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SAFLII Note: Certain personal/private details of parties or witnesses have been redacted from this document in compliance with the law and SAFLII Policy

 “IN THE HIGH COURT OF SOUTH AFRICA”

NORTH WEST DIVISION, MAHIKENG

                                                   CASE NUMBER:  1897/2013

In the matter between:-

M[…] M[…] obo G[…] M[…]                                                                    Plaintiff

And

MEMBER OF THE EXECUTIVE COUNCIL FOR

DEPARTMENT OF HEALTH, NORTH WEST PROVINCE                        Defendant

JUDGMENT

GUTTA J.

A.        INTRODUCTION

[1]        M[…] M[…] (plaintiff) instituted an action in her personal and representative capacity as mother and natural guardian of her son G[…] M[…] (G[…]) against the Member of the Executive Council (MEC) for Health, North West Province(defendant) for breach of an agreement alternatively a duty of care to examine, treat and care for plaintiff and G[…] and to provide  gynaecological and obstetric services with skill, diligence, competence and care reasonably expected of doctors and nursing staff.

[2]        Plaintiff alleged inter alia that:

2.1       defendant’s staff at the Moses Kotane Hospital (MKH):

          2.1.1   failed to diagnose abruptio placentae timeously;

           2.1.2   failed to call a doctor when they diagnosed abruptio placentae in the

early hours of 16 October 2010;

           2.1.3   failed to monitor the condition of plaintiff and the foetus;

           2.1.4   failed to do an emergency caesarean section after diagnosing an

abruptio placentae;

2.2       defendant’s staff at the MKH and the Job Shimankana Tabane Hospital (JSTH), previously Paul Kruger Hospital:

2.2.1   failed to diagnose a foetal heartbeat;

2.2.2   made an incorrect diagnosis of abruptio placentae with intra-uterine death and allowed plaintiff to deliver vaginally.

B.        COMMON CAUSE

[3]        It is common cause that:

(i)            At all relevant times, medical staff involved in the treatment of plaintiff at the MKH and the JSTH were employed by defendant and were acting within the course and scope of their employment;

(ii)          Plaintiff attended the Mogwase Health Centre (the clinic) on 7 October 2010 when she was 38 to 39 weeks pregnant. The clinic referred her to the MKH because of hypertension;

(iii)         At the MKH, she was sent back to the midwife unit and was put on antihypertensive treatment;

(iv)         On 13 October 2010, the clinic again referred her to the MKH and she was admitted;

(v)          On 14 October 2010 at 10:00, plaintiff was induced with cytotec solution that she took seven times every two hours;

(vi)         The last cytotec solution was given to plaintiff at 22:00 on 15 October 2010;

(vii)        Plaintiff was not monitored from 22:00 on 15 October 2010 until 3:00 on 16 October 2010;

(viii)       On 16 October at 3:30 she was seen by a nurse who recorded early signs of labour. The foetal heart rate was 148;

(ix)         At 4:00 on 16 October 2010, the doctor was called. Plaintiff had lost approximately 1liter of blood;

(x)          Plaintiff suffered an abruptio placentae;

(xi)         No foetal heart was seen at the MKH. The presence of a small retroplacental clot was observed;

(xii)        At around 8:00, she was transferred to the JSTH hospital;

(xiii)       An ultra sound was done at the JSTH and no heartbeat could be detected;

(xiv)      Her membranes were ruptured and at 11:10 she was fully dilated and delivered vaginally at 11:20 on 16 October 2010 and G[…] was born;

(xv)       The recorded Apgar scores was 6 at one minute and 9/10 at five minutes; and

(xvi)      Cerebral Palsy (CP) with microcephaly was diagnosed.

C.        ISSUES IN DISPUTE

[4]        What is in dispute is whether the medical staff at the MKH and the JSTH were negligent and whether such negligence caused G[…]’s CP.

D.        PLAINTIFF’S EVIDENCE

[5]        The first witness for plaintiff was Professor Stefanus Cronje (Prof Cronje), an obstetrician and gynaecologist. He obtained a MMED degree from Stellenbosch and the fellowship of obstetrics and gynaecology. He obtained a doctorate from the College of Medicine.  From 1985 to 2011, he was head of Obstetrics and Gynaecology at the University of the Free State. Since 2012 he has only been practicing gynaecology. He published 131 articles nationally and internationally and is the author of four text books. In 2017 he received a lifetime achievement award from South African Society of Obstetrics and Gynaecology.

[6]        He said, Plaintiff was 32 years old and pregnant with her second child. She was significantly overweight and being overweight brings complications. She had a body mass index of 39. More than 35 is classified as morbid obesity. She suffered from mild hypertension which is typical of a patient who is obese. At her last stage of pregnancy she developed mild to moderate hypertension. Hypertension in pregnancy is 140/90 or higher. On 7 October 2010, her blood pressure was 140/90. On 12 October, her pressure was 168/76 and she had protein in her urine. On 13 October her pressure was 138/80. They started induction on 14 October with a drug called cytotec which is used to induce labour and to prevent the abruptio placenta. He said, the indication for induction was correct as the longer you wait the higher the risk.

[7]        He said when a patient is induced she is at a high risk level as you can overstimulate the uterus and if you overstimulate then there is a higher risk of foetal distress. He explained that when the uterus contracts the muscle contracts and it compresses the mother’s blood vessels, so less oxygen means less blood will reach the placenta and less oxygen to the baby. Also with overstimulation, the uterus can also rupture leading to the death of the baby and the mother. Prof Cronje said plaintiff was high risk and should have been delivered at a higher level hospital. There were three factors that put plaintiff at high risk, namely:

a)      She was overweight;

b)      Hypertension and

c)      Induction.

[8]        At 22:00 on 15 October, plaintiff had a show. This is when the cervix opens up and the muscles plug comes out. She was then in true labour as she had:

a)     Enforcement of the cervix.

b)     A show.

c)     Spontaneous rupture.

d)     Painful contradictions.

He differed with Prof Adam who said at 3:30 she had mild contractions with a dilation of tip of finger. He said definition of labour does not have anything to do with dilation. It is effacement, that is the thickness of the cervix. He said there was abnormal bleeding due to the abruptio, it was antepartum haemorrhage and not a show.

[9]       Plaintiff needed the following meticulous monitoring:

a)        the foetal heart rate every 20 minutes;

b)        Plaintiff’s blood pressure hourly;

c)         Measure the number of contractions within 10 minutes and duration of the

  contractions;

d)        take temperature on an hourly basis;

e)        every two to four hours the urine output and fluid intake must be monitored.

[10]      On 16 October at 1:00, plaintiff experienced acute pain. This was the beginning of abruptio placentae which is when the placenta which is attached inside the womb and attached to the baby by the umbilical cord becomes separated. As the placenta separates the amount of oxygen from the mother to the baby decreases and there is bleeding and the bleeding caused a clot between the placenta and uterus. If not separated, the clot will be small. The clot can remain in the uterus with no bleeding. This is a concealed abruptio and there is no bleeding through the vagina. In most cases there is bleeding. This is an anti-partem haemorrhage and an abruptio placentae is one of the main causes of anti-partem haemorrhage. Prof Cronje explained that with the abruptio placentae if –

a)       the separation is 10% - the baby survives.

b)       the separation is 20% - the foetal heart will start being abnormal.

c)       the separation is 30% - the foetus will show abnormalities in the foetal

 heart.

d)        the separation is 40% or more – there is foetal distress which means that

the baby suffers from acute deficiency of oxygen.

[11]      Every person in obstetrics is made aware of the symptoms and if they suspect an abruptio placentae and if there is pain they must determine the heart rate before, during and after contractions. He said from the records, there is no evidence of any monitoring between 12:00, 1:00 and 3:00. This is very serious as plaintiff was a high risk patient. She was overweight and at risk for abruptio. The fact that she was not monitored for 3 hours is negligence. The first inscription of foetal heart of 148 was at 3:30. A vaginal examination was also done and plaintiff was ½ to 1cm dilated. At this stage although the cervix was slightly dilated, plaintiff was in true labour. At 4:30, plaintiff had the abruptio. Her blood pressure was 83/54 and she had 1litre of blood loss. They did an ultra sound and found no foetal heart rate. It is extremely unusual to miss the heart beat on an ultra sound. In his practice of over 40 years, he has never seen a case where the heartbeat was missed. If the ultra sound is done properly and foetal heart is present and you suspect abruptio placenta, the baby must be delivered within 20 – 30 minutes by emergency caesarean section. A hospital that is not equipped for caesarean section should not induce and is grossly negligent if it induces.  Plaintiff should have been referred to a bigger hospital before the induction.

[12]      The fact that the foetal heart rate was not diagnosed at 4:30 had huge implications because an emergency caesarean was necessary. The baby had to be delivered at 5:00. If the baby was delivered, the possibilities are that G[…] would be normal without brain damage because the time period exposed to low oxygen was shorter and the baby would have coped. At 7:00, plaintiff was losing blood through the vagina. A vaginal examination was done. A transfer was arranged due to PV bleeding. She felt foetal movement because the baby was still alive. Plaintiff delivered after 11:00, that is, seven hours after the diagnosis of abruptio. This was too long and many complications could have occurred.

[13]      The implications in the delay from 4:00 to 7:00 is that:

13.1      The placenta can separate more and the baby can die;

13.2      Plaintiff’s blood does not clot anymore and she can bleed from any orifice in the body, for example the nose and anus.

13.3      Due to the massive amount of blood loss, plaintiff can develop organ failure.

13.4      Both mother and baby are at risk. To let the abruptio continue for so long is dangerous for baby and for mother and is substandard obstetrical practice.

[14]      In his report Prof Cronje said “since the baby was not dead and cerebral palsy was diagnosed later on. It is clear that the baby was exposed to insufficient oxygen in the uterus. In retrospect the abruptio was not severe”. He explained that the abruptio took place and the placenta started to separate but it did not separate completely, there was still part of the placenta allocated to the uterine wall through which oxygen was transferred to the baby and that kept the baby alive. But the oxygen was not enough to ensure normal organ activity within the baby and normal brain function. As the oxygen was insufficient, that caused certain cells in the brain to die and the baby developed brain damage. The hospital records state that there was a small retroplacental clot. If it was a large clot, then it is unlikely that G[…] would be alive at the time of birth.

[15]      The Apgar score was 6/10 and 9/10. He said the Apgar score is an inaccurate determination or description of G[…]’s condition at birth. It is well proven in literature that it is not very accurate. With respiration, muscle tone, responsiveness to stimulation and colour, G[…] scored 1 point at birth. If it is normal, you assign 2 points and if it is abnormal, 1 point, if absent 0. For heart rate, G[…] scored 2 points. After five minutes G[…] scored 2 points. But it was overwritten. He said, Apgar score was not grossly abnormal but the first test was on the low side. He said an abruptio over a period of seven hours with a baby that is alive is unusual as most babies would have been dead by this time. It is very dangerous to let an abruptio be present for seven hours. This is also negligent behaviour by the staff. The general policy is that if you think there is an abruptio or when you make the diagnosis you do an emergency caesarean section. This is a very important principle or rule in obstetrics.

[16]      Under cross examination, he confirmed that since 2012 to date he has a limited private practice doing mostly urogynaecology.  He prepared his report in 2013 and pursuant thereto he received new documents which he included in the minutes which deals with the diagnosis of abruptio placenta. When he compiled his report he had the hospital records and plaintiff’s report. He did not consult with plaintiff. He said that morbid obesity is associated with hypertension and an abruptio placenta. Obesity also makes certain diagnosis more difficult to detect for example, the detection of the foetal heartbeat. In his report he states that, “the patient visited the Mogwase Health Center on 7/10 where her pressure was 140/90 which is mild hypertension and that this was indication for induction with the intention of preventing abruptio because she was term, had hypertension and was overweight. She was referred to Moses Kotane hospital and they sent her back to the midwife unit. This was substandard treatment”. He said even if plaintiff’s blood pressure was normal afterwards, plaintiff remained a hypertensive patient and should have been induced as she was overweight and she was on treatment for hypertension.             

[17]      Prof Cronje in his report said the abruptio occurred between 1:00 and 3:00 because plaintiff reported active pain at 1:00 and this is a symptom of abruptio. Plaintiff should have been monitored very closely from point of induction. The other possibility is that the abruptio started at 4:00 and plaintiff only delivered at 11:00 which is gross negligence. In his report he said the crucial time in the course of labour was from 00:00 to 00:30 or 04:00 on 16 October 2010. This is when the abruptio must have been diagnosed followed by action. From 01:00 to 4:00 plaintiff should have been closely monitored, namely; foetal heart, pulse, blood pressure and contractions. He did not accept that at 3:30 there was nothing wrong with plaintiff and at 4:00 there is a full blown abruptio. If plaintiff was examined properly at 3:30 they would have picked up abnormalities, because the abruptio happens over a period of time. If the abruptio was picked up at 4:00, a caesarean section should have been done between 04:00 and 05:00 and the chances were very good that G[…] would not have had brain damage. The nurses made mistakes in their entries, for example when they wrote that the labour started at 11:00 on the 15 October 2018. If the MKH was not equipped to do caesarean sections they should not have induced a high risk patient. It was negligent to induce plaintiff and she should have been referred to Rustenburg before induction. Plaintiff was at risk for abruptio placenta. Everything was not normal when they started inducing her as she was grossly overweight and she had hypertension and was at term which means the later the pregnancy goes the higher the risk of an abruptio placenta.

[18]      The next expert witness was Dr Thomas Ignatius Wessels (Dr Wessels). He received a BMBCH Cum Laude at the University of the Orange Free State. He achieved the MMed in paediatrics in 1985. In 1986 he achieved the Fellow of College of paediatricians from the College of Medicines. From 1987 he worked as a private paediatrician and also worked in two local public hospitals. He did 20 locums as a paediatrician in the Netherlands. He also runs a neonatal unit which manages thousands of births a year in both the private and G[…] child and studied the expert witnesses’ reports of the obstetrician and the radiologist.

[19]      He said in the early morning of 16 October 2010, plaintiff was in a poor clinical condition and a diagnosis of abruptio placenta was made. An ultra-sound examination was done and they could not find a foetal heart. A clinical finding of intrauterine death was made despite the fact that plaintiff told them that she could feel foetal movements. This is critical from a paediatric point of view because the focus should be the baby. All the negative effects from 3:00 that morning until the baby was born at 11:00 had a detrimental effect on the condition of the baby. The baby was ignored from 4:00 “and that is the condition where we as paediatricians receive a baby in a very poor condition and at that stage there is very little you can do to turn around the damage that has already been done. If the baby is not looked after and monitored and decisions made on the well-being of the baby, then it is too late when we receive the baby and that is exactly what happened here”.

[20]     He said from a medical point of view the monitoring was as good as none. There was one foetal rate of 148 and that one foetal heart rate in that period of times means absolutely nothing. Without continuous monitoring you do not know what the condition of the baby is. To say that the baby was in good foetal health at that stage is untrue. That is why they use CTG as this gives you a minute to minute indication of the condition of the foetus. He said the explanation that they could not detect the foetal heart rate because of obesity is absolute nonsense. 50% of the patients in the maternity ward look like plaintiff and there is no problem in detecting the foetal heart rate.

[21]     He said to prove the cause of brain damage and to implicate birth asphyxia, you must prove that the baby had HIE or encephalopathy, that is where the brain was affected by a lack of oxygen. There are no clinical notes available about G[…] and its management for the two weeks that he was in hospital. There is a prescription on the medical chart that G[…] received Phenobarbitone syrup which is an anticonvulsant given to babies who develops fits after birth. Anticonvulsants after birth is one of the critical findings in a baby with neonatal encephalopathy indicating birth asphyxia. G[…] could not suck or swallow and was tube fed for two weeks. On discharge he was not able to swallow and had to be cup fed and often vomited because feeding and swallowing was difficult. This also points to early encephalopathy or damage to the brain. Further the fact that G[….] was in hospital for two full weeks after vaginal delivery means something ‘big’ was wrong with the baby. This is an indicator that he had neonatal encephalopathy.

[22]     Cerebral Palsy (CP) is the clinical expression of damage that occurred to the brain due to a single insult to the brain that caused injury. A normal brain at some point in time experienced an insult which could be hypoxia, trauma, infection etc. At four months the G[…] was diagnosed with CP. The injury to the brain must have happened during pregnancy or labour or immediately after birth up to four months.           The only insult they can identify is the hypoxia that occurred during the last eight hours of the labour process. The eight hours is from the time that there was probable compromise to the intrauterine unborn baby. From the reports up until the time she went into labour there was nothing of note that could have caused injury to the baby.

[23]     The MRI was in keeping with a Hypoxic Ischemic injury of the acute profound nature and there were also features of partial prolonged hypoxic ischemic event. Hypoxia is lack of oxygen and ischemia means lack of perfusion or blood flow through the brain. With acute profound you find dyskinetic type of CP where there is abnormal movements of the muscle while with partial prolonged hypoxia you get spastic CP. G[…] has predominately spastic CP. Therefore it fits in with prolonged partial hypoxia. Acute profound means total lack of oxygen to the whole body and the brain does not get any oxygen. So the most active parts of the brain will experience the worst damage because it needs the most oxygen and energy while in prolonged asphyxia it is not complete obstruction. With partial prolonged, the baby starts experiencing hypoxia and needs more oxygen, there is a reflex in the blood vessels and the blood gets shunted from the non-essential organs, for example, the muscles, liver and the skin. So initially during a partial prolonged phase there is still some oxygen and it is functioning on reserves and when the reserves are used up and something else happens, there are no reserves to manage another acute problem and slowly the brain get less and less oxygen and that is when progressive brain damage sets in. Then the superficial parts of the brain develops problems before the deepest structures of the brain. The insult is the episode that happens which leads to injury. The severity of the insult and the duration of the insult determines the severity of the damage.

[24]     The placenta that is attached to the uterus gets blood and oxygen supply from the uterus. With a contraction it causes pressure on the blood vessels in the uterus and the placenta. It constricts and during that time there is low perfusion and oxygen supply to the baby. That is why the length of the contractions must be monitored so that it does not become too long to cause problems to the baby. With every contraction the oxygen and blood supply to the baby decreases. With the acute episode of abruptio the baby is functioning on reserves and every contraction of the uterus leads to accumulative damage to the baby’s brain. After the acute profound episode, if the baby is delivered it will be fine. After about 20 minutes, progressive brain damage will set in. If the baby is not delivered by 40 to 45 minutes during acute profound asphyxia the baby will die. Dr Wessels said, “if the abruptio placentae was so profound, so acute that it was near terminal event, if you do not act, it is terminal to the baby. If you act immediately you can save the baby. The fact that the abruptio was not the acute profound episode means that the baby would have been much better off if he was delivered at that stage. His initial compromise was aggravated by further compromise due to the labour process taking place. The mother must have had significant contractions at that stage because the baby was expected and it was a big baby. Hence I don’t agree that the abruptio in itself was so bad that it caused the clinical condition. This is further confirmed by the fact that the baby came out crying with not a good but not a bad Apgar. Babies with acute profound are born with a low Apgar. The baby should have been monitored and if there were signs of foetal distress the caesarean should have been done. This would have been immediately after the abruptio”.

[25]     Under cross examination he acknowledged that management of the labour is in the field of the obstetrician except when it affects the baby and relates to the baby’s well-being and condition. In his report he says that plaintiff had a show at 20:00. He said he got this from Prof Cronje’s report but it is immaterial to the case pertaining to the baby and it pertains to obstetrics also the fact that her pains got worse during the night and at some stage she developed vaginal bleeding is also relevant to the management of the labour process. His concerns as a paediatrician starts from the point of the abruptio. If PV bleeding indicates an incident where there is a compromise to the foetal well-being then it is important.

[26]     He said although plaintiff was in active labour during the course of the night, there is only one measurement of the foetal heart rate after induction on 15 October at 22:00. This is poor monitoring of foetal well-being. He said Prof Cronje said there should be foetal monitoring every 10 minutes during active labour process. What is important is how many times was the foetal heart monitored before the delivery of the baby, after the abruptio because you are looking for signs of foetal distress. The pattern of the heart rate is more important than a single recording. It is important to do continuous measurements with the CTG. He did not accept that the heart rate reading between 3:00 and 4:00 of 148 was done using a CTG and explained that a CTG does not give you a single reading. It gives you a continuous reading. You get a single reading with a fetoscope.

[27]     He said there was no clinical notes on the hospital management of G[..] during his stay in the neonatal high care unit. This is important as it describes the condition of the baby, what treatment was given, how he responded, how he improved or deteriorated. He deduced that G[…] experienced HIE or encephalopathy due to birth asphyxia. The discharge and prescription note are available which indicates that G[…] had birth asphyxia. He said it is very suspicious that in birth asphyxia cases, the neonatal records disappear as the notes from birth to discharge are important because that is where the evidence lies. G[…] could not feed and was unable to suck or swallow. He was tube fed for the first two weeks after birth. That is typical of birth asphyxia and HIE. He said the Apgar score is a point of controversy in birth asphyxia cases. The one minute Apgar score was such a degree that G[…]needed active resuscitation which means that he experienced foetal distress immediately before birth. If the five or ten minutes Apgar score is low the baby is more at risk for brain damage. Although G[…] scored better in the five and ten minutes Apgar, he has severe brain damage. This does not correlate with the facts.

[28]     He was questioned about the MRI finding that it was acute. He said the abruptio initiated the hypoxic episode that carried on for eight hours. The abruptio in itself was not the only cause for the damage. It started the process because that is when a part of the placenta became loose from the uterus. That is when G[…] started experiencing hypoxia and asphyxia and this was aggravated by the fact that he was not delivered immediately. If the abruptio was the sole cause of the acute profound event, G[…] would have died after 15 to 20 minutes. The radiologist do not know what happened in labour. In Dr Wessels’ opinion the acute profound event is a combination of the abruptio plus the prolonged period of labour during which contractions took place and caused the chronic asphyxia to the baby. A caesarean section was supposed to be done as soon as the diagnosis of abruptio was made before hypoxic damage sets in. The only point of difference between him and Prof Cooper is that Prof Cooper opines that the abruptio was so severe that it caused the brain damage in the first 30 minutes after the abruptio and the baby developed his complete brain damage at that period and that the seven hours after did not have an impact on G[…]’s brain damage and Dr Wessels disagrees.

[29]     M[…] P[…] M[…], (plaintiff) is 40 years old. In 2010 she was 32 years old. Her highest standard of education is Grade 11. In 2010, she had an 8 year old daughter and was pregnant with G[…]. During her pregnancy, she visited the clinic and she also went once to a private doctor. She said on 7 October 2010, she was at the clinic for a check-up and the midwife gave her a letter saying that she has blood pressure and she should go to the MKH. At the hospital a doctor examined her and she said she does not have blood pressure. She returned to the clinic on 12 October 2010 where the midwife gave her another letter and told her to go to the MKH the next day. On 13 October, she went to MKH where she was admitted.

