Dela Rosa v Accident Compensation Corporation (Personal Injury & Treatment Injury)

IN THE DISTRICT COURT AT WELLINGTON ITE KOTI-A-ROHE KITE WHANGANUI-A-TARA (2018] NZACC 195 ACR 032/16 UNDER THE ACCIDENT COMPENSATION ACT 2001 IN THE MATTER OF AN APPEAL UNDER SECTION 149 OF THE ACT BETWEEN ACCIDENT COMPENSAT CORPORATION Appellant AND JOHANNA DELA ROSA (as litigation guardian) Respondent Hearing: 13 November 2017 Appearances: Ms Rushbrook and T Morrison for the appellant Mr H de Groot for the respondent Judgment: 19 December 2018 RESERVED JUDGMENT OF JUDGE JH WALKER [s 20 Personal Injury; s 32 Treatment Injury; and s 33 Treatment Accident Compensation Act 2001] Background to the proceedings.......................". Positions of the Parties................... Events Prior to Birth .... Events Post Birth... The Appeal Considerations..... ......... / Application for Cover ... 8 The Law ......... .9 Medical Reports and Opinions............... ..... 11 Eliza Cloete ....... 11 Dr Ngan Kee ............ ..... . 12 Ms Davis ........... . . ... . 14 First Report Associate Professor Westgate .. 15 Professor Stone .... 19 Second report Associate Professor Westgate................ ......25 Or Tony Baird .... ..33 Final report Associate Professor Westgate. ..................... ......37 Position of the Appellant................................................ . . . ..... 42 Position of the Respondent .................."." ..... 52 Section 33(1)(d) - Failure to Treat...... 56 Discussion and Conclusion.............. ..... 60 Prior to admission ....................."." .... 63 Subsequent to Admission........ ..........."."" 65 Orders.........*.*.*.************* *..............75 [1] The Accident Compensation Corporation (the Corporation) is the appellant in this matter and Johanna Dela Rosa, the litigation guardian of Jia Dela Rosa (an infant) is the respondent. The appeal is pursuant to s 149 of the Accident Compensation Act 2001 (the Act). [2] The appeal is in respect to a review decision by Reviewer Ms Sandra Gay made on 23 December 2015 which overturned the Corporation's decision of 14 January 2014 to decline Jia cover for a treatment injury pursuant to s 20 of the Act. [3] Prior to the hearing before me, on 13 November 2017 a joint memorandum was filed, appointing Johanna Dela Rosa as litigation guardian of her daughter Jia(infant). [4] For ease of reference Jia Dela Rosa will be referred to as Jia. Background to the proceedings [5] Jia was born on 20 August 2013. She was Ms Dela Rosa's first child. Jia suffered cerebral palsy as a result of a bradycardia during her birth by caesarean section following induced labour, which resulted in a Hypoxic Ischemic Encephalopathy (HIE) and basal ganglia changes on MR of brain. [6] An application for cover was lodged with the Corporation by Liza Colete, the Auckland Hospital Board's authorised representative, on 13 September 2013. The injury diagnosis is stated as: Fetus and newborn effected by other specified complications of labour and delivery [7] A report, dated 6 December 2013, was obtained from Dr Ngan Kee, specialist in obstetrics and gynaecology. A report was also obtained from Suzanne Davis, paediatric neurologist from Starship, dated 30 December 2013. A further report dated 14 January 2014, was received from Dr Ngan Kee. [8] A decision, dated 31 January 2014, was made by the Corporation, declining cover for a treatment injury. [9] Subsequently John Miller Law on behalf of Jia lodged an application for review. The review was heard before Reviewer Ms Sandra Gay on 26 November 2015 and concluded on 7 December 2015. [10] The Reviewer issued her decision on 23 December 2015 quashing the Corporation's decision and giving Jia cover as of 20 August 2013, the date of injury, for Hypoxic ischemic encephalopathy with basal ganglia changes on MRI of brain (brain damage). Positions of the Parties [11] The Corporation's position is that Jia's personal injury was not a treatment injury . [12] The position of the respondent is that Jia suffered a personal injury caused by giving of treatment, or alternatively a failure to provide the appropriate treatment. [13] Counsel for both parties filed written submissions in respect to this appeal. [14] Counsel advised me in June 2017 that the forthcoming Court of Appeal decision of Adlam v Accident Compensation Corporation would be relevant to these proceedings. [15] The Court of Appeal decision of Adlam was issued on 16 October 2017 and Counsel for the appellant filed submissions dated 3 November 2017 and provided the Court with a Bundle of Documents and Bundle of Authorities. [16] Counsel for the respondent failed to file further submissions until the day before the hearing. It is understood these had not been served on counsel for the appellant until shortly before the hearing nor received by the Court in sufficient time to be read prior to the hearing. 2 17] Counsel for the appellant, at the commencement of the hearing sought leave, if necessary, to file further submissions. Events Prior to Birth [18] The mother Johanna Dela Rosa, is a Philippino nurse. At the time of Jia's birth, she was aged 26. [19] This was her first child. It would seem that Ms Dela Rosa's pregnancy proceeded uneventfully. It is noted in the booking form/antenatal record that her menstrual cycle was regular, that her last menstrual period was 30 October 2012 with the word sure circled. Based on those dates, the delivery was estimated as 6 August 2013. The estimated delivery date by scan was 10 August 2013. The mother was stated to be "fit and well". [20] Ms Dela Rosa had a growth scan at 34 weeks and 5 days of gestation which showed normal growth with abdominal circumference of the 50th centile. The estimated fetal weight (EFW) of 2.5 kilos was just above the 50" centile. This assessment depended on the correct maternal height and weight being entered into the programme to calculate the expected growth rates. In the report from Dr Westgate, it is noted that Ms Dela Rosa may have been shorter and heavier, in which case the EFW may have been a little under the 50th centile. [21] A further growth chart was done at 39 weeks and 2 days of gestation which showed an interval growth of abdominal circumference (around the 50th centile) a slight drop in head circumference and femur length and a narrowing of the biparietal diameter. The EFW was 3.4 kg, just above the 50" centile in the customised chart. [22] However, the liquor volume was reported as being low for gestation, with a maximum pool depth of two centimetres. As a result of the scan report, on 5 August 2013, the same day the scan was done, Ms Dela Rosa was referred to the Women's Assessment Unit for consultant review. 3 [23] No appointments were available until 13 August 2013 and the specialist who reviewed the referral was of the view there was no need to see Ms Dela Rosa before that date. [24] On 13 August 2013 at 40 weeks plus 3 days, Ms Dela Rosa was seen at the Day Assessment Unit (DAU) by senior practitioner Dr Nicholas Walker. Dr Walker recorded fetal movements were good, clinically adequate liquor volume, and good fetal growth on the scan done on the 5th. [25] A cardiotocograph (CTG) was undertaken, and was normal. It was noted there was no induction booking vacancies until 20 August 2013, so he booked Ms Dela Rosa for an induction, then arranged for her to return on 16 August 2013 for a formal scan and CTG. The plan stated: Booked with DAU ROERS - 930 scan slot for formal scan and clinical review, low threshold for IOL to be considered on Friday. 16/8/13 [26] On 16 August 2013 Ms Dela Rosa was seen at the DAU by specialist Dr Tony Baird. She was 40 weeks and 6 days gestation. Dr Baird recorded she was anxious but found no reason for induction. The CTG done that day was normal. A scan was also done. It states: Fetus Atatus Alive Fetal Activity: >2 minutes Presentation Cephalic Placement Position: Posterior fundal Amniotic fluid: Normal. The umbilical artery Doppler PI = 0.59. Comments: Active foetus. BPP 8/8. Two measurable pockets of liquor; 2.3 cm. and 1.9 cm. Normal umbilical artery Doppler. [27] No growth measurements were taken as it was less than two weeks since the previous scan. Arrangements were made for Ms Dela Rosa to be seen again on 19 August 2013. 28] On 19 August 2013 at 41 weeks and 2 days Ms Dela Rosa was seen in DAU by Dr Haddad, a specialist. Fetal movements were described as active. A CTG was done and was normal. Another ultrasound showed there was no measurable pockets 4 of liquor free of umbilical cord. The umbilical artery Doppler was normal and BPP was 6/8 (missing 2 due to low liquor). It is noted that Dr Haddad who performed the scan herself, has a diploma in diagnostic ultrasound. Induction was booked for "tonight' 7pm. [29] The sequence of events that followed were as follows: At 2030 on 19 August 2013 Ms Dela Rosa was admitted for induction. A CTG was done and was normal. A vaginal examination showed that the cervix was unfavourable with a Bishop's score of only 2. At 2115, as a result of the Bishop's score, 2 mg of prostaglandin gel was administered vaginally with Ms Dela Rosa's consent. . At 2215 a CTG done after the prostaglandin was normal and CTGs were continued. . CTG recorded between 0005 and 0050 normal and showed sleep/wake cycle. At 2350 a CTG showed some periods of low variability so the recordings continued. At 0055 a note was made that Ms Dela Rosa felt fetal movement but they were reduced in number. She was experiencing cramping pains but no tightening was palpable. . At 0100 CTG was recommenced. At 0140 the registrar was asked to review the CTG due to reduced variability. At 0145 (note these hospital notes were written in retrospect due to busy ward) an IV line was set up and IV fluids were administered to Mrs Dela Rosa. 5 . At 0220 it was noted there was a small amount of moderate meconium stained liquor on gown. CTG normal and continues to be normal with little uterine activity shown. At 0220 Ms Dela Rosa felt a small "pop" and felt a small trickle. It was noted she had ruptured her membranes (SROM). At 0240 it was noted "pink spot on pad" further trickling. Ms Dela Rosa was feeling some tightenings when palpitated. CTG continues. . Suddenly at 0301 the fetal heart rate drops to less than 60 bpm within three minutes and does not recover. Emergency calls are put out and Ms Dela Rosa is transferred to the theatre at about 0312/0315. Senior Registrar in attendance. Delivery by emergency caesarean section (CS) occurs at 0324/0327. There was no evidence of abruption in at the time of the CS and no comment on the position of the umbilical cord. Thick meconium liquor was present. (Times based on hospital notes and report of Associate Professor Westgate.) Events Post Birth [30] Baby Jia was delivered in very poor condition. She weighed 3420 grams (30.7th centile on a customised chart for maternal BMI of 25, 28.3th centile on a customised chart for maternal BMI of 25, 28.3 centile on a customised chart for material BMI of 31 and 38 on a population chart). Jia had Apgar of one, zero and zero at 5 and 10 minutes. Her cord gases had an arterial pH of 7.01, Base Excess - 16 mmol/L, venous pH 7.19, Base Excess - 7 mmol/L. She required active resuscitation and only regained a heart rate at 13 minutes of age. 6 She was treated for hypoxic ischemic encephalopathy with head cooling for 72 hours. [31] MRI scans at two weeks of age showed evidence of moderate hypoxic HIE. [32] In January 2016 Jia's clinical problems were listed by her paediatrician as being that of global development delay, evolving dyskinetic cerebral palsy and a past history of growth concerns with failure to thrive and bruxism (teeth grinding). 33] Placental histology showed a small placenta (3rd centile for weight) with one infarct which measured 4 x 4 cm. The villous maturation was normal for gestation age. The umbilical cord was described as showing a spiral every 10 mm and is described as being hypercoiled. An association between hypercoiled cords and adverse fetal outcome, possibly due to abnormal cord blood flow was noted in the pathology report (Associate Professor Westgate's report). [34] Jia's placenta was forwarded for diagnosis and a report was received for Dr Jeanette Mcfarlane Perinatal and Paediatric Pathologist dated 20 August 2013. The comment states: The placental weight (285 grams) lies below the third centile and the disc contained a large infarct. The umbilical cord shows increased coiling. Hypercoiled cords are thought to be more susceptible to abnormal blood flow and are associated with adverse outcome including fetal distress Diagnosis: placenta - weight below third centile, hypercoiled umbilical cord, infarct. [35] It is accepted that Jia suffered bradycardia during her birth by caesarean section following induction of labour, which resulted in Hypoxic-Ischemic Encephalopathy (HIE) and basal ganglia changes of the brain. The Appeal Considerations [36] The appeal requires consideration of all of the evidence, particularly that of the expert medical witnesses, Professor Stone, Dr Baird, Associate Professor Westgate and Dr Ngan Kee. 7 [37] The main areas of disagreement in relation to the expert evidence are: [a] Whether any earlier intervention by induction of labour or caesarean section was required; [b] Whether the administration of prostaglandin gel to induce labour caused the claimant's injury; [c] Whether the claimant's personal injury is wholly or substantially caused by her hypercoiled cord. Application for Cover [38] The application for cover for Jia was lodged by Eliza Cloete, the Auckland Hospital Board authorised representative, dated 13 September 2013. [39] As noted an independent advisor's report, dated 6 December 2013, was received from Dr Ngan Kee, whose specialty is obstetrics and gynaecology. Subsequently a report was obtained from Suzanne Davis, Paediatric Neurologist from Starship dated 30 December 2013 A further report was obtained from Dr Ngan Kee dated 14 January 2014. [40] A decision was made by the Corporation dated 31 January 2014 declining cover for a treatment injury for hypoxic ischaemia encephalopathy with basal ganglia changes on MRI of brain. [41] As noted, subsequently, John Miller Law, on behalf of Jia, lodged an application for review. [42] The review was heard before Reviewer Ms Sandra Gay on 26 November 2015 and concluded on 7 December 2015. The Reviewer issued her decision dated 23 December 2015. 