Grobler v Accident Compensation Corporation

IN THE DISTRICT COURT AT WELLINGTON [2013] NZACC 115 UNDER The Accident Compensation Act 2001 IN THE MATTER OF an appeal pursuant to section 149 of the Act (Appeal No. ACR 808/10) BETWEEN AMELIA BARRINGTON GROBLER Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent Hearing: 11 March 2013 Appearances: Ms ML Bagnall for appellant Mr J P Coates for respondent Judgment: 24 April 2013 RESERVED JUDGMENT OF JUDGE D A ONGLEY [1] This appeal concerns a treatment injury claim. Baby Amelia was born on 12 September 2009 after a compromised delivery. She developed seizures within 24 hours and was diagnosed with hypoxic ischemic encephalopathy. [2] During labour, there were several indicators that the baby was at risk. Steps were taken to accelerate delivery, first by assisted vaginal delivery and then by caesarian section. Some five hours before delivery, the mother was pyrexial (heightened temperature indicating infection) and there was evidence of meconium staining of her liquor. Two and a half hours before delivery it was apparent that the mother was septic with a fever that peaked at 39.7. The mother had increased heart rate and the fetal heart rate had risen from 160 to 200 per minute, [3] Once a decision was made for assisted delivery, delay was caused by difficulty turning the baby into the proper anterior occiput position. When she was prepared for caesarian section, there were delays, first by failure of the epidural anaesthetic when she was able to feel the scalpel, and secondly by a difficulty with intubation for general anaesthesia. [4] The basis for the treatment injury claim is that Amelia suffered hypoxic ischemic encephalopathy (HIE) caused by asphyxia during an avoidable delay in delivery. The appellant does not allege a negligent failure to treat, but a series of decisions that can be seen in hidsight to have prejudiced Amelia's safe delivery, therby causing or axacerbating HIE. [5] There are three central questions: (a) whether Amelia's hypoxic ischemic encephalopathy was caused by treatment; (b) whether it was not a necessary part or ordinary consequence of treatment; and (c) whether it was caused wholly or substantially by an underlying disease condition of chorioamnionitis. [6] Examination of the placenta confirmed that Ms Grobler-Barrington had stage 3 chorioamnionitis which is an inflammation of the fetal membranes due to bacterial infection. There is no doubt that this contributed to Amelia's HIE, but experts consulted by the appellant considered that delay in delivery contributed to a material extent and that the injury was not caused wholly or substantially by chorioamnionitis. The appellant's arguement depends on that opinion together with expert opinion that avoidable delay was a significant contributing cause of the extent of injury suffered by Amelia. Labour and delivery [7] Following the usage in the appellant's submissions, I will refer to Ms Grobler- Barrington as Carla and to her daughter as Amelia. The "appellant" describes either mother or daughter according to the context. [8] The course of labour and delivery is well documented. Carla went into spontaneous labour at around 9.00 pm on 11 September 2009. She was at 40+3 weeks gestation, and was admitted to Christchurch Women's Hospital around midnight and into the care of her lead maternity carer (LMC). At 12.05 am Carla's blood pressure was 130/80 and her temperature was raised at 37.5 C with a pulse rate of 98. The fetal heart rate was found to be 140 beats per minute (bpm), which is within normal limits. [9] There was little change by 2.00 am but by 3.00 am Carla had begun to vomit and an intravenous line was inserted. At this point, her temperature had risen to 37.7C with pulse rate of 100. [10] At 3.25 am Carla's membranes ruptured spontaneously during vaginal examination revealing fresh meconium. The midwife requested a review by Dr Monique Stravens, obstetric registrar. Dr Stravens noted that the cardiotocographic (CTG) variability had improved so she agreed to the insertion of an epidural anaesthetic and advised the LMC to continue CTG monitoring. [1 1] The epidural was inserted at 4.17 am and Dr Stravens reviewed Carla again at 4.50 am. [12] At 5.55 am, the LMC noted the fetal heart baseline was 155-160 bpm with reduced variability and no accelerations or decelerations. Carla's temperature was recorded as 37.8C. When she was encouraged to push, a gush of thick meconium was noted. An epidural top-up was administered at 6.12 am and at 6.22 a relieving midwife administered paracetamol because Carla felt cold and shivery. [13] At 7.00 am the midwife recorded the fetal heart rate over a 20 minute interval as 120-170 bpm with decreased variability of 3-10 bpm and no decelerations. She advised Dr Stravens of the CTG changes at 7.13 am and also that the maternal temperature had increased to 39.7 C with pulse rate of 167 bpm. The Obstetric Senior House Officer commenced IV augmentin antibiotics and at 7.27 am Carla was noted by the LMC to be very unwell with possible obstruction or sepsis. The LMC noted Carla's pulse rate was 179 bpm and the fetal heart rate was now 203 bpm. Carla's care was handed over to the secondary care team. At 7.40 am, Dr Jim Bingham, Obstetric Consultant, attended and examined Carla and noted the maternal pyrexia, fetal tachycardia and the presence of thick meconium. The fetal heart rate was 180 bpm with no decelerations and this was assessed as fetal tachycardia secondary to the maternal pyrexia. His assessment was that Carla needed delivery and transfer to theatre was arranged. Section 32 [14] Treatment injury is defined in s 32 of the Act, the relevant part of which is as follows 32 Treatment injury (1) Treatment