 [30]    On 15 October, they induced her every 2 hours from10:00 until 22:00. She said before she drank the last induction at 22:00 she went to the toilet and when she wiped herself with a toilet roll she felt that she was becoming wet. She went to the nurses and showed them the toilet roll. She described it as “a gel, some dirtiness”. The nurses told her to throw it in the dustbin and gave her the last induction at 22:00. She said after the last induction she went to the nurses and informed them that she has pains. One sister Modikwe told her to go into the labour ward and place a sheet on top of the bed. She was in pain as she walked back to find a sheet. She walked and stopped because of the pain. She felt pain on her abdomen and stomach going to her waist. She placed the sheet on top of the bed and waited for the nurses. While on the bed, she cannot recall the time she felt like something like water was coming out from her vagina. It was not water but blood. There was no nurse with her. She screamed for the nurses but they did not come. She became dizzy and everything was spinning and she couldn’t remember what happened thereafter. She regained consciousness in the morning.

[31]     She said in the morning she observed that both the night staff and morning staff were present. She said the staff change at 7:00. The doctor was also present. The nurses asked her questions about herself and she answered but not fully as she was not breathing properly and she felt as if she was suffocating. The doctor used a sonar to check the baby. The doctor told her that there is no heart beat and she told the doctor that she felt movement. The doctor told her that her mind was telling her that she was going to have a baby. She observed that the sheet that was full of blood had been replaced with a clean sheet and they washed her.

[32]     She said they called an ambulance and took her to the JSTH. At the JSTH she was attended to by three doctors. One doctor suggested they do a caesarean section and the other said no as she had lost a lot of blood. They did a sonar and told her that they don’t hear the heartbeat. She told them that she can feel movement and that the baby is alive. She told a midwife, Masego that she could feel movements. The midwife became angry and told her not to give her a stroke. G[…] was delivered at 11:20. The nurse only came in when they heard the baby cry.

[33]     She was told to breastfeed G[…] and she tried but he was making choking/gasping sounds. The following day she was discharged. G[…] was kept in the ward for premature babies. He was kept in an incubator and fed with a drip and given oxygen and after three days, G[…] was fed with a feeding tube and was sleeping. He was discharged after three weeks on 4 November 2010. She was not told about his condition. On discharge she was given epilepsy medication for G[….]. She could not breastfeed him and fed him by putting milk into the lid of the bottle and placing it on the mouth so he could drink. G[…] is now 8 years old and cannot walk, sit or speak and has not developed like a normal child.

[34]     Under cross examination, it was put to her that the times she gave in her affidavit differ to the times she gave her attorneys. Her affidavit is signed in March 2017 while the attorney received information before November 2013. In the particulars of claim it is alleged that she had contractions at 19:00. She said that before she took the glass at 20:00 she had labour pains. It was put to her that she told Dr Wessels that she was experiencing contractions at 18:00. She said she started to feel pains after 18:00 and that Dr Wessels misunderstood her. She said after she took the glass of liquid at 18:00 she felt pain and that is when she became aware of what was on the tissue. She showed the nurses what was on the tissue after 18:00. She denied the correctness of the letter of demand and the affidavit for condonation which said that she went to the toilet at 22:00. She reiterated that it was after 18:00. She said the time when she showed the nurse the tissue, she started to feel pain but it was not painful. Hours passed and then she drank the liquid at 22:00 and the pain was stronger and that is when she went to the nurses to report the pain and was sent to the labour room to look for a sheet.

[35]     She was asked to explain the discrepancy between Dr Wessels report where he states that she was seen by a nurse at 23:00 while the letter of demand states that a nurse checked on her at 24:00. She said at 23:00 the nurse did not examine her but picked up a scissor and said “we forgot about you”. At 24:00 she was inside the labour ward and was not seen by a nurse. She said her labour started on 15 October and not 16 October. It was put to her that at 3:30 sister Modikwe conducted a PV (vaginal examination) which she could not have done if she was bleeding. She disputed this. She did not recall being attended to at 4:00 or 4:30. She could only recall when she awoke in the morning and saw both the night and day staff. She was able to recognize the different nurses as she was admitted for 3 days prior to that. She could recall that they called the doctor. She said when she ‘blacked out’, they woke her by slapping her and asking her questions. They called the doctor when they saw that she was bleeding. It is the same doctor that she saw when she regained consciousness and who she told that she could feel the baby move. She did not know why the letter of demand states that no sonar was done a JSTH when it was done. She admitted that she did not have a clear recollection of the times.

[36]     Defendant’s first witness was Dr Susile Parvataneni (Dr Parvataneni). She is a medical doctor who qualified in 1976. She worked in Zambia at a University teaching hospital for 3 years from 1978 to 1984. From 1984 to 1989 she worked at the Zimbabwe Neuro Provincial hospital in the obstetrics and gynaecology departments. She has worked in South Africa since 1990 in the maternity department at the MKH. In 2010 she had 32 years of obstetrics and gynaecology experience. She received training in conducting ultra sounds and performs approximately 12 – 15 ultra sounds daily. She received special awards:

a)      2005 – best performing doctor;

b)      2008 – MEC Excelled awards – First place in the North West Province.

[37]     On 15 October 2010 she was a Grade 3 medical officer at the MKH in the maternity section. Her work included performing normal caesarean sections. She said in complicated cases they refer it to a level 1 hospital. She saw plaintiff on 15 October 2010 when she was full term. Her blood pressure was 115/75 and she had pregnancy induced hypertension. At that stage there was no concern. According to the clinical notes on 15 October 2010, plaintiff was to receive 200mg of cytotec in 200ml water, 3 doses of 20mls and 3 does of 30ml and a last dose of 40ml. On 16 October 2010, she saw plaintiff at 4:00. Her blood pressure was 63/54 which is indicative of very low pressure. Plaintiff had lost blood and was in shock.  Plaintiff’s abdomen was tender She did a sonar using an ultra sound machine and a foetal heart rate was not heard. With the sonar, she observed a retro placental clot. She diagnosed an abruptio placentae and requested a full blood count. She remained with plaintiff from 4:00 to 4:30, because plaintiff’s blood pressure was low and she lost 1litre of blood. She was able to say that plaintiff lost 1 litre of blood as she measured the clots and from the bed linen that were soaked in blood. She resuscitated plaintiff by giving her two drips which included 1 unit of blood which is 500ml. The resuscitation was successful as plaintiff’s blood pressure went up. There was no active bleeding. She said, it is protocol to refer an abruptio placenta in 30 minutes. She contacted Doctor Sereke at Rustenburg hospital and agreed to transfer her to the JSTH. She completed the transfer form at 4:30. The sister calls the ambulance. The JSTH is approximately 45 minutes away. She did not see the patient again after 4:30.

[38]     She said she worked 32 years doing sonars. Her explanation for not detecting the foetal heart is plaintiff’s weight. She said before she used the sonar she first used the foetal scope and could not detect the heartbeat. Had she detected a heartbeat she would have referred plaintiff to a level 2 hospital as she would need a specialist anaesthetist also her blood pressure was low, she was in shock and the placental bleeds a lot during the caesarean which is a risk to the mother’s life. Also a level 1 hospital does not have a blood bank. They only keep a few units for emergency cases. She explained that they are a level 1 district hospital where they manage mild to moderate hypertension in pregnancy where the systolic is 140-159 and the dystolic is 90-109. If the blood pressure is more than 160/110 this is severe hypertension and eclampsia and in terms of their protocol, the patient must be transferred to a level 2 hospital.

[39]     Dr Parvateneni admitted in cross examination that it is a possibility that the induction of a woman with mild to moderate high blood pressure could lead to an abruptio plancentae as well as because in the last two weeks of pregnancy, the placenta is ‘not sufficient enough’ because of the hypertension in pregnancy. They would therefore induce to prevent foetal death. She said they would not allow a lady in the last two weeks of pregnancy to go into spontaneous labour. She admitted that if they have a patient with high blood pressure who is obese and they induce, there is an increased risk of an abruptio and they should be monitored every 4 hourly and once they go into labour, there should be hourly observations of the mother and the foetus, namely, the blood pressure, foetal heart and the contractions. She said by inducing they are initiating the labour and once the labour starts, the patient is not given the cytotec solution. She said the maximum dose is 7 every two hours if the labour does not start. Plaintiff had 7 doses up to 22:00.

[40]     She said she is relying mostly on the clinical notes for recollection of the events. When she saw plaintiff at 4:00, there was only slight bleeding as she had already bled and at 4:30 there was no active bleeding. She explained the method she used in looking for the heartbeat, namely, from the bottom where the baby is present, the head or the leg which is called breach and then the thorax where they test the heart beat and then up to the placenta. She said “because of the abruptio I was looking for placental clot”. She wrote in her note “retroplacentae clot after internal examination was 2cm, the opening of the womb and the cervix is thick”. She explained that this means that there was no effacement. Usually if the lady goes into labour the cervix will become thin and will be soft. Plaintiff’s cervix was still thick which mean that she was not really established in labour.

[41]     Regarding the emergency transfer to Rustenburg, she said sometimes the ambulance may be busy with other patients or it may not be working. Then it may take one and a half to two hours. Dr Parvateneni did not dispute that plaintiff had blanked out and when she came to she was told that her baby is dead and plaintiff told her that she could feel movement. She said it is common that mothers do not accept it immediately. She said at 4:30 there was no active bleeding but at 7:00 there was PV bleeding. There was slight bleeding as the bleeding does not stop completely. There is no mention of how much bleeding. If it was excessive bleeding a doctor would have been called. She said the information contained in the ‘Summary of labour’, namely the date and time of the first stage of labour, that is when the labour starts until the patient is 4cm dilated, (11:00 on 15 October 2010) is incorrect. The document was only signed by one Tlhalefang Dijale, a student and should have been signed by all the nurses who attended plaintiff.

[42]     Sister Modikwe is a professional nurse with qualifications in general nursing and in midwifery, management and administration. She received her nursing training at the George Shimankane Hospital and qualified in 2000 and midwifery at the Mmabatho College of Nursing in 2006. In October 2010 she was a midwife in the maternity ward at the MKH. She has been employed there since 2006.

[43]     She was on night duty on 15 and 16 October 2010. She said the protocol in the ante natal unit when a patient is in the early stage of labour is to monitor her four hourly.

On 15 October, she also signed four entries in respect of plaintiff in the antenatal ward and two entries on the clinical notes when cytotec was administered. She also completed the initial assessment form when labour was reported for the first time at 3:00 on 16 October. On this form she noted pregnancy induced hypertension (PIH). She said she got this from the antenatal care history. Under general examination plaintiff’s blood pressure (PB) was 114/69 and her temperature was 36⁰ C. She looked good. Plaintiff was 9 months and the examination showed that she was close to labour. The head in correspondence with the abdomen was 4/5 which means that the baby “was still high from the bones of the waist”, the pelvis. Her contractions were less than 20 seconds. The foetal weight was estimated at 3.5kg. The foetal heart (FH) was normal. From the vaginal examination, the membranes were intact and there was no blood and the cervix was thick. At 3:00 when she did the PV examination, plaintiff was not bleeding. The pelvic assessment was normal which means that plaintiff will deliver normally. Under risk factors, PIH is noted.  She said PIH is high risk and they anticipate the foetal distress, that is when the baby is having low heart rate or increased heart rate and they anticipate postpartum haemorrhage, that is bleeding after delivery. Based on the assessment at 3:00, there was no cause for concern.

[44]     She noted that at 3:30, plaintiff reported labour and a PV was done which showed that she was in labour and the contractions were mild. Her PB was 114/69 and the FH was 148. This is normal. When asked whether there was a cause for concern at this stage, she replied “yes, apparently there was a concern because this patient was in labour at 3:00 and immediately after 30 minutes she came again crying with the severe pain or what, I don’t remember, because it is a long time ago”. When questioned how she recorded the FH, she replied “I used a foetal scope, I mean the CTG to test the foetal heart rate because this patient apparently was obese and then with the foetal scope, it fails to hear it, … I use the foetal scope I mean the CTG here. Using the CTG I listened to the foetal heart rate, the rhythm and the readings on the foetal, on the monitor and then that’s how I came to write 148 beats per minute”. She said she was certain that she used a CTG and not a foetal scope because plaintiff was obese and it is difficult to detect the foetal heart rate with the foetal scope. She said the foetal heart rate reading correlated with the rhythm of the foetal heart rate on the monitor. A normal foetal heart rate ranges from 160 to 180. When asked to explain, she said it was normal between 140 and 180 beats per minute.

[45]     She called Dr Parvateneni at 4:00 because of the pain that plaintiff reported which didn’t correlate with the cervical dilation. She said she didn’t recall plaintiff at all and was relying on the notes. She said after Dr Parvateneni did the scan she said there was no FH rate and she there is a placentae abruptio and diagnosed antepartum haemorrhage. They estimated the blood loss from the blood they observed and from the soaked linen.  She said she called the ambulance 10 minutes after Dr Parvateneni wrote her entry.

[46]     In cross examination she admitted that she was supposed to write down that she contacted the JST and the ambulance for transfer and because of nine deliveries per night she probably didn’t note that she called the hospital. She denied that the nurse on duty at 7:00 is the one who arranged the transport. She said the nurse got the report from night staff and she only noted that ‘the transport was arranged’ and not that she arranged the transport. She said they have a CTG print out when she took the foetal heart rate at 3:30. She admitted that she did not record that this was a CTG recording. She said the FH rate is recorded even if there is no tracing paper and they correlate it with the beat that they hear and they will pick up if there is foetal distress. She admitted that the CTG without the print out does not give you a single number like 148. She was confident that a CTG was used as she said plaintiff was obese and the FH rate is difficult to detect with the foetal scope. Another reason for using the CTG was that and they could not use the foetal scope because plaintiff was experiencing extreme pain and with a foetal scope you have to go deeper and press the abdomen very hard. She said Dr Parvateneni used the foetal scope as she has more skill.

[47]     Bafedile Sinah Malope, trained as a nurse from 1979 to 1981 and worked at the Moreteletsi hospital. In 1986 she studied midwifery for 2 years at the Kuruman hospital and worked as a midwife at the Moreletsi Hospital until she was transferred to George Shimankane Hospital in 2004. In 2005 she did a diploma in General Nursing. From George Shimankane she was transferred to the MKH where she worked in the maternity until 2014 when she went on pension. In 2010 she was a midwife, a psychiatric nurse and a community science nurse.

[48]     On 15 October 2010 she gave plaintiff cytotec at 18:00. Plaintiff’s BP was 120 and the FH beat was 140 beats per minute. In the clinical notes, she recorded on 16 October 2010 at 7:00 that she “found plaintiff in the labour ward at 7:00 having PV bleeding, PV not done. Transfer arranged due to PV bleeding which commenced at 4:00”. She said before the night staff leaves both the day and night staff go to the ward where the patient is. The midwife gives her a report and examines the patient and writes down, listening to the vitals and foetal heart and will show it to her and she will also confirm same. She said plaintiff was a high risk patient who had been examined by the doctor who found placenta abruptio. She corroborated Sister Modikwe evidence that it was sister Modikwe, who arranged the transfer to the JSTH. She is certain that arrangements were made for transfer because the doctor who is transferring the patient writes on the clinical notes and fills in a transfer form and Sister Modikwe informed her that plaintiff was supposed to be transferred to JSTH. She said in the clinical notes, she wrote FH not heard after she took the foetal scope to listen for the FH.  She said she is good at using the foetal scope as she was taught in 1987. She also said that at the time she took the report with sister Modikwe, sister Modikwe had checked the FH using the CTG and did not find a heartbeat and that is the reason why she used the foetal scope. She said she was the third person to check the FH and did not find it. Plaintiff was obese and this could be the reason why the FH was not heard. She could not recall plaintiff specifically because it was four years ago and she relied on her notes.

[49]     Under cross examination she said they take the patient’s vital signs when the patient is given cytotec. She was directed to the entries made when cytotec was administered and it was put to her that there were only three entries when plaintiff’s vital signs were noted on 15 October 2010. She said when a patient is in labour without bleeding and cytotec is administered they monitor the patient every four hours and the foetal heart every 30 minutes. She said they work hand in hand with the patient who must inform them when the pain start. When a patient is not having labour pains and cytotec is administered, the patient will be monitored every six hours. From the record it is noted on the 15 October 2010, that plaintiff’s BP and FH was monitored at 6:00, 8:00,18:00 and 22:00

[50]     Prof Adam is a professor of Gynaecology and Obstetrics. She is presently the clinical head of Obstetrics and Gynaecology at the Chris Hani Baragwanath hospital and in 2015 – 2016 she was the academic head and prior to that she was in private practice. Professorship was conferred on her in 2015. As clinical head she is responsible for everything that has a clinical outcome and she is also involved in teaching midwives, medical students, nursing students, clinical associates and post graduate students. She has completed several research studies in various topics including causes of stillbirth, babies with hypoxia and obesity in pregnancy. She also did research in emergency caesareans and how long it took from the time they take a decision to do a caesarean section. A further study she conducted is, “The effect of maternal weight on obstetric outcomes” in which study they looked at whether different mothers’ BMI affected maternal outcomes and perinatal outcomes such as stillbirth or easy neonatal deaths and low birth weight babies. She wrote several journals and articles. In one of her presentations they considered whether the induction of labour using misoprostal (cytotec) was associated with poorer outcomes in both the mother and the foetus and whether there was poor outcomes to those babies and if there were, whether it was related to the induction or something else.

[51]     In her report, she states that plaintiff’s BMI was 38.85 which falls under obesity class 2. She said plaintiff was admitted to the MKH which is a level 1 district hospital. There was a formalised referral process which she explained was a pyramid, where at the bottom you have the least complications and at the tip there are fewer patients but the resources and skills are greater than at the bottom. The American College guidelines recommends 50 micrograms. She said the way cytotec was administered to plaintiff was the protocol. She said the protocol is normally 12 doses of misoprostol (cytotec). The JSTH went up to 7 doses. If after 12 doses the mother is still in labour, they rest her for 24 hours and start the misoprostol the next day with up to 7 doses.

[52]     In terms of the intrapartum guidelines for South Africa published in 2012, there are patients, who are referred to district (level 1) hospitals for induction due to hypertension or women who are post-date, that is more than 41 weeks. The maternity case guidelines which was updated in 2015 refer patients upwards from a level 1 hospital if their BMI is 40 and above. It depends on the hospital, for example with the Albert Luthuli hospital in KZN, the criteria is BMI of 50. She said they would induce mothers who are hypertensive at 38 weeks. With a ruptured placenta they would deliver if it was a live baby but do a caesarean if the baby is not alive. She said plaintiff is classified as high risk because she came in with hypertension.  A high risk woman in South Africa is classified as a woman who cannot deliver in a midwife obstetrics unit.

[53]     In her report she states that plaintiff was referred to the hospital on 7 October 2010. She was 38 weeks pregnant and should have been admitted and probably induced on that day. No one can say if she was induced on that day, the outcome would have been different. In her report she states that “a rupture placenta is an accident and whether there are risk factors associated with the condition, it cannot be predicted and therefore not presented”. A ruptured uterus or a cord prolapse is a sentinel event. She said an acute profound event occurs when there is a sentinel event and you have a sudden reduction of oxygen to the baby’s head, then those areas in the foetus which have a higher metabolic rate for example, the brain, are very susceptible to the sudden loss of oxygen.  A prolonged event occurs when there is foetal distress with recurrent decelerations or with ongoing hypoxia and every time there was a contraction you would get a prolonged effect. The prolonged effect would give you other effects not just in the head, but also for example an acute kidney injury.

[54]     Professor Adam stated that at 3:00 on 16 October, Sister Modikwe did an initial assessment and plaintiff’s cervix was dilated by 1cm and the contractions was less than 20 seconds in duration. This means that plaintiff was in the early or latent phase of labour. The early signs of labour are regular painful contractions with any changes in the cervix or with a show which is a mucous plug coming out of the cervix with rupture of membrane. You have to distinguish whether it is the latent phase of labour. If there is a change to the cervix it is the early labour. The appropriate monitoring for a patient in this phase is maternal monitoring every hour and the FH rate every two hours in the latent phase. She explained that an abruption placenta is a premature separation of the placenta from the uterus (maternal circulation). When the placenta separates prematurely there can either be a clot behind the placenta where you will not see the blood loss or you could have the blood coming out which is a haemorrhage where the mother’s health is at risk. In this condition, the mother is in shock and her heart rate goes up and her blood pressure is reduced. With the clot formation there is also blood loss. The body takes up the clotting factors and tries to stop the bleeding and then the bleeding becomes worse. Where you don’t see the blood at all, that is a concealed abruptio. For the baby the separation means a reduction in oxygen and other nutrients. The baby’s heart rate goes down when the mother is challenged and where you get the FH rate going down you call it a bradycardia, which by definition is a heart rate in a baby that is under 100. It is sudden and has an acute effect on the baby.

[55]     Plaintiff was in shock as her BP had dropped and she had lost “large amounts of blood, a significant amount of blood”. It was recorded that she lost 1litre of blood.  She needed resuscitating to get her systolic BP above 90.  The fact that the doctor at the JSTH noted a small retro placenta clot means that most of the bleeding was seen. She said the grading of the abruptio is the level of severity. The most severe is where there is intrauterine death. Grade 2 is where there is some effect on the foetus. She said they gave plaintiff 3 units of FFP (Fresh Frozen Plasma) and 4 units of blood. Based on this she said the rupture was severe, 4 units of blood in 24 hours is almost a replacement of the blood volume and 5 units is a replacement. She said Dr Parvateneni’s response to resuscitate plaintiff was correct, a reading of 93/54, indicates that it is responsive. BP was then appropriate to do a caesarean section. They had to resuscitate plaintiff before they could do a caesarean section.

[56]     Standard protocol once you diagnose an abruptio is to do a caesarean within 30 minutes while resuscitating the mother. Plaintiff’s BP was responsive. The fact that a caesarean was not done within 30 minutes would not have changed the outcome. She said, what we know about abruptio is that even if the caesarean was performed within 25 minutes, it may not have been adequate. Prof Adam disputed that the size of the retro placental clot equates with the outcome. She agreed with Prof Cronje that the abruptio could happen within minutes or over a period of time. If it is concealed you would not see it which could mean that it is happening over some time. It can happen as a sudden event and you can see the amount of bleeding. It was put to her that Prof Cronje said that it is impossible that everything was normal at 3:30 (normal heart beat). She said it is possible that you have a completely normal tracing and then you have an abruption. “Those are accidental things which you cannot see”.

[57]     Prof Adam also states that “once a sentinel event occurs, the risk of perinatal morbidity is high. In these times it is the severity of the sentinel event and not the time to delivery which is the most important factor. When looking at the MRI and the fact that plaintiff’s pressure dropped significantly one can conclude that the sentinel event was a catastrophic event”. In her report, she states that the sentinel event such as the placenta abruption caused the acute profound injury and is responsible for the subsequent neurological damage. She explained that “It was a big bleed that caused plaintiff’s blood pressure to drop. As it was significant to the mother it was significant to the baby…in the light of the MRI without any further effects or an effect of ongoing hypoxia and also the fact that there was no ongoing bleeding in the mother and in the light of the paediatric report. I would say that this was the sentinel event.” In response to Dr Wessels hypothesis or theory that there was a sentinel event just prior to delivery, she said there was no recording of ongoing bleeding. If there was another event, then one would say it was a concealed abruption and with the delivery of the placenta you would see a clot. The blood in this case was a little over a cup. When she looked at the summary of labour from the hospital, she said the total blood loss is 300 ml which is the blood after delivery which is measured. Hence there was no post-partum haemorrhage which is 500ml with a normal delivery. “There was a small retro placental clot which was added to the blood loss to come to 300ml. There certainly was not another abruptio that we could see evidence of”.