8 [43] In her review, the Reviewer states: The issue in Jia's claim is whether treatment resulted in the diagnosed Hypoxia injury. Treatment includes failure to diagnose and failure to treat. . .. The first flag indicating that something had changed was at 39 weeks 2 days. It was found that her amniotic fluid was reduced from 7cm (at 34 weeks, 5 days) to 2cm. This was described as "borderline" [44] The conclusion of the review decision stated: Conclusion: For the reasons stated above, I quash ACC's decision, substituting it with a decision that Jia has cover for Hypoxic ischemic encephalopathy with basal ganglia changes on MRI of brain (brain damage) and that the date of injury is 20 August 2013. [45] An appeal was lodged by the Corporation dated 18 January 2016. Subsequently further medical reports have been obtained. The Law [46] The key statutory provisions which require consideration are as follows: [47] To obtain cover a claimant must prove, on the balance of probabilities, that he/she satisfy the requirements of section 20(1) of the Act. 20 Cover for personal injury suffered in New Zealand (except mental injury caused by certain criminal acts or work-related mental injury) 1) A person has cover for a personal injury if- (a) he or she suffers the personal injury in New Zealand on or after 1 April 2002; and (b) the personal injury is any of the kinds of injuries described in section 26(1) (a) or (b) or (c) or (e); and (c) the personal injury is described in any of the paragraphs in subsection (2). [48] Section 20(1)(a) and (b) are not in dispute in these proceedings. 9 [49] In respect to s 20(1)(c) the issue is whether Jia has suffered a "treatment injury" as defined in s 32 of the Act. [50] The second relevant section in these proceedings is s 32. The relevant parts of s 32 are: 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 ii) receiving treatment from, or at the direction of, 1 or more registered health professionals; or (ifi) referred to in subsection (7); and 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- 1) the person's underlying health condition at the time of the treatment; and 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: [51] In respect to the term "treatment" this is defined in s 33. The relevant parts of that section are: 33 Treatment (1) For the purposes of determining whether a treatment injury has occurred, or when that injury occurred, treatment includes- (a) the giving of treatment: (b a diagnosis of a person's medical condition: (c) a decision on the treatment to be provided (including a decision not to provide treatment): (d) a failure to provide treatment, or to provide treatment in a timely manner: [52] Accordingly, the matters required to be addressed in this case are: [a] Has there been a treatment injury (in terms of's 33 of the Act);' 10 [b] Has Jia suffered a personal injury caused by: [i] the giving of treatment ($ 33(1)(a)) [ii] or alternatively a failure to provide treatment being a failure to deliver at an earlier date (s 33(1)(d)); [iii] or alternatively a failure to provide treatment being a failure to deliver at an earlier time on 20 August 2013 ($ 33(1)(d)). [53] Both Counsel have made substantial submissions on the law which will be referred to later in this decision. Medical Reports and Opinions Eliza Cloete [54] It is noted the ACC Treatment Injury Claim dated 25 September 2013 was filed by the treatment provider Eliza Cloete, Occupational Neonatologist Newborn Services. [55] The form, details as follows: Injury caused by the treatment: Hypoxic ischaemic encephalopathy Basal ganglia changes on MRI of brain. Signs and symptom of the injury: Required respiratory support for 7 days. Seizures required 2 doses of Phenobarbit Aspiration with sucking feeds. Central hypotonia. How the injury affects daily activities: Jia is unable to take sucking feeds and is therefore receiving feeds via a nasogastric tube. The full extent of the injury will become apparent as Jia gets older. What treatment gave rise to the injury: 11 Maternal management will have to be reviewed. The obstetric team are in a better position to give information. Events or circumstances which led to the injury: Johanna Dela Rosa (TH9533) was admitted on the 19 August 2013 for induction of labour at 41 + 2 weeks gestational age. There was oligohydramnios. The fetus developed severe bradycardia and an emergency caesarean section was performed. Jia Dela Rosa was delivered at 3.27 am on 20 August 2013. She was in poor condition at birth. Her Apgar scores were 1 at 1 minute and 0 at 5 minutes. A heart rate was detected after 13 minutes of cardiopulmonary resuscitation. Whole body cooling was commenced at 1.5h of age and continued for 72h. Dr Ngan Kee [56] Prior to the review decision Dr Digby Ngan Kee, Obstetrician, Gynaecologist, Endoscopic Surgeon made two reports which provide a survey of events. In his report of 8 December 2013, he states: However at 0305 hours the Obstetric Registrar was called urgently to the ward as a sudden fetal bradycardia had developed. He found that Ms Dela Rosa was not in labour, and the cervix was not dilated. A prolonged bradycardia was still present, and therefore a "crash" caesarean section was arranged. By this time there had been a bradycardia for approximately 9 minutes. Ms Dela Rosa was transferred rapidly to theatre and a rapid caesarean section carried out. The baby was born at 0324 hours with a decision to deliver interval of less than 15 minutes. [57] Dr Ngan Kee, in his report answered a number of questions: Was the obstetric care" reasonable and appropriate for the client? Ms Dela Rosa had a normally grown baby, but a scan near term revealed liquor volume at the lower limit of normal. Follow-up was therefore arranged at the antenatal assessment unit which was initially satisfactory. However, when assessed at 41 weeks oligohydramnios was found on scan and therefore induction of labour was arranged that day. In my opinion these were appropriate decisions that would commonly be made in this situation. Induction of labour was commenced with prostaglandin gel, and subsequently spontaneous rupture of membranes occurred. CTG monitoring revealed essentially normal tracing but unfortunately a sudden, and prolonged bradycardia developed, before Ms Dela Rosa became actively contracting. Examination of CTG tracing reveals a normal baseline and reactivity just before the bradycardia. The registrar was called urgently and an emergency caesarean section was carried out rapidly, with a decision to delivery time of less than 15 minutes. 12 These actions were appropriate, and there did no appears to be any significant delay in effecting delivery. The decision to delivery interval is also within international standards. Unfortunately Ms Dela Rosa appeared to have reduced placental function at 41 weeks gestation that was reflected by the oligohydramnios. Placental reserve is likely to have been severely reduced, and most likely the prostaglandins caused increased uterine tone, precipitating the fetal bradycardia. The sudden bradycardia is an unusual response to this situation. ... In summary the decision taken in the management of Ms Dela Rosa were those that the majority of obstetricians would have made, and in my opinion her obstetric care was reasonable and appropriate ... Could, and should an alternative treatment pathway have been actioned by the obstetric team at any point that would likely to have altered the outcome for this baby'? Please explain your reasoning. If an immediate caesarean section had been carried out when the oligohydramnios had been diagnosed on scan, the fetal outcome would probably have been favourable. However this is not a course of action that most obstetricians would have followed ... Unfortunately in this case the fetal compromise was sudden and unpredictable. [58] In his second report of 15 January 2014 Dr Ngan Kee answered additional questions. Was the small amount of meconium stained liquor noted at 0200 hours significant? i.e. was it a clinical sign that should have meant a different treatment pathway be taken or was it a non specific clinical sign? Meconium stained liquor is relatively common in post-term pregnancies and is, in general a non-specific clinical sign that has a poor correlation with fetal distress. There are also different grades of meconium staining of the liquor. Thin, dilate meconium liquor, as seen in Ms Dela Rosa's case, is infrequently associated with fetal compromise. ... In my opinion the type of meconium seen at 0200hrs in the case of Ms Dela Rosa should not be considered a clinical sign of significant importance to have meant an alternative clinical pathway should have been taken. If a different treatment could and should have been taken at this point, would in your opinion this have altered the outcome? In my opinion, at 0200hrs there was not sufficient deviation from normal labour to justify intervention. There was no indication to have taken a different treatment pathway at this point. Please comment on the use of prostaglandin, was the dose used within normal limits, and was this of any significance in the overall outcome of events' Ms Dela Rosa was primigravida and had a very unfavourable cervix with a Bishop's score of 2 out of 10. In this situation it is appropriate to attempt to 13 induce labour with prostaglandin gel, and the dose of 2mg was usual in the circumstances. Uterine hypertonus can also occur in an unpredictable pattern, independent of the prostaglandin dosage. Furthermore the progressive placental dysfunction and reduced placental reserve may not be obvious before induction begins, and signs of fetal stress may occur even when mild contractions commence after prostaglandin is administered. Hence the necessity of carefully monitor the fetal heart electronically following administration of prostaglandin. Ms Davis [59] A short report was obtained from Ms Davis, Paediatric Neurologist dated 31 December 2013. [60] In answer to questions Ms Davis states that she reported the child's EEG on two occasions but was otherwise uninvolved with the care of this infant. She answered a number of questions with regard to the care of baby Jia: This claim has been lodged for hypoxic ischaemic encephalopathy and basal ganglia changes secondary to fetal bradycardia in labour. Are you aware of any additional physical injuries for this client? As far as I'm aware from the medical record there was no injury reported except for the prenatal hypoxic ischaemic insult If possible, please identify the mechanism of treatment which caused the client's hypoxic ischaemic encephalopathy, providing reasoning for your answer. The baby suffered an acute hypoxic ischaemic insult during the immediate prenatal period as evidenced by her condition at birth, including absent heart beat and metabolic acidosis. The findings of borderline oligohydramnios, and thick old meconium at birth, suggests factors acting prior to the induction of labour contribute to this outcome. . . . If possible please identify the mechanism of treatment that caused the client's basal ganglia changes? The basal ganglia are typically a site of injury in hypoxia ischaemic encephalopathy in the term infant. This area of brain is susceptible to injury because of the relatively high metabolic demands and the autonomy of blood flow in the area at this age. [61] On the basis of this medical information the Corporation reached its decision of 14 January 2014 to decline cover. 14 First Report Associate Professor Westgate [62] A Treatment Injury Advise report was obtained by the Corporation from Associate Professor Jenny Westgate dated 28 April 2016. [63] Attached to the report was Associate Professor Westgate's CV, including her qualifications. She is presently Honorary Associate Professor in Obstetrics and Gynaecology at the University of Auckland. She refers to her Research publications of some 42 in number publications dating back to 1986, 11 reviews, chapters, 6 letters with comments, 4 published extracts and 34 abstracts in Conference Proceedings. She states her primary research studies are aimed at improving fetal monitoring for which she has a number of clinical and experimental publications as a result. She is also an expect advisor to ACC and the Health and Disability Commissioner. [64] Associate Professor Westgate reviews the summary of clinical events leading up to the claim. [65] She states that she reviewed the CTGs which have been referred to, in particular those from 19 and 20 August 2013. She states: The pre and post PG recordings are normal. The CTG recorded at 2354 did not photograph well, has no gridlines showing and seems to have been reduced in size. There are no decelerations but it is not of sufficient quality to interpret. The CTG recorded between 0005 and 0050 are normal and show sleep wake cycle. Very little uterine activity was recorded The CTG recorded from 0102 showed reduced heart rate variability until 0145 when variability became normal again. Very little uterine activity was recorded At 0220 the SRM (Spontaneous Rupture of Membranes) CTG was normal at this point and continued to be normal with little uterine activity shown. 