injury means personal injury that is- (a) suffered by a person- (i) seeking treatment from I or more registered health professionals; or ) receiving treatment from, or at the direction of, 1 or more registered health professionals; or (ifi) referred to in subsection (7); and b) caused by treatment; and (c) not a necessary part, or ordinary consequence, of the treatment, taking into account all the circumstances of the treatment, including - (i) the person's underlying health condition at the time of the treatment; and (ii) the clinical knowledge at the time of the treatment. (2) Treatment injury does not include the following kinds of personal injury: (a) personal injury that is wholly or substantially caused by a person's underlying health condition: (b) personal injury that is solely attributable to a resource allocation decision: (c) personal injury that is a result of a person unreasonably withholding or delaying their consent to undergo treatment. (3) The fact that the treatment did not achieve a desired result does not, of itself, constitute treatment injury. . . .. [15] By 7.30 am fetal distress was evident. In the presence of maternal pyrexia there was a need to intervene. The situation was described in the following ways by medical professionals and consultants whose reports and opinions were put before the Review and later on before the Court in this appeal. Midwife Barbier [16] Christine Barbier, Midwife and Lead Maternity Carer, reported delivery details. She recorded that at 3.00 am Carla's temperature was 37.7 pulse 100 and blood pressure 146/90. She then began continuous monitoring of FHR (fetal heart rate) on a CTG machine. At 6.00 am temperature was 37.8 pulse 121 blood pressure 117/50. At 6.22 paracetmol was given orally for fever when Carla was feeling cold and shivery. Ms Barbier recorded the CTG between 6.50 am and 7.10 am showing four FHR decelerations then suddenly the baseline rose to 200 bpm and stayed there until baby was born at 8.44 am. Dr Bingham [17] Dr Bingham later reported: "I met Carla at 0740hrs. I had taken over the on call duty at 0700h and had been called in earlier to assess another patient I noted Carla to be pyrexial with thick meconium and a fetal tachycardia. The fetal heart rate was around 180 bpm with some reactivity and no evident decelerations, and my diagnosis was of an uncomplicated tachycardia secondary to maternal pyrexia. On vaginal examination, there was a soft anterior lip of cervix and the fetal station was at spines 0. There was no evidence of caput or moulding. I decided that delivery was necessary and arranged transfer to theatre for reassessment and trial of vaginal delivery or delivery by caesarean section as appropriate. Gentamicin was added to the antibiotic regime." [18] This record of fetal heart rate was lower than Midwife Barbier had reported from the CTG. The evidence indicates that the FHR was significant for decision making in a situation of maternal pyrexia. Midwife Ansell [19] Midwife Ms Leslie Ansell was asked to advise the Corporation concerning the midwifery care. She said that Amelia's injury was not caused by a failure of midwifery care. That is not disputed in the appeal. Concerning the situation at 7.40 am she wrote: "12. At 07.30hrs Midwives Barbier and Handorf handed over clinical responsibility for Carla's care to the hospital team. This was an appropriate handover as Carla was requiring tertiary level care. Both midwives elected to remain in a supportive role with no clinical responsibilities, to support Carla and her partner. This is in accordance with good practice. 13. At 07.40 Carla was reviewed by an Obstetrician (Dr Bingham), who decided that Carla should be transferred to theatre for a trial of vaginal delivery or lower segment caesarean section, CTG monitoring was discontinued at 07.50hrs presumably when Carla was transferred to theatre. At this time there was a marked fetal tachycardia, with normal variability and no decelerations. There is no further CTG recordings available until 08.55hrs (as charted on CTG recording)." Dr Richardson [20] Paediatric advice on the treatment injury claim was given to the Corporation by Dr V F Richardson, Paediatrician. Dr Richardson noted that a mildly raised temperature is common in labour (without infection) and when it was clear that an infection was present, this appeared to be acted on appropriately. Dr Ngan Kee [21] Dr Digby Ngan Kee is a specialist in obstetrics and gynaegology. He was critical of a failure to expedite delivery even at 6.00 am. In an opinion given to ACC's Medical Misadventure Unit he wrote: "Although an admission CTG tracing was not carried out, the CTG tracing from early in labour revealed a non-reactive tracing that became progressively more tachycardia as the labour progressed. In my opinion, at 0600hrs there was sufficient cause for intervention. At that stage the maternal temperature was 37.8C and the CTG revealed a fetal tachycardia of 160BPM with reduced variability. In my opinion there was sufficient reason at this stage to question the fetal well-being. Either delivery should have been expedited at this stage by emergency caesarian section, or an ancillary test such as a fetal scalp pH or lactate should have been carried out to clarify the fetal status." Dr Battin [22] Finally, the appellant obtained a report and opinion from Dr Malcolm Battin, Specialist Paediatrician and Neonateologist. Dr Battin produced a report before the review hearing which took place on 26 October 2010, and he updated his report in some minor respects. There are three slightly different copies of Dr Battin's report, all without identifying dates. "... An epidural was inserted at 04:17 and two hours later Carla developed a