[58]     She explained that in obstetrics an emergency caesarean section must be done in 30 minutes. This is endorsed by the American College and the Royal College. But subsequent thereto there have been other studies a 2010 meta-analysis where they found that the outcome for babies may be worse in those babies that were born before 30 minutes. In her report she states that “a caesarean section is indicated when there is a placental abruption and a live baby and when the mother is not imminently deliverable vaginally. This incorrect diagnosis is a major concern and resulted in there being no fatal monitoring”. She said she referred to it as a major concern because it changed the medical management going forward, because if they found a foetal heart they would have done a caesarean section which might not have changed the outcome but it changed the management. She said there had been occasions in her hospital when the FH was not heard when the mother was obese or when the staff were junior and inexperienced. An intern doctor in her hospital cannot make a diagnosis but a conserve doctor (3years) can make a diagnosis.

[59]     She and Dr Cronje prepared a joint minute as there was a difference of opinion. She disagreed with Dr Cronje that because plaintiff was high risk (obese, induction and high blood), there should have been monitoring every 20 minutes. She said there is no different monitoring for patients who are above in terms of time. The timing of monitoring for induction is every 2 hours and every 4 hours. Every 2 hours is a FH and every 4 hours is maternal monitoring and patients who are hypertensive have their BP checked every 4 to 6 hours. She disagreed that the onset of labour was at 22:00 on 15 October 2010. There is also no evidence in the hospital records of acute pain from 22:00. Pain is a sign of labour and not abruptio. The first change in the cervix when plaintiff was in labour with mild contractions was at 3:30. Dr Pavarteneni examination at 4:00 is consistent with sister Madikwe clinical notes at 3:00 that there was no effacement which is the thinning of the cervix. Prof Adam said it is not possible to state that the abruptio started at 01:00.

[60]     Under cross examination she said the reason for induction in a patient who is hypertensive is not to prevent abruptio, it is to prevent the ongoing effects of the hypertension in the mother. The effects of hypertension in the mother is that the mother could become pre eclamptic and would be at risk for a stroke and for renal disease. These are the main reasons for inducing at 38 weeks. She admitted that gestational hypertension is an independent risk factor for placental abruptio but said it is not the reason why they induce mother. Although today at her hospital they induce patients who are hypertensive at 38 weeks. In the intrapartum guidelines for 2012, they induced at 40 weeks. She denied that if plaintiff was induced at 38 weeks, the chances of her getting an abruptio during the labour would be less. She said nobody can say that because an abruptio is an accident.

[61]     She said as plaintiff’s BMI was less than 40 she did not fit into the high risk classification. She agreed that induction can lead to hypertonic contractions with foetal decelerations which if it continues for too long, leads to possible hypoxia of the foetus. She said the high risk factors such as hypertension, obesity and induction do not affect each other separately and they follow the intrapartum guidelines on which protocol to follow which is updated by research and doctors. For obesity she would not be induced only for hypertension. They consider each risk and put the benefits against it separately. The risks are not additive. They have good evidence that they do not affect each other. She denied that because plaintiff was obese and hypertensive that she should have been referred to a higher hospital. She said abruptio occurs in 0, 5% of all women (1 out of 200). She said the hospital is a district hospital and they should have the ability to do a caesarean section. She however denied that they were negligent in inducing plaintiff when they do not have the ability to perform caesarean sections because she said they have guidelines and protocols which allow them to induce hypertensive patients.

[62]     She said, plaintiff’s blood pressure and pulse should have been monitored every two hours after induction. She agreed that according to the medical records there was monitoring of the FH up until 22:00. The next monitoring was at 3:00 or 3:30. Hence there was no monitoring for a period of 5 hours. She reiterated that failure to see the FH with a sonar is unacceptable, but she does not know that the outcome would have been different. In her report she states that “the fact that the baby did not die is an indication that the abruptio was not complete even at the time of birth. The baby was born with a good Apgar”. G[…] had an Apgar of 6 and 9. A 9 Apgar means it has a normal heart rate. G[…]’s heart beat recovers completely.

[63]     Prof Adam admitted that she is assuming that the acute profound damage to the brain of the baby was at the time of the abruptio at 4:00 and that the baby recovered which gave him a normal heart rate 7½ hours later. She agreed that the areas of the brain that is damaged during an acute profound insult is the central core of the brain, referred to as the Brainstem, thalamus and that the damage that you get with partial prolonged damage is to the cortical matter of the brain, the outside of the brain. She said a prolonged insult is a repeated insult and initially the baby can compensate because you have various stages inter alia compensatory mechanisms. Prof Adam was questioned on the article, “Review how long have we got to get the baby out” by Janet Rennie and Lewis Rosenbloom[1]. This article looked at profound or acute damage. She said a normal heart rate of a baby is between 110 and 160 and bradycardia is a low heart rate that is usually below 110 beats per minutes, a severe bradycardia would be down to 80 or more severe down to 60. In the article the authors state that the data supports the evidence provided by the private studies regarding a worse outcome if an acute near – total insult is superimposed on the previous episode of partial hypoxia.

[64]     Prof Adam was questioned on an article written by Joseph Pasternak[2] called “The Syndrome of Acute Near – Total Intrauterine Asphyxia in the Term Infant”. In the article, they describe the radiological features of acute neonatal intrauterine asphyxia and they selected infants who experienced a prolonged persistent bradycardia. The authors said the patients in the study experienced a prolonged persistent bradycardia. The hypoxia ischemic insult occurred at the end of labour and was acute and severe. Dr Adam said in this case the acute insult occurred at 4:00 and plaintiff had the effect, namely the big bleed and there are no indications of late decelerations or even any decelerations before this happened. There is no clinical evidence that there was an abruption before 4:00. She said the Pasternak’s study was a retrospective study and they took patients who had the outcome and they were looking back. It was put to her that in the second phase of labour the mother is 10 centimetres dilated and the contractions usually increase during the first phase until it gets to the second phase and the baby is expelled. She denied that the contractions have the effect that while there is a contraction at the late stage, the arteries are contracted and you have a normal deceleration of heart rate, she said this is speculation. She admitted that during contractions the arteries contract and for a short period of time, the baby gets less oxygen and the baby’s heart beat may go down and it goes up when the contractions passes but said it does not happen in all babies. She said not all normal babies have this pattern of deceleration. There is a way for them to say which ones are normal and which ones are pathological. She denied that during a contraction less oxygen goes to the brain and said it will take oxygen from other organs. She said most foetuses would not have decelerations in the second stage. She accepted that there will be less oxygen going to the brain whether they show a deceleration or not. She said the contractions are always 60 seconds in the second stage. She denied that because the contractions increase in strength and intensity in the second stage that it may result in the baby becoming hypoxic.

[65]     In further cross examination, Prof Adam said the studies done on the animals are not the same as the studies on the humans. Also that the bradycardia is not a total shutdown of oxygen and that one does not know exactly how long the bradycardia was that caused the damage. Prof Adam was referred to the article by Andrew Macnab[3].  The Etiology and Evolution of Foetal Brain Injury, it reads: “in applying this data to the human foetus it is recognised that what occurs most often is a near total profound interruption of brain blood flow and oxygen delivery rather than an event where hypoxia and ischemia are absolutely total in nature”…. “it is generally agreed that approximately 15 minutes and possibly up to 20 minutes of sudden profound asphyxia can be tolerated by the human foetus prior to brain damage…. then after this grace period damage to the brain begins to occur and over a further period of 15 to 20 minutes the extent and severity of the injury becomes progressively more profound over time and beyond this period a human foetus is usually born dead”. Prof Adam said the article is not talking about severe hypoxia but hypoxia generally. The degree of hypoxia is as important as the duration. She was also referred to the article by Volpe[4], the author or editor in chief of the handbook that is used in the wards regarding neonatal neurology. His article is called “Hypoxic – Ischemic Injury in the term infant. Pathophysiology.” She said the picture from the MRI scan is that many cells in the deep core that govern life died. Because the baby was born alive, the basal ganglia and the brainstem were not totally destroyed. She said it is not an all or none phenomenon. You do not get the total necrosis of the entire area. In response to Volpe that “the large majority of insults occur in the late intra uterine inter partum period. This occurs generally from 10 to 46 minutes before delivery”. She said it is “large” and not “all”. Since Volpes article there have been many differences and changes. Pasternak’s work is also late 1990. She said textbooks look at generalities. She referred to Rennie’s article supra where the conclusion for half of the patients was that if the baby is already compromised then the effect of asphyxia would be greater, she said that in those patients that were compromised they had similar effects but you cannot take it that all of the babies who have acute profound event had been compromised prior to that. She said in that study half of them had CTG’s before the event and half did not and Volpe says it’s a generality. She said when interpreting literature from 1985 to 1990 you must also consider the new literature.

[66]     It was put to her that according to Volpe what is likely to occur after a brief repeated hypoxia insult is that it first causes accumulative deleterious effect on the cardio vascular function and that can result in severe blood insult and that is when the damage is done. She replied that Rennie supra says differently, where half of the babies had an acute insult and half of them had abnormal tracings, so half had normal and the other half abnormal. It was in babies who had asphyxia and those babies who did not. It was put to Prof Adam that the data in both Volpe and Rennie supports the evidence in the studies regarding a worse outcome if an acute near total insult is super imposed on previous episodes of partial asphyxia. She reiterated that in the study not all of them had evidence of asphyxia so the near total insult could cause a severe abnormality. With regard to Pasternak’s article, she said retrospective studies are bias and there was also an inclusion criteria for the study, namely seizures with bradycardia at the end of delivery. You can only generalise this information to babies who had seizures and to babies who had bradycardia at the end of their delivery.

[67]     It was put to Prof Adam, that plaintiff’s loss of 1litre of blood is not a significant loss of blood, especially since a pregnant woman has 2 litres more blood than a non-pregnant woman. Prof Adam replied that if you look at the effect on plaintiff, it was a considerable and significant bleed as it caused her to go into shock and it reduced her systolic pressure by 50%. She said a pregnant woman’s blood pressure is slightly lower in pregnancy but in the third semester it goes up. Plaintiff’s BP dropped to half of what was before. This she said is considerable. Her pressure dropped to 63 over 54. The diastolic was 54 which means she is in shock. It fits clinically with a severe abruption namely, a big bleed, hard uterus and one cannot detect the FH with the ultra sound. She said in her minutes when she wrote that “the indications are that this is not a complete abruptio”, she was saying that because the baby survived. If it was a complete abruptio, the baby would not have survived. She admitted that in her minute she did not write that it was a severe abruption.

[68]     It was put to her that having regard to the literature, it is unlikely that the abruption would cause an acute profound or near total asphyxia effect on the foetus given that the small clot was graded as one or two. Prof Adam said the incomplete abruption was severe and there is no second abruption. All the medical staff that examined plaintiff going forward said there was no bleeding and plaintiff’s blood pressure was stable at the JSTH. She said the nurses’ recorded at 7:00 on 16 October 2010, “bloody OSS dilated”. This means that there was a little bit of blood on examination. In obstetrics if there is significant bleeding, the staff will write that there is bleeding and they would call the doctor. She denied the fact that because the baby survived that it does not mean that it was not acute. She said from the literature there are babies that were born who had bradycardia and were delivered even after 45 minutes, those babies were resuscitated and they had good Apgar’s of 6 and 9. She referred to the article by Benjamin Y Huang[5] Hypoxic – Ischemic Brain Injury: Imaging findings from birth to adulthood, where they evaluated 33 cases of placental abruption which found that the babies had poor outcomes with abruption placenta. It was put to Prof Adam that if you have hypoxia, the longer you stay in the mother before you are born, the more likely you are going to have damage. She said that is only if there is ongoing hypoxia and they do not have evidence on the MRI that there are watershed areas of the brain that are affected. What appears on the MRI is that the deep brain matter was affected.

[69]     In her minutes she said “abruption placenta with brad needs to be delivered within 30 minutes to prevent hypoxia”. She said she took 30 minutes as a guideline but subsequently the SA guideline is to deliver within 75 minutes. She said abruptio placenta with bradycardia needs to be delivered before abruptio placenta without bradycardia which needs to be delivered in 60 minutes if you have a live baby. She said they do not know whether the abruptio led to a bradycardia and admitted that she is speculating that it was severe bradycardia which explains why they did not see a foetal heart. She clarified her earlier testimony that all contractions last not for 60 seconds but between 20 and 60 seconds. It was put to her that during contractions there was ongoing hypoxic insults. She said that is speculation as there is no FH rate. There are labours with even 3% insufficient placenta or with placental insufficiency where they induce and they do not have an effect so it is not an all or nothing. So even if there is placental insufficiency, you could have a baby that is fine.

[70]     Prof Adam was questioned whether there is any literature and protocol that suggests that the damage to the foetus brain happens only during the period of the acute abruption. She referred to the article by Tolcher et al[6], Decision to Incision Time and Neonatal Outcomes where 33 cases of placental abruption were evaluated and showed a statistically lower rate of poor neonatal outcomes with shorter decision to delivery intervals. “That the findings in the METO analysis of worsening foetal status within 30 minutes are confounded and that in the clinical situations including …placenta abruption… which result in acute hypoxia because of lack of foetus perfusions expeditions’ delivery is clearly advantageous”. The result is that babies born after 30 minutes do better which is an indication of the severity. She agreed that the quicker you can deliver a baby in the case of an abruptio the better the chances are that they are going to prevent a bradycardia or the duration of the bradycardia but you would not do that if you have an unstable mother as the mother has to be resuscitated before you go to theatre.

[71]     Professor Allan Cooper is a paediatric neonatologist. A paediatric neonatologist is a paediatrician who subspecialised in neonatology, that is new born medicine. He is presently an emeritus professor at the School of Clinical Medicine Facility of Health Sciences at the University of Witwatersrand. He was practicing as a neonatologist prior to 1992. He is an International Paediatric Association representative on the board of the Partnership for Maternal New-born and Child Health. He is also a member of the National Perinatal Morbidity and Mortality Committee from 2008 to 2010, which committee looked at mothers who died with pregnancy related complications and examined the date and makes recommendations. Prof Cooper wrote several articles and journals which were published. In one article which he co-authored it was a study dealing with Apgar scores and asphyxia results and proposals for clinical grading. They considered whether there were factors in the early neonatal period that might predict whether the baby showed signs of neonatal encephalopathy and subsequent brain damage. He was Head of the neonatal division at Chris Hani Baragwanath hospital for eight years and also continued to practice as a neonatologist. He has extensive experience of asphyxiated babies.

[72]     Prof Cooper did not examine G[…] and relied on hospital records and medical reports. He said plaintiff’s BMI was 38.5 which is classified as ‘grossly obese’. He said a normal heart rate for the foetus is between 110 and 160 and at 3:30 on 16 October 2010, the foetal heart rate was 148 per minute. A bradycardia is less than 110 per minute. Plaintiff’s blood pressure of 63/54 at 4:00 was extremely low which could compromise the foetus severely and therefore the management as far as the foetus is concerned is to resuscitate the mother. He said “there was a lot of blood at 4:00 and there was obviously some bleeding into the amniotic cavity as well as in addition to the retro placental clot, it added up to a large amount of bleeding”.

[73]     G[…] was delivered at 11:20. His Apgar were 6 and 10 at one and five minutes. The score of 6 is an intermediate score which does not reflect or suggest severe preceding hypoxia and the fact that the Apgar score was 10 at five minutes is a perfect score which indicates that G[…] responded to oxygen and suction extremely well. This is telling that G[…]’s condition at that stage was not reflective of a severe hypoxic ischemic even within the preceding hour. He referred to the article by Pasternak supra which has a table listing 11 babies with amongst others, uterine rupture. In the first minute, the Apgar scores for 5 babies were two 1 and three 0, which is technically stillbirths. These babies would have required extensive resuscitation. If the heart rate is less than 60, they would commence with ventilation, cardiac massage. Most of the babies required extensive ventilatory support. This is evidenced by the ten minutes Apgar score where the highest score is 7. The majority are 4 and 5. Most still required assisted ventilation. He said that is what one would expect in a preceding severe acute hypoxic ischemic episode. He said when looking at the notes, if correct, there was no obvious sign of neurological abnormality but subsequently there were and this is in keeping with an insult that occurred several hours earlier rather than an hour to delivery. The neurological symptoms are a baby that is not active, with poor tone. They test certain reflexes, primitive reflex for example a grasp reflex, a more reflex and the sucking reflex. Sucking is very important because it requires a certain integrity of the nervous system and the development of convulsions is very common.

[74]     He said G[…]’s weight was 3.6 grams which is above the average weight of 3.25 – 3.33 grams. In in his report, he stated that “abnormalities noted on the First Examinations Tick List were that his colour was blue, the respiratory rate was slow, less than 40/ minutes and he had a hoarse cry. It was stated that he responded well after resuscitation”. He said less than 30 is a slow respiratory rate and he wasn’t sure why they noted it as slow. He said the admission diagnosis was Respiratory Distress Syndrome (RDS). He said this was also surprising because the main symptom with RDS is a rapid respiratory rate above 60 and recession of the chest wall and central cyanosis and a grunting noise on expiration. There are two possible causes for RDS, namely either transient tachypnoea or congenital pneumonia. There was a recording that G[…] had seizures when he was 9 days old. After an asphyxia insult one would need to know when the seizures started.

[75]     Prof Cooper said an acute profound hypoxic ischemic event is where there is near total asphyxia that comes on very rapidly or usually without much in the way of prior warning or precipitated by central event. He said an acute profound event may also follow prolonged partial asphyxia. With the prolonged partial event, the basal ganglia which is the deep grey matter is preserved and the watershed areas which is the cortical area, the white matter is affected. When there is an acute profound event, the brain is unable to preserve blood flow to the deep grey matter or the basal ganglia and those are the ones that gets preferentially affected and can be differentiated on the MRI scan even years later because the areas are damaged very differently. You sometimes see a combination of the two so there are signs of acute profound as well as partial prolonged. The clinical manifestations are different. In the acute profound you get a dystonic or dyschromatic form of CP whereas in partial prolonged it is mainly spastic type of cerebral palsy. With dystonic CP you have abnormal movements and very low muscle tone while with spastic CP the limbs are very stiff and after some time they develop fixed contractures and they have brisk reflexes for example, knee reflexes and the ankle and the reflexes of the upper limbs. You also get a combination of the two. He said spasticity is an injury to the motor system within the brain, high up in the spinal cord. The effect is that muscles are inflexible and stiff. Also the reflexes become exaggerated. Dystonia is another form of CP and is a result of damage to the basal ganglia. There may be some increase or decrease in tone, particularly in the neck and spinal area but it manifests with abnormal movements, namely writhing type of movements. The reflexes are variable. Microcephaly in the context of this case is where there was normal head size which reflect normal brain growth but subsequently the head growth is poor and at a year or two or later the head is below the normal for that age which usually indicates that the insult occurred somewhere around the time of birth because brain growth had been normal up until then.

[76]     Prof Cooper’s opinion of what caused the acute profound event, is “well if one looks at the time of the abruption when it was diagnosed, the mother had extensive blood loss, her blood pressure had dropped dramatically….. the mother has verbalised with Doctor Mogashoa in her report that she could not remember anything after that until the morning which suggests that she had a depressed level of consciousness ….. it is all in keeping with a sudden acute loss of a significant amount blood”. He said her haemoglobin on admission was 10g and when she arrived at the JSTH, her haemoglobin was 8.1g which represent a 25% drop which was a very significant drop when this was about five to six hours after the bleeding. It takes eight-twelve hours to re-establish blood volume so the blood was going to fall further up to eight to twelve hours which would be more than 25% as well as her ongoing blood loss. If there is a loss of a significant amount of blood, the blood vessels to the brain, the heart, the myocardium and the kidneys remain dilated, there is a constriction to all the ‘non-vital organs’ and the uterus is a non-vital organ, so if the mother had a depressed level of consciousness it was an indication of a very severe cardiac output which was confirmed by the blood pressure. So in the period there must have been a severe insult on the foetus and the picture of acute profound injury on the MRI confirms this and “this could not have happened in the hours before delivery because the Apgar scores would have been much lower…. at birth and you would need much more resuscitation abnormal neurological signs very soon after birth”.  He said “regardless of whether this was a very severe abruption or a moderate size the most important thing was the loss of blood which compromised both the mother and the foetus”. He said “any bradycardia in the foetus automatically translates into poor perfusion of all the organs including the brain and a heartrate below 60 is going to be inadequate and if it goes on for any length of time and certainly beyond ten minutes, it is likely that brain damage will start developing”. In the animal model they took seven minutes for the bradycardia.

[77]     In his report he refers to a note on 18 November 2010 which speaks of a moderate birth asphyxia, HIE (Hypoxic Ischaemic Encephalopathy). He said they use the SAUNAT classification which is divided into mild, moderate and severe. He relied on Volpe and said that although the APGAR scores were not suggestive of a severe insult, the information available is indicative of a moderate neonatal encephalopathy which is a sine qua non for attributing later neurological handicap to intrapartum hypoxia ischemic. The MRI also excluded other potential causes. The brain injury was caused by the severe hypoxic ischemic event. The MRI scan is conclusive that hypoxia ischemia occurred around the perinatal period of the term infant.

[78]     In his report he said “The MRI scan was in keeping with hypoxic ischemia injury of the acute profound nature in a term infant however the description of the areas of the brain that were involved it seems also features of partial prolonged hypoxia ischemia event.” He said Dr Ranchod mentioned white matter injury but he was not specific about which areas of white matter were showing abnormalities and also bearing in mind they had found increase tone it made him think that there was a partial prolonged element to the injury as well. However he said subsequently, Dr Taylor described only features of acute profound and the joint minute confirmed that there were no features of partial prolonged and he accepts the findings of the radiologists that the features were in keeping with an acute profound hypoxic ischemic injury in a term infant. This he confirmed in his addendum report.

[79]     Prof Cooper said when the abruptio was diagnosed it would not have been possible to perform an immediate caesarean section because of plaintiff’s condition. She was in shock, had a low blood pressure and had a depressed level of consciousness. An immediate caesarean section would have threatened her life. He said with every teaching and ethical principles, the mother’s life is a priority in this situation even if it means detrimental effects on the baby to save the mother’s life. He said he cannot say when hypoxia damage set in as they did not find a foetal heart. If they picked up the foetal heartrate, one would have access to the pattern that was displaying whether there was evidence of foetal distress and this is a guide of whether hypoxic damage had already set in. He said in the instance of an acute profound injury, one would need to act within 45 minutes but that would not necessarily prevent the brain damage. If one intervened at 30 minutes, the brain damage might have already been there.

[80]     With regard to Dr Wessels theory of the foetus response to contractions, Prof Cooper said where there has been foetal growth restriction like hypertension that has been going on for some time that will affect the growth of the foetus. The foetus has already been affected by poor supply of oxygen and nutrients and is more vulnerable during a normal labour. Prof Cooper said the fact that G[…]did not die within the 40 to 45 minutes period means that there was restoration of the oxygen supply. He said the damage might have already occurred, only those parts of the brain that have not been damaged would be restored to normal function as would the heart muscle and other organs. A foetus may cope with the first 10 minutes and beyond that the foetus will not cope and when you get to 40-45 minutes they would not be coping.