15 Suddenly at 0301 the fetal heart rate drops to less than 60 bpm within three minutes and does not recover. [66] Associate Professor Westgate answered a number of questions in this report: Were there any factors that indicated an early SC should have been performed (caesarean section)? 5/8/13 routine ultrasound for growth at 39 weeks and 2 days showed normal interval growth of abdominal circumference and EFW but maximum liquor pool depth of 2cm, which is low for 39 weeks. 13/8/13 DAU review at 40 weeks and 3 days - normal fetal movements, normal CTG 16/8/13 DAU review at 40 weeks and 6 days, ultrasound showed normal liquor volume for gestation, normal umbilical Dopplers, normal BPP, normal CTG. (Only 1 1 days since previous growth scan so too early to repeat growth measurements). 19/8/13 DAU review at 41 weeks and 2 days - normal fetal movements, normal CTG, likely bedside scan by obstetrician showed no measurable liquor pocket (that means no liquor pocket without umbilical cord in it as opposed to absent liquor), normal umbilical Doppler and normal fetal breathing and movements on scan. 19/8/13 Admission for induction - both pre and post-PG CTGs were normal. Given the sequence of events I cannot identify any factor that indicates a CS should have been performed earlier. More generally could and should an alternative treatment plan have been followed? Based on the information available to me I do not believe that an alternative treatment path should have been followed. Mrs Dela Rosa appears to have been anxious about her pregnancy given the scan findings at 39 weeks and 2 days. However she continued to report normal fetal movements and all assessments of fetal wellbeing were normal so there were no indication to intervene earlier. If an CS had been done earlier or an alternative treatment plan followed, what effect would this have had on Jia's outcome? Jia's poor outcome was due to the sudden unexpected bradycardia which occurred at 0301. Had a CS been performed before this in the antenatal period I have no doubt that Jia would have been born in good condition. Had the induction process been commenced one week earlier it is impossible to say with any certainty that the prolonged bradycardia which caused her injuries would have been avoided. 16 Do you consider that Prostaglandin Gel use was appropriately used in this case? Yes, Prostaglandin Gel use followed the induction protocol. Specifically, the antenatal movements, CTGs and umbilical artery Dopplers were all normal. The cervix was very unfavourable. Therefore it was appropriate to follow the standard induction protocol. Do you consider that the use of Prostaglandin Gel contributed to or caused the ultimate outcome? This is an interesting question because the exact cause of the sudden bradycardia suffered by Jia is unknown. The evidence which needs to be considered is as follows: a. There is no suggestion that Mrs De La Rosa's uterus was hyperstimulated as a result of the prostaglandins. b. Mrs De La Rosa was not in yet established labour. She was experiencing recurrent crampy abdominal pain but the recording of uterine activity on the CTGs does not show much uterine activity. This could be because the uterine tightenings were still very mild or the tocometer device was not well applied and/or it was due to maternal body habitus. Mrs De La Rosa did rupture her membranes which indicates that uterine activity was occurring but the evidence suggests that Mrs De La Rosa was not yet in established labour. C. The FHR pattern before the bradycardia was normal. If Jia as a feus had encountered progressive hypoxia as a result of mild uterine activity we would have expected to see progressive changes in her heart rate. In fact her FHR pattern before the bradycardia was normal. The CTG pattern in the hours prior to the sudden bradycardia showed periods of reduced variability followed by periods of normal variability. The baseline remained stable and there were no decelerations. I interpret the FHR appearance as showing sleep/wake cycles which is evidence of adequate fetal oxygenation to allow normal physiological processes. d. Sudden unexpected prolonged bradycardia was the cause of her poor condition at delivery and her subsequent outcome. The occurrence of sudden unexpected prolonged fetal bradycardia is something I have observed regularly but infrequently over the last 30 years given my special interest in fetal physiology and FHR monitoring. . .. e. Jia's placenta was very small and had one moderate sized infarct which measured 4x4cm. It is likely that she had not grown much over the last two weeks of the pregnancy. Her progressive decrease in liquor volume is consistent with fetal compensation for reduced oxygen supply by prioritising blood flow to her heart, brain, adrenals and placenta. The passage of meconium is related to gestational age and meconium is common after 41 weeks. Thick meconium indicates reduced liquor volume which reflects 17 compensation for a degree of fetal hypoxia. However, in the antenatal period the evidence is that Jia's oxygenation levels were sufficient to maintain normal fetal movements, normal Doppler flows and a normal FHR on CTG. However, her late onset growth restriction will have reduced her capacity to cope with additional hypoxia. f. Jia's cord was described as being hyper-coiled and an association between this and poor outcome was noted by the pathologist. Studies have reported that an increase in the number of coils in the umbilical cord is associated with fetal growth restriction, abnormal fetal heart rate changes and low birth weight ... It does appear that the vessels in Jia's cord were significantly more coiled than usual and it is possible that this has played a significant role in the events as I will explain later. Whether or not it contributed to the small placenta and the placental infarct is less clear to me. However, it would be unusual to have two independent pathologies. . . . g. The cord gases taken at delivery show a large discrepancy between the arterial and venous values. The results are consistent with a sudden prolonged bradycardia which is due to cord occlusion. In other causes of prolonged bradycardia, such as abruption or uterine rupture both the arterial and venous pH are very low - less than 6.9 for the arterial pH and less than 7.0 for the venous pH. In Jia's case the venous pH was lower than normal for very early labour and is consistent with a degree of hypoxia. But it is not consistent with chronic prolonged fetal hypoxia and acidemia. It is very likely that the prolonged bradycardia contributed to the degree of acidosis seen in the vein. My point is that at the onset of the bradycardia it is possible that the cord venous and arterial pHs were still in the normal range (perhaps at the lower end) seen in early labour. This would be consistent with normal fetal movements being reported by Mrs De La Rosa and seen on scan and normal Doppler studies and the preceding day and the normal CTG seen leading up to the bradycardia. h. After considering all of the above, it is my conclusion that the most likely cause of the sudden bradycardia was in-utero cord occlusion secondary to both rupture of the membranes with the loss of the small amount of liquor present and the mild contractions caused by the Prostaglandin Gel. I suspect the cord became compressed between parts of the fetal body or between the body and uterine wall. The hyper-coiled nature of the cord may have made the cord more susceptible to compression. Unfortunately, due to low liquor volumes and on-going (albeit mild) contractions the cord remained compressed which resulted in prolonged bradycardia. The cord compression would have been 18 released once the uterus was opened at the time of CS and would not have been obvious to the doctor who delivered the baby. . .. Unfortunately, this type of sudden and prolonged cord complication cannot be predicted. I suspect it is likely that the hyper-coiled cord has played a role in these events. Based on the information available about Jia's condition before the induction I cannot find any indication she should have been delivered by caesarean section [67] Associate Professor Westgate in her report also refers to a number of studies in respect to FHR patterns associated with neurologically high risk infants and studies in respect to the definition of increased coiling and the possible outcome. Professor Stone [68] A report, requested by the respondent from Professor Stone, was filed on 22 November 2016, and included an addendum dated 1 February 2017. There was also an undated curriculum vitae attached. [69] Professor Stone lists his previous appointments and his current position as the Professor of Maternal Fetal Medicine at the University of Auckland. He sets out his qualifications and notes that he has practiced in all aspects of obstetrics including intrapartum care since commencing obstetric training in 1977 until recently and has taught fetal heart rate monitoring as well as having been on the first international cerebral palsy task force chaired by Professor MacLennan and published in 1999. He stated that currently he is the obstetrics advisor to the Health and Disability Commissioner and a member of the Health Profession Disciplinary Tribunal and advice to the neonatal encephalopathy task force. [70] With regard to Ms Dela Rosa and Jia, Professor Stone notes: Joanna Dela Rosa booked very early in her first ongoing pregnancy, with sure menstrual dates which were in keeping with the early ultrasound scanning. . The dating is certain and can be based on the menstrual data. For some reason the booking midwife changed the dates to an "agreed date" of EDD being 10/08/2013. 19 A morphology scan was reported to show no abnormalities. The booking blood pressure was 100 over 60. . The fetal growth initially reported to be as expected. On 5 August 2013 (39 weeks 2 days by scan and 39 weeks 6 days by menstrual dates) following a community scan which showed a single pool of amniotic fluid at 2 centimetres in depth (the lower limit of normal) Ms Dela Rosa was referred to a hospital antenatal clinic for specialist review. The request for review stated the reduced liquor volume on scan at 39 weeks as the reason and a review of the referral was performed by a specialist who stated she should be seen "at term" Prudent surveillance should have been to either review the patient face to face or arrange an outpatient fetal assessment and recheck the amniotic fluid volume which can change over 3-4 days. An unsigned and undated annotations on the antenatal assessment form dated 6 August 2013 stated: This should be given priority due to the fact of oligohydramnios 10/08/2013. The next available date is the comment "overdue three days". Ms Dela Rosa was seen at the clinic on 13 August 2013. The specialist seemed to have reported "clinically adequate liquor volumes, good fetal growth (this means that the amniotic fluid volume was not reviewed by scan at that time because clinical means by clinical examination, that is palpitation of the abdomen)". An ultrasound was booked for a Day Assessment Unit review on 16 August 2013. There was a comment stating "low threshold for IOL (induction of labour). 20 A further CTG was undertaken on 13 August 2013. The CTG was hardly adequate as over the 20-minute period the fetus could have been in state IF, (quiet sleep) but if so, then the CTG should be run long enough (up to 45 minutes) to ascertain if fetal reactivity occurred. . The problems with a CTG is that it is very difficult to assess liquor volume clinically except in a patient with an increased BMI at this stage of pregnancy. It is not clear what a low threshold means: it is not stated what clinical symptoms or signs should have been sought by the patient or the LMC midwife and a suboptimal CTG. On 16 August 2013 an antenatal assessment was done by another specialist and it would seem no scan was done. Subsequently he notes that a scan was done however as the assessment record is annotated, the clinician was acting as though no scan had been done. It is unclear if any further formal scan assessment of amniotic fluid was done. It would have been prudent or even essential to check this given the previous scan in the post term situation. A long assessment of the CTG would have resolved whether the tachycardia was transient, related to fetal activity of more importance. Also given the AVHC induction policy it is unclear why the specialist wrote "anxious but I see no reason for IOL at the moment". Even by the ultrasound dating, that specialist seeing her on the 16/8/2013 could have been expected to plan an induction given the difficulties of getting bookings, and/or could have performed a membrane sweep. It is written by the LMC midwife notes that it is suggested this was done but may have proved too difficult (as the midwife note of 17/8/2013 states "VE cervix unfavourable for stretch plus sweep)". Further assessments were arranged for three days' time and the patient was reviewed by a different specialist. A scan was done that showed "no measurable pocket of liquor" and the specialist arranged IOL for that evening. A CT performed at 10.40 that morning seemed normal with 21 normal baseline and normal long-term viability but few accelerations with movement. The induction commenced at 2115 hours that evening and the Bishop's score was found to be 2 which suggests there would need to be a considerable time for cervical priming to occur before active labour or membrane would be feasible in the normal course of events. A CTG was commenced and showed a wandering baseline before the prostaglandin