tachycardia. Carla had been noted to be pyrexial on admission at 37.5 degrees and had other temperatures noted between 37.4 and 37.8 degrees between admission and 6 am. At 07:13 the temperature had risen to 39.7 degrees and Carla was commenced on IV augmentin. At 07:40 Carla was reviewed by the specialist O&G, at this point fetal tachycardia and thick meconiuxn was noted. The fetal heart rate was 180/min with no decelerations and was assessed as fetal tachycardia secondary to the maternal pyrexia. It was arranged for transfer theatre for trial of vaginal delivery proceeding to Caesarean section if required. ..." [23] Dr Battin considered that the chorioamnionitis created a situation in which the baby was vulnerable to a reduction in her oxygen supply. He said that the chorioamnionitis may have set up a situation where there was little reserve in supply but there were warnings that the baby was stressed. As early as 3.25 am it was noted that the liquor was meconium stained. He said that, although a healthy fetus can compensate for a decrease in oxygen supply during labour ultimately the supply needs to match requirement if fetal compromise is to be avoided. [24] The appellant's argument is that maternal pyrexia and signs of fetal distress set the scene for intervention by way of early delivery at the very least by 7.40 am if not earlier. After 7.40 am - medical commentary [25] After 7.40 am there were unwanted delays through events and circumstances that were not anticipated, but which were not caused by any individual want of proper care. Midwife Barbier [26] After handover to the delivery team occurred at 7.40 am, Ms Barbier recorded that Dr Bingham first did a manual rotation of baby from OP (occipital posterior) to OA (occiptal anterior) then put the Kiwi Cup on and it came off with the second pull. The Kiwi Cup seals by vacuum to the baby's crown in order to turn the baby to the correct delivery position. Dr Bingham then put forceps on but removed them because the baby rotated. He then tried positioning the Kiwi Cup again, contractions became infrequent and the cup came off. At 8.29 am he had Neville Barnes forceps in place and said that the baby would come with the next contraction. However she did not, and he said "baby doesn't want to come vaginally we need to deliver baby by Caesarean" [27] However when Dr Bingham started operating at 8.35 am, Carla became distressed with pain (from the scalpel). She was given pethidine down the epidural but it was not satisfactory and the plan changed to general anaesthetic. "There was failed intubation after induction of GA and I remembered seeing an anaesthetic chart in her old notes during the night that mentioned difficult intubation at her laparoscopy, found it and showed it to Anaesthetist Dr Knoesen. She wasn't pleased. I was unaware antenatally of this and Carla and Jordon didn't mention it. Subsequently Carla told me she really hadn't been told that it was something that might cause problems again and never thought to mention it. Baby Amelia was born within 4minutes of the GA according to the CWH documentation." [28] The failed intubation caused a delay that could have been avoidable if the anaesthetist had been able to anticipate the problem. Ms Barbier recorded: "The time that elapsed from fetal distress at 0700 - to delivery at 0844 (1hr 44mins) meant Amelia required resuscitation and has been diagnosed following two MRIs two weeks apart with a brain injury. The atmosphere in theatre before the GA was calm and there seemed no urgency to expedite delivery. The Neonatal Nurse Specialist did not seem concerned about the prolonged tachycardia nor did the Obstetrician." [29] Ms Barbier did not clarify whether some additional step could have been taken to expedite delivery. The fact was that there were two phases of delay, first when Dr Bingham attempted vaginal delivery and secondly when the epidural failed and intubation proved difficult. Leaving aside questions of individual responsibility, the question is whether delay caused some significant extent of Amelia's injury that would otherwise have been avoided. If so, it would follow that the outcome was not a necessary part, or ordinary consequence of treatment. There is no medical opinion to the effect that the delay itself was no more than an ordinary process or mecessary part of treatment in the circumstances of the case. Dr Bingham [30] Dr Bingham recorded the conditions on transfer to theatre as follows: "Carla was transferred to theatre and her epidural was topped up sufficient to allow a caesarean section. I reassessed her at 081 1h in delivery suite theatre. The fetal heart rate was now 190, the cervix was fully dilated, the fetal position was leit occipital posterior with the station about spines+ 0. There was good descent and some rotation with maternal effort and I was easily able to manually rotate baby's head to a direct occipital anterior position. The baby's head would rotate back to its original position when I removed my hand. Taking into account Carla's condition and what I felt to be excellent prospects of a vaginal delivery, I decided to proceed with Kiwi cup rotational ventouse." [31] He then described how the Kiwi Cup was not effective and failure to achieve delivery with Neville Barnes forceps, leading to a decision for caesarian section at 8.31 am. He described: "We proceeded immediately to caesarean section under the epidural anaesthetic which had previously been topped up and appeared adequate however Carla experienced significant pain at the level of the rectus sheath and after discussion with the anaesthetists we decided to proceed to general anaesthetic. The anaesthetist experienced difficulty with the intubation and called for assistance. She