[81]     In his joint minute with Dr Wessels, they both agree that if foetal monitoring had been done during the labour process is it highly likely that signs of foetal distress would have been identified which should have led to an emergency caesarean section. Dr Wessels stated that if proper monitoring and management had taken place during labour, the adverse outcome could have been prevented while Prof Cooper stated that,  “It is not possible at this stage to speculate how much brain damage had already occurred even if an emergency caesarean section was performed”. Prof Cooper said that at the stage when he prepared the joint minutes he was uncertain about how much might have been acute profound and how much was partial prolonged. He said now that he has a definitive report of the MRI scan and Dr Mogashoa’s report that it is predominantly dystonic CP, his opinion is that all or a vast predominance was when plaintiff was in shock.

[82]     Prof Cooper said the Pasternak study describes acute profound hypoxia ischemia injuries occurring during labour and then babies born subsequently and manifesting with neurological signs of HIE and basal ganglia damage. He said it was a retrospective study. The study also found that with partial prolonged you get evidence of other organ damage while in acute profound there is seldom evidence of other organ damage. Further the study found that all the babies were born severely depressed at birth requiring extensive resuscitation. The article also looks at the timing where the shortest duration in their cases was 10 minutes and the longest duration was 46 minutes. This confirms the window period in which damage occurs but beyond 45 or 46 minutes, death ensues. This is if there is ongoing severe bradycardia. In this case the Apgar scores are out of keeping with what is described in the Pasternak table 1 and there was not a lot of resuscitation. He said the Rennie study reviews the animal data and the human data and does not represent any of their own cases. He agreed with the Rennie study that the question whether G[…] was able to recover depends on the extent of the brain damage. He said another important point is that the majority of cases are in the last hour before delivery but that is not necessarily the case as there are some cases that occurred before labour. His opinion of what was the main contribution to the damage is, “The main contribution in my view is what occurred immediately after the abruption where there was major blood loss resulting in maternal shock and inadequate profusion across the placenta to the foetus with an acute profound hypoxia ischemic injury”. When questioned whether other management would have resulted in a different outcome, he said “well I think there was potential as the joint minutes reflected that there could have been an additional partial prolonged injury after that, but the MRI scan does not show evidence of that, so in terms of the acute profound injury I do not think that was preventable at all”.

[83]     In cross examination, Prof Cooper agreed that as a clinician you always look at the clinical manifestations of the patient and then get a MRI scan. He agreed that you may not always see everything on an MRI scan. He said potentially there could have been partial prolonged damage but it was not seen on the MRI scan. He accepted that the fact that it was not observed on the MRI does not mean that it was not there. He said he raised it as a possibility in his report because at that stage he did not have clinical information about the current situation. In his report he reports feeding difficulties, abnormalities of tone and visual problems. Although there are consistent with partial prolonged injury, these signs were picked up in the early months after birth and the changing picture in the first two years made them unreliable but it raised the possibility which is what he considered. He said that based on Dr Mogashoa’s report there must have been an element of partial prolonged injury.

[84]     Prof Cooper said it was highly unlikely that the acute profound damage occurred in the last hour before birth because of the Apgar score, the description of the amount of resuscitation that was required and the admission diagnosis which did not mention birth asphyxia. He disagreed that plaintiff’s description of the baby after birth namely that the baby cried for a short moment, attempted to suckle for a short period and then made grunting noise was irreconcilable with Apgar score of 10. He said it is noted that there was grunting respiration. He said the baby showed signs of respiratory distress and it is quite common for babies to have normal Apgar scores. If they have pulmonary disease, they show signs of respiratory distress. He said he does not think the signs of encephalopathy were there immediately after birth which you would expect if there had been an episode an hour before delivery. He reiterated that the only grunting respiration that was documented was respiratory distress. There was nothing about abnormal neurological signs at that stage. They developed presumably later. One cannot say with any confidence that the grunting respiration was due to acidosis. There are other possibilities. He acknowledged that Apgar scores are not always accurately done but he said the score excludes a baby who requires cardia compressions, prolonged assisted ventilation with bag and mask or tracking. He said whether the scores are out by 1 or 2 points is quite possible but it does not correspond to an Apgar score of 0 or 1 at one minute and less than 5 at five minutes. He was asked “you would not expect a baby with an Apgar score of 10 out of 10 to receive oxygen for 18 days”. He said “I think you are talking about two different things. The first is to change the baby from intrauterine fluid environment to an extra uterine an environment, this involves the Apgar score of 6 is not normal, it required suctioning and oxygen was given appropriately. The Apgar score of 9 or 10 is normal and did not require ongoing oxygen”. He said there may be a reason for oxygen being needed later on if the baby has a respiratory disease or neurological problems such as HIE. He accepted that the oxygen that was given for 18 days was because of a neurological problem. He reiterated that it does not do anything to disprove what the recorded Apgar scores are.

[85]     He said the first examination tick list is the initial physical assessment and it had nothing to do with the Apgar score at all. It does not change the Apgar score. He agreed that on the first examination tick list, it reflected that the baby was blue which is part of respiratory distress. The respiratory rate was below 40 but he said they regard 30 as the lower limit of normal. He said it does not make sense as one would expect with respiratory distress for there to be a rapid respiratory rate. Although it was not noted he agreed that there was grunting sounds and the cry was hoarse. He said after resuscitation there were still some abnormal signs but in the last column, it reads that the reflexes are normal. These are primitive reflexes and they would not be normal if there are already severe signs of encephalopathy. He accepted that subsequently the reflexes were not normal. It was put to him that there were signs of encephalopathy that also manifested in seizure activity which was caused by a severe hypoxic ischemic injury to the brain and you have a profile of acute profound injury which normally occurs 10-44 minutes before birth and that the injury on the MRI was caused in the last period of 10-44 minutes according to literature. Prof Cooper replied that “No, I could not disagree more strongly. The condition of the baby at birth, the Apgar scores and the amount of resuscitation makes it highly, highly unlikely. I never say impossible because it is highly, highly unlikely”.

[86]     It was put to him that resuscitation carried on for a long time and oxygen was given for a very long time. Prof Cooper said that is not resuscitation but it is ongoing management of a condition and it has nothing to do with resuscitation. Resuscitation is done immediately after birth. The outcome of the resuscitation was good because the 10 minutes Apgar score was 10 or 9. Subsequently we are seeing signs of brain damage and we are now looking at when that might have occurred. He said, in his opinion it did not occur in the first hour prior to delivery. He said Volpe article refers to studies in the lamb which “indicate that the severe terminal insult that results in injury to deep nuclear structures especially may be likely to occur after brief, repeated hypoxic ischemic insults first cause a culmination deleterious effect on cardiovascular function that presumably then can result in a severe late insult”. He said this is the exception where there is repeated insults. He referred to the Rennie article supra which refers to the Meyer’s[7]7article study monkeys were studied where there were all single prolonged acute profound hypoxia and not repeated episodes. He said all the animals’ models and the human descriptions do not have repeated short episodes but have one prolonged episode. There is no evidence that the sheep example occurred in a human situation.

[87]     Prof Cooper was asked whether there could have been damage after the acute profound insult, he said not according to the MRI but Dr Mogashoa reported some features consistent with partial prolonged. He said he does not think that happened before the rupture and said it is possible that aspect of the injury occurred after the acute profound injury. He said the foetus was totally unmonitored, it had already been compromised, “so it is a possibility or perhaps even a probability, because the partial prolonged could not have happened before the rupture”. He admitted that there is no literature on this but said everyone accepts that “the mechanism and timing is really a black box, but looking logically what the baby’s condition was at birth, the acute profound episode could not have occurred in the hour prior to delivery and therefore logically the only time it could have occurred was at the time of abruption”.

[88]     The article, ‘The Apgar Score’ by the American College of Obstetricians and Gynaecologist and American Academy of Paediatrics[8] refers to the limitations of the Apgar score. They said that the Apgar score should not be used to implicate in asphyxia or to be used for long term prognosis. They also say that if the Apgar score at five minutes is 7 or greater, it is unlikely that hypoxia ischemia caused the neonatal encephalopathy. In re-examination, Prof Cooper reiterated that the MRI is conclusive that there is an acute profound event. However, he accepts that the MRI has limitation and one cannot rule out the fact that there was some evidence of partial prolonged due to partial prolonged insults.  His concludes that the acute profound insult could only have happened during the period between 4:00 and 4:45.

[89]     He said both Rennie and Volpe say that it is not always possible to time the damaging event with precision. He said the initiation of resuscitation at least by 40 – 45 minutes resulted in the reversal of the bradycardia but obviously left severe brain damage. He said with shock the important thing is the re-establishment of adequate vital organ profusion. That does not depend on haemoglobin. The blood pressure is more important. The fact that plaintiff’s pressure improved at 4:30 is the beginning of a successful resuscitation. He reiterated that the cause of the profound event is the acute blood loss suffered by plaintiff at 4:00 resulting in shock, hypertension and low blood pressure an inadequate profusion of her vital organs and of the foetus. In reply to the Court’s question whether if there was a partial prolonged injury did it contribute in any way to the baby’s condition, he said that he would have difficulty in assigning a number because Doctor Mogashoa says it was predominantly dystonic CP with elements of spasticity. He said it certainly would have contributed but it was a relatively small component of the overall damage.

[90]     Dr VR Mogashoa is the Head of Department of Paediatrics at the Military Hospital in Pretoria. She is registered as a paediatric neurologist which is a paediatrician who specialises in neurology. She works with children with disability and epilepsy, CP and all disorders of the brain. She has a limited private practice at Life Groenkloof Hospital in Pretoria. She brought out two reports dated 27 July 2018 and 19 October 2018. She said her initial report was a provisional report which was rushed as defendant requested an urgent report for trial and it was done without consulting with plaintiff and G[…]. It was based on the records that were emailed to her. She subsequently interviewed plaintiff and examined G[…] and produced her final report. She consulted with plaintiff in her mother tongue, Tswana as her evidence was taken through an interpreter. She said there was some inconsistency in the days given by plaintiff and the medical records for example, according to plaintiff a decision was made by the doctor to start induction of labour on 15 October 2010 while the record states the instruction to start induction was 14 October 2010.

[91]     At the trial, Dr Mogashoa referred to her written notes which she recorded when she consulted with plaintiff. Her notes read:

·   “around 18:00 went to bathroom, had thick discharge, not sure if blood. Shown to nurses.

·   pain from ±18:00.

·   never checked from time started induction.

·  last dose taken at 22:00 thereafter reported to nurses pain intensity, did not check her. Showed her where to get linen, instructed her to make own bed.

·  Felt fluid on genitalia, blood, no recollection from then till morning….”.  

Dr Mogashoa said that plaintiff’s last recollection after the massive gush of blood, was when she awoke at the JST hospital. In her written notes she states that “the baby cried a bit at birth, she was given to mom who put him on the breast. He started sucking but then developed abnormal rolling movements of the eyes. Ms M[…] called nurses who took the baby to the nursery”. Under Neonatal History, she states,

·   “according to Ms M[…] she saw the baby on 16 October 2010.

·         baby was nursed in an incubator.

·         he was on supplemental oxygen and was fed through a nasogastric tube.

·         The baby did not have any seizures but was always sleeping according to mom.

·         The baby was discharged on 4 November 2010.

·         He was given Phenobarbitone on discharge”.

[92]      She examined G[…]at age 7 years and 11 months. She said there was marked drooling of saliva which is what you usually get with extrapyramidal signs. It is a sign of dystonia most of the time and his breathing was abnormal because of abnormal control of his muscles. He had very noising breathing which you get when children have marked truncal hypertonia because all functions in the body are controlled by the brain and the areas of the brain controlling the functions, such as sucking, swallowing, sight are impaired. She said you evaluate for central tone which is control of the axial muscles like the neck and the trunk. G[…] had signs of truncal or axial tone “marked truncal hypertonia” and that usually signals that the problems are in the brain. There was obvious microcephaly, as the head is very small. There was rigidity of all limbs. She said, “When you put him down he becomes rigid, almost like a board, he becomes very stiff and rigid. But in actual fact when the child relaxes then that rigidity almost goes away and it becomes a bit of a variable tone. …when a child is spastic but it is a variable form of spasticity or rigidity that speaks to a basal ganglia sign then if a child is permanently spastic even in their sleep. The variable tone and that variable rigidity is actually a sign of more basal ganglia than a sign of pure, pure spasticity and it is important to differentiate the two because when one is doing a physical examination you are also trying to establish where is the lesion and what type of lesion you are dealing with in this patient…Variable tone when he is more relaxed speaks more to basal ganglia involvement than cortical spinal traits”. She noted in her report that the “Basal ganglia signs were rigidity and dystonia of the hands and feet… His muscular skeletal abnormalities were contractures of the hips and archilles tendons bilaterally”. She explained that anything that results in reduced movement will result in contractures. In this case what makes G[…] prone to contractures is that he is not moving much and the fact that there is rigidity and abnormal contraction and relaxation because of lack of proper coordinated control by the brain.

[93]      Under summary of physical findings in her report, she said she concluded that “he has microcephally, mixed cerebral palsy predominantly dystonic, strabismus with cortical visual impairment uncontrolled epilepsy and lower limb contractures”. With regards to her finding of ‘mixed cerebral palsy predominantly dystonic’ she explained that there are different types of CP. With spastic CP you get increased tone. G[…] tone was increased but the tone was variable and not consistent. At times the tone is floppy and at times it feels spastic. She said there are two big group of muscles, namely the skeletal tone which is the tone in the muscles of the limbs and the exhale tone which tone of the axis, namely in the trunk and the neck. Children who have dyskinetic CP or dystonic CP such as G[…] have low tone of the axial muscles whereas tone in the spastic CP is usually elevated in the axial muscles. “G[…] tone was not strictly spastic but at times he was spastic but at times he felt a bit floppy, it was variable and that is more for dystonia but he did not have brisk reflexes which is also for spasticity. That is why it is a mixed CP because he has features of spasticity and he also has features of dystonia which falls under dystonic CP”. She said she concluded that it was ‘predominantly dystonic’ based on the fact that he has more variable tone with rigidity which is more for dyskinetic CP. All these abnormal movements stem from basal ganglia involvement.

[94]      She explained that under the classification of CP, there is spastic CP which has different groups depending on the limbs which are affected for example spastic hemiplegic where half the body is involved or spastic quadriplegia in which all four limbs are affected. She said “most of the time you get features of spastic with dyskinetic and that is the reason why one has to decide clinically what it is that is predominant that you see”. Different causes of CP will give you different types of CP. She said if the injury occurs at term then depending on the type of injury you will get either mixed CP or spastic quadriplegic or dyskinetic. She said when doing a physical examination you determine the type of CP it is clinically, what your clinical findings are and whether the clinical findings fit with the history that was obtained and with the MRI. In her report, under the heading ‘what caused G[…] neurological impairment’, she put together the history, the physical examination, the clinical records and the radiology to formulate a conclusion. She said radiology is a different speciality of medicine and all clinicians work together with radiologists. They depend on the radiologists to give them clinical information and to explain the clinical information so that they can come up with a diagnosis.

[95]     She said the definition of neonatal encephalopathy by the American College of Obstetricians and Gynaecologists (ACOG) is, “a clinically defined syndrome of disturbed neurologic function in the earliest days of life in an infant born at or beyond 35 weeks of gestation manifested by subnormal level of consciousness or seizures and often accompanied by difficulty with initiating and maintaining respiration”. She used the ACOG statement to look at G[…]’s clinical status in the neonatal, during birth and at birth in the neonatal period and the subsequent outcome, to determine if he fits the criteria for intrapartum hypoxia. Dr Mogashoa said ACOG sets out certain requirements before you can diagnose encephalopathy on hypoxic ischemic injury, that the cause of the encephalopathy in the baby is secondary to intrapartum hypoxia. ACOG looks at:

1)   the condition of the baby at birth and refers to the Apgar scores.

2)   the condition of the baby in the neonatal period that speaks to neonatal encephalopathy and the staging.

3)   is there muscle system involvement is imaging done in the neonatal period.

4)  was there a sentinel event.

[96]      ACOG says look for risk factors during the labour, called proximal risk factors and then look at how the labour was managed. She said ACOG helps one to conclude when the insult occurred. According to ACOG 2014 an Apgar score less than 5 at five and at ten minutes is supportive of intrapartum hypoxia. The Apgar score remain helpful to determine what the condition of the child was at birth, the need for resuscitation and the response to resuscitation and as one goes on with the resuscitation, the lower the Apgar remains, the more likely the chance of morbidity. She said G[…]’s Apgar were 6 and 9 or 10. They were not below 5 at five and ten minutes but he did need resuscitation. According to ACOG if one does neuro imaging in the neonatal period and one sees features of hypoxia then one can say that hypoxia occurred in the intrapartum period and they elaborate with the use of MRI and sonars. ACOG also says there must be a presence of multi system organ failure. On 23 October, the kidney’s function test was normal. In this case some information required by ACOG is not available for example, blood results or blood gas. It is stated in ACOG 2014 that if there is a documented sentinel event then that points to hypoxic secondary to intrapartum hypoxia.

[97]      She said she uses the SARNAT stages while others use Volpe or Thompson. SARNAT graded the severity of neonatal encephalopathy in infants with perinatal asphyxia into 3 stages of hypoxic ischemic encephalopathy (HIE). She concluded that based on both the history from plaintiff and the clinical records, that G[…] had features of moderate HIE stage 2 because he had seizures in the prolonged hospital stay and depressed reflexes and a depressed level of consciousness in the neonatal period. She said this assessment would be done in the neonatal period and not at birth.  One considers what else could have caused the encephalopathy. She said G[…]’s clinical picture was not in keeping with genetic or metabolic disorders or damage caused by meningitis. She said although stroke is another common cause of a depressed baby in the neonatal period, the MRI was not in keeping with a stroke. She said his Apgar was 6 and 9 or 10 at one and five minutes respectively, he had shallow breathing at birth and was cyanosed, he was resuscitated and this suggest there may have been HIE.

[98]      In her report she deals with when the insult occurred. The first stage is the antepartum stage, that is before the onset of labour. She said problems identified during her pregnancy was pregnancy induced hypertension and she had obesity. With the intrapartum period, that is, during labour, she said signs of labour were noted on 16 October at 3:30, there was ‘show’, cervix admitted a tip of the finger. At 4:00, the doctor was called, plaintiff was in hypovolemic shock, her blood pressure was 63/54 she had lost 1 litre of blood vaginally and she was pale, the abdomen was tender on palpitation. A diagnosis of abruptio placenta was made. In respect of the postpartum period, that is, after birth she noted inter alia that G[…] had normal growth parameters at birth, that is in respect of the weight, length and head circumference. G[…]was resuscitated at birth, his airways suctioned and oxygen administered by mask. At birth G[…] was blue in colour and had slow grunting respiration. He had HIE in the neonatal period. He had neonatal seizures and an HIE score of 12. She opined that the G[…]’s neurological problems was intrapartum. She said the imaging findings according to both Dr Ranchod and Dr Tracey were features of acute profound hypoxia and there were no features of partial prolonged injury.

[99]      In her report under the heading “what caused G[…]’s neurological impairment”, she said the following:

·           “G[…] impairments are secondary to hypoxic brain injury.

·           Identifiable distal risk factors are material obesity and hypertension.

·           Identifiable proximal factors are abruptio placenta”.

She said distal means far away from the labour process. Hypertension and obesity are a risk factors for intrapartum hypoxia. She said she looked at everything because ACOG says do not just focus on the labour. The proximal risk factors are those close to the time of delivery. In this case an identifiable problem occurred, namely the sentinel event that occurred with the abruption placenta and subsequent hypovolemic shock. How the labour period was managed is the domain of the obstetricians. In her summary she states inter alia that “I am of the opinion that G[…]’s impairments are secondary to intrapartum hypoxia due to acute profound hypoxia from a sentinel event which is abruptio placental. At the time when the sentinel event was diagnosed, Ms M[…] was in hypovolemic shock requiring resuscitation with volume expanders and blood. I am of the opinion that the injury to G[…] brain occurred during the time of the diagnosis of the sentinel event. She said G[…]’s neurological impairment, fits in with the most severe motor impairment, GMFCS 5. The scale she used to measure looks at the gross motor function of G[…] such as mobility, head control, sitting and independent mobility. He fits in with GMFCS 5 because he has poor control of his neck. He will need a mobility device for all mobility requirements.

[100]   With regards the Apgar score, Dr Mogashoa said that at one minute, the sister assigned a 2 to the baby’s heart rate. She said they were happy that the baby was not bradycardia. She said bradycardia would be a low pulse rate of less than 100. She said as the baby’s respiration was not adequate, they gave him 1 and the baby had some reflection of the extremities and they assigned 1 for all the other features except the heart rate which was 2 and the total Apgar was 6 at one minute and at five minutes the Apgar was 9. She said the Apgar “tallies a little bit with what mom said on her history that the baby cried a little bit”. Dr Mogashoa referred to the pitfalls of Apgar scoring and said that is the reason why one cannot just look at the Apgar score and say there was no HIE simply because the Apgar’s were above 5 in one and five minutes. She said from the history that plaintiff gave and from the Apgar scores the baby did not need a lot of resuscitation at birth. “This is not an Apgar score of zero or one or something dramatic like that, the fact that the sisters even gave the baby to the mom and she said the baby cried a little but at birth says this baby was not bad at birth. The baby was depressed but not grossly depressed. ….What these Apgar’s tell me is that this hypoxic injury was not in the last 30 -45 minutes of birth because when we look at our bundles we know that babies who are hypoxic, especially acute profound hypoxic occurred in the last 30 minutes, those babies are going to be grossly depressed”.

[101]   She opined that because of the predominance of dystonia that an acute profound abrupt insult occurred at the time when plaintiff needed resuscitation. Plaintiff had sudden bleeding, she was in hypovolemic shock and there is definitely a sentinel event. With the sentinel event when plaintiff was in hypovolemic shock that is when the insult to the baby’s brain occurred because the mother cannot be in shock and have a baby that is spared and completely normal. The baby’s circulation is dependent on the mother’s circulation and at the time of diagnosis the mother had no circulation and the doctors had to intervene. For an acute profound insult to occur there is a sudden loss of BP to the baby and with that sudden loss closer to delivery the baby will be more depressed and this is a baby who was not depressed based on the history and the Apgar scores. She referred to the article by Pasternak where the studies show the scores of baby’s who had acute profound or total asphyxia close to the time of delivery and the babies were extremely depressed. None of them had Apgar’s of more than 5 at five minutes and the acute profound insults were close to the time of delivery. Had G[…]’s acute profound insult occurred close to the time of delivery, he would have been extremely depressed and he was not extremely depressed. He needed suctioning and oxygen by mask and he was given a respiratory stimulant. But he did not need chest compressions which is given to a baby who had bradycardia (a pulse rate of less than 100).

[102]   Dr Mogashoa was asked to explain the entry on the summary of labour ‘grunting respiration’. She said this means difficulty in breathing and that usually children who have respiratory problem or neurological problems will have difficulty in breathing. She said it is a sign of laboured breathing and there are many causes of laboured breathing such as respiratory problems, neurological problems and acidosis. She said it is breathing and should not be confused with gasping respiration which is what you get with pre-terminal breathing and that is what you usually get in children who have just had acute profound hypoxia and are delivered soon thereafter. There is a big difference between the two. In the summary of labour, the time between the second and third stage of labour is approximately 10 minutes. She said there is no indication that the period between the second and third stage was prolonged. A prolonged second stage is associated with intrapartum hypoxia. In a hospital admission from which details the demographic information of the patient, she said the provisional diagnosis was RDS (respiratory distress syndrome). They thought that G[…] had respiratory difficulty and were more concerned about difficulty in breathing. Their diagnosis relates to the diagnosis at birth of grunting. The final diagnosis was birth asphyxia in November 2010. She said when G[…] was born they were not particularly worried because the baby was not so depressed at birth and only had a little bit of respiratory difficulty. They were not worried of a possibility of HIE because the baby did not need a lot of resuscitation. But when the baby developed signs of HIE they changed the diagnosis to the correct diagnosis of birth asphyxia on discharge.