gel was inserted into the posterior fornix of the vagina to start the induction. It is difficult to interpret but at least from 2010 to 2050 there appear to be accelerations of fetal heart with maternal contractions and some commentators have concluded this is a stress response to fetus. Whilst this does suggest that the fetus had the ability to respond, it nevertheless indicates the fetus is mounting a sympathetic nervous system response to urinary activity. From 0150 to 0220 the CTG appears to be within normal parameters. Clinical notes state "Small amount of moderate meconium stained liquor on gown ... Joanna ... felt a little trickle" (note this is a moderate not thin or faint). . This is further evidence the fetus is under stress. . The ECG remained within normal parameters until 0257 when the variability reduced and shortly thereafter was followed by a terminal bradycardia and an emergency caesarean section was arranged and the baby was born at 0327. What can be said is that the baby was acidotic and clinically showing all the signs of a hypoxic/ischaemic episode. . The baby was born with metabolic acidaemia, and in the absence of any other identifiable cause for this, it is reasonable to state that the baby had 22 hypoxic/ischaemic insult during the labour and birth and had neonatal encephalopathy. Hypercoiled cord is of insignificance and it is unclear if this is a finding which occurs secondary to poor placental function and reduced placental perfusion or as a primary measure. In this case the placenta was small and had a large infarct-dead area - but the placenta cannot be held responsible for the outcome. That is to say the outcome reflects a failure to synthesise the indicators of progressive placental dysfunction meaning that Jia had inadequate reserves to cope with the stresses of labour. In summary, this was a pregnancy complicated by possibly slowing of fetal growth (at least the head measures) and reduction of amniotic fluid volume (signs of placental "failure") further complicated by proceeding past term. The feto-placental reserve was reduced and once induction of labour was commenced, the fetus had insufficient reserves to cope with the hypoxic stresses which occur in all labours. The lack of amniotic fluid and the hypercoiled cord which may have become compressed repeatedly during uterine contractions is a consistent part of the scenario. This is the outcome of a post term pregnancy with reduced to absent amniotic fluid is predictable and the main way of avoiding this is to intervene by whatever method (caesarean section or induction of labour) earlier so not to get into the situation. The mechanisms to the problem that Associate Professor Westgate states are really a corollary to poor placental reserve as compressed cord may be a result of no amniotic fluid. [71] At page 7 of his report, Professor Stone states: There appears to have been an opportunity to offer a different care plan which would certainly have led to a different outcome. The care provided to Johanna Dela Rosa was clearly planned by specialists and as serial post term assessments continued and the labour was finally induced there clearly was an intervention plan based on their clinical judgment. Thus, the patient underwent treatment, from which there was a poor outcome. 23 . . . ... I would say that the comments of Dr Ngan Kee do not reflect a holistic or overarching view of the case. While some of his comments are correct, the issue is that there were opportunities in this case to act differently. Also, as stated in my report, there are times when the CI'G was not normal and it does not appear that any detailed consideration was given to this in the context of the whole case. So Dr Ngan-Kee takes the view that the clinicians were powerless to influence the outcome whereas I would take the view that inaction as well as action may constitute treatment. It could not really be accepted that during the labour the CTG would have been regarded by most specialists as satisfactory, for over 1 hour 20 minutes between 0025 hours and 0145 hours the baseline variability was abnormal and after review intravenous fluids were given to the mother. The subsequent change in the fetal heart rate variability was ascribed to the mother's improved fluid balance. I would submit that many specialists, seeing that period of reduced baseline variability and noting that the cervix was still "unfavourable" would have opted to cease the induction and deliver by caesarean section. Taking the CTG from 0145 in isolation from anything which had happened beforehand, it is likely that some obstetricians and many registrars would have accepted that portion as satisfactory and then would have been surprised by the terminal bradycardia at around 0302hours. It is a totally reasonable and a biologically plausible comment to make, that an abnormal CTG may reflect a baby who is in trouble and indicates loss of reserve, the baby may then adapt but has of course lost some reserve - the CTG may now seem normal but it does not mean that the baby has recovered entirely. Sometimes there may be an obvious factor which can be readily corrected and which leads to a subsequently totally normal C TG such as finding the mother lying on her back and then correcting this by turning her on her side - but in this case there were no such issues, the problem was loss of reserve. Experts in reading CTGs such as Dr Westgate, but also many experienced specialists would have taken the CIGs plus the lack of cervical change and progress in labour - let alone the meconium as bad signs and would have delivered earlier. The abnormal antenatal CI'Gs that I commented upon with the fetal tachycardia are again clearly abnormal to experienced staff and many would have acted at that time, i.e. delivered and if the cervix had been unfavourable, would have suggested a caesarean section. Moreover, while I do not want to get into complex fetal physiology, there would be some scientific debate about whether fetal behavioural states (awake sleep cycles) that Dr Westgate mention actually occur in labour - they may in early labour which really strengthens the point that there was poof to no labour progress. . .. In the application for review ... it states "the brain injury occurred in the context of treatment but was due to underlying undiagnosable and precipitous health conditions". I would submit that this is not correct as the condition was diagnosable - namely an earlier scan (repeated after the "virtual clinic referral") would have seen reduced or absent amniotic fluid before the day of induction and thus the subsequent events would not have been "precipitous" 24 [72] In the addendum dated 1 February 2017 added to his report, Professor Stone states: I have had the opportunity to review an ultrasound scan report relating to the episode of care on 16/08/2013. In the first place, I do not think though we should over-rate this scan because it is only one part of the clinical scenario. There is the induction policy and also the system issue that the doctor seeing the patient may not have had the scan result whether or not it had been done. From my understanding of the clinical episode, it is stated in the clinical notes that the doctor seeing the patient did not have a scan report. Thus whether or not the scan was done, the clinical care was being determined in the absence of the scan result. Therefore, the scan result did not appear to influence the clinical decisions that were made. . . . I am not entirely certain that cord occlusion alone was the mechanism because we all know (including Dr Westgate) that in cord prolapse if the baby who is otherwise healthy is delivered with 20-30 minutes, the outcome is good. ... I emphasise that this is difficult territory for ACC to be in, but under the definitions of treatment, she was having medical care and as Dr Westgate has noted she had prostaglandins which she states contributed to the events. The scenario is not uncommon and could potentially occur in many post-term or even term deliveries with reduced placental reserves. However, I am arguing for elements of the outcome to have been avoidable by treatments and thus I believe that this is a treatment injury. [73] To his report, Professor Stone attached an article entitled 'Perinatal Outcomes Associated with Oligohydramnios in Uncomplicated Term Pregnancies'. Second report Associate Professor Westgate [74] A Second Report received from Associate Professor Westgate dated 28 April 2017, relates to specific questions put to her from Counsel. She notes that she has reviewed the following documents: . Her previous report of 8 April 2016. Observation of Professor Stone's initial report dated 18 December 2016. . Dr Stone's updated report of 1 February 2017. . Dr Ngan Kee's report of 14 January 2014. 25 [75] Associate Professor Westgate was again asked a number of questions. Question 1: Were there sufficient signs of progressive deterioration of placental function at any of the following points in the treatment timeline to suggest that, on the information available at the time, a different treatment path was available and should have been followed (for example, performing a caesarean section or induction of labour earlier)? [76] Professor Westgate gave an expansive answer: 5 August 2013 (39 + 2 weeks) An USS was done for growth 5/8/13. No clinical concerns noted prior to the scan. An antenatal assessment done 1/8/13 by LMC noted fetal movements were ++ and fetal height normal for gestation. Two previous growth scans were done 29 weeks and 34 weeks both showed normal growth. The liquor volume was reported as showing maximum pool depth of 2 centimetres which is at the lower limit of normal for gestation. The Bio Physical Profile score (BPP), a measure of three ultrasound assessments of fetal movement and tone and of liquor volume was 8/8. Prof Stone's suggestion that a slight decrease in head measurements could indicate reduced growth is incorrect and he should know that head measurements alone are not used to diagnose intrauterine fetal growth restriction. It was appropriate for lead maternity carer (LMC) to refer Mrs Dela Rosa for obstetric opinion on the scan findings of liquor volume but no other features of concerns in clinical history or scans indicate urgent assessment. Ideally mother should have been seen on Monday 12 August a week after the previous scan for review, a CTG and a repeat liquor volume assessment. There was obviously a high demand for antenatal assessments and it was reasonable to see Mrs Dela Rosa in eight days rather than in seven. There was unsigned and undated annotation of the antenatal assessment form which states This should be given priority due to the fact of oligohydramnios.' Other unacknowledged comments are also noted in what appears to be similar handwriting These annotations were probably made after the events by someone who reviewed Jia's case. Comments about the appointment timing illustrates outcome bias and refers to Hendriksen and Kaplan, 2003 where authors state: 26 Rather than use hindsight to show where people went wrong, investigators should focus prospectively on foresight and reconstruct the conditions experienced by those actively engaged in sense making at the time. In conclusion, based on the information available at the time the referral was triaged and with the resource constraints, the timing was acceptable. Tuesday 13 August 2013 (40 + 3 weeks) Mrs Dela Rosa seen by Assessment Unit reported good fetal movements and CTG was normal. No ultrasound was performed to check liquor volume but rather clinical assessment and she agrees with Professor Stone this is an inadequate method of liquor volume assessment. I believe that an ultrasound assessment of liquor volume was required and this could easily have been achieved by the obstetrician but not clear from the notes why this was not done. The LMC was advised about come by telephone and also advised that all induction of labour appointments were fully booked until 20 August. Friday 16 August 2013 (40 + 6 weeks). Mrs Dela Rosa had a formal scan performed by senior radiologist and reported normal liquor volumes. She was then seen by a senior obstetrician who reported she was anxious but there was no indication for induction at that stage. LMC were contacted by phone and asked to see Mrs Dela Rose in the next two days to perform stretch and sweep of her cervix. A review was scheduled on 19 August. CTG was performed after the obstetric review and was signed off by a midwife. The CTG showed a baseline of 160 to 165 with frequent accelerations of the fetal heart. There were no decelerations. Unfortunately, the CTG was discontinued before the baseline rate had reached normal and therefore cannot be regarded as a normal CTG. I am confident that the elevated baseline was due to frequent fetal movements. This is not uncommon. It should have been continued. Professor Stone and I are in agreement there. It is noted Professor Stone completed his report without access to the scan done at the assessment of 16 August. It was assumed it had been done but not printed, and a copy was requested and then supplied to Professor Stone. This scan is absolutely critical, without it, the management of Mrs Dela Rosa would have been concerning Professor Stone has written his report on the miscomprehension that an important investigation had not been made. The scan shows a normal post dates liquor volume and a normal BPP. In Mrs Dela Rosa's case the levels were 2.3 cms and 1.9 cms based on the scan, there is no indication to offer induction. The obstetrician did arrange a follow up scan and review in three days. It would have been reasonable to consider induction over the weekend given Mrs Dela Rosa's gestation, anxiety