advised us to continue with the procedure and baby was delivered without difficulty at 0844hrs. Baby was noted to be in occipito anterior position at delivery confirming the findings from the vaginal examination. Blood loss was 1400ml which was above average but not particularly unusual for this type of caesarean section. Meanwhile, the anaesthetic team had maintained Carla's airway with a laryngeal mask. Baby Amelia was born weighing 4340g with apgar scores of 6, 7 and 8 and arterial blood gas pHs of 7.058, arterial 7.117 venous, with base excess of -15.2, arterial -13.9 venous. Examination of baby confirmed appropriate placement of the Kiwi cup on the flexing point. During the recovery period Carla became hypotensive and required some resuscitation. There was no evidence of vaginal or intraperitoneal blood loss and she was quickly resuscitated. From the surgical point of view she subsequently made an uncomplicated recovery. Meanwhile, baby Amelia required CPAP and was noted to be unsettled and irritable in the neonatal unit. She was pyrexial and treated with antibiotics. Within the first 24 hours she developed seizures and a likely diagnosis of hypoxic ischemic encephalopathy was made. This has subsequently been confirmed by the MRI appearances. Subsequent investigations of placental pathology have confirmed stage 3 chorioaranionitis. Swab results from placenta and from Carla revealed no definite pathogens however the placental swabs culture a non-haemolytic streptococcus the significance of this is uncertain. In summary, baby Amelia has been diagnosed with hypoxic ischemic encephalopathy following a labour which was complicated by meconium staining of liquor, occipito posterior position, chorioamnionitis with evidence of sepsis, and finally an unsuccessful attempt at vaginal instrumental delivery culminating in caesarean section under general anaesthetic with failed intubation. It is difficult to be certain when the main hypoxic event occurred. In the presence of chorioamnuitis babies are known to be particularly susceptible to hypoxic insult. The blood gases at delivery showed pHis which would not inevitably result in an adverse outcome for baby however the base excess results from the cord bloods suggest loss of buffering capacity in baby's blood consistent with hypoxia over a longer period of time. Taking everything into account, it is my opinion that the unsuccessful attempt at vaginal delivery contributed significantly to the outcome. The additional delay this produced was around 20 minutes. I do not think the anaesthetic complication, whilst potentially very serious, contributed in any significant way to the outcome for Amelia. Recognising the vulnerability of the fetus and I am naturally very conservative in this clinical scenario preferring not to attempt vaginal delivery unless I consider this assured. In this particular case, it was my opinion that baby would deliver more rapidly and with less risk to mother by the vaginal route. I was proved wrong in this respect. Given the ease with which she rotated to the occipital anterior position and continued to descend, I am not sure why Amelia did not deliver vaginally. Her weight of 4340g was perhaps a factor. With respect to causation the obstetric management was not the cause of the underlying conditions which resulted in hypoxic ischemic encephalopathy. However I am in little doubt that the unsuccessful attempt at vaginal delivery delayed Amelia's delivery and contributed to the severity of her condition. In this respect it would be reasonable to call this a treatment injury. We can never know what the outcome for Amelia would have been had we proceeded direct to Caesarean Section at 081 1h. It is possible that significant hypoxia had occurred before then." [32] There is no room for certainty in any aspect of causation. Dr Bingham said that it is difficult to be certain when the main hypoxic event occurred. He stated that, in the presence of chorioamnionitis, babies are known to be particularly susceptible to hypoxic insult, and that the unsuccessful attempt at vaginal delivery contributed significantly to the outcome. Dr Bingham thought the period from 8.11 to 8.31 was a significant cause of hypoxia. It can be logically inferred that the whole period from 8.11 to 8.44 was significant. The attempt a vaginal delivery represented a loss of an opportunity to go immediately to caesarian section. The baby may by then have reached a stage of exhausation that resulted in hypoxia during the caesarian section. Either way, the delay of 20 minutes was an event that, otherwise avoided, may have enabled a better outcome. The difficulty lies in weighing probabilities without speculating. Dr Richardson [33] When advising the Corporation, Dr Richardson stated: "I believe that the neurological damage that occurred was substantially due to the underlying condition of chorioamnionitis in combination with labour. Chorioamnionitis can have profound effects on the baby's brain probably related to reduced perfusion, in turn related to the condition of use 'septic shock' noted in 'non-fetal' patients. The effects on brain perfusion are probably worse prior to delivery and cord clamping, as the placental circulation is of low resistance and this interferes with the infant's ability to boost their brain perfusion while still attached to the placenta. Inflammatory cytokines in the bloodstream have also been implicated in the pathogenesis of brain damage associated with chorioamniontlis. Earlier delivery may have reduced (slightly) the extent of this damage, but I do not believe would have prevented it." [34] Dr Richardson's view that chorioamnionitis alone would have caused the whole or substantial injury though reduced perfusion