[103]   It was put to her that Dr Wessels opined that G[...] is suffering from spastic quadriplegic CP with mental retardation and microcephaly. She disagreed and said he has four limb involvement and that is four quadriparesis. “He has features of spasticity with rigidity but the predominant feature in this child is actually dystonia”. She said Dr Wessels doesn’t mention dystonia anywhere. She said his assessment is incomplete, that G[…] has marked dystonia. G[…]is not clear cut spastic quadriparesis. She said “I am not sure how much experience Dr Wessels has with neurology, strictly neurology but it is very easy for clinician who does not do neurology every day to just label all four limb involvement as spastic quadriparesis. He has involvement of all four limbs and I understand how he could have made the mistake. But it is not pure spastic quadriparesis. He has got predominantly dystonia but he has variable tone and that puts it more on the side of dyskinetic cerebral palsy”.

[104]   She agreed with Dr Wessels that there is a once off insult to the brain and that the insult damages the brain and leads to CP and the physical features evolves over time. She referred to the article by Volpe supra which describes the evolution of pyramidal and extra pyramidal signs in CP. She said dyskenitic CP tends to evolve over time. Earlier the signs of dystonia athetosis and dyskinesia may not be evident and the only features that one can see earlier would be a little bit of increased tone. As time goes on the features evolve. Dyskinetic CP is a disorder of movement and posture and that movement and posture is what evolves depending on the mood, pain, infection and many things. Volpe article reads “of particular interest and not readily explicable is the finding that the onset of extrapyramidal abnormalities is not clearly apparent until after 6 to 12 months and after much later. Thus, most such infants develop overt choreoathetosis or dystonia or both between 1 and 4 years of age. Abnormal motor development and hypertonia commonly are obvious before the time (as early as 6 months of life)”. She said the above speaks to the evolution of symptoms, that symptoms can vary and that children with predominantly dyskinetic CP from basil ganglia involvement ealier look like children who have spastic quadriplegic but in actual fact the damage is really to the basil ganglia and the thalamus.

[105]   She said the MRI picture support the clinical findings of predominately dystonia or disconnected CP because that area of the brain is the area that gets damaged with an acute profound insult. She said neo-radiology or patha-radiology in HIE is very well described. Radiologists look at the pattern of injury and the pattern of injury in hypoxia is well described. The radiologists agree that there was predominately basil ganglia involvement with the thalmic involvement and they speak of prothalmic involvements. And those are the hallmarks of acute profound insults to the brain. With a partial prolonged injury you get watershed injury. She explained that a brain has critical parts which are the basil ganglia in the brain stem and these are the most metabolically active parts of the brain. The brain stem is also responsible for breathing. The body will always try and spare the most critical parts of the brain like the centre that is responsible for breathing and the basil ganglia, the most metabolically active part. With partial prolonged hypoxia, the brain has time to compensate and it spares the critical parts of the brain, namely basil ganglia and the brain stem. There is more affixation with the top parts of the brain like the white matter and in particular with hypertension there is watershed injury in the area of the boundary between the vascular supply and those areas. There are distinct and well described radiology patterns. She said none of the radiologists’ allude to elements of partial prolonged injuries. The MRI has many issues and that is the reason why they work together with the radiologists to give them clinical information and they must interpret the MRI together with the clinical information.

[106]   Dr Mogashoa agreed with Prof Adam that it is possible that a sentinel event such as a ruptured placenta caused the acute profound injury that is seen on the MRI and is responsible for the subsequent neurological damage. Dr Mogashoa said anything that causes a sudden loss of supply of oxygen to the baby would then be a sentinel event. And where there is a sudden loss of blood, the brain does not have enough time to compensate and there is a sudden loss of oxygen and blood supply to the brain and that explains the acute profound nature of the injury on the MRI because the brain does not have time to compensate, unlike a sustained bradycardia and a little bit of oxygen, the brain over a couple of hours, has enough time to compensate. The article by Huang and Castillo supra supports this theory. She said with a sentinel event, the literature says you have about 10 to 15 minutes to save the baby’s brain. With most sentinel events, there is not enough time to save the baby’s brain and almost all of them once there is a sentinel event, there is definitely damage to the baby’s brain. She said in this case there is a clear documentation that there was a ruptured placenta. This is a case of a clear abruption that resulted in hypovolemic shock and low blood pressure in plaintiff, so this is not a mild abruption. She said, “The low blood pressure from the abruption in the mother at the same time there is a loss of supply to the baby and that is a clear sentinel event”.

[107]   In cross examination, she said she qualified as a paediatric neurologist in 2014 and as a paediatrician in 2009. She said the field of paediatric neurology also entails neonatal neurology. She admitted that the bulk of the work of a paediatric neurologist would be to look after children who are a little bit older as opposed to new babies.  She reiterated that Apgar scores have to be taken in context and in this context the baby cried a bit at birth which means that the baby was not grossly depressed at birth. Although Adcock says that once the Apgar scores are above 5 and 10 minutes it is not likely that it is peripartum but in this case there was a sentinel event and G[…] subsequently had features of moderate encephalopathy. One has to look at the whole case in totality. She says Adcock says it’s unlikely and not impossible. It was put to her when looking at Adcock, the inference to be drawn is that the Apgar score of 9 or 10 is inaccurate. She said the Apgar is what is documented. She reiterated that if the insult occurred close to the time of delivery, the Apgar would be extremely low but if the insult is far away from the time of delivery the Apgar might be close to normal. Other factors are that G[…]cried a little at birth and had a pulse of more than 100 which leans to the fact that he was not so depressed at birth.

[108]   It was put to her that if the baby was blue at one minute, the score should be 0 and not 1 and if the body is pink and the extremities blue then the score is 1. She said it depends where the blue is. If the blue is just the extremities, you get 1, but if G[…] is blue everywhere you get 0. We are not sure whether G[…] was blue centrally or peripherally, it could be a 0 or 1. She said the blue in the 30 minutes assessment could be a baby who is blue peripherally and not centrally. To say blue is 0 is stretching it. She reiterated that she was happy to take it from 2 to 1 for the 5 minutes Apgar and that G[…] was centrally pink but peripherally blue based on the fact that he cried and the midwife was happy with the respiration. At one minute they ticked 1 which is the baby pink and extremities blue. Further it was put to her that at five minutes, the score is 10 but the respiratory rate is less than 40. She agreed that if its less than 40 it cannot be 10 out of 10. The respiratory rate should be 1 not 2. In respect of the hoarse cry, she said she didn’t know whether it was weak or just hoarse. The reflexes are recorded as normal. She said the reflexes in the new born are not the same as the reflexes seven years later. In the neonatal period they are speaking of primitive reflexes. She agreed that if there was anything wrong with the brain, the reflexes would not be normal. With muscle tone is depends whether the muscle tone at birth was depressed so if the baby is encephalopathic, you get depressed muscle tone and the baby is floppy. She agreed that from the initial assessment the score should have been less than 10. She said probably a 7 or 8 out of 10 at five minutes based on the physical examination. She reiterated that although the Apgar scores have pitfalls they are generally quite reliable. She said it is possible that the five minutes Apgar was not 9 or 10 but 7 or 8 but there was no reason to doubt the one minute. G[…] cried a little so he was not really depressed. A cry is very important at birth, it is very reassuring. There is no reason to give a baby who cries an Apgar of less than 6. A cry is equivalent to an Apgar of 6. A baby who is blue, pale and lifeless is not going to cry. If there was bradycardia of under 100, the Apgar would be less than 6. They assigned a 1 for respiration at one minute which is in her view correct.

[109]   In respect of the blood loss, she explained that if you have extra litres of blood as with pregnant women and you lose blood at a rapid pace there is not enough time to compensate and that is what happened with plaintiff. If she was able to compensate, she would not have been in shock and she would not have lost consciousness. She resuscitated with 1litre of blood and a Voluven expander which is an intravenous fluid which allows the blood to run rapidly. Dr Mogashoa said the ‘bulk of the injury was secondary to the sentinel event on the basis of the hypovolaemic shock”. When questioned about the rest of the damage, whether it happened right up to the time of birth after the abruptio she replied “the injury in this case occurred at the time of abruptio”. She later conceded that she does not know what happened after the abruptio.

[110]   Dr Mogashoa said it is important to clarify the articles by Pasternak and Volpe supra and the context under which the articles were written. She said these articles speak predominantly to when you don’t have a sentinel event. She said there are two scenarios, the one is where you have a sentinel event that occurred which resulted in a severe acute profound insult and the other scenario is where there is a partial prolonged insult and at the end there is a sudden acute profound insult, as referred to in the article. In this case there was a sentinel event where there was a sudden loss of oxygen and blood to the baby and this correlates with the radiology of acute prolonged insult and a period when we don’t know what happened. She said there is no radiology or evidence of partial prolonged insult from 3:00 until 11:00 which would give you specific MRI changes. The radiology is well described in all the literature. “If there was significant partial prolonged hypoxia after the acute profound, we would’ve seen the radiology”…. “the bottom line is that there is no radiological signature that there was continuous damage of partial prolonged”.

[111]   She reiterated that it is a possibility that the lesser damage was done after the abruptio but nobody knows what happened after the abruptio and after the resuscitation. “There is a possibility that nothing happened and that the baby was fine and there is possibility that there may have been a bit of cellular damage to the baby….. we do not know … we do not have evidence radiologically that there was continuous damages to this baby”. Dr Mogashoa said there was hypertension and probably hypoxia to the baby at the time of the sentinel event. Counsel relied on Volpe to support the hypothesis of a partial prolonged insult followed by an acute profound insult. She said she agrees with the two scenario she mentioned previously and that there is a possibility of a partial prolonged with repeated insults and then you get an acute profound insult but stressed that in those circumstances you would get a signature of partial prolonged insult, radiological features of a partial prolonged insult and then eventually an acute profound. She said an MRI will always pick up partial prolonged and acute profound injuries. She said the pitfalls of MRI is in the new born baby but when you do an MRI much later it helps to understand the mechanism of injury. The MRI is a proven investigation that helps to prove the mechanism of injury. She was questioned about her evidence that the MRI must be assessed in conjunction with clinical features and that she found clinical features that were compatible with partial prolonged. She said “just because the child has spasticity and increased reflexes, it is not equivalent to partial prolonged” … we shouldn’t make that mistake to say there is increased tone and rigidity therefore this is a partial prolonged injury. In this child there are changes which are in keeping with acute profound. There is a degree of white matter which signal extension of the acute injury. She said symptoms evolve and children with only basal ganglia can present with a degree of spasticity. One should move away from the inference that if there was spasticity that means partial prolonged injury. Spasticity is damage to the white matter but you cannot say that damage to the white matter is equivalent to partial prolonged”. She was asked whether she differs with Prof Cooper who said that spasticity is indicative of partial prolonged. She said, “spasticity is damage to white matter but she cannot say that damage to white matter is equivalent to partial prolonged.” She reiterated that in this case there is no radiological signature of a partial prolonged injury.

[112]   Dr Mogashoa referred to the animal models in Meyer’s article supra where it says that there was an acute profound insult and then volume was restored. In the monkeys the experiment on acute profound damage, where asphyxia was produced by tying the umbilical cord completely and placing a rubber bag over the head of the foetus to prevent breathing. The insult produced bradycardia, gushing and metabolic acidosis within minutes. The PH fell from 7.3 to 6.8 in about 12 minutes. In spite of complete cessation of the circulation the heart continued to beat at 60 to 70 beats per minute and the circulation could be restored by resuscitation. Thus they were able to establish volume after resuscitation.

[113]   The Court asked the question whether a partial prolonged can cause shock. Dr Mogashoa’s said no, that if one loses a lot of blood suddenly this results in low blood pressure. Clinical features of shock is low blood pressure and decreased level of consciousness. Shock in the mother results from the sudden blood loss from the abruption and the sudden shock is what gives you the acute profound injury. In this case you have a radiological pattern and a clinical pattern of predominantly acute profound injury and that injury is because there was a sudden loss of blood pressure and the brain did not have enough time to compensate. The abruptio placenta caused the shock in plaintiff. She said a sudden severe hypotension is not partial profound. This was an acute profound insult. There mere fact that she bled almost to death suggests that there was a significant loss of blood pressure. With a minor abruption the degree of blood loss would be minimal and will not result in severe hypotension. It was a sudden gush of blood that was lost and the sudden gush of blood was associated with a loss of level of consciousness. That is a sudden, acute severe loss of blood from the placenta.

E.        THE APPLICATION FOR ADMISSIBILITY OF HEARSAY EVIDENCE

[114]   Before evaluating the evidence, it is necessary at this juncture to consider defendant’s application for the admission of hearsay evidence. Defendant applied for admission of certain sections of plaintiff’s record in terms of Section 3 of the Law of Evidence Amendment Act 45 of 1998 for reasons that two of the personnel at the JSTH, namely, Sister Mogopodi and Dr Moosa are deceased alternatively untraceable and that their notes cannot be confirmed through oral evidence. Defendant’s application was not opposed and Plaintiff also relied on certain entries by the said personnel. Having considered the reasons furnished for admitting same, I am of the view that plaintiff will not be prejudiced if the documents are admitted and failure to admit same will in fact prejudice defendant as the exclusion of the entries will lead to a fragmented and incomplete sequel of events that transpired at the JSTH which may lead to this Court being unable to arrive at a fair, just, balanced and equitable decision. Accordingly the application for admission of hearsay evidence is granted.

F.        EVALUATION

WRONGFULNESS

[115]   In order to establish liability in delict, defendant’s conduct must have been wrongful. This is a conclusion of law that a court draws from the facts before it[9]. Wrongfulness is a distinct and separate enquiry for delictual liability and is a requirement quite apart from the negligence of the defendant’s conduct. The wrongfulness issue is logically anterior to the fault enquiry and only when it is established that defendant acted wrongfully does the question arise as to whether the objectively wrongful conduct can be imputed to the defendant[10]. Fault does not presuppose the existence of wrongfulness and is irrelevant unless wrongfulness is established. Put otherwise negligence is unlawful and actionable only if it occurs in circumstances that the law recognises as making it unlawful. In broad terms conduct is wrongful if it infringes a legally recognized right of the plaintiff or constitutes a breach of a legal duty owed by the defendant to the plaintiff [11].

[116]   Plaintiff in her pleadings alleges that, ”the Plaintiff and the Defendant through the doctors and professional staff in `defendants employ concluded an express, alternatively tacit agreement in terms of which the hospital through the doctors and other professional staff or nursing staff in its employ, undertook to examine, treat, care for and provide gynecological and obstetric services to the Plaintiff and the minor with the skill, diligence, competence and care reasonably expected of doctors and nursing staff employed by a hospital” alternatively “the doctors and professional staff  assumed a duty to the Plaintiff and the minor to provide professional medical services including examining, caring for and providing gynecological and obstetric services to the Plaintiff and the minor with the skill, competence, diligence and care reasonably expected of doctors and nurses employed by a hospital”. Plaintiff alleged further that, “As a result of breach of the agreement, alternatively negligent breach of duty of care, the minor is brain damaged and has cerebral palsy”.

[117]   Defendant in its plea alleged inter alia that, the medical practitioners exercised the

necessary skills and diligence reasonably expected of them in their care and treatment of the plaintiff in accordance with the applicable and/or standing protocols. And denied any breach of contractual obligations, negligence and duty of care.

[118]   The enquiry as to whether defendant has contravened the duty is objective. The imposition of a legal duty depends on the particular circumstances of the case. In casu, defendant admitted to performing the skills and diligence reasonably expected of them and as the duty is recognized in law, it follows that a breach of that duty for the purposes of liability is wrongful[12]. The existence of the legal duty (which is admitted) and its breach (the harm caused against the legal duty) would render defendant’s conduct wrongful. The breach of that legal duty is implicit with the finding that harm was caused. Thus the question is not whether defendant was at fault but whether defendant complied with the legal duty imposed upon him.

            NEGLIGENCE

[119]   The test as regards professional negligence is whether a reasonable practitioner in the circumstances would have foreseen the reasonable possibility of his conduct injuring another and would have taken reasonable steps to guard against its occurrence, and whether the practitioner concerned failed to take such step[13].The Supreme Court of Appeal (SCA) in Mkhatswa v Minister of Defence[14] approved the above stated test for negligence, subject to the following qualification:

“It is probably so that there can be no universally applicable formula which will prove to be appropriate in every case… Notwithstanding the wide nature of the inquiry postulated in para (a)(i) of Holmes JA’s formula – and which has earned the tag of the absolute or abstract theory of negligence – this Court has….. acknowledged the need for various limitations to the broadness of the inquiry where the circumstances have so demanded. For example, it has been recognised that, while the precise or exact manner in which the harm occurs need not be foreseeable, the general manner of its occurrence must indeed be reasonably foreseeable..Too rigid an approach in borderline cases could result in attributing culpability to conduct which has sometimes been called negligence …in the air …..Inevitably the answer will only emerge from a close consideration of the facts of each case and ultimately will have to be determined by judicial judgment …..whether or not conduct constitutes negligence ultimately depends upon a realistic and sensible judicial approach to all the relevant facts and circumstances that bear on the matter at hand. What also needs to be emphasised is that what is required to satisfy any test for negligence is foresight of the reasonable possibility of harm. Foresight of a mere possibility of harm will not suffice.” (own emphasis)

[120]   In Mukheiber v Raath[15] the Court held that the ultimate analysis is whether in the particular circumstances the conduct complained of fell short of the standard of a reasonable person, or in this matter, the appropriate standard for the relevant medical personnel applicable. In respect of medical practitioners and nurses this is a profession that demands special knowledge, skill and care and the measure is the standard of competence that is reasonably expected of a member of that profession[16]. The relationship between doctors, nurses and the patient they treat, involves the duty to act with reasonable care and skill and is a duty imposed by the law of delict. Wessels JA in Van Wyk v Lewis[17] said the following on the standard of competence of a surgeon “… the surgeon will perform the operation with such technical skill as the average medical practitioner in South Africa possesses and that he will apply that skill with reasonable care and judgment… (he) is not expected to bring to bear on a case entrusted to him the highest possible professional skill but is bound to employ reasonable skill and care and is liable for the consequences if he does not.”

[121]   The onus of proving negligence rests on plaintiff. The SCA in Goilath v MEC for Health Eastern Cape said the following:

[11] In Sardi v Standard and General Insurance Co Ltd  1977 (3) SA 776 (A) at 780C-H, Holmes JA made plain that it is inappropriate to resort to piecemeal processes of reasoning and to split up the enquiry regarding proof of negligence into two stages. He emphasized that there is only one enquiry, namely whether the plaintiff, having regard to all of the evidence in the case, has discharged the onus of proving, on a balance of probabilities, the negligence averred against the defendant. In that regard the learned judge of appeal stated:

‘As INNES, C.J., pertinently insisted in Van Wyk v Lewis,   1924 AD 438 at p. 445, lines 8 - 9, "It is really a question of inference". It is perhaps better to leave the question in the realm of inference than to become enmeshed in the evolved mystique of the maxim. The person, against whom the inference of negligence is so sought to be drawn, may give or adduce evidence seeking to explain that the occurrence was unrelated to any negligence on his part. The Court will test the explanation by considerations such as probability and credibility; see Rankisson & Son v Springfield Omnibus Services (Pty.) Ltd.,  1964 (1) SA 609 (N) at p. 616D. At the end of the case, the Court has to decide whether, on all of the evidence and the probabilities and the inferences, the plaintiff has discharged the onus of proof on the pleadings on a preponderance of probability, just as the Court would do in any other case concerning negligence. In this final analysis, the Court does not adopt the piecemeal approach of (a), first drawing the inference of negligence from the  occurrence itself, and regarding this as a prima facie case; and then (b), deciding whether this has been rebutted by the defendant's explanation. See R. v Sacco,  1958 (2) SA 349 (N) at p. 352; Grootfontein Dairy v Nel, 1945 (2) P.H. 15 (A.D.); Arthur v Bezuidenhout and Mieny,  1962 (2) SA 566 (AD) at pp. 574 - 576.’

[13] Medical negligence cases do sometimes involve questions of factual complexity and difficulty and may require the evaluation of technical and conflicting expert evidence. But the trial procedure, which is essentially the same as in other cases, is designed to deal with those and thus no special difficulty ought to be involved in determining them….

[17] When an inference of negligence would be justified and to what extent expert evidence would be necessary would no doubt depend on the facts of the particular case.

[122]   Plaintiff relies on breach of an express alternatively tacit agreement concluded between plaintiff and the staff at the Moses Kotane Hospital (MKH) and the Job Shimankana Tabane Hospital(JSTH), previously the Paul Kruger Hospital, alternatively breach of a legal duty. With regards to negligence, plaintiff’s case rests inter alia on the following:

(i)         The nursing staff failed to diagnose abruptio placentae timeously when there were clinical indications to that effect;

(ii)          The nursing staff failed to call in a doctor when they did diagnose abruptio placentae during the early hours of 16 October 2010;

(iii)         The nursing staff failed to monitor the condition of the Plaintiff and the foetus during the course of labour;

(iv)         The medical and nursing staff failed to detect a foetal heartbeat both at the Moses Kotane Hospital and the Paul Kruger Hospital;

(v)          The medical staff made an incorrect diagnosis by diagnosing abruptio placentae with intra uterine death and allowing the Plaintiff to deliver vaginally when there was no death of the foetus and an emergency caesarean procedure would have been the appropriate treatment regime.

[123]   In Lee v Minister of Correctional Services[18], Nkabinde J said the following:
“(41) In the case of “positive” conduct or commission on the part of the defendant, the conduct is mentally removed to determine whether the relevant consequence would still have resulted. However, in the case of an omission the but-for test requires that a hypothetical positive act be inserted in the particular set of facts, the so-called mental removal of the defendant’s omission. This means that reasonable conduct of the defendant would be inserted into the set of facts. However, as will be shown in detail later, the rule regarding the application of the test in positive acts and omission cases is not inflexible. There are cases in which the strict application of the rule would result in an injustice, hence a requirement for flexibility. The other reason is because it is not always easy to draw the line between a positive act and an omission. Indeed there is no magic formula by which one can generally establish a causal nexus. The existence of the nexus will be dependent on the facts of a particular case”.

THE ISSUES

[124]   The issues under negligence to be determined are the following:

1.    Was there inadequate monitoring of plaintiff and if there was, were the medical staff negligent in not properly monitoring plaintiff?

2.    Were the medical staff negligent in diagnosing placentae abruptio with intra-uterine death and allowing plaintiff to deliver vaginally?

3.    Was the medical staff negligent in not performing a caesarean section?

4.     Was defendant negligent by inducing plaintiff at a level 1 hospital?

5.    Did the doctors and professional staff at the MKH and JSTH act with reasonable care and skill in their treatment of plaintiff and G[…]?