and liquor volume. It was absolutely clear 27 she would need reassessment and ongoing monitoring. But if we look at what was known on the day - normal liquor volume, normal BPP, normal fetal movements and no indication of vacancies over the weekend, what action should be taken? Given the circumstances, the option to review Mrs Dela Rosa after the weekend and to ask her LMC to visit on the weekend was acceptable The main concern at this point was the low normal liquor volume seen in the scan at 39 weeks and 2 days. Growth on that scan was normal. The BPPs done then and on 16 August 2013 were normal, dopplers were normal. Fetal movements were always reported as good. The scan on the 16th reported a greater volume of liquor than the scan at 29 weeks and 2 days. There is a struggle to find any evidence of progressive fetal dysfunction. Professor Stone quotes a 2004 study of outcomes of pregnancy with women with isolated oligohydramnios around term. Professor Stone points out we do not use AFI but rather maximum pool depth and we do not know Mrs Dela Rosa's AFI at 39 week and 2 days. The term isolated oligohydramnios means fetal growth on scan was normal, which suggests that Professor Stone agrees that this was the case with Mrs Dela Rosa. In post term pregnancies, IO (isolated oligohydramnios) is associated with increased risk of obstetric intervention with outcomes that are similar to those of pregnancies with normal AF. In conclusion, a key point is that the obstetrician followed the ADBH Guideline for induction in post date pregnancies on 16 August 2016. The maximum liquor pool depth was above the level at which induction was recommended and there is no other clinical indicators (such as reduced fetal movement) to indicate induction should have been offered. I do not believe that an allegation of substandard practice can be substantiated when the institutional guidelines were followed 19 August 2013 (41 + 2 weeks). Mrs Dela Rosa was visited by her LMC on Saturday 17th August who reported fetal movements were good and fetal heart rate was normal. 19 August 2013 she had a further scan for liquor volume. There was a bedside scan done at the assessment unit which showed no measurable pockets of liquor. A CTG done during the visit was normal. The fetal movements were normal and the BPP was 6/8 - 2 points were lost for low liquor. In accordance with the guideline she was offered and agreed to induction to commence that evening. This was the first time in her pregnancy that intervention was required. Questions 2: Is your answer impacted by the fact that Mrs Dela Rosa was seen within the public hospital system rather than the private care system described on page 7 of Professor Stone's report? Have you got any other comments on 28 Professor Stone's suggestion that there was a failure to synthesise the information available? [77] She responds: No, my answer is not impacted by the fact that Mrs Dela Rosa was seen in the public system, nor do I believe that her care was compromised as a result of this. Prof Stone suggested that because the obstetrician requested the LMC to visit Mrs Dela Rosa on either 17th to 18th August that this somehow indicates lack of clarity with respect to who was making management decisions. it is very common practice to ask an LMC to perform such visits and tasks when the secondary obstetric services have been consulted, particularly prior to an induction (ADHB Guideline, Induction of Labour, 2012, page 6). In Mrs Dela Rosa's case there was never any confusion about lines of responsibility for her care, nor did this affect her care in any way. Question 3: Do you have any comment on the CTG performed on 13 August 2013 which Professor Stone suggests is suboptimal and should have been run for longer at page 3 of his report? [78] She responds: No, the CTG is not suboptimal; it is normal. It ran from 1337 to around 1412 which is 35 minutes. The print out of the machine used has a more compressed scale and the photocopy is poor. However, the first 10 minutes showed frequent accelerations and the next 25 showed two clear accelerations and no decelerations. This fulfils the criteria for a normal CTG. Question 4: Was there any need for reassessment of fetal growth by an expert as referred to in page 2 of Professor Stone's report. [79] Associate Professor Westgate states: It appears to me that Prof Stone is concerned by the finding of a normal growth scan at 39 weeks and 2 days but a fundal height measure as performed and recorded by the LMC which changed from 38 cm at 38 weeks and 5 days gestation on Ist August to 35 cm one week later on 8th August. This last measurement occurred 3 days after a scan which reported normal growth and low normal liquor. Fundal height measures are known to be subjective but I believe they can be useful as a screening measure, albeit a fairly crude one. Where a fundal height measure is unusually low, a scan for growth is recommended to more accurately assess fetal size and growth. I have never seen a low fundal height measure 29 trump a normal growth scan as far as fetal assessment of growth goes. Nor have I seen any suggestion that such a scenario should be an indication to refer such a woman to a materno-fetal (MFM) subspecialist as opposed to a general obstetrician. I don't think our MFM specialist colleagues would welcome a host of referrals for this reason. Question 5: Is there an indication at any point in the post-induction CTG that a caesarean section should have been performed prior to the occurrence of the sudden, unexpected bradycardia? [80] Associate Professor Westgate states: No, I do not see any indication a caesarean section (CS) should have been performed, nor was there any evidence of a progressive decline in fetal condition due to fetal hypoxia. [81] She also responds to Professor Stone's observation in the presence of accelerations with movement on the CTG prior to the prostaglandin administration and notes: ... the tocograph pattern does not show the usual smooth shape of increased pressure which accompanies uterine contractions. The increases in pressure recorded are irregular in timing and quite spiky and are much more likely to be due to maternal movement than contractions. ... There is no evidence to support such a claim, nor does Prof Stone provide any references to support his suggestions that the ability to mount a sympathetic nervous system response to uterine activity indicates a fetus at risk. [82] She also refers to Professor Stone describing CTG 0025 to 0150 and states: I agree that there was a period of reduced variability alone (normal baseline, no decelerations) between 0025 to 0052 when the CTG was removed to allow Mrs Dela Rosa to go to the bathroom. The CTG was recommenced 10 minutes later and the variability improved from 0140. The CTG record also shows a marked reduction in the frequency of fetal movements and I believe this is evidence of fetal 'sleep' state. The presence of sleep/wake cycles of fetal activity (fetal behavioural state) is normal and generally viewed as evidence of central nervous system integrity. She refers to some literature references. [83] She continues: Medical staff were notified of the CTG appearance at 0140 and attended promptly at 0145. Intravenous fluids were commenced but by then the variability had already begun to improve. There was no indication to deliver by CS at this time. 30 [84] Professor Westgate refers to further comment by Professor Stone in respect to the CTG from 0150 to 0220. I agree with the CIG interpretation but not the comment on the significance of the meconium which I will address in answer to your next question. Thus, we both agree the CIG was normal from 0150 to 0220, some 30 minutes of recording. Therefore, it is simply not possible to support the contention that the recording showed a progressive deterioration in fetal condition. Question 6: Was the presence of meconium during labour an indication that a caesarean section should have been performed sooner? [85] Associate Professor Westgate states: No, the presence of meconium is primarily related to gestational age and race. A review of nearly 500,000 deliveries found that crude meconium-stained AF rates in preterm, term, and post-term births were 5.1% ... 16.5% ... and 27.1% ... respectively. The incidence of meconium also varies by race. ... They concluded that the overall risk of adverse outcomes in meconium stained AF is low. . . . [86] Professor Westgate notes the women classified as South Asians in this study came from the Indian subcontinent and Sri Lanka. Although she has been unable to find a rate for Filipinas, the rate of South Asians is 3% and 7%. Question 7 was: Professor Stone comments at page 7 that a terminal bradycardia does not happen without prior indications except in the rare case of placental abruption or major maternal cardiovascular collapse such as with an amniotic fluid embolism or maternal myocardial infarction. Could you comment on the nature of the bradycardia that occurred in this case and whether you agree that it could not have occurred without earlier diagnosable indications of distress? [87] The response from Associate Professor Westgate states: Prof Stone says a terminal fetal bradycardia does not occur out of the blue and I agree. But I did not use the term terminal bradycardia, I used the term sudden unexpected bradycardia. A terminal bradycardia occurs when the fetal heart rate pattern becomes progressively more and more abnormal due to continued fetal 31 hypoxia until eventually the heart rate falls to 60 bpm or so and does not recover until fetal demise. If you read my report you will note that I referred to a sudden unexpected bradycardia with a preceding normal FHR. I also reviewed the literature to show that this was a well reported phenomenon in cases with poor outcome. I also pointed out in my previous report that discrepancy in the arterial and venous cord gases indicates a sudden onset bradycardia as the cause of the asphyxia rather than a progressively developing asphyxia. [88] Question 8: Professor Stone comments at page 7 that the outcome in this case was predictable in a post term pregnancy with reduced amniotic fluid and that the main way of avoiding this outcome would be to intervene earlier. Do you agree that the outcome was predictable in this case and that an earlier intervention should have occurred? [89] Associate Professor Westgate responds: The evidence does not support Prof Stone's contention. In Section Ic of this report I discussed the outcome of post term pregnancies with low liquor volume compared to post term pregnancies with normal liquor volume. One study showed low liquor pregnancies had higher rates of low birth weight but no other differences in neonatal outcome. A meta-analysis of 4 studies reported no difference in neonatal outcome at all. Thus, there is no evidence that I can find that would support a policy of automatic CS for all women with low liquor between 41 and 42 weeks. [90] Question 9: Would using an EDD based on the menstrual date of 6 August 2013 rather than the "agreed date" of 10 August 2013 have had a material effect on the treatment decisions made? [91] Associate Professor Westgate states that she does not believe that it would make a difference. She refers to the ADHB guidelines on induction of labour and the margin of error rate in the first trimester scans. She states: Mrs Dela Rosa's first trimester scan was done at 6 weeks and 6 days. The margin of error for gestations less than 7 weeks is +/- 3 days so I believe there was justification for using the scan EDD in her case. 32 [92] Question 10: Is there any reason why these events would only have occurred during labour induced through prostaglandins and would not have occurred during spontaneous labour? [93] Associate Professor Westgate states: There is no evidence that these events occurred due to a complication of prostglandin use such as hyperstimulation (contractions which occur too frequently) or hypertonus (contractions last too long). Therefore, in my opinion it is possible that the same events would have occurred in spontaneous labour. We do not know the exact cause of Jia's sudden bradycardia but we know it was not due to an acute abruption, a cord prolapse or a ruptured uterus. It would appear that another event of sudden onset was responsible for the sudden and unexpected bradycardia. I suggested that a sudden cord occlusion due to the cord becoming 'kinked' between Jia's body parts or between her body and the uterine wall may be the cause. Her cord was hyper-coiled and may have been more susceptible to occlusion, especially after her membranes ruptured. The pathologist noted that blood flow through very coiled cords is thought to be reduced or impaired so it may be that a lesser degree of 'kinking' produced a greater degree of blood flow restriction than would have been seen in a normally coiled cord. ... However, cord occlusion in utero is not analogous to a cord prolapse because in a cord prolapse the degree of cord occlusion varies from case to case. Often cord prolapse occurs because the presenting part does not fit into the pelvis and therefore there may be inadequate pressure on the cord to cause a complete cord obstruction. [94] In respect to further general observations Professor Westgate states: If one avoids hindsight bias and relies only on the information available to the clinicians at each encounter and an understanding of the resource constraints with respect to appointment and induction availability, then each clinical encounter (bar 13" August) was acceptable and followed institutional guidelines Dr Tony Baird [95] In his report of 20 September 2017, Dr Baird states: I am familiar with the processes that led to the birth of baby Jia. It is my opinion that there were opportunities to intervene earlier with a better outcome. I have seen the electronic records at Auckland City Hospital and, on that basis, I can say that some aspects of care were less than optimal. There is no doubt that Joanna underwent treatment, from which there was a poor outcome, regardless of the causation of that poor outcome. 