was not accepted by Dr Ngan Kee and Dr Battin. Dr Richardson did not dismiss a compounding effect of delay in delivery, but he thought it minimal. Dr Sharpe Dr Graham Sharpe, Consultant Anaesthetist, was critical of the midwife for not conveying the history of a previous difficult intubation to the anaesthetist before coming to theatre. During the attempts to secure the airway, Carla's oxygen saturations fell to 60%. From Dr Sharpe's reading of the notes and the anaesthetic record, her saturations were below 90% for about a minute or so. Whilst this was not ideal, Dr Sharpe thought it was extremely unlikely to have had any impact on the final outcome for Amelia. He stated that the blood pHs at birth showed base excess results consistent with prolonged hypoxia rather than a short episode just prior to delivery. That is to say that the short drop in oxygen saturation did not cause the level of hypoxia shown in blood Ph. Dr Sharpe went on to say: 'I note the labour history of foetal tachycardia, meconium, maternal pyrexia and a failed attempt at vaginal delivery via ventouse (Kiwi Cup) and then forceps. All of these are likely to have compounded to affect Amelia, and the anaesthesia problems, whilst unfortunate and undesirable, are unlikely to have had any major impact on the final outcome. I also note Amelia's heart rate was 100 at delivery, whereas acute hypoxia (lack of oxygen) usually causes slower heart rates in new babies (100 being regarded as satisfactory)." [35] In excluding acute hypoxia Dr Sharpe seems to have repeated the point that acute hypoxia was not caused by the brief drop in oxygen saturations, while acknowledging that it might have been caused by delivery events and chorioamnionitis. Dr Ngan Kee [36] Dr Ngan Kee described Carla as having developed a severe maternal pyrexia with an attendant severe fetal tachycardia, immediate delivery became imperative. Dr Ngan Kee said that the consultant obstetrician was placed in a difficult situation as to whether an instrumental vaginal delivery, or an emergency caesarian section was the most likely way to effect rapid delivery. In hindsight his decision to attempt a vaginal delivery was incorrect. He said: "However there were several indicators suggesting that caesarian section may well have been the better option. Firstly the eventual birth weight was 4340g, indicating that clinically Ms Grobler-Barrington should have been assessed on examination to have had an above average size baby. Secondly on vaginal examination the presenting part was only at station 0 with an occipito-posterior position. In conjunction with a large baby and a severely abnormal CTG, the examination findings should not have indicated confidence in a successful vaginal delivery. [37] Dr Ngan Kee noted that the caesarian section was complicated by a difficult intubation and some delay while a consultant anaesthetist was called. There was a brief period of maternal oxygen desaturation down to approximately a Pa02 of 60. Carla had experienced a difficult intubation in the past but that history had not been conveyed to the anaesthetist. Dr Ngan Kee said: "While it is not clear whether the history of a difficult intubation had been conveyed to the LMC midwife, if this had been known, it should have precipitated a referral for an anaesthetic assessment prior to delivery. Furthermore, Ms Grobler-Barrington's weight prior to pregnancy was 106kg, equating to a BMI of 35. This is a major risk factor for dystocia, macrosomia and anaesthetic complications and is another reason for both careful Obstetric and Anaesthetic assessment prior to labour. In conclusion, it appears that obvious risk factors were not taken into consideration prior to labour. Furthermore, during labour indicators of fetal compromise were not recognized and the opportunity to effect delivery prior to possible fetal compromise was not considered. Therefore it is my opinion that the overall standard of care did [not] reach an appropriate standard in this case." [38] The evidence overall points to the probability that the HIE would not have occurred but for the chorioamnionitis. Dr Ngan Kee was asked for his opinion whether the injury was caused by treatment or was more likely to have been caused wholly or substantially by underlying health conditions. He said: "It is highly likely that the cause of fetal compromise in this case was chorioamnionitis. Although this is an underlying health condition, there were sufficient indicators during labour to suggest that delivery should have been expedited. In this context I believe that failure to treat was the predominant cause of the injury, resulting in hypoxic ischaemic encephalopathy." [39] Dr Ngan Kee repeated that the extent of the injury was exacerbated by failure to act on clinical indicators of fetal compromise during labour. He stated: "This may well have resulted in an improved fetal outcome. Not only were these factors in labour not heeded, but also serious risk factors during the pregnancy (previous failed intubation, maternal obesity) were not recognized and sufficiently assessed prior to labour. Specialist consideration of these factors may well have resulted in a different birth plan, heightened consideration of risk factor and possibly earlier intervention." [40] There is plenty of evidence of the loss of opportunity to expedite delivery. The central question in this case is not whether there was a failure of treatment (whether negligent or not), but whether some or all aspects of that failure caused a significantly worse outcome, judged on the balance of probabilities. Dr Ngan Kee said that a different course "may well have resulted" in a better outcome. He did not say a probably better outcome, but medical evaluation