6.    Did their conduct fall short of the appropriate standard for doctors and nurses?  

Was there inadequate monitoring of Plaintiff

[125]   Prof Adam said a patient who is hypertensive is monitored in the same way as a woman who is not in labour, namely six hourly blood pressure, six hourly temperature and listening to the foetal heart. The timing of monitoring for induction irrespective of whether you are high risk or not is every two hours the FH and every two hours maternal monitoring of BP and pulse. Prof Adams said the management changes when a patient is in labour. From 3:00 on 16 October 2010, plaintiff was in the early stage of labour. She said, the appropriate monitoring for a patient in this phase of labour is maternal monitoring every hourly and foetal heart rate every two hours. (own emphasis)

[126]   There is a dispute between the parties as to when plaintiff was in labour. Prof Cronje in the joint minute said, “From 19h00 on 15 October 2010 her contractions had started and by definition she was in true labour from 22h00” Prof Adams in the joint minute said, “The diagnosis of labour is made if there are painful uterine contractions accompanied by at least one of the following:-

·         Cervical effacement

·         Rupture of membranes or a show

·         At 3:30 she had mild contractions with a dilation of ‘tip of finger’. It is not possible to state that labour started at 22:00.”

            In the ‘Labour – Initial Assessment Form’, the date and time for the onset of labour is noted at 3:00 on 16 October 2010. The doctor in the application for transfer says she started bleeding at 3:30. There is inconsistency in plaintiff’s evidence, particulars of claim, letters of demand and affidavit for condonation. Plaintiff’s recollection of the times when she experienced pain, when she was in labour and when she spoke to the doctor is contradictory and cannot be relied upon. Prof Cronje said, the reason why he said that the labour started at 22:00 on 15 October was because of the show which information he got from plaintiff’s report. Plaintiff’s report did not form part of the records before Court. Prof Cronje said the bleeding at 3:00 was not a show but it was part of the abruptio placenta. The entry made by the nurse in the clinical notes at 3:30 reads “ward patient reported labour. PV done cervix tip of finger, show marked, contractions mild”. This is by definition labour. According to the nurse’s record, 3:00 was the initiation of labour and not 22:00. Plaintiff had labour pains at 3:00 and was 1 cm dilated. This court accepts that labour commenced at or around 3:00 when plaintiff experienced labour pains and was 1 cm dilated.

[127]   The monitoring of plaintiff and the foetus is found in the medical records. It is not disputed that plaintiff and the foetus were monitored from 14:00 on 13 October 2010 until 22:00 on15 October 2010 and then at 3:00, 3:30 and 4:00 and 4:30 on 16 October 2010. Dr Paravataneni diagnosed the abruptio placenta with intrauterine death at 4:00 on 16 October 2010. There is no evidence that plaintiff and the foetus were monitored from 22:00 on 15 October 2010, which was the time of the last induction, until 3:00 on 16 October 2010. Plaintiff and the foetus were accordingly not monitored every two hours after induction. Prof Cronje said the fact that plaintiff was not monitored for at least 5 hours is a very serious omission which he regards as being negligent. He said the foetal heartrate of 148 at 3:00 on 15 October 2010 is meaningless because there is no indication whether there was any decelerations. Dr Wessels opined that the monitoring was as good as none. One foetal heartrate in that period means absolutely nothing. If you don’t have continuous monitoring, you do not know what the condition of the baby is. Dr Wessels was of the view that the FH was not monitored as it should have been and that led to foetal distress not being detected.

[128]   In cross examination Prof Adam agreed that according to the medical records there was monitoring of the FH up until 22:00 and the next FH recorded was at 3:00 or 3:30 and that there was no monitoring for five hours. Both Dr Wessels and Prof Cooper in their joint minutes agree that, “If foetal monitoring had been done during the labour process, it is highly likely that signs of foetal distress would have been identified which should have led to an emergency caesarean section”.

[129]   According to Prof Cronje, a woman who has been induced requires vigilant monitoring because it can be dangerous and overstimulate the uterus. If you overstimulate the uterus there is a higher incidence of foetal distress. The risk of placenta abruption is always present. High blood pressure is a forewarning of a possible abruption that may take place. Dr Parvateneni said that when there is an induction of labour of an obese patient, there is a risk for foetal distress and a risk of abruptio placenta. Prof Cronje and Prof Adam agreed in their joint minute that because of the induction, obesity and hypertension and plaintiff’s pulse and blood pressure she should have been monitored every two hours. As plaintiff was not monitored from 22:00 on 15 October 2010 until 3:00 on 16 October 2010, I am of the view that the medical staff foresaw the reasonable possibility that by failing to monitor plaintiff and the foetus, it would cause harm to plaintiff and the foetus and they would have to take reasonable steps to guard against such harm, and they failed to take such steps. Accordingly defendant was negligent in failing to monitor both plaintiff and the foetus according to the standard protocol required after the last induction at 22:00 on 15 October 2010.

Were the medical staff negligent in diagnosing placenta abruptio with intra-uterine death and allowing plaintiff to deliver vaginally instead of performing an emergency caesarean?

[130]   Dr Parvateneni testified that she failed to detect the FH using both a foetal scope and a sonar at 4:00 on 16 October 2010. Although she explained in cross examination how an ultrasound examination is conducted, she did not have any independent recollection of plaintiff and relied on the medical notes. Her only explanation for not detecting the FH was plaintiff’s weight. According to Prof Adam, Plaintiff’s BMI was 38.85 which falls under obesity class 2. It is common cause that the FH was detected seven times on 15 October 2010 and also at 3:30 on 16 October 2010. Hence plaintiff’s weight did not prevent the medical staff from finding the FH on 15 October 2010 and at 3:30 on 16 October 2010.

[131]   Dr Adam said that plaintiff’s clinical picture fits the reason why the FH was not heard, namely, she had a hard uterus, a big bleed and was in shock. Counsel for defendant submitted that plaintiff’s blood pressure dropped to 63/54 and that the experts, Prof Cooper and Dr Mogashoa testified that when a mother is experiencing an adverse event such as an in this case, the baby will always be adversely affected. The extent of the shock which in this case was sudden and severe, would have led to the baby having experienced a sudden and catastrophic reduction of blood flow and which would have led to a bradycardia. Prof Cooper submitted that plaintiff’s weight coupled with the bradycardia would have been ‘the likely’ reason why a FH went undetected. The test however is whether it is the probable reason and not the likely reason. Dr Adam said when there is a bradycardia the difficulty is that you do not know which is the mothers’ heart rate and which is the baby’s heart rate.  She said that the ultra sound is the gold standard and if you do not pick up the FH with the ultra sound, you would not with a CTG. She however admitted that it is speculation that Dr Parvateneni did not see the FH because there was a bradycardia. She agreed in her joint minute with Prof Cronje that the failure to detect the FH with a sonar is unacceptable. Prof Cronje said that “an ultrasound examination is not altered and is very accurate”. He said that “it was unusual to miss a foetal heart on ultrasound”. (own emphasis)

[132]   Dr Wessels and Prof Cooper agree that a wrongful diagnosis of intrauterine foetal death was made twice by the treating doctors on the basis of not finding a FH. Thereafter the wellbeing of the unborn baby during labour was ignored, as the foetus was assumed dead and no foetal monitoring was done. I am of the view that Dr Parvateneni and the medical staff at MKH and JSTH foresaw the reasonable possibility of their conduct in failing to detect the FH causing harm to plaintiff and the foetus and that they would take reasonable steps to guard against such harm, and they failed to take such steps. They failed to exercise the degree of skill and care which a reasonable practitioner would exercise. This is also not a case of applying hindsight in the consideration of the facts as both the experts for plaintiff and defendant, Prof Cronje and Prof Adam, agree that the failure to detect the FH with a sonar is unacceptable. A reasonable competent doctor in the same circumstances as Dr Parvateneni who is a general practitioner with several years of obstetrics experience, with the exercise of reasonable skill and care would have detected a FH. In the circumstances, I am of the view that the doctors at both MLH AND JSTH were negligent in not detecting G[…]’s FH.

[133]   Dr Wessels said a caesarean should have been done within an hour of the abruptio’s detection.  Prof Adam said that in obstetrics according to standard protocol when you diagnose an abruptio a caesarean should be performed within 30 minutes while resuscitating the mother. In the Rennie[19] article, the authors state that,

 “We are aware that for obstetricians the accepted decision-to-delivery interval is 30 minutes and that the evidence provided in this paper is that that this is too slow to avoid hypoxic brain damage in a small number of foetuses…while there is clear variability both in the foetal reserve and in the duration and degree of an insult, we are now of the opinion that the concept that damage begins to accrue after 10 minutes if an acute profound hypoxic ischaemic insult..”

[134]   Prof Adam said that Dr Parvateneni response to resuscitate plaintiff was correct. Her BP was then appropriate to do a caesarean section. They could not take plaintiff into theatre before 30 minutes. Thus when Dr Parvateneni diagnosed the abruption, it was necessary to first resuscitate plaintiff and then transfer her urgently to a level 2 hospital so that an emergency caesarean could be performed. Dr Wessels said from the time the diagnosis of abruptio was made, G[…] was disregarded and that all the negative effects that played out from 3:00 until G[…] was born at 11:20 had a detrimental effect on his condition.  Prof Cronje said the fact that the abruptio was present for seven hours is negligent behaviour by the staff, because the longer the abruptio lasts, the worse the consequences.  I am of the view that Dr Parvateneni took reasonable steps to resuscitate plaintiff before arranging plaintiff’s transfer to JSTH. There is however no reasonable or acceptable explanation proffered by defendant why plaintiff was only transferred to JSTH more than 5 hours after she had the abruptio and not earlier and why an emergency caesarean section was not done. I am accordingly of the view that defendant was negligent in not transferring plaintiff to a level 2 hospital as soon as was reasonably possible and not performing a caesarean section.        

Was defendant negligent by inducing plaintiff at a level 1 hospital?

[135]   Both Prof Cronje and Dr Wessels testified that an induction of a high risk patient should

not be done if the hospital is not equipped to do a caesarean section for abruptio placenta. They said that as plaintiff presented with PIH and obesity she ought not to have been induced at a level 1 hospital and that it was negligent for defendant to have done so.  These allegations were introduced in their oral evidence and were neither in their expert reports nor in defendant’s particulars of claim.  I have considered this issue even though it was not pleaded, as it was dealt with by defendant’s experts.

[136]   Dr Parvateneni said that they are a level 1 district hospital where they manage mild to moderate hypertension in pregnancy where the systolic is 140/159 and the dystolic is 909/109. If the blood pressure is more than 160/110 this is severe hypertension and in terms of their protocol, the patient must be transferred to a level 2 hospital. Dr Parvateneni said in 2010 they could not perform emergency caesareans as they did not have specialist anaesthetists. They do not have a blood bank and are not equipped to deal with an abruptio placentae.  Since 2013 they have a specialist anaesthetist who performs emergency caesareans. Prof Adam stated that the MKH is a district hospital and they should have the ability to do a caesarean section. She however denied that they were negligent in inducing plaintiff when they do not have the ability to perform caesarean sections because she said they have guidelines and protocols which allow them to induce hypertensive patients. Prof Adam denied that because plaintiff was obese and hypertensive that she should have been referred to a higher hospital. She said abruptio occurs in 0, 5% of all women (1 out of 200). She said today they induce mothers who are hypertensive at 38 weeks but according to the 2012 Intrapartum guidelines they induce at 40 weeks.

[137]   Counsel for plaintiff submitted that plaintiff’s rights in terms of the provisions of section 27(1) (a) of the Constitution of the Republic of South Africa, 1996 were violated as she should have been referred to a higher level hospital.

Section 27 of the Constitution reads as follows:

“27 (1) Everyone has the right to have access to— (a) health care services, including reproductive health care; (b) sufficient food and water; and (c) social security, including, if they are unable to support themselves and their dependants, appropriate social assistance.

       (2)  The state must take reasonable legislative and other measures, within its available resources, to achieve the progressive realisation of each of these rights.

       (3) No one may be refused emergency medical treatment.”

            Section 36 of the Constitution provides for a limitation of Rights and reads:

“ 36(1) The rights in the Bill of Rights may be limited only in terms of law of general application to the extent that the limitation is reasonable and justifiable in an open and democratic society based on human dignity, equality and freedom, taking into account all relevant factors, including— (a) the nature of the right; (b) the importance of the purpose of the limitation; (c) the nature and extent of the limitation; (d) the relation between the limitation and its purpose; and (e) less restrictive means to achieve the purpose. (2) Except as provided in subsection (1) or in any other provision of the Constitution, no law may limit any right entrenched in the Bill of Rights.”

[138]   Section 3(1)(a) of the National Health Act,2004 provides for access to health care service with what resources are available and is affordable. The existence of treatment guidelines and the categorisation of hospital according to resource needs, is the practical manifestation of a limitation within the definition of a law of general application[20]. In terms of the maternity case guidelines published in 2015, they only refer patients upward from a level 1 hospital if their BMI is 40 and above. From the evidence of Prof Adam, neither the maternity guidelines applicable at the time nor the current national guidelines contradict the induction of a patient presenting as plaintiff did at the time, from being treated in a level 1 hospital. The Court cannot ignore the 2012 Intrapartum guidelines which provides that level 1 hospitals such as the MKH is equipped to deal with the induction of hypertensive patients at 40 weeks and that in emergency and complex cases, patients would be referred to a level 2 hospital. In the circumstances when considering the guidelines and protocols, I am of the view that the medical staff at the MKH were not negligent in inducing plaintiff who had not reached 40 weeks, whose BMI was 38.85 and who had mild to moderate pregnancy induced hypertension.

CAUSATION

[139]   Plaintiff must allege and prove the casual connection between the negligent act relied upon and the damages suffered. It is for plaintiff to allege and prove her damages. The legal test for causation has been formulated in a number of cases. In ZA v Smith[21] the court at paragraph 30 held that: 

“The criterion applied by the court a quo for determining factual causation was the well-known but-for test as formulated, e.g. by Corbett CJ in International Shipping Co (Pty) Ltd v Bentley. What it is essentially lays down is the enquiry – in the case of an omission – as to whether, but for the defendant’s wrongful and negligent failure to take reasonable steps, the plaintiff’s loss would not have ensued. In this regard this court has said on more than one occasion that the application of the ‘but for test’ is not based on mathematics, pure science or philosophy. It is a matter of common sense, based on the practical way in which the minds of ordinary people work, against the background of everyday life experiences. In applying this common-sense, practical test, a plaintiff therefore has to establish that it is more likely than not that, but for the defendant’s wrongful and negligent conduct, his or her harm would not have ensued. The plaintiff is not required to establish this casual link with certainty”.

[140]   Nugent JA in Minister of Safety and Security v Van Duivenboden[22] 22 said the following:

‘A plaintiff is not required to establish the causal link with certainty, but only to establish that the wrongful conduct was probably a cause of the loss, which calls for a sensible retrospective analysis of what would probably have occurred, based upon the evidence and what can be expected to occur in the ordinary course of human affairs rather than metaphysics”.

[141]   The above test was applied in Lee v Minister of Correctional Services[23], where the Constitutional Court said:

“45 In the case of “positive” conduct or commission on the part of the defendant, the conduct is mentally removed to determine whether the relevant consequence would still have resulted. However, in the case of an omission the but-for test requires that a hypothetical positive act be inserted in the particular set of facts, the so-called mental removal of the defendant’s omission. This means that reasonable conduct of the defendant would be inserted into the set of facts. However, as will be shown in detail later, the rule regarding the application of the test in positive acts and omission cases is not inflexible. There are cases in which the strict application of the rule would result in an injustice, hence a requirement for flexibility. The other reason is because it is not always easy to draw the line between a positive act and an omission. Indeed there is no magic formula by which one can generally establish a causal nexus. The existence of the nexus will be dependent on the facts of a particular case”.

56 Even if one accepts that the substitution approach is better suited to factual causation, the preceding discussion shows that there is no requirement that a plaintiff must adduce further evidence to prove, on a balance of probabilities, what the lawful, non-negligent conduct of the defendant should have been. All that is required is “the substitution of a hypothetical course of lawful conduct and the posing of the question as to whether upon such a hypothesis the plaintiff’s loss would have ensued or not”.¹¹⁶ What is required is postulating hypothetical lawful, non-negligent conduct, ¹¹⁷ not actual proof of that conduct. The law recognises science in requiring proof of factual causation of harm before liability for that harm is legally imposed on a defendant, but the method of proof in a court room is not the method of scientific proof. The law does not require proof equivalent to a control sample in scientific investigation.

57  Postulating hypothetical lawful, non-negligent conduct on the part of a defendant is thus a mental exercise in order to evaluate whether probable factual causation has been shown on the evidence presented to court. It is not a matter of adducing evidence, as the Supreme Court of Appeal appears to have found. I accept that the postulate must be grounded on the facts of the case, but that is not the same as saying that there is a burden on the plaintiff to adduce specific evidence in relation thereto.

58….. Substitution and elimination in applying the but-for test is no more than a mental evaluative tool to assess the evidence on record. In my view, this hypothetical exercise shows that probable causation has been proved.

63  The implication of that kind of inexorable logic is that factual causation under our law can never be proved where the specific incident or source of infection cannot be identified. This means that even wrongful and negligent conduct of correctional facility authorities can by no means, in those instances, lead to delictual liability. Fortunately, in my view, our law relating to factual causation does not require that kind of inflexibility in determining factual causation.

    102     This is not to say that normative considerations bearing on what wrongs should be compensable in our constitutional system play into determining factual cause and effect – but, rather, these considerations make the case for relaxing the over-rigid strictures of but-for factual inferences. Should the common law be developed, the causation inquiry remains a question of fact, though now the question is a wider one, that is easier to answer in cases like Mr Lee’s: would reasonable measures have reduced the overall risk of infection? And, then, should the extent of risk to which the defendant’s negligent conduct exposed the claimant lead to recovery for the injury that was suffered.

104 The test for causation the Supreme Court of Appeal applied, while adequate for cases where a claimant can identify the source of his injury, may not be sufficient where he or she cannot know the source. On the existing test, the Court correctly found that because Mr Lee cannot specify the source of his infection, he cannot show on balance of probabilities that the prison authorities caused his injury. But this approach rejects all prospect of recovery even where the court finds that the defendant’s negligence increased the risk of injury. This seems unjust. And it may be constitutionally unsustainable. The law has never required perfection in imposing standards of care. It has only ever required reasonable conduct. Reasonableness permits a defendant to fall short of perfection. This means that there are legally countenanced levels of risk of harm – as well as levels of risk that the law should not countenance. (own emphasis)

[142]   The human body and its reactions are of such a complex nature that it is imperative for a plaintiff to provide expert medical evidence regarding the issue of causality. In assessing the most probable cause of the CP, this court must assess the facts of this matter and the objective opinion of the experts for both plaintiff and defendant. The facts upon which the opinion is based must be found to exist[24].

[143]   Regarding the roll of an expert witness, the SCA in Jacobs and Another v Transnet

Limited t/a Metrorail and Another[25] held that:

“It is well established that an expert is required to assist the court, not the party for whom he or she testifies. Objectivity is the central prerequisite for his or her opinions. In assessing an expert’s credibility an appellate court can test his or her underlying reasoning and is in no worse a position than a trial court in that respect.”

[144]    An expert witness’s objectivity and the credibility of his opinions may be called into question, namely, where he or she:

•      accepts to perform his or her mandate in a restricted manner;

•      presents a product influenced as to form or content by the exigencies of litigation;

•      shows a lack of independence or a bias;

•    has an interest in the outcome of the litigation, either because of a relationship with the party that retained his or her services or otherwise;

•    advocates the position of the party that retained his or her services; or

•   selectively examines only the evidence that supports his or her conclusions or  accepts to examine only the evidence provided by the party that retained his or her services.

[145]   In Pricewaterhousecoopers Inc v National Potato Cooperative Ltd[26], the SCA

examined the admissibility of expert opinion, and the duties and responsibilities of an expert witness in civil cases:-

“[97] Opinion evidence is admissible „when the Court can receive “appreciable help” from that witness on the particular issue‟. That will be when: „… by reason of their special knowledge and skill, they are better qualified to draw inferences than the trier of fact. There are some subjects upon which the court is usually quite incapable of forming an opinion unassisted, and others upon which it could come to some sort of independent conclusion, but the help of an expert would be useful.‟ As to the nature of an expert’s opinion, in the same case, Wessels JA said: „… an expert's opinion represents his reasoned conclusion based on certain facts or data, which are either common cause, or established by his own evidence or that of some other competent witness. Except possibly where it is not controverted, an expert's bald statement of his opinion is not of any real assistance. Proper evaluation of the opinion can only be undertaken if the process of reasoning which led to the conclusion, including the premises from which the reasoning proceeds, are disclosed by the expert. (Own emphasis)

[146]   In Michael and Another v Linksfield Park Clinic Ltd and Another[27] the court said the following:

‘ [35]  ……in the absence of evidence of the general practice prevailing in a specialist field, or a collective or representative opinion in relation to that practice it is difficult to determine the general level of skill shown by practitioners in that field. The court is often faced with conflicting medical opinions in regard to what constitutes proper treatment of a patient with the particular condition under treatment. It must then evaluate this conflicting expert testimony.

 [37]  The court is not bound to absolve a defendant from liability for allegedly negligent medical treatment or diagnosis just because evidence of expert opinion, albeit genuinely held, is that the treatment or diagnosis in issue accorded with sound medical practice. The court must be satisfied that such opinion has a logical basis, in other words that the expert has considered comparative risks and benefits and has reached “a defensible conclusion. (at 241 G - 242 B).

[38]   If a body of professional opinion overlooks an obvious risk which could have been guarded against it, it will not be reasonable, even if almost universally held (at 242 H). 

[39]    A defendant can properly be held liable, despite the support of a body of professional opinion sanctioning the conduct in issue, if that body of opinion is not capable of withstanding logical analysis and is therefore not reasonable. However, it will very seldom be right to conclude that views genuinely held by a competent expert are unreasonable. The assessment of medical risks and benefits is a matter of clinical and it would be wrong to decide a case by simple preference where there are conflicting views on either side, both capable of logical support. Only where expert opinion cannot be logically supported at all will it fail to provide “the benchmark by reference to which the defendant’s conduct falls to be assessed” (at 243 A-E)”.

[147]   In AM.obo KM. v The MEC for Health, Eastern Cape, Z.M[28]. Nhlangulela said, “A court of law can only weigh up the proved fact without concerning itself with speculating an evidence that was never adduced, or which does not follow by reasonable inference from the proved facts. The case of Bates Lloyd Aviation (Pty) Ltd v Aviation Insurance Co. 1985(3) SA 916 (A) is instructive. There the appellate court stated as follows at p 939I-J and 940A_B:

            ‘Inference, it was observed by LordWright in Cawell v Powell Duffryn Associated Colliers Ltd [1939] 3 ALL ER 722(HL) at 733, must be carefully distinguished from conjecture or speculation: There can be no inference unless there are objective facts from which to infer the other facts which it is sought to establish. In some cases the other facts can be inferred with as much practical certainty as if they had been actually observed. In other cases the inference does not go beyond reasonable probability.  But if there are no positive facts from which the inference can be made, the method of inference fails and what is left is mere speculation or conjecture.”