33 [96] Dr Baird refers to gestational dates and states: Changing the date by four days to 10th August may not seem a major issue but it can be and, it has been in my practice over forty three years doing obstetric clinics, to check with the women, many of whom know when they ovulated and the timing of their conception on which I would rely rather than an ultrasound scan which has a margin of error of three or four days during the early months of pregnancy Over recent decades, the recommended "best practice" has changed in regards to the time to induce labour if it has not occurred spontaneously. During 2013 at Auckland City Hospital, the guidance has been 41 weeks and 3 days by the accepted EDD. Some specialists hold the view that 39 weeks is the best time in a pregnancy that is normal. Individual assessment is essential with, at each visit, a careful review of all information. The Passage of Meconium The passage of meconium has never been described as normal in my experience and although there may be studies that conclude that the rate of adverse outcomes is low when there is meconium in the amniotic fluid, the presence of meconium cannot be dismissed as inconsequential. Clinically, it must be assumed that there has been some fetal distress with the potential for hypoxia, neonatal encephalopathy (as it is now known) and cerebral palsy. [97] With regard to the antenatal referral to secondary care, Dr Baird states: The referral by the independent midwife to the antenatal clinic was appropriate in this case. It is done by sending details to the Greenlane Antenatal Clinic where, on certain days of the week, a specialist obstetrician will be in attendance for a virtual consultation. [98] He notes the referral was reviewed on 8 August after the ultrasound of 5 August when it showed the amniotic fluid level was lower than normal and states he agrees with Professor Stone that at the time a plan should have been made rather than just stating "see intern". He states: In my assessment [a clinical assessment] should have been undertaken the next day at the latest. [99] Regarding the assessment of 13 August Dr Baird states: It seems clear from the notes that there was some concern, sufficient to consider induction of labour and there should have been more than just a clinical assessment of the amniotic fluid. There is a scanning machine within the Women's Assessment unit on level 9 of Auckland City Hospital, it is very easy 34 to use and to look at the fluid around the baby. Given the concern and the mention of induction, it would have been a good opportunity to do an assessment of Joanna's cervix and do a "stretch and sweep". This is a safe procedure that can help stimulate labour naturally [100] On 13 August, the gestation was 41 weeks by menstrual dates. A cardiotocography was done. He states: In my view there is a significant change in the pattern of that CTG, it is short, and cannot be called reassuring. [101] Dr Baird refers to Associate Professor Westgate using the expression "resource constraints" in respect to the public health system service. He also refers to discussions and studies on booking induction and the "weekend effect" outcomes: ... postulating that the absence of senior medical staff during the weekend leads to more poor outcomes. The findings are not conclusive in those studies, but it is not by any means unusual for the Auckland City Hospital to be short of staff and beds. ... The provision of good quality care in obstetrics with all its uncertainty, should not be constrained by fixed policies. I would agree with whoever wrote, in regard to the induction of labour for Joanna, "this should be given priority due to the fact of oligohydramnios", with the addition of the prolongation of the pregnancy. [102] He states in respect to the second assessment of 16 August: Regardless of the delay in arranging a date for induction when Joanna was seen on 13th August, the review on 16th August should have involved a full study of all the events, including the dates, the scans, the estimated fetal weight, the finding of amniotic fluid at the lowest level of normal and Joanna's anxiety. ... Whenever a woman expresses anxiety, there is another question that should be asked about the reasons for her feelings. There is nothing in the records that I have seen to show that this question was asked [103] Dr Baird states that Associate Professor Westgate has written she does not believe that using EDD based on the menstrual dates would have made a difference. He states that he disagrees and that there would have been a better outcome if induction had been done on 16 August. 35 He states: The CTG during the induction of labour showed diminished variability and a tachycardia at times which I would have called non-reassuring. [104] In his view there is enough information to show this was not a sudden event. He states: The previous signs may have been subtle and intermittent but there was meconium noted during the induction process. [105] He refers to Dr Suzanne Davis' report for ACC stating: The findings of borderline oligohydramnios, and thick old meconium at birth, suggest factors acting prior to the induction of labour contributed to the outcome. [106] He also states: I would also question the decision to give prostaglandin gel in this particular case. It is unusual for a woman to have such an unfavourable cervix at 42 weeks of pregnancy, there is no explanation beyond the fact, that for some women, the uterus does not work effectively. I would also question the decision to give prostaglandin gel in this particular case. ... It is unusual for a woman to have such an unfavourable cervix at 42 weeks of pregnancy; there is no explanation beyond the fact that, for some women, the uterus does not work efficiently . . . With the benefit of hindsight, which is unavoidable in this review of care, the examination prior to inserting prostaglandin gel would have been an opportunity to pause, to review previous assessments and the unlikelihood of a short efficient labour. I have looked at the references quoted by Professor Westgate in section 5 of her report of 8/4/2016 and I do not find them helpful. The causes of the brachycardia are not given and it is not clear what sort of sentinel event had occurred. Each case needs to be considered on its own, a sudden brachycardia that is terminal will often have previous events, the terminal event itself may be relatively mild if the baby is already compromised, rather than a healthy fetus suddenly dropping its heart rate which can occur with a total placental abruption and a cord prolapse neither of which was found this time. [107] Dr Baird concludes that: On the balance or probabilities, I think that the injurious hypoxia occurred following the insertion of prostaglandin gel, compounding the milder, intermittent insults and reduction of placental reserve. 36 [108] There is an addendum attached to his report dated 5 October 2017 which states: All of my comments were made before I was able to see a note from Joanna's independent midwife which has an entry for 16.8.13 "DAU Reviewed by Dr Tony Baird" On the 16th August 2013 I was on-call for gynaecology in the Auckland City Hospital from 8.00 am to 5.00 pm or whenever the need finishes. All my comments were made before I was able to see a note from Johanna's independent midwife which was an entry for 16/8/13 "DAU reviewed by Dr Tony Baird". On 16 August 2013 I was on call for gynaecology at Auckland Hospital from 8am to 5pm or whenever the need finishes. For Joanna Dela-Rosa, it is clear that I failed to do a full assessment for which I am deeply regretful. I must take some responsibility for the delay in the birth of Jia. Final report Associate Professor Westgate. [109] A further report was received from Associate Professor Westgate date 18 October 2016. In this report, she responds to the issues commented on by Dr Baird: 1. Gestational dating Mr Baird picks up Professor Stone's point that the due date (EDD) was changed from 6 August 2013, calculated from Ms Dela Rosa's dates to 10 August 2013 based on the ultrasound done at 6 weeks and 6 days of gestation. In my response to Professor Stone's comments I referred to the ADHB Guidelines on Induction of labour - Post dates Pregnancy (2012). The Guideline gives the following margin of error rate of first trimester scans by gestation; 6 wk +/- 3 days 7 wk +/- 4 days 8 wk +/- 4.5 days 10 wk +1- 5.5 days Mrs Dela Rosa's first trimester scan was done at 6 weeks and 6 days. The margin of error for gestations less than 7 weeks is +/- 3 days so I believe there was justification for using the scan EDD in her case. The Guideline states: Gestation should be calculated from the woman's last menstrual period. If ultrasound dating differs from the menstrual dating then the margin of error of the scan should be considered. If the discrepancy between the menstrual dating and scan dating is more than the margin of error for the scan and the menstrual dating is sure, then the menstrual dating should be confirmed as correct. 37 For example Gardosi et al (1997) concluded:! Most pregnancies undergoing post-term induction are not post-term when assessed by ultrasound dates. And Even if the date of the last menstrual period is recalled with accuracy, delay in ovulation can result in over-estimation of the true gestational age, which results in an apparent prolongation of pregnancy. It is common practice to change an EDD on the basis of scan results, particularly if the scan is early, as the margin of error in an early scan is low. 2. Timing of Induction. Mr Baird correctly states that in 2013, induction of labour for post dates pregnancy at ADHB was offered at around 41weeks and 3 days (41w3d). Currently, the recommendations are to induce closer to 42 weeks. 3. Meconium Liquor. Mr Baird states that he believes that meconium is 'never normal' and in the presence of meconium liquor it 'must be assumed that there has been fetal distress and a potential for hypoxia, neonatal encephalopathy and cerebral palsy'. Mr Baird's views are not substantiated by data, nor indeed by clinical outcomes. [1 10] Associate Professor Westgate referred to her responses to Professor Stone's comment on the presence of meconium: In my response to Professor Stone's comments on this issue, I noted that the presence of meconium is primarily related to gestational age and race. I summarised a review of nearly 500,000 deliveries which found that crude meconium-stained AF rates in preterm, term, and post-term births were 5.1% ... 16.5%, ... and 27.1% ... respectively. The incidence of meconium also varies by race. ... They concluded that the overall risk of adverse outcomes in meconium stained AF is low.2 [1 11] As to antenatal referral to secondary care she states: Mr Baird maintains that Ms Dela Rosa should have been reviewed by 9 August 2013 following the scan which showed normal growth and low normal liquor on 5 August 2013. I disagree. As I previously stated, in the presence of normal movements and no other concerns about the pregnancy, a review in a week was appropriate. ... Gardosi J, Vanner T, Francis A. Gestational age and induction of labour for prolonged pregnancy. Br J Obstet Gynaecol. 1997 Jul; 104(7): 792-7. 2 Balchin 1, Whittaker JC, Lamont RF, Steer PJ. Maternal and fetal characteristics associated with meconium-stained amniotic fluid. Obstet Gynecol 2011 Apr; 117(4) doi: 10.1097/AOG.06013e3182117a26. 38 Mr Baird also states that Mrs Dela Rosa should have been seen earlier because her antenatal scans had shown a significant fall off in customised centiles of the estimated fetal weight (EFW) on scans. ... Unfortunately, Mr Baird has not realised that the EFW plotted at 29 weeks was actually the EFW from the scan done at 34w5d [34 Weeks 5 days]. Professor Stone and I both realised this and Professor Stone noted this on page 2 of his report of February 2017. [112] In respect to the assessment of 13 August 2013, Associate Professor Westgate states: Both Professor Stone and I are in agreement that a bedside scan for liquor volume should have been performed. However, I point out, that given what we know of the scan result on 16 August 2013, it is most likely that any scan done on 13 August 2013 would have shown liquor volume of at least 2cm and possibly more .. . Sometimes it can be tricky to find a pool of liquor without cord if the cord is long or positioned in the areas where liquor is normally measured. Thus, there can be some variation in liquor pool depth between scans. Both Professor Stone and I agree that the first 10 minutes of the cardiotocography (CTG) recorded on 13 August 2013 was normal with fetal heart rate (FHR) accelerations ... This CTG fulfils the criteria for a normal antenatal CTG Mr Baird states that CTG interpretation is not 'an exact science'. However, I point out that the criteria for a normal antenatal CTG have been established since the mid 80s and have not changed since then. [1 13] Associate Professor Westgate refers to the fact that Dr Baird includes as a CTG interpretation summary from a well known textbook in respect to his concerns in respect to CTGs but the page he copied applied to intrapartum CTGs rather than antenatal CTGs. [1 14] Associate Professor continues: 6. Booking an induction. Mr Baird points out that an induction was not booked on 13 August 2013, presumably in reference to the comment that there were no available induction vacancies until 20 August 2013. He states that specialists have to prioritise clinical care and should not be constrained by fixed policies. I agree. But in Ms Dela Rosa's case neither I nor the clinicians responsible for Ms Dela Rosa's care in 2013 felt there was sufficient indication to prioritise Ms Dela Rosa's induction above those women already scheduled for induction. 