is frequently expressed in such tentative language. More significant, in my view, was his earlier direct opinion that "I believe that failure to treat was the predominant cause of the injury". Dr Battin [41] Dr Battin's view was firmly opposed to that of Dr Richardson that neurological damage that occurred was substantially due to the underlying condition of chorioamnionitis in combination with labour. In his preliminary remarks, Dr Battin agreed that the delay in treatment was not the cause of the encephalopathy, that is to say the HIE would probably have occurred in any case. But in his view it was "possible that treatment related events could have potential to worsen Amelia's eventual condition". Dr Battin's reasoning was that, if the placenta was not supplying the fetal brain with enough blood and oxygen to match metabolic requirements, then injury could be made worse by factors that either (a) increased demand, (b) decreased supply of these essentials, or (c) increased the duration of exposure to this hostile environment. Dr Battin explained that pyrexia increases metabolic requirements. When Carla was pyrexial in labour, there would have been a significant increase in fetal requirements. In utero, the fetus can only loose heat via the mother. Although intravenous antibiotics and delivery are appropriate actions, there were delays in the delivery that could have exacerbated injury. He referred to the same point made by Dr Bingham. Dr Battin went on to say; "In my opinion the causal link for the brain damage is an inadequate blood and oxygen supply to the fetal brain prior to delivery. I do not agree with the opinion that the neurological damage that occurred was substantially due to the underlying condition of chorioamnionitis. Neither do I agree with the model proposed for chorioamnionitis reducing perfusion in a manner analogous to septic shock. Also of note the postnatal blood cultures were negative. ... In Carla's case we see a pattern of brain damage on MRI that is much more typical of asphyxia as a mechanism for injury. Asphyxia is a continuous process that may occur to a variable degree. The occurrence, severity and distribution of brain injury depend on several factors including the severity and nature of the insult, gestation of the fetus or infant and presence of systemic stress or fever. It is well recognised that the incidence of antenatal and intrapartum asphyxial insult is higher in complicated pregnancies, particularly those with diminished placental reserve or those with elevated requirements. Conditions such as maternal fever in labour (Impey, Greenwood et al. 2001) and pre-eclampsia (Impey, Greenwood et al. 2001) are also associated with an increased risk of NE. There are two main changes that occur in response to hypoxia in utero. Firstly the tissues may extract an increased fraction of the oxygen available Richardson 1989) and secondly blood flow may be redirected to the brain, heart and adrenal glands and away from the skin, gut and kidneys (Cohn, Sacks et al. 1974). Although a healthy fetus can compensate for a decrease in oxygen supply during labour ultimately the supply needs to match requirement if fetal compromise is to be avoided. In situations of chronic placental deficiency when reserve is already utilised the fetus may poorly tolerate the extra stress of labour. The chorioamnionitis may have set up a situation where there was little reserve in supply but there were warnings that the baby was stressed. As early as 03:25 it was noted that the liquor was meconium stained. Although a healthy fetus can compensate for a decrease in oxygen supply during labour ultimately the supply needs to match requirement if fetal compromise is to be avoided." [42] Dr Battin restated that position in the following terms: "I do not agree with the opinion that the neurological damage that occurred was substantially due to the underlying condition of chorioamnionitis. Neither do I agree with the model proposed for chorioamnionitis reducing perfusion in a manner analogous to septic shock. In addition to the fact that postnatal blood cultures were negative, I consider that the mechanism of injury is considerably more likely to be one of hypoxia ischemia causing asphyxia. Although chorioamnionitis can be associated with placental insufficiency and may produce pyrexia that will increase metabolic demand, an adverse outcome such as neonatal encephalopathy and MRI abnormality is not inevitable. - With this mechanism of injury delays, particularly those occurring after failure of the fetal compensatory mechanisms, may be responsible for causing injury or exacerbating established injury in the fetal brain. In this case there were signs of potential fetal distress as early as 03:25 when the meconium liquor was noted. In addition, a fetal tachycardia was present 1 hr prior to delivery. At delivery Carla had features supportive of asphyxia causing compromise in-utero including low Apgar scores of six and seven at 1 and 5 minutes, requirement for resuscitation and acidosis on cord gases (Arterial pH 7.06). The cord gases and depressed Apgar scores strongly support hypoxia ischemia as the injury mechanism. In contrast clinical chorioamnionitis has been reported to not have an independent effect on cord blood gas values in term pregnancies not complicated by any other disease (Arnon Samueloff 1994)." [43] Dr Battin annexed a number of research publications. The Samueloff study identified deliveries involving chorioamnionitis without other complications. The conclusion reached by Samueloff et al. was: "We therefore suggest that, although chorioamnionitis may be associated with neonatal morbidity and mortality, it is rarely associated with intrapartum asphyxia, as