[148]   The question for consideration is whether defendant’s negligence as stated supra, caused G[…]’s CP. Is there a nexus between the failure to monitor G[…], the failure to detect a heartbeat, the delay in transferring plaintiff to the JSTH for a caesarean section, causing her to deliver vaginally and G[…]’s CP or put differently but for the defendant’s wrongful and negligent conduct, would the harm to G[…] not have ensued. There are several issues in dispute which require consideration, namely:

·   The type of CP G[….] has?

·   whether plaintiff suffered an acute profound insult and/or a partial prolonged insult?

·   The timing of the acute profound insult.

·   Whether proper management and monitoring and conducting an emergency caesarean section could have prevented the outcome?

[149]   With regard the issues in dispute, is trite that when there are two different versions before Court, plaintiff can only succeed if she satisfies the Court that her version is true and accurate and therefore acceptable, and the version of defendant is therefore false and falls to be rejected.  In deciding whether the evidence is true or not, the Court will weigh up and test plaintiff’s allegations against the probabilities.  If the balance of probabilities favour plaintiff, then the Court will accept her version as being probably true.  If however the probabilities are evenly balanced, plaintiff can only succeed if the Court nevertheless believes plaintiff’s witnesses and is satisfied that the evidence is true and defendant’s version is false[29]. 

[150]   The duty of this Court therefore is to establish, on the balance of probabilities, which of the two versions is more probable and more likely.  The procedure to be adopted in such a case has been aptly set out in Stellenbosch Farmers’ Winery Group Ltd & Another v Martell et Cie & Others[30], where the Court stated as follows:

“The technique generally employed by courts in resolving factual disputes of this nature may conveniently be summarized as follows.  To come to a conclusion on the disputed issues a court must make findings on (a) the credibility of the various factual witnesses, (b) their reliability, and (c) the probabilities.”

[151]   As stated supra, it is common cause that there was an acute profound insult. What is in dispute is the timing of the acute profound insult and whether a partial prolonged insult preceded the acute profound insult. I turn to consider the evidence in respect of the factual disputes referred to supra. Both Dr Wessels and Prof Cooper in their joint minutes agreed that: “Mrs M[…] experienced an acute incident early in labour, later diagnosed as a partial abruptio placenta, leading to fetal compromise.” Dr Wessels in his report states that, “..the findings was reported by the experienced radiologist as confirming the chronic sequelae of severe hypoxic ischemic brain encephalopathy, secondary to an acute profound event in a term infant. This would correlate with the clinical history of placenta abruptio during the delivery period. The significant thalmic and lentiform nucleus changes are typical of a profound event of an acute onset such as abruptio placenta”. Prof Cronje in his report said that, “Since the baby was not dead and cerebral palsy was diagnosed later on, it is clear that the baby was exposed to insufficient oxygen in the uterus. In retrospect, the abruptio was not severe- severe enough to cause an insufficient oxygen supply to the baby but not to such an extent that the baby died”.(own emphasis)

[152]   Prof Cronje testified that the abruptio was not severe. The placenta started to separate but did not separate completely. There was still part of the placenta attached to the uterine wall through which oxygen was transferred to the baby and kept the baby alive. Dr Wessels explained that, “Impaired oxygenation, though it can cause harm to the foetus, does not necessarily mean that injury has occurred. It is important therefore to recognise the distinction between an insult and an injury. Where oxygenation to the foetus is impaired but the foetus is compensating for the decreased oxygenation, it can be said that there is an insult but no injury. The foetus is equipped with a number of compensatory strategies that allow it to withstand this impaired oxygen gas exchange for hours if not days. Prolonged partial asphyxia causes a gradual increase in the build-up of acids in the blood leading to metabolic acidosis. The foetus has three main compensatory responses to increasing acidosis. These compensatory measures help the foetus avoid any permanent injury from arising acidosis. The initial response to a build of acids is called ‘ buffer stage’. The foetal blood contains natural alkaline (base) chemicals which are said to buffer or neutralise the acids when they build up. The buffering capacity of the blood can hold off the acidification of the blood for some time. During the buffer stage there is no risk of neurological injury to the foetus. The cardiovascular stage of foetal compensation for increasing acidosis involves a change in blood flow. First, blood is directed from non-essential organs to essential organs (heart, brain and adrenal glands). The second aspect of the cardiovascular response is to cause blood vessels to be dilated and foetal blood pressure to increase allowing a greater volume of blood to be circulated. In this way the essential organs continue to be adequately perfused with blood. During the cardiovascular stage of foetal compensation, the brain is protected from injury. As the acidosis in the foetal blood worsens, the foetal brain may require more protection to avoid injury. Following the cardiovascular stage, there is another compensatory measure (the brain auto regulatory stage) that provides added protection to the brain. During this stage, blood is diverted from the outside of the brain to protect the inner core. This results in a ‘watershed’ brain pattern injury referred to by radiologists as prolonged partial hypoxia ischemia. When the foetus has already been subjected to prolonged partial asphyxia, the ability to withstand a period of total profound asphyxia is reduced. In other words, a foetus with a prior period of hypoxia due to prolonged partial asphyxia will have already become somewhat acidotic with a low pH, which means that it will take less time during a profound total asphyxia to reach the critical level of acidosis where things start to fail catastrophically. The magnitude of the insult is maximal with profound total asphyxia. The longer the prolonged partial hypoxia ischemia, the greater the risk of injury of a subsequent profound total asphyxia. Where the foetus is exposed to a period of prolonged partial asphyxia followed by a period of profound total asphyxia, the outcome tends to be worse than those exposed to either prolonged partial asphyxia, the greater the risk of injury from a subsequent profound total asphyxia.”

[153]   Plaintiff relies on the following inference: Plaintiff had a partial abruptio placenta which led to systemetic hypotension at 4:00 on 16 October 2010. There was a blood pressure drop to 63/54, which was rapidly increased during the resuscitation to 93/54. The abruptio was not complete as a small retroplacental clot was found. Plaintiff lost 1 litre of blood. Within half an hour, plaintiff was in a condition good enough for a caesarean to take place. Plaintiff’s blood pressure increased to 105/64 at 8:00. At the time of abruption there was a diminished cerebral blood flow secondary to hypotension. This endured for hours. The haemoglobin which was 9.1 dropped to 8.1 at 10:00. When the contractions increased in severity from 10:00 and became stronger until birth, the placental insufficiency became evident and by virtue of the brief repeated hypoxic ischemic insults from the contractions it caused a cumulative deleterious effect on the cardiovascular function that then resulted in a severe insult which is evident on the MRI scan as acute profound damage. Counsel submitted that Volpe supports an acute profound damage occurring in the late intrauterine/intrapartum period. This severe insult according to Rennie et al[31] occurs between 10 and 46 minutes before birth. He relied on the authorities namely, Rennie, Pasternak, Volpe and Andrew McNab[32] to submit that the injury likely occurred after 10 minutes of an acute profound occlusion of the artery supplying blood to the brain, in other words a bradycardia where there would have been a heartbeat of less than 110 bpm. This lasts for approximately 40 to 45 minutes before death would ensue. Pasternak[33]found acute near total intrauterine asphyxia at the end of labour. Pasternak said if the baby is not born between 10 and 46 minutes after the acute profound insult, the baby is usually dead.

[154]   Counsel for plaintiff, submitted that as the baby was not dead, it was clear that this acute bradycardia happened during the last period when plaintiff was bearing down. He said that on the probabilities, drawing inferences from the established facts, it must therefore be that there was insufficient oxygen supplied to the baby’s brain during the hours following the diagnosis of abruptio but only during the last hours the foetus’ ability to tolerate the insults became compromised leading to partial prolonged damage (spasticity). He submitted further that the above inference is the only logical explanation of how the damage probably occurred. He submitted further that had the caesarean section taken place at any time at approximately 10:30 on 16 October 2010, this last acute period when the blood supply was totally or severely occluded, damage would have been prevented and G[…] would have been born without the acute brain damage.  He submitted that the bad outcome is directly related to the failure to diagnose a heartbeat and to do a caesarean section and to monitor the foetus.

[155]   Plaintiff quoted from Volpe[34]

“Factors related to the severity and the temporal characteristics of the insult appear to be of particular importance in determining the major pattern of selective neuronal injury in the newborn. Severe and prolonged insults result in diffuse and marked neuronal necrosis, involving the many levels of the neuraxis described earlier as the diffuse pattern of injury. The cerebral–deep nuclear pattern of neuronal injury appears to be related to insults that are less severe and prolonged, often termed partial, prolonged asphyxia . The deep nuclear–brain stem pattern of injury to basal ganglia–thalamus–brain stem has been described in human infants with a severe, abrupt event, often termed total asphyxia . It is postulated that the severe, abrupt event prevents the operation of major adaptive mechanisms normally operative with asphyxial events (see Chapter 13). The most important of these may be the diversion of blood from the cerebral hemispheres to the vital deep nuclear structures. Because the latter have high rates of energy utilization and also a high content of glutamate receptors, these nuclei are particularly likely to be injured. In the more prolonged and less severe insults, the diversion of blood to deep nuclear structures occurs at least to a degree, and thus the cerebral regions are more likely to be affected. Studies in the near-term foetal lamb indicate that the severe terminal insult that results in injury to deep nuclear structures especially may be likely to occur after brief, repeated hypoxic-ischemic insults first cause a cumulative deleterious effect on cardiovascular function that presumably then can result in a severe late insult. the large majority of insults occur in the late intrauterine/intrapartum period. In the living infant MRI studies can be valuable in delineating approximate timing, albeit not with extreme accuracy (see Chapter 20). 

Classic studies with term fetal monkeys by Myers and co-workers provide insight into the relation of timing and duration of hypoxic-ischemic insults to certain patterns of injury. For example, the deep nuclear-brain stem pattern was produced by total asphyxia in the term foetal monkey. The sequence of events was rapidly progressive foetal hypoxia, hypercarbia, acidosis, hypotension, and brain injury within approximately 10 to 15 minutes. … neuroimaging after such sentinel events occurring generally from 10 to 46 minutes before delivery. 

Term foetal monkeys subjected to a partial rather than total interference with respiratory gas exchange (produced by halothane-induced hypotension) developed physiological derangements over longer periods), so-called prolonged partial asphyxia. The maternal event resulted in more slowly evolving hypoxia and acidosis, followed by late decelerations of the foetal heart rate, diminished cardiac output, hypotension, and evidence for cerebral ischemia. Brain injury became apparent after several hours, and the topography involved cerebral cortex (especially in paracentral areas), basal ganglia, and thalamus, as in human infants (see Table 19.1 ) If the insults were especially severe and prolonged, brain stem was also involved, as in the diffuse pattern noted in Table 19.1.

[156]   Counsel for plaintiff submitted that the above quotation is applicable to plaintiff’s situation with one caveat, namely that the signature of the MRI was acute profound damage. Counsel said that the clinical features found in G[…] must be take into account with the MRI and the spasticity found in G[…] is indicative of partial prolonged. Hence the clinical picture is acute profound and partial prolonged.

 [157]   Counsel for plaintiff relies on the Lee case supra to submit that defendant’s stance is that because they do not know when the foetal heart decelerations occurred, plaintiff had not proved that the damage was preventable. The effect of this is that even though defendant was negligent, plaintiff is denied the opportunity of proving causal damage. Counsel for plaintiff submits that by not doing a caesarean section within an hour or even later, before 10:00, the risk of damage to the foetus through hypoxia was significantly increased, which satisfies the test in Lee. On the traditional ‘but for’ test, causality would then also had been proved. That if defendant was not negligent in not diagnosing a foetal heartbeat, it would have been detected. That at some stage there was distress and a caesarian section should have followed upon that distress. In any event a caesarean section should have been done within an hour because of the abruptio. According to Cronje, Wessels, and Adam, defendant was negligent in not monitoring the FH and not detecting a foetal heartrate and not transferring plaintiff to Rustenburg for a caesarean section where they were once again negligent in not detecting a heartbeat and not doing a caesarean section immediately, If a caesarean section had been done, the probabilities are that the acute profound damage, would not have occurred as this probably occurred within the last 40 or so minutes before birth. This damaging causing insult could thus have been prevented as well as probably all the partial prolonged damage which carried on for many hours before the actual birth. Counsel submitted that the ‘but for’ test as well as the ‘risk test’ as enunciuated in Lee supra has been satisfied.

[158]   Defendant’s experts Prof Adam, Prof Cooper and Dr Mogashoa opined that an acute profound insult was the most likely cause of the hypoxic ischaemic encephalopathy. Prof Adam in her report states:

            “The abruptio placentae was significant in that the doctor notes that the blood loss was 1L and the patient’s blood pressure dropped significantly. This event could definitely cause the changes on the MRI which is ascribed to an acute profound effect. Once a placental abruption occurs there is a 14 times higher risk of foetal acidosis (marker of hypoxia) and 4 times increased risk of the neonate requiring resuscitation”.  She states further that “Hypoxic ischaemic encephalopathy is associated with a sentinel event such as cord accident, uterine rupture or a placental abruption. (as occurred in this case). There is some evidence that once a sentinel event occurs the risk of perinatal morbidity is high. In these times it is the severity of the sentinel event and not the time to delivery which is the most important factor”. Prof Cooper in his report states that, “Ms M[…] had a major abruptio placenta, which can result in a significant hypoxic ischaemic insult to the foetus. Although the Apgar scores were not suggestive of a severe such insult, the limited information available to me is indicative of moderate neonatal encephalopathy, a sine qua non for attributing later neurological handicap to intrapartum hypoxia/ischaemia”…The MRI brain scan was in keeping with a hypoxic ischaemic brain injury in a term infant but a paediatric-trained radiologist should review the scan…..With the limited information available it seems probable that the brain injury was caused by a severe hypoxic ischaemic event as a result of the abruptio placenta”.(own emphasis)

[159]   Dr Mogashoa, the paediatric neurologist opined as follows, “I am of the opinion that G[…]’s impairments are secondary to intrapartum hypoxia due to acute profound hypoxia from a sentinel event, abruptio placenta. At the time when the sentinel event was diagnosed, Ms M[…] was in hypovolaemic shock requiring resuscitation with volume expanders and blood. I am of the opinion that the injury to G[…]’s brain occurred during the time of the diagnosis of the sentinel event.” The radiologists for both plaintiff and defendant also agree that, “The MRI Brain scan dated 16^th Sept 2014 on MASTER G[…] M[…] , demonstrates features consistent with the sequelae of a previous acute profound hypoxic ischemic brain injury, this is demonstrated by the central pattern of injury present involving the Putamina, Thalami, Peri-Rolandic cortex and Hippocampi. There are no features to suggest partial prolonged event.” (Own emphasis)

[160]   Plaintiff’s aforesaid hypothesis based on the literature was put to Dr Mogashoa, namely that, there was a partial abruptio that caused hypotension in plaintiff that started causing insults to the foetus. It was prolonged and there was partial prolonged damage done as confirmed by Dr Mogashoa’s finding of spasticity and the findings of Dr Wessels and then as Volpe and others said that after accumulative minor insults the baby was set up for severe damage which occurred close to birth when plaintiff was bearing down and the contractions were strong and the blood flow gets depleted. It is already compromised by the partial placental abruption. There is then an acute profound event where there is near total occlusion of the artery supplying the brain causing acute profound damage to G[…]. Dr Mogashoa said it is a logical explanation but it is not supported by science. The science says there was hypotension in the morning around 3:30, there was a sentinel event and the sentinel event was accompanied by shock and plaintiff was resuscitated and received fresh frozen plasma. During the time of the sentinel event, plaintiff’s condition was bad, she was dying. She was in shock as evidenced by her blood pressure and loss of consciousness which speaks to sudden severe loss of blood. When there is a sudden severe loss of blood there is also sudden severe loss of oxygen to the brain of the baby and that is the sentinel event. Subsequently she was resuscitated. G[…] was depressed at birth but according to Pasternak not so grossly depressed at birth and if you look at these articles including the ACOG statement it fits the picture of what happened that is a clinical picture of predominance of dystonia which is commonly caused by an acute profound insult with damage to the basal ganglia as supported by the imaging. The problem with counsel explanation is that there is no radiological evidence for partial prolonged injury and the radiological evidence is well described. She said it does not make sense why there would be foetal bradycardia from 3:30 to 7:30 and there is no evidence on the MRI to support a partial abruption. There would be an MRI pattern that showed a mixed pattern of partial prolonged and acute profound. The radiological signature of partial prolonged is well described, even by Volpe who refers to the extensive damage to the white matter and damage to the top to the brain as the brain is trying to spare its most critical and deep parts. In this case there is an identifiable sentinel event and it is important that we do not disregard the identifiable sentinel event. She reiterated that if you look at the radiology there is no radiological signature of partial prolonged but one does not know whether after plaintiff was resuscitated there was any other injury and whether subsequently there may have been a bradycardia. She said, “It is unlikely that the child would have been 100% okay after the sentinel event”.

[161]   Dr Wessels in the joint minute opines that G[…] has spastic quadriplegic CP with mental retardation and microcephaly. Dr Wessels said the MRI was in keeping with a Hypoxic Ischemic injury of the acute profound nature and there were also features of partial prolonged hypoxic ischemic event.  He said with acute profound you find dyskinetic type of CP where there is abnormal movements of the muscle while with partial prolonged hypoxia you get spastic CP. He said G[…] has predominately spastic CP which fits in with prolonged partial hypoxia. Plaintiff relies on the fact that G[…] has spasticity to lend support to the inference that a partial prolonged insult preceded the acute profound insult as a partial prolonged insult supports a finding of spasticity.

[162]   Counsel for plaintiff submitted that although the MRI report finds that it was consistent with an acute profound ischemic brain injury and the features do not suggest a partial prolonged event that this does not exclude partial prolonged damage as the clinical manifestations are to be correlated with the scans. He submitted that the MRI is not the be all and end all and that the experts namely, Prof Cooper, Dr Mogashoa, Dr Wessels agree that there was partial prolonged damage in that G[…] manifests features of spastic quadriplegia(caused by partial prolonged damage) and dystonia(caused by acute profound damage).

[163]   Dr Mogashoa opined that G[…] has a mixed CP, namely features of spastic quadriplegia and dystonia, predominantly dystonia. Dr Mogashoa said different causes of CP will give you different types of CP. She said if the injury occurs at term then depending on the type of injury you will get either mixed CP or spastic quadriplegic or dyskinetic CP. She said when doing a physical examination you determine what type of CP is this clinically, what your clinical findings are and whether the clinical findings fit with the history that was obtained and with the MRI. She acknowledged Dr Wessels’ experience as a paediatrician but said that when one spends time in a specific area one is able to fine tune your skills and she has spent more time looking at children with CP. She reiterated that if you do not spend much time in neurology it would be easy to say it is spastic quadriplegia when it is not. She said Dr Wessels doesn’t mention dystonia anywhere and that his assessment is incomplete as G[…] has marked dystonia. She said “I am not sure how much experience Dr Wessels has with neurology, strictly neurology but it is very easy for a clinician who do not do neurology every day to just label all four limb involvement as spastic quadriparesis. He has involvement of all four limbs and I understand how he could have made the mistake. But it is not pure spastic quadriparesis. He has got predominantly dystonia but he has variable tone and that puts it more on the side of dyskinetic cerebral palsy”. A variable tone is suggestive of dystonia. But because there were features of spasticity with elevated reflexes she could not say that this was dystonic CP only, that is the reason why she said G[…] has mixed CP in that there are features of spasticity with increased reflexes but the predominant feature was dystonia.

[164]   She referred to the article by Volpe supra which describes the evolution of pyramidal and extra pyramidal signs in CP. She said dyskenitic CP tends to evolve over time. Earlier the signs of dystonia athetosis and dyskinesia may not be evident and the only features that one can see earlier would be a little bit of increased tone. As time goes on the features evolve. Dyskinetic CP is a disorder of movement and posture and that movement and posture is what evolves depending on the mood, pain, infection and many things. Volpe article reads “of particular interest and not readily explicable is the finding that the onset of extrapyramidal abnormalities is not clearly apparent until after 6 to 12 months and after much later. Thus, most such infants develop overt choreoathetosis or dystonia or both between 1 and 4 years of age. Abnormal motor development and hypertonia commonly are obvious before the time (as early as 6 months of life)”. She said the above speaks to the evolution of symptoms, that symptoms can vary and that children with predominantly dyskinetic CP from basil ganglia involvement earlier look like children who have spastic quadriplegic but in actual fact the damage is really to the basil ganglia and the thalamus. It was put to her that Dr Wessels examined G[…] when he was 3 years which would be during a period where it was not dystonia. She did not accept this and said that from the records at Chris Hani Baragwanath there were features of dystonia even earlier. One of the doctors describes G[…] as having opisthotonic posturing and this is one of the very early signs of dystonia.

[165]   With regards the examination of G[…] at age 7, she said the motor examination revealed poor head lift on prime. He could not lift his head while lying on his stomach and this is a sign of generalised hypertonia. She said the rigidity of the limbs can be both spasticity and dystonia. Increased tone is spasticity. He had increased tone when more relaxed.  She explained “reflexes were brisk in all limbs, planters were upgoing”, this is spasticity. She said if there is brisk reflexes of all four limbs that is four limbs involvement with quadriplegia. She said even without quadriplegia, any brain abnormality is going to give G[….] increased reflexes. G[…] did not have a ‘Babinski sign’ an upgoing blunt response which is definitely for spasticity. She said “this child does have four limb involvement, he does have long track signs which are primordial signs. And as evidenced by tone that is elevated at times, evidenced by increase reflexes with upgoing planters, so he does have a positive Babinski response, but over and above that when you look at both signs, the signs that are predominant are actually the signs of dystonic.”.

[166]   She said the imaging findings according to both Dr Ranchod and Dr Tracey were features of acute profound hypoxia and there were no features of partial prolonged injury. She said the MRI picture support the clinical findings of predominately dystonia or disconnected CP because that area of the brain is the area that gets damaged with an acute profound insult. She said neo-radiology or patha-radiology in HIE is very well described. Radiologists look at the pattern of injury and the pattern of injury for partial prolonged and acute profound in hypoxia is well described. She said both Volpe and the article by Rennie supra go into detail about the radiological signature. The radiologists agree that there was predominately basil ganglia involvement with the thalmic involvement and they speak of prothalmic involvements. And those are the hallmarks of acute profound insults to the brain. With a partial prolonged injury you get watershed injury. She explained that a brain has critical parts which are the basil ganglia in the brain stem and these are the most metabolically active parts of the brain. The brain stem is also responsible for breathing. The body will always try and spare the most critical parts of the brain like the centre that is responsible for breathing and the basil ganglia, the most metabolically active part. With partial prolonged hypoxia, the brain has time to compensate and it spares the critical parts of the brain, namely basil ganglia and the brain stem. There is more affixation with the top parts of the brain like the white matter and in particular with hypertension there is watershed injury in the area of the boundary between the vascular supply and those areas. There are distinct and well described radiology patterns. She said none of the radiologists’ allude to elements of partial prolonged injuries. A lot of research has gone into describing the radiological pattern of injury and also therefore trying to understand the events that damaged the brain of the child. One cannot downplay the role of MRI but one has to be aware of its pitfalls and its significance. She did not accept that the MRI scan does not always show everything and you have to see what the clinical signs are and correlate the two. The MRI has many issues and that is the reason why they work together with the radiologists to give them clinical information and they must interpret the MRI together with the clinical information. Dr Wessels in his report also states that “A MRI investigation is a very sensitive tool to determine the cause of the neurological damage, and gives a very good indication of the timing and of the extent of the insult to the brain.”