39 [115] With reference to the second assessment on 16 August 2013, Associate Professor Westgate states: Mr Baird makes a number of criticisms of care offered at this assessment but apparently only realised after completing his review that he was actually the specialist that saw Ms Dela Rosa on that occasion. In doing so, Mr Baird illustrates the point I made in my response to Professor Stone's comments about management of her case. In real time, in 2013 Mr Baird did not see any reason to revert to Ms Dela Rosa's period dates; he did not see any reason to offer induction of labour on the weekend, despite her anxiety; and he did not see any reason to bring her back to the hospital for review on the weekend. Yet, in his retrospective review he demonstrates hindsight bias by criticising all these aspects of his own management (before he realised he was the treating clinician at the time). [116] She refers to his addendum and states: It is highly likely that Ms Dela Rosa's case would have been reviewed in some official forum or another at ADHB in the months that followed her delivery. Possibly Mr Baird did not participate in these reviews or possibly he did not regard his clinical care as lacking at the time. [1 17] In response to his comments, Associate Professor Westgate states: Mr Baird notes that the CTG recorded on the 16 August 2013 showed a high baseline rate and should have been continued longer. Both Professor Stone and I agree on this point. Mr Baird also states that he regards the CTG recorded during the induction process as non-reassuring at times. Both Professor Stone and I have provided detailed analysis of the CTGs. We both agree that following a period of reduced variability which was identified and responded to, the CTG returned to normal prior to the sudden bradycardia. [1 18] On comments on "sudden bradycardia" Associate Professor Westgate states: Mr Baird quotes Dr Suzanne Davis, a paediatric neurologist who provided a report about Jia to the ACC in late 2013. She stated that: "The findings of borderline oligohydramnios and old thick meconium at birth suggest that factors prior to the induction of labour contributed to the outcome." With the benefit of hindsight, this is likely to be true. Placental examination showed Jia's placenta was small, with a weight of less than the 3rd centile, it had one infarct of 4 x 4 cm and the umbilical cord was hypercoiled. A hypercoiled cord offers more resistance to blood flow and is more likely to result in complete occlusion if kinked between the fetus and the uterus or between parts of the baby or if wrapped around a limb or the neck of the fetus. So Jia's placenta and cord were both abnormal. 40 Jia's birth weight was 3420 grams which suggests she has not grown much over Jia's birthweight was 3420g, which suggests that she had not grown much over the last two weeks. However, the fact that her movements remained normal and her CTGs were normal meant that she was still getting enough oxygenation in the antenatal period. In the last week of her pregnancy, Ms Dela Rosa was monitored more closely in view of the liquor volume being at the lower end of the normal range. But in the presence of a normal growth scan and 39w2d, normal movements and CT G, there was no indication that she required delivery by caesarean section prior to the sudden bradycardia. We know in retrospect that it was very likely that Jia would get into trouble once she began to experience uterine contractions for two reasons. The first, and most common, relates to her small placenta. During a uterine contraction there is a temporary reduction in oxygen supply to the fetus. Most fetuses have more than enough oxygen to compensate for this so contractions do not cause problems for them. But in a fetus with a small placenta, with one infarct, like Jia had, this is not going to be the case. Therefore, Jia was likely to experience problems in a spontaneous labour, or an induced labour, whether the induction was on the weekend of 17/18 August 2013 or on 19 August 2013. Now, normally where the onset of even mild contractions (as Ms Dela Rosa experienced) causes significant hypoxia the fetal heart rate will show predictable changes - decelerations during the contractions, a rise in the baseline heart rate and a reduction in the heart rate variability. Mr Baird expresses the view that Jia's fetal bradycardia was due to reduced placental reserve of the fetus in response to increasing contractions. However, the clinical notes recorded that Ms Dela Rosa was only just beginning to experience tightenings at 0240 but these were not palpable. If these mild tightenings caused progressive hypoxia then this should have manifested as progressively abnormal CTG changes as described above. But, in fact, the CTG was normal from 0220 to 0300; the bradycardia occurred a few minutes after this. This evidence is not consistent with progressive hypoxia caused by the onset of contraction but rather suggests a sudden event occurred to reduce Jia's oxygen supply. This relates to the second abnormality found on examination of her placenta; the hypercoiled cord. [119] Associate Professor Westgate refers to Mr Baird being unhappy about prostaglandins being used in the induction. She states: The alternative to prostaglandins is placement of a catheter balloon through the cervix, inflation of the balloon so that it stretches the cervix thus mechanically releasing prostaglandins from the woman's cervix. However, in Ms Dela Rosa's case her cervix was closed and insertion of a balloon to perform the induction would not have been possible. [120] In summary Associate Professor Westgate states: Mr Baird's review of this case as an expert witness is quite extra-ordinary given he was directly involved in Ms Dela Rosa's care. His criticism of his own management of her care was made before he realised his involvement and illustrates a marked hindsight bias which pervades the entire report. 41 In my view careful assessment of the information available at the time of each clinical encounter (and without the benefit of hindsight) shows that the decisions taken were reasonable apart from the lack of a liquor volume scan on 13 August 2013. However, even if this had been done it is unlikely to have changed the management. There was no indication to delivery Jia by caesarean section before her sudden bradycardia in the early hours of 20 August 2013. Furthermore, the hypoxia she sustained was most likely due to sudden cord occlusion that was not heralded by CIG changes. It was probably related to a combination of a hypercoiled cord, position of the cord and a recent spontaneous rupture of the membranes. [121] Dr Baird provided a final brief e-mail dated 27 October 2017 in response. Position of the Appellant [122] Counsel for the appellant in his written submissions refers to the fact that a number of ACC appeal cases have addressed the issue of how the Court should deal with competing expert evidence and refers to the High Court decision of Martin v Accident Compensation Corporations stating the Judge must apply "a traditional approach" in analysing competing expert evidence: . . . Factors such as (non exhaustive) the extent and relevance of the practitioners [sic] qualifications and experience, the comprehensiveness of the evidence gathered, the quality of the report, where the predominance of opinion lies and the validity of criticism of other medical opinions ... [123] Counsel states that in preferring the evidence of one expert or set of experts above others the Court must give reasons that are rationale and/or consistent with the facts with reference to Ellwood v Accident Compensation Corporation+; Beckham v Accident Compensation Corporations. [124] In respect to the witnesses, Counsel states: 48. Assistant Professor Westgate is highly qualified and extensively published in obstetrics and gynaecology, with a research focus on fetal monitoring. Both Professor Stone and Dr Baird acknowledge in their reports that Associate Professor Westgate is an expert in interpreting fetal CTGs. 39. Likewise, Dr Ngan Kee is a highly qualified specialist in obstetrics and gynaecology. His qualifications are set out in the front page of each of his reports. [2009] NZLR 701 (HC) at para [31]. 2007] NZAR 2015 at [37] [2016] NZACC 92 at [12]. 42 . . . 50. As the Court will see, Associate Professor Westgate, in particular, has taken a thorough approach to producing her reports, including checking medical authorities, requesting further hospital documents, and carefully considering and reviewing all relevant documents. Associate Professor Westgate has also prepared her reports with an active focus on the context of each treatment and the information involved to those treating Mrs Dela Rosa at the time, saying (28 April 2017 page 12): If one avoids hindsight bias and relies only on the information available the clinicians at each encounter and an understanding of the resource constraints with respect to appointment and induction availability. 51. By contrast, Dr Baird, for example, notes in his report that "benefit of hindsight" is unavoidable in this review of care. [125] In his written submissions counsel refers to the legal issues that require comment from the medical reports referred to: 52. Based on the arguments advanced at review, ACC anticipates that the claimant will argue, in reliance on the evidence of Professor Stone and Dr Baird, that she has suffered a treatment injury on the basis that: (a) an induction of labour or delivery by caesarean section should have occurred sooner and that earlier intervention would have prevented her personal injury; and b) the administration of prostaglandin gel to induce labour caused the claimant's personal injury. 53. The following sections set out why ACC says that the claimant cannot satisfy the requirements necessary to obtain cover for a treatment injury. This discussion is structured as follows: (a) there was no failure to provide treatment or provide treatment in a timely manner in relation to not performing an induction of labour or caesarean section sooner (ss 32(1)(b) and 33(1)(d)), because i) there was no clinically indicated and available alternative treatment; and (ii) further while earlier intervention by way of caesarean would likely have prevented the claimant's personal injury, earlier induction of labour would not likely have prevented the claimant's personal injury. (b) the giving of treatment by administering prostaglandin gel did not cause the claimant's personal injury (ss 32(1)(b) and 33(1)(a)); and (c) the claimant's personal injury was most likely wholly or substantially caused by her underlying health conditions (s 32(2(a)). 43 [126] Counsel goes through the events in a chronological manner as to when matters arose: 54. The Court of Appeal in Adlam v ACC held that for there to be a failure to provide treatment, the claimant must show that there was an alternative treatment that was both available and clinically indicated. 55. Further, the clinical indication that a treatment that was not provided should have been provided must assessed at the time of the failure. 56. The Court of Appeal's emphasis on an indication at the time of the failure, makes it clear that this is not an assessment to be made with the benefit of hindsight. 57. ACC submits that in this case, the claimant cannot point to a sufficient clinical indication that, at the time of any of the relevant treatment decisions, one of the following treatments should have been provided: a) an earlier induction of labour; or (b) an earlier delivery by caesarean section. 58. In considering whether an induction of labour was clinically indicated, Professor Stone and Associate Professor Westgate refer to the ADHB Induction of Labour - Post Dates Pregnancy Guideline ("ADHB Guideline"), which states that: (a) induction of labour should occur the same day if an ultrasound scan shows the depth of the deepest pocket of liquor is 2.0 cm; and (b) induction of labour when there is no medical indication other than prolonged pregnancy should occur after 41 weeks and 3 days, and up to 42 weeks gestation. 59. The following section will discuss the expert evidence on whether an alternative treatment was clinically indicated at the time that each of the elevant treatment decisions, outlined at above, were made. Referral for assessment on 5 August 2013 and review on 6 August 2013 by Or Wise 60. Professor Stone suggests that rather than the obstetric assessment being arranged for the next available date, 13 August 2013, it would have been prudent to review the patient face to face or arrange an outpatient assessment and recheck of liquor volume. Dr Baird, in his report of 20 September 2017, also stated that an obstetric assessment should have been undertaken by 9 August 2013. 61. However, Associate Professor Westgate notes that there were no clinical appointments available before 13 August 2013, and that given the good growth and BPP, and the lack of concerning features shown in the previous scan of 5 August 2013, it was reasonable for Mrs Dela Rosa to be assessed on 13 August 2013. 44 62. Associate Professor Westgate's assessment was that it was appropriate for the LMC to refer Mrs Dela Rosa for obstetric assessment on the basis of low liquor volumes, but as there were no other features of concern there was no clinical indication for an urgent assessment or for early delivery. 