reflected by cord blood profile. In trying to prevent asphyxia in chorioamnionitis-complicated pregnancies, special attention should be paid to the presence of meconium, and efforts should be made toward shortening the length of labor, selecting the appropriate method of delivery and using pitocin cautiously." [44] The study supported Dr Battin's opinion that, while chorioamnionitis in combination with labour might have caused HIE, there was also avoidable asphyxia that was not a usual outcome of chorioamnionitis and would have been caused by prolonged delivery. [45] The sequence of Dr Battin's three reports is not clear but his overall opinion is clear. In one report he tabulated his reasons for considering treatment delay as a cause when he wrote: "On the balance of probabilities I consider that some aspects of treatment may have worsened Amelia's injury. Specifically, the delay in delivery would have likely contributed by exacerbating neurological injury. As stated in my original report I do not agree with the opinion that the neurological damage that occurred was a result of the chorioamnionitis. The reasons for this are explained fully in my previous report and in the following paragraphs but it should be noted that: postnatal blood cultures were negative . the mechanism of injury was likely that of hypoxia ischemia, causing asphyxia . asphyxia is supported by the umbilical cord gases recorded at birth . the pattern of injury seen on the MRI is suggestive of hypoxia ischemia . the attending clinical staff made notes referring to hypoxic ischemic insult . the presence of renal. impairment supports hypoxia ischemia insult rather than chorioamnionitis." [46] Dr Battin referred to the balance of probabilities for the conclusion that some aspects of treatment "may" have worsened Amelia's injury, and the delay "would" have likely contributed. The respondent submits that his conclusions remained no higher than the level of possibility but the appellant argues that his meaning was that delay was a probable cause of asphyxia contributing to the severity of injury. Mr Coates for the respondent referred in particular to a paragraph at the end of Dr Battin's third report, in which his language was more tentative, when he said: 'In summary Amelia's condition was consistent with HIE and renal impairment secondary to sub optimal condition at birth. Chorioamnionitis may have contributed by affecting placental function and increasing fetal metabolic demand via pyrexia. However, any delay in delivery but particularly a delay after there was sign of distress in the fetus could potentially have exacerbated the injury." Submissions [47] I will not cover the findings in the review decision because they cover the same ground. The Reviewer found that there was insufficient evidence that the delay had caused a distinct injury in terms of a significantly worse outcome than would otherwise have occurred. [48] Ms Bagnall for the appellant submitted: (a) that the medical evidence supports the position that there was significant delay in Amelia's treatment (b) there is a large consensus between the medical specialists (Drs Bingham, Ngan Kee and Battin) that the Amelia's HIE injury was made worse by the delay in providing appropriate treatment and in a timely manner. (c) the extent of delay is indicated by Dr Ngan Kee's opinion that there were indications for earlier intervention at 6.00 am, and Dr Battin's opinion that urgent intervention was needed when fetal tachycardia was present at about 7.00 am. Ms Barbier also believed that intervention should have been made at 7.00 am; (d) Dr Bingham considered that the unsuccessful attempt at vaginal delivery caused a delay of some 20 minutes and this would have contributed significantly to the severity of outcome; (e) the delays at a crucial stage of delivery were compounded by the failed attempt at vaginal delivery, failure of the epidural and avoidable difficulty with intubation; (f) Dr Ngan Kee did not believe that vaginal delivery sould have been attempted in the circumstances; (g) a substantial consensus of specialist opinion did not agree with Dr Richardson's opinion that the neurological damage that occurred was substantially due to the underlying condition of chorioamnionitis. (h) there was a pattern of brain damage on MRI that is much more typical of asphyxia as a mechanism for injury (i) chorioamnionitis may have set up a situation where there was little reserve in supply but there were warnings that Amelia was stressed. (j) an adverse outcome such as neonatal encephalopathy and MRI abnormality is not a usual outcome of chorioamnionitis alone. [49] Ms Bagnall referred to the Samueloff study of 2200 deliveries which showed that clinical chorioamnionitis did not by itself contribute to change in arterial cord blood pH. Differences were attributed to other factors including labour, mode of delivery, method of delivery and presence of meconium. [50] Mr Coates for the respondent referred to the medical evidence, and in particular the following: (a) Dr Richardson stated that chorioamnionitis can have profound effects on the baby's brain probably related to reduced perfusion with an effect of septic shock. He did not believe that delay in delivery was a significant cause (b) Dr Sharpe did not believe that the anaesthetic delay was a cause; (c) Dr Ngan Kee accepted that it was highly likely that the cause of fetal compromise in this case was chorioamnionitis (d) Dr Battin acknowledged only a possibility when he said at the end of his final opinion that a delay could "potentially" have exacerbated the injury [51] Mr Coates referred to ACC v Ambros [2007] 1 NZLR 340 (CA) and submitted that this is not a case in which the probability of causation