“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.”
“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 ...” 23. (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.”
“(1) On Sunday6 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.”
“(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.”