether the Court of Appeal erred in failing to find that Mrs Lezama died as a result of complications from AFE.
The submissions of the appellant and the respondent
The Board’s view on the pleading point
The Board’s view on negligence and causation
(i) The appellant should have taken steps to source and administer blood and blood products at an earlier stage (paras 85-86).
(ii) Blood was available in cases of emergency from the blood bank and the appellant ought to have made a request for blood at an earlier stage (para 87).
(iii) The appellant failed to call for help in a timely manner (paras 91-92).
(iv) The appellant failed to administer sufficient medication to stop the bleeding (para 94).
(v) There was only one intravenous access in operation which contributed to Mrs Lezama’s lack of hydration (para 95).
(vi) The appellant failed to exercise all due care and diligence in the treatment of Mrs Lezama in all the circumstances of the case (para 94).
(i) AFE is rare. Uterine atony leading to PPH commonly occurs.
(ii) The appellant’s immediate response to the bleeding was to carry out or to instruct others to carry out uterine massage. His later explanation for four hours of uterine massage, namely that it was prophylactic, was rightly accorded little weight by the Court of Appeal.
(iii) The appellant told no one of his opinion that it was AFE during the hours between 5:00 pm and 10.00 pm when he and others were seeking to treat and save the life of Mrs Lezama.
(iv) Dr Chang who arrived at 7.50 pm and thereafter worked with the appellant in attempting to resuscitate Mrs Lezama and provide supportive therapy stated that the “working diagnosis” was PPH. The clinicians worked for some two hours to save the life of Mrs Lezama and a working diagnosis would have been at the clinical core of their efforts. There is no mention of AFE in Dr Chang’s evidence which was compelling and unchallenged.
(v) There is nothing in the appellant’s medical notes made immediately following Mrs Lezama’s death which makes any reference to AFE. On the contrary, they refer to treating PPH. The notes are the closest to a contemporaneous recording of the appellant’s opinion.
(vi) The death certificate is silent as to AFE. The purpose of the death certificate is to record the conclusion of the appropriate medical practitioner as to the cause of death. The appellant’s subsequent explanation that it was only a presumptive diagnosis does not provide an adequate explanation as to why, in this important document, the treating clinician omitted any reference to what he now says was the working diagnosis. It is of note that his own expert, Dr Jibodh, stated that it would have been reasonable to include this diagnosis on the death certificate.
(vii) At para 17 of his witness statement the appellant, in describing AFE states that the “reaction takes the form of a combination of acute respiratory distress, acute cardiovascular collapse and usually coagulation defect, which means that the patient has difficulty clotting and is at much greater risk of bleeding”. Undisputed was the evidence of haemorrhaging, DIC and eventually cardiovascular collapse. The cardiac arrest did not occur until some two hours after the bleeding commenced. The evidence of acute respiratory distress is not mentioned until 7.30 pm, two and a half hours after the bleeding started. It was an observation by Dr Manning-Alleyne who stated that Mrs Lezama was demonstrating “air hunger”, she was “… thrashing. She was thrashing about and she had lost consciousness as such. She was no longer communicative.” It was the opinion of Dr Manning-Alleyne that by 7.30 pm Mrs Lezama had died.
(viii) No signs particular to AFE were present. No signs were present which could not be explained by the presence of uterine atony, leading to PPH and DIC. No factor was present which ruled out uterine atony leading to PPH and DIC.
(ix) The factors identified by Dr Singh Bhola at para 37 of the judgment, which in her opinion made the appellant’s diagnosis of AFE questionable, have not been demonstrated to be unsound or unreasonable.
(x) If the appellant believed that Mrs Lezama was suffering from AFE, given his evidence that he had previously treated five patients for this condition four of whom had survived he, better than many, would have known what to do. That being so, he failed to call for blood or blood products, he did so knowing that his relationship with St Clair’s Medical Centre was such that he could demand blood or blood products.
Conclusion