is higher than 50%; that it is not a case in which the burden of proof is discharged by the appellant. Mr Coates submitted that the evidence is that the obstetric delay could have had some effect, but was not a causative element. In that regard the circumstances are similar to Manning [2012] NZACC 294. He submitted that chorioamnionitis was wholly or substantially the cause of Amelia's HIE. Decision [52] In his judgment in Manning Judge Beattie decided that there was "simply no evidence, or at least insufficient evidence, to identify that for the hours following [ the baby's] birth, during which his blood glucose level was low, that situation of treatment within the meaning of the Act, was causative of the subsequent personal injury of PVL". In that case the injury was periventricular leukomalacia or PVL, a specific type of brain lesion. The appeal was decided on that basis, which differs from the present appeal in which the injury is a diffuse brain injury caused by the secondary effect of the underlying chorioamnionitis and also other asphyxial insults. [53] In the present case, there is no dispute about the first two essentials of s 32 treatment injury. Baby Amelia suffered an injury, hypoxic ischemic encephalopathy, and the injury occurred when she was receiving treatment. [54] The next question is whether the injury was caused by treatment. There is consensus that HIE was caused by chorioamnionitis in combination with labour, but there is a dispute about Dr Richardson's view that the mechanism was an effect on the baby's brain related to reduced perfusion. There are closely allied questions, first whether asphyxia was a contributing cause of HIE to some degree, and whether the cause was nevertheless wholly or substantially chorioamnionitis. [55] All the opinions admit of contribution, in some combination, by both chorioamnionitis and delay in delivery carrying a risk of asphyxia. The differences concern the level of risk and hence the level of contribution of the two possible causes. Although cover is not allowed on the basis of risk (see Ambros), this is a case in which risk assists to indicate probability. If the delay carried a serious risk, then it is more likely that it brought about significant birth asphyxia. [56] Dr Battin was highly qualified and had a longstanding research interest, including publications, in the field of neonatal encephalopathy. He offered a carefully argued opinion with references to research concerning the occurrence of neonatal encephalopathy, clinical signs and associated causes at birth. [57] There is substantial concordance between the views of Dr Ngan Kee and Dr Battin. Dr Bingham, and the midwifery advisor Ms Ansell, also believed that the delay during attempted vaginal delivery was likely to have contributed to the severity of Amelia's encephalopathy. The drop in blood oxygenation during delay in intubation was probably not a cause of hypoxia on its own, it was the overall delay in delivery that is implicated in hypoxia causing added brain damage. [58] Although opinions are not expressed with a high degree of confidence, that is only to be expected in a medical scientific analysis. Most significant are the expressions of medical judgment, such as Dr Ngan Kee's opinion "I believe that failure to treat was the predominant cause of the injury"; and Dr Battin's opinion 'In my opinion the causal link for the brain damage is an inadequate blood and oxygen supply to the fetal brain prior to delivery. " It is possible to read parts of the opinions that refer to "possibilities" as medical propositions subsidiary to the specialist's overall conclusions. My reading of the opinions is that both specialists referred to the potential causes of exacerbation of HIE and then expressed an opinion of probability resting on the circumstances of the case. [59] I am satisfied that those two specialists considered that delay in delivery was a cause of significant worsening of the hypoxic ischemic encephalopathy suffered by baby Amelia. Their view is hardly contradicted by other opinions except that of Dr Richardson who considered that chorioamnionitis was a sufficient explanation on its own. I think that the carefully argued opinions of Dr Ngan Kee and Dr Battin should be preferred. [60] The conclusion to be drawn is that delay in delivery caused a period of decreased oxygen supply when Amelia's resources were already overloaded by the effect of chorioamnionitis and when she was vulnerable to asphyxia. The result was a worsening of hypoxic ischemic encephalopathy initially caused by chorioamnionitis. [61] The delay occurred in the course of treatment and was not a necessary part or ordinary consequence of treatment because it could have been avoided by more effective decision making and better communication over the history of difficulty with induction. There is no expert evidence that the delay was a necessary part or ordinary consequence. [62] The remaining question is whether the injury was caused wholly or substantially by an underlying health condition, that is to say by chorioamnionitis. It follows from the findings that I have made that chorioamnionitis was not a whole or substantial cause in the sense in which the exclusion has been applied by this Court in other cases. While it could be described as a substantial cause, the expression "wholly or substantially" in this context is interpreted to refer to a cause that is close to the whole cause. [63] For those reasons the appeal is allowed with the effect that the review decision is quashed and the appellant will have cover for hypoxic ischemic encephalopathy as a treatment injury. The appellant will have costs of $3,000 and reasonable disbursements. Judge D A Ongley District Court Judge