[167]   Counsel for plaintiff, submitted that Prof Cooper is an unreliable witness for the following reasons:

·    In his first report he said he did not know when the damage occurred.

·    In his subsequent report, he excludes additional partial prolonged hypoxic ischemic insults.

·    In cross examination, he concedes that there were partial prolonged insults and damage.

Prof Cooper explained the reason for the difference of opinion in his two reports. In his report he said “The MRI scan was in keeping with hypoxic ischemia injury of the acute profound nature in a term infant however the description of the areas of the brain that were involved it seems also features of partial prolonged hypoxia ischemia event.” He said Dr Ranchod mentioned white matter injury but he was not specific about which areas of white matter were showing abnormalities and also bearing in mind they had found increase tone it made him think that there was a partial prolonged element to the injury as well. However he said subsequently, Dr Taylor described only features of acute profound and the joint minute confirmed that there were no features of partial prolonged and he accepts the findings of the radiologists that the features were in keeping with an acute profound hypoxic ischemic injury in a term infant. This he confirmed in his addendum report. He further explained why he was of the view that there was partial prolonged damage and deferred to Dr Mogashoa who is an expert in this field. I am of the view that Prof Cooper is a reliable witness.

[168]  When considering the totality of evidence, I am of the view that the probabilities are that G[…]’s impairments are secondary to intrapartum hypoxia due to an acute profound hypoxia from a sentinel event, abruptio placentae which occurred  at the time of the abruptio and not in the last hours before birth. and that the acute insult was not preceded by partial prolonged insult. I accept the opinions of Prof Cooper, Prof Adam and Dr Mogashoa as their opinions are supported by scientific evidence as set out more fully hereinbelow:

(1)  An abruptio placenta occurred according to Dr Parvateneni and Sister Modikwe at 3:30 – 4:00 on 16 October.  The abruptio placentae was significant in that Dr Parvateneni noted that the blood loss was 1 litre and plaintiff’s blood pressure dropped significantly. Prof Adam said in this case the acute insult occurred at 4:00 and plaintiff had the effect, namely the big bleed and there are no indications of late decelerations or even any decelerations before this happened. There is no clinical evidence that there was an abruption before 4:00. She said, “It was a big bleed that caused plaintiff’s blood pressure to drop. As it was significant to the mother it was significant to the baby…in the light of the MRI without any further effects or an effect of ongoing hypoxia and also the fact that there was no ongoing bleeding in the mother and in the light of the paediatric report. I would say that this was the sentinel event….when looking at the MRI and the fact that plaintiff’s pressure dropped significantly one can conclude that the sentinel event was a catastrophic event”. Dr Mogashoa and Prof Cooper corroborated Prof Adam and said when there is a sudden severe loss of blood there is also sudden severe loss of oxygen to the brain of the baby and that is the sentinel event. The sentinel event was accompanied by shock and plaintiff was resuscitated and received blood. Dr Mogashoa said “in my view the damage to the baby occurred at the time of the blood loss with hypotension and this was the sentinel event that occurred. We know that there was a sentinel event. The abruption was significant enough to cause hypovolemic shock and according to ACOG sentinel events will result in acute profound insults as in this case”. Prof Adam said you can have a partial abruptio which is so severe because of the bleeding and it causes the mother’s blood pressure to drop significantly as in plaintiff’s case. She said the acute profound is associated with a sudden catastrophic effect like an abruption. The FH recovers but the damage at that time was so severe that the baby had damage to the brain.

(2)  The undisputed fact is that plaintiff lost approximately one litre of blood and was in shock. Prof Adam said, they gave plaintiff 3 units of FFP (Fresh Frozen Plasma) and 4 units of blood. Based on this she said the rupture was severe, 4 units of blood in 24 hours is almost a replacement of the blood volume and 5 units is a replacement. According to Dr Mogashoa even though pregnant women have two litres more blood than non-pregnant women, a 1 litre loss is a significant loss and plaintiff had to be resuscitated with two drips. Plaintiff was resuscitated within half an hour and the blood pressure increased from 63/54 to 93/54 and 105/64 at 8:05. The haemoglobin was 9.1 before resuscitation. 10 is regarded as normal.

(3)  Dr Mogashoa explained that peripartum refers to the time of labour. It is the time from onset of labour to just after delivery. She said you need to look at everything in totality which includes the Apgar scores and the events that transpired. The Pasternak article says if there is an acute profound disaster close to the time of delivery the Apgar scores will be lower and the baby will be more depressed suggesting in this case that the insult was not very close to delivery. She said the Apgar score is a standardised form while the assessment of new born babies is just a physical examination that is ticked after the baby is born.

(4)  G[…]’s Apgar were 6 at one minute and 9 or 10 at five minutes. Dr Mogashoa said that the Apgar score at five minutes was probably 7 or 8 and not 9 or 10. Both Dr Mogashoa and Prof Cooper corroborated each other that the Apgar’s in the Pasternak samples were very low, namely 1 at one minute while in this case it was 6 at one minute which suggests that the damage to G[…] could not have occurred in the last hour. Dr Mogashoa said G[…] cried a little so he was not really depressed. A cry is very important at birth, it is very reassuring. There is no reason to give a baby who cries an Apgar of less than 6. A cry is equivalent to an Apgar of 6. Dr Wessels also said “the baby came out crying with not a good but not a bad Apgar. Babies with acute profound are born with a low Apgar.”  A baby who is blue, pale and lifeless is not going to cry. If there was bradycardia of under 100, the Apgar would be less than 6. They assigned a 1 for respiration at one minute which is in her view correct. G[…] was depressed at birth but according to Pasternak study not so grossly depressed at birth to conclude that the acute profound event occurred in the last stage of labour. The Apgar’s were not indicative of a severe insult in the last hour.  Although this court accepts that the Apgar’s are not always reliable and accurate, I accept Dr Mogashoa’s opinion that Apgar score remain helpful to determine what G[…]’s condition was at birth, the need for resuscitation and the response to resuscitation and as one goes on with the resuscitation, the lower the Apgar remains, the more likely the chance of morbidity. The American College of Obstetricians and Gynaecologists (ACOG)[35] looks at the condition of the baby at birth and also refers to the Apgar scores. Dr Mogashoa said ACOG helps one to conclude when the insult occurred. According to ACOG 2014 an Apgar score less than 5 at five and at ten minutes is supportive of intrapartum hypoxia.  The article on Apgar scores by the American College of Obstetricians and Gynaecologists and American Academy of Paediatrics reads “the Apgar score provides an accepted and convenient method for reporting the status of the new born infant immediately after birth and the response to resuscitation if needed. The Apgar score alone cannot be considered to be evidence of or a consequence of asphyxia, does not predict undivided neomortality or neurological outcome and should not be used for that purpose”. Accordingly I have taken the Apgar scores into consideration when viewing the evidence in totality.

(5)  Prof Cooper also corroborated Dr Mogashoa evidence supra and said that it was highly unlikely that the acute profound damage occurred in the last hour before birth because of the Apgar score, the description of the amount of resuscitation that was required and the admission diagnosis which did not mention birth asphyxia. Prof Cooper said there must have been a severe insult on the foetus and the picture of acute profound injury on the MRI confirms this. He disagreed that plaintiff’s description of G[…] after birth namely that he cried for a short moment, attempted to suckle for a short period and then made grunting noise was irreconcilable with Apgar score of 10. He said it is noted that there was grunting respiration. He said G[…] showed signs of respiratory distress and it is quite common for babies to have normal Apgar scores if they have pulmonary disease and show signs of respiratory distress. He said he does not think the signs of encephalopathy were there immediately after birth which you would expect if there had been an episode an hour before delivery. He reiterated that the only grunting respiration that was documented was respiratory distress. There was nothing about abnormal neurological signs at that stage. They developed presumably later. One cannot say with any confidence that the grunting respiration was due to acidosis. He acknowledged that Apgar scores are not always accurately done but he said the score excludes a baby who requires cardia compressions, prolonged assisted ventilation with bag and mask or tracking. He said whether the scores are out by 1 or 2 points is quite possible but it does not correspond to an Apgar score of 0 or 1 at one minute and less than 5 at five minutes. He was asked “you would not expect a baby with an Apgar score of 10 out of 10 to receive oxygen for 18 days”. He said “I think you are talking about two different things. The first is to change the baby from intrauterine fluid environment to an extra uterine an environment, this involves the Apgar score of 6 is not normal, it required suctioning and oxygen was given appropriately. The Apgar score of 9 or 10 is normal and did not require ongoing oxygen”.

(6)  Prof Cooper also referred to the article by Pasternak supra which has a table listing 11 babies with amongst others, uterine rupture. In the first minute, the Apgar scores for 5 babies were two 1’s and three 0, which is technically stillbirths. He said what one would expect in a preceding severe acute hypoxic ischemic episode are babies who require extensive resuscitation. If the heart rate is less than 60, they would commence with ventilation, cardiac massage. He said that the damage did not occur in the last hour before birth because resuscitation of G[…] was not extensive. What we know is that G[…] was given oxygen and that he was placed in an incubator on oxygen with a feeding tube. The nurse documented that he responded well to resuscitation. Counsel for plaintiff’s submission that G[…] was in a bad condition before the resuscitation is in the light of the aforegoing evidence unfounded.

(7)   Prof Cooper said when looking at the notes, there was no obvious sign of neurological abnormality but subsequently there were and this is in keeping with an insult that occurred several hours earlier rather than an hour to delivery. The neurological symptoms are a baby that is not active, with poor tone. They test certain reflexes, primitive reflex for example a grasp reflex, a more reflex and the sucking reflex. Sucking is very important because it requires a certain integrity of the nervous system and the development of convulsions is very common. He said the Rennie study reviews the animal data and the human data and does not represent any of their own cases. He agreed with the Rennie study that the question whether G[…]was able to recover depends on the extent of the brain damage

(8)  Prof Cooper said the initial assessment was completed by a professional nurse who usually has extensive experience of baby’s both at birth and in the early period after birth so he has no problem with her assessment. He said that with acute profound damage as found on the MRI, the baby would be dead after approximately 40 minutes if not delivered but in this case at 4:30, plaintiff’s blood pressure partially recovered and fluid was given to plaintiff so if the condition of the mother improved the condition of the baby as supplied by the placenta would also improve. Because there was recovery to plaintiff’s vital signs there would be recovery to the foetus as the baby was still alive. The baby will only die if the bradycardia continues without foetal improvement. Pasternak said the insult might occur in some cases prior to labour. So in this case there must have been some insult and there was recovery prior to labour.

(9)  Although counsel for plaintiff submitted that the Apgar’s were not proved by calling the author and is accordingly not evidence before court, no objection was made during the trial proceeding and both parties referred to the Apgar scores.  According to Volpe, it is inappropriate to use the Apgar score alone as it does not predict individual neonatal mortality or neurological outcomes. Prof Cooper submitted that the encephalopathy that occurred and the Pasternak study shows that 7 out of 11 babies had moderate encephalopathy after birth therefore placing G[…] who had moderate encephalopathy, within the category of injuries as found by Pasternak. This court cannot ignore the empirical evidence which clearly indicates much reduced Apgar scores in babies where the mothers experienced acute profound damage in the last hours. There is no evidence of good Apgar scores where the baby suffered the acute profound injury in the last hours before birth.

(10)Dr Wessels in his report said G[…] is suffering from a “clear picture of spastic quadriplegic cerebral palsy with mental retardation and microcephaly while Dr Mogashoa in her report said “G[…] has microcephaly, mixed cerebral palsy predominantly dystonic” Dr Mogashoa opined that because of the predominance of dystonia that an acute profound abrupt insult occurred at the time when plaintiff needed resuscitation. This Court accepts Dr Mogashoa opinion for the following reasons:

·  Dr Mogashoa is a paediatric neurologist and her field includes neonatal neurology while Dr Wessels is a paediatrician.  Dr Mogashoa spent more time than Dr Wessels looking at children with CP and was able to fine tune her skills. This is corroborated by Prof Cooper who said Dr Wessels in his report said G[…] is suffering from a “clear picture of spastic quadriplegic cerebral palsy with mental retardation and microcephaly while Doctor Mogashoa in her report said “G[…] has microcephaly, mixed cerebral palsy predominantly dystonic”. Prof Cooper deferred to a neurologist who differentiate the types of rigidity and can classify it as either being predominantly dystonic or spastic. Prof Cooper said he would accept Dr Mogashoa’s report as she is trained as a paediatric neurologist and this is her field of expertise.  Dr Mogashoa said it is very easy for a clinician who does not do neurology every day to just label all four limb involvement as spastic quadriparesis. G[…] has involvement of all four limbs and she understood how Dr Wessels could have made the mistake.

·   Dr Mogashoa provided the Court with a detailed explanation of the different types of CP. She conducted a physical examination of G[…] and she determined the type of CP G[…] has clinically, what the clinical findings were and whether the clinical findings fits with the history that was obtained and with the MRI.

·   She admitted that she found indications of spastic quadriplegics but said it is not pure spastic quadriparesis. G[…] has got predominantly dystonia but he has variable tone and variable tone is more suggestive of dystonia than spasticity.

·   Dr Mogashoa said that although the acute profound supports the finding of dystonia and partial prolonged supports a finding of spasticity she reiterated that many patients who have purely dyskinetic CP or deep basal ganglia thalmic involvement also have motor sign involvement evidenced by spasticity.

·   Dr Wessels did not find any features of dystonia and his assessment is incomplete.

·  Prof Cooper said the change in the clinical presentation is mainly in the first two years because the motor track is complete by 18 months to 2 years. There is not much change thereafter. There may be some changes but not a complete reversal of the findings. He said what is surprising is that Dr Wessels didn’t find dystonic CP and that should have been well established.

·    The MRI findings according to both Dr Ranchod and Dr Tracey were features of acute profound hypoxia and there were no features of partial prolonged injury. Both Volpe and Rennie supra go into detail about the radiological signature. Dr Mogashoa, Prof Adam and Prof Cooper accept the finding of the MRI. Dr Mogashoa said one cannot downplay the role of MRI but one has to be aware of its pitfalls and its significance. She said the MRI has many issues and that is the reason why they work together with the radiologists to give them clinical information and they must interpret the MRI together with the clinical information. Dr Wessels in his report also states that “A MRI investigation is a very sensitive tool to determine the cause of the neurological damage, and gives a very good indication of the timing and of the extent of the insult to the brain.”

·   This Court has when considering the totality of evidence accepted the MRI findings which supports the clinical findings of predominately dystonia or dyskinetic CP. The radiologists agree that there was predominately basil ganglia involvement with the thalmic involvement and they speak of prothalmic involvements. And those are the hallmarks of acute profound insults to the brain. With a partial prolonged injury you get watershed injury. There are distinct and well described radiology patterns and there is no trace of any watershed injury. None of the radiologists’ allude to elements of partial prolonged injuries. (own emphasis) The radiological signature for partial prolonged and acute profound is well described and detailed. There is no evidence to gainsay the MRI picture coupled with the evidence of defendant’s experts supra.

[169]   Plaintiff relies on inferences to support her claim against defendant. It is trite that plaintiff need not prove that the inference it asks the court to draw is the only reasonable inference, it suffices that the inference it advocates is the most readily apparent and acceptable inference from a number of possible inferences[36]. From the aforegoing, I am of the view that the inference that plaintiff asks the Court to draw is not the most apparent and acceptable inference. Plaintiff has not proffered any factual evidence of the existence of a partial-prolonged event or insult or injury. There are no objective facts from which to infer a partial prolonged insult. It is void of any factual basis. I am of the view that this is pure conjecture and speculation. When considering the totality of evidence, the Pasternak study, defendant’s expert opinions based on the clinical records and the radiologists MRI findings which is decisive, as well as G[…]’s Apgar scores, his condition at birth,  namely, that he cried, he suckled and he did not require extensive resuscitation, then I am of the view that G[…]’s impairments are secondary to intrapartum hypoxia due to acute profound hypoxia from a sentinel event which occurred at or around 4:00 on 16 October 2010.

Would proper monitoring and management and doing an emergency caesarean section have prevented the outcome?

[170]   Dr Wessels in the joint minutes states that, “if proper monitoring and management had taken place during labour, the adverse outcome could have been prevented.” Prof Adam referred to the fact that no FH was detected as a major concern because it changed the medical management going forward, because if they found a FH they would have done a caesarean section which might not have changed the outcome but it changed the management. She said careful monitoring with a CTG would not have prevented the abruption. Prof Adam said it is possible that you have a completely normal tracing and then you have an abruption. “Those are accidental things which you cannot see”. In her report she states that “Abruptio placentae is an ‘accident’ and whilst there are risk factors associated with the condition, it cannot be predicted and therefore not prevented…… There is some evidence that once a sentinel event occurs the risk of perinatal morbidity is high. In these times it is the severity of the sentinel event and not the time to delivery which is the most important factor”. Prof Cronje agreed with Prof Adam that an abruptio is an accident which is unpredictable and cannot be prevented. (own emphasis)

[171]   Prof Cooper in the joint minute opined that, “At the time the abruptio placenta was diagnosed, Ms M[…] was extremely hypotensive and remained so for at least the next 30 minutes and possibly longer in spite of fluid resuscitation. The combination of the abruptio placenta and prolonged maternal hypotension would have resulted in severe foetal compromise. It is not possible at this stage to speculate how much brain damage had already occurred even if an emergency caesarean section was performed.” Prof Cooper said in the instance of an acute profound injury, one would need to act within 45 minutes but that would not necessarily prevent the brain damage. If one intervened at 30 minutes, the brain damage might have already been there. Prof Cooper said the fact that G[…] did not die within the 40 to 45 minutes period means that there was restoration of the oxygen supply. He said the damage might have already occurred, only those parts of the brain that have not been damaged would be restored to normal function as would the heart muscle and other organs. A foetus may cope with the first 10 minutes and beyond that the foetus will not cope and when you get to 40-45 minutes they would not be coping. Prof Cooper said at the time of the abruptio, plaintiff was in shock, had a low blood pressure and had a depressed level of consciousness and an emergency caesarean section would have threatened her life. He said with every teaching and ethical principles, the mother’s life is a priority in this situation even if it means detrimental effects on the baby to save the mother’s life. Prof Cooper said he disagreed with Dr Wessels who felt that the well-being of the foetus was the primary concern and said Dr Wessels seems to disregard plaintiff’s well-being and that it was life threatening. The situation at the time was that the condition of the foetus was uncertain, probably damaged and plaintiff was still salvageable so plaintiff’s life should be the priority. (own emphasis)

[172]   Prof Adam said that in obstetrics an emergency caesarean section must be done in 30 minutes. She said she took 30 minutes as a guideline but subsequently the South African guideline is to deliver within 75 minutes. She agreed that the quicker you can deliver a baby in the case of an abruptio the better the chances are that they are going to prevent a bradycardia or the duration of the bradycardia but corroborated Prof Cooper’s evidence that you would not do that if you have an unstable mother as the mother has to be resuscitated before you go to theatre. She said when the abruptio was diagnosed it would not have been possible to perform an immediate caesarean section because of plaintiff’s condition.

[173]   Dr Mogashoa agreed with Prof Adam that a sentinel event such as a ruptured placenta caused the acute profound injury that is seen on the MRI and is responsible for the subsequent neurological damage. It is stated in ACOG 2014 that if there is a documented sentinel event then that points to hypoxic secondary to intrapartum hypoxia. She said this is a clear case of an abruption that resulted in hypovolemic shock and low blood pressure in plaintiff. Dr Mogashoa said, the big question is whether G[…] could have been saved, put differently, could G[…] have been normal after the sentinel event. She said she did not think so because from all the information there was a severe shut down to the brain from hypotension which is the acute profound insult and one has about 10-15 minutes to save the baby’s brain. After 10-15 minutes there will be damage. Dr Mogashoa said with a sentinel event, the literature says you have about 10 to 15 minutes to save the baby’s brain. With most sentinel events, there is not enough time to save the baby’s brain and almost all of them once there is a sentinel event, there is definitely damage to the brain. She said the ‘bulk of the injury was secondary to the sentinel event on the basis of the hypovolaemic shock”. When questioned about the rest of the damage, whether it happened right up to the time of birth after the abruptio she replied “the injury in this case occurred at the time of abruptio”. She later conceded that she does not know what happened after the abruptio. She reiterated that it is a possibility that the lesser damage was done after the abruptio but nobody knows what happened after the abruptio and after the resuscitation. “There is a possibility that nothing happened and that the baby was fine and there is possibility that there may have been a bit of cellular damage to the baby….. we do not know … we do not have evidence radiologically that there was continuous damages to this baby”. (own emphasis)

[174]   From the aforegoing, when applying the ‘but for’ test supra it is clear that proper monitoring of plaintiff and detecting a FH after the abruptio would not have prevented the abruptio as the experts have opined that an abruptio is an accident which is unpredictable and cannot be prevented. Furthermore I accept Dr Mogashoa opinion that there is direct evidence when the bulk of the damage occurred, namely within 30 minutes of the sentinel event and it would not have been possible to perform a caesarean section within that time frame as plaintiff was unstable. Hence when applying the ‘but for’ test, supra,  I am of the view  on probabilities that had defendant conducted an emergency caesarean section and caused plaintiff not to deliver vaginally, it would not have changed the outcome as the bulk of damage to G[…]’s brain occurred with the sentinel event.  Further, according to the MRI there was no damage to the watershed areas in G[…]’s brain. As there is no evidence of further damage to G[…]’s brain, one cannot speculate that there may have been damage after the sentinel event. This is in any event not plaintiff’s case. I am also of the view that plaintiff cannot rely on the ‘risk test’ in Lee  supra as Dr Goitsemodimo said you can identify the source of the  injury which was the sentinel event and there is no evidence that any reasonable measures would have reduced the overall risk.  Hence there is no evidence that by not doing a caesarean section within an hour or even later, before 10:00, the risk of damage to through hypoxia was increased.

G.        CONCLUSION

[175]   There is in my view no causal relationship between the breach of defendant’s duty to monitor plaintiff, to detect a foetal heartbeat or to do an emergency caesarean section and causing her to deliver vaginally and the damage caused to G[…]. This Court cannot infer the causal relationship from the evidence before me.          Plaintiff failed to prove on objective facts, that defendant’s negligence caused the CP. The facts are that the abruptio, a sentinel event and an accident was the trigger and the cause for the damage to G[…], I am of the view that, ‘but for’, defendant’s wrongful and negligent failure to take reasonable steps, plaintiff’s loss would still have ensued. In the circumstances, plaintiff failed to discharge the onus of proving that defendant’s negligence caused the CP.

H.        ORDER

[176]   In the result, plaintiff’s claim is dismissed with costs.

_________________________

N. GUTTA

JUDGE OF THE HIGH COURT

APPEARANCES

DATE OF HEARING                                  : 13 DECEMBER 2018

DATE OF JUDGMENT                              :  08 AUGUST 2019

(Complete transcribed record was received on 30 April 2019)

ADVOCATE FOR PLAINTIFF                  : ADV J J WESSELS

ADVOCATE FOR DEFENDANT              : ADV H CASSIM

ATTORNEYS FOR PLAINTIFF                :  Smit Stanton Inc.

                                                                     (Instructed by: Munro, Flowers & Vermaak)               

ATTORNEYS FOR DEFENDANT            :  MAPONYA ATTORNEYS

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