63. Dr Ngan Kee commented that while an immediate caesarean at the time oligohydramnios was diagnosed (5 August 2013) would have had a favourable outcome, this was "not a course of action that most obstetricians would have followed" 64. Dr Baird makes an additional comment that the customised growth chart showed a "significant drop" in estimated fetal weight ("EFW") at 5 August 2013, sufficient to indicate a need to intervene rather than continue to observe. Associate Professor Westgate explains in her report of 18 October 2017, that this comment is based on a clear error. The EFW recorded on the growth chart at 29 weeks is actually the EFW from the scan performed at 34 weeks and 5 days. This means that growth was in fact normal, both Associate Professor Westgate and Professor Stone realised this point. 65. ACC submits that there was no clinical indication to induce labour or deliver by caesarean section. Obstetric assessment on 13 August 2013 66. The expert witnesses agree that the clinical assessment of liquor volume on 13 August 203 was not appropriate and that an ultrasound scan should have been performed. ACC submits, however, that even if this scan were performed it would not have altered the course of treatment that was clinically indicated. 67. Professor Stone has commented that an ultrasound scan performed at this stage "would have seen reduced or absent amniotic fluid before the day of induction". This comment was made before Professor Stone had the opportunity to review the results of the scan on 16 August 2013 which revealed that liquor depth was above 2 cm. 68. After reviewing the scan from 16 August 2013, Professor Stone added an addendum to his report dated 1 February 2017. Professor Stone maintained that even with the scan, the information available at this date was non-reassuring, and there were indications of progressive placental dysfunction. 69. This evidence is strongly refuted by Associate Professor Westgate in her report of 28 April 2017: As far as I can see the only concern to this point was the low normal liquor volume seen on the scan at 39 weeks and 2 days. Growth on that scan was normal. The BPPs done then and on 16th August 2013 were normal. Dopplers were normal. Fetal movements were always reported as good. The scan on 16th reported a greater volume of liquor than the scan at 39 weeks and 2 days. I struggle to find any evidence of a progressive fetal dysfunction. 45 70. Associate Professor Westgate observes that as the subsequent scan result on 16 August 2013 showed adequate liquor volume, "it is most likely that any scan done on 13 August 2013 would have shown liquor volumes of at least 2 cm and possibly more". As the ADHB Guideline did not require induction on 16 August 2013 (see the analysis at [75] below), it would not have required induction on an earlier date. 71. While an ultrasound scan of liquor volume should have been performed, ACC submits that it would not have provided a sufficient clinical indication to induce labour or deliver by caesarean section sooner. Obstetric assessment on 16 August 2013 72. Professor Stone commented in his report of 22 November 2016, that the CTG performed on 16 August 2013 was suboptimal, showing a baseline tachycardia. Further, he noted that it was unclear why the specialist saw no reason for induction, because the ADHB Guideline states induction should occur after 41 weeks and 3 days gestation, which would have been 16 August 2013. Professor Stone's comment is made in reliance on the gestational age of the original EDD of 6 August 2013, based on menstrual dating. 73 . The gestational age in this case was in fact 40 weeks and 6 days not 41 weeks and 3 days as Professor Stone suggests. As noted [9], the treating obstetrician was using an EDD of 10 August 2013 reflecting dating based on an early ultrasound scan. Associate Professor Westgate has commented that it is very common for the EDD to change as early scans have a low margin of error, and the vast majority of clinicians would accept an EDD based on an early scan as accurate. 74. Professor Stone's comments were made before he was able to review the ultrasound scan result from 16 August 2013, however in the addendum to his report of 1 February 2017 he suggests that the scan result did not change the clinical situation. 75. This is strongly contested by Associate Professor Westgate who states that this scan was "absolutely critical". The ultrasound scan on 16 August 2013 showed a normal BPP and recorded a maximum depth of liquor volume of 2.3 cm. Associate Professor Westgate notes that as the maximum liquor pool depth was greater than 2 cm, and there were no other clinical indicators, the ADHB Guideline was followed and there was no clinical indication that induction of labour should have been offered. 76. Dr Baird has suggested that the next obstetric review should have been scheduled for 17 August 2013 rather than 19 August 2013. However, Associate Professor Westgate has stated that even if the assessment had occurred on 17 August 2013, given the subsequent results of the assessment of 19 August 2013, "[Mrs] Dela Rosa would have reported normal fetal movements, the CTG would have been normal and it is quite possible that there would have been no change in liquor on a bedside scan only 24 [hours] after the previous scan" and "it is very unlikely that the management would have changed". 46 77. While Dr Baird is now critical, in retrospect, of his care on 16 August 2013, Associate Professor Westgate's assessment is that the treatment decisions on 16 August 2013 were appropriate: The obstetrician then appropriately did arrange a follow-up scan and review in 3 days' time [19 August 2013] (i.e. after the weekend) and also arranged for the LMC to visit Mrs Dela Rosa on the weekend (which she did and reported normal fetal movements) 78. ACC submits that there was no clinical indication to perform an induction of labour or deliver by caesarean section. Obstetric assessment of 19 August 2013 79. Neither Professor Stone or Dr Baird make any substantive comment on the obstetric assessment of 19 August 2013. 80. Associate Professor Westgate says that Mrs Dela Rosa's referral for induction on 19 August 2013 was in accordance with the ADHB Guideline that induction should be arranged for the same day where the maximum liquor pool depth is less than 2 cm, and that "this was the first time in Mrs Dela Rosa's pregnancy that intervention was required". 31. Associate Professor Westgate's evidence is very clear that: Based on the information available about Jia's condition before the induction I cannot find any indication that she should have been delivered by caesarean section. 82. ACC submits that induction of labour was in accordance with the ADHB Guideline and there was no clinical indication to deliver by caesarean section. Induction of labour with prostaglandin gel on 19 August 2013 83. Dr Baird has questioned the use of prostaglandins in this case and suggests that this was an opportunity to pause and review previous assessments rather than proceed with induction. However, Dr Baird does not suggest that delivery by caesarean section should have occurred at this time. Likewise, Professor Stone does not make any statement to suggest that induction with prostaglandin gel should not have occurred at this point. 84. The ADHB Guideline required that induction of labour occur on this date because measurable liquor was now below 2.0 cm. Associate Professor Westgate has said that the alternative to induction by prostaglandin gel would have been induction by way of catheter balloon and that this would have been impossible in Mrs Dela Rosa's case as her cervix was closed. 85. Dr Ngan Kee comments that it was appropriate to attempt to induce labour with prostaglandin gel in this situation and that the dosage, 2 mg, was both usual and appropriate. 47 86. ACC submits that there was no clinical indication to induce labour by a different method or to deliver by caesarean section. CTG monitoring during induced labour 87. Professor Stone in his report of 22 November 2011, discusses the results of the CTG run during the induced labour. He observes that the CTG results between 12:25 am and 1:45 am showed abnormal baseline variability and would not be regarded by most specialists as satisfactory. Dr Baird also states that the CIG showing diminished variability was "non-reassuring". Professor Stone states that many specialists would have opted to cease induction and deliver by caesarean at this point. 88. As noted above, Professor Stone and Dr Baird acknowledge that Associate Professor Westgate is an expert in interpreting fetal CTGs. 89. Associate Professor Westgate explains that the period of reduced variability referred to by Professor Stone was accompanied by a marked reduction in the frequency of fetal movements. She argues that this is evidence of fetal sleep state and that the presence of sleep/wake cycles of fetal activity is both normal and sign of central nervous system integrity. 90. Associate Professor Westgate maintains that the CTG monitoring during labour did not show any evidence of a progressive decline in fetal condition nor any indication to perform a caesarean section. Her evidence is clear that: In real time, there was no clear indication that delivery by caesarean section was required at any time before the sudden bradycardia occurred. Ms Dela Rosa reported normal fetal movements and her CTGs on Monday 19 August 2013 were all normal. 91. ACC submits that there was no clinical indication to deliver by caesarean section based on CTG results during labour. Presence of meconium at 2:20am on 20 August 2013 (see paragraph 22) 92. Professor Stone in his report of 22 November 2016 suggests that the presence of meconium was evidence that the fetus was under stress. However, neither Professor Stone nor Dr Baird suggest that it was a sufficient indication for delivery by caesarean. 93. Dr Ngan Kee states that the type of meconium seen in Mrs Dela Rosa's case is infrequently associated with fetal compromise. In his opinion, this should not be considered a clinical sign sufficient to suggest that an alternative clinical path should have been taken. 94. Associate Professor Westgate's evidence is that meconium is primarily related to gestational age and race. She cites a study of nearly 500,000 cases which concluded that the overall risk of adverse outcomes in cases of meconium stained amniotic fluid is low. The presence of meconium in this case was not an indication that a caesarean section should have been performed sooner. 48 95. ACC submits that there was no clinical indication to perform a caesarean section based on the presence of meconium liquor. Sudden bradycardia and emergency caesarean (see paragraph 23-26) 96. Dr Ngan Kee in his report of 6 December 2013, called the actions after the claimant's sudden bradycardia occurred "appropriate" and noted that there was no delay in delivery with the decision to delivery time being "within international standards". Associate Professor Westgate agrees, commenting that: This was a very rapid response. There has never been any suggestion that there was an undue delay in the recognition and management of Jia's unexpected bradycardia. 97. ACC submits that there was no clinical indication to perform a caesarean section any sooner following the claimant's sudden bradycardia. Conclusion 98. As the expert evidence outlined above indicates, there was no sufficient clinical indication for an alternative treatment at the time of any of the relevant treatment decisions in this case. 99. Neither Professor Stone nor Dr Baird have identified a clear point at which an alternative treatment could and should have been adopted by those involved in the claimant's care. Their focus in places is on "opportunities" where a different approach could have been taken, rather han on identifying a particular point at which a different approach could and should have been taken. Professor Stone says that "[there would appear to have been opportunities to offer a different care plan which would almost certainly have led to a different outcome. " Similarly, Dr Baird comments that (i) there were opportunities to intervene earlier with a better outcome; and (ii) there were some personal and systemic failures resulting in lost opportunities to deliver the claimant in a good condition 100. Professor Stone's report has also suggested that the outcome in this case was predictable in a post term pregnancy with reduced amniotic fluid and the main way of avoiding this would have been to intervene sooner. In response, Associate Professor Westgate noted that an analysis of four studies revealed no difference in neonatal outcomes in post term pregnancies with low liquor volumes. She emphasised that: There is no evidence that I can find that would support a policy of automatic [caesarean section] for all women with low liquor between 41 and 42 weeks. 101. In contrast to Professor Stone and Dr Baird's evidence that there were opportunities to provide different treatment, the clear assessment of Dr Ngan Kee is that: In summary the decisions taken in the management of Ms Dela Rosa were those that the majority of obstetricians would have made, and in my opinion her obstetric care was reasonable and appropriate, despite the unpredictable adverse outcome. 49 102. Dr Ngan Kee's evidence is consistent with the assessment of Associate Professor Westgate who concludes: In my view careful assessment of the information available at the time of each clinical encounter (and without the benefit of hindsight) shows that the decisions taken were reasonable apart from the lack of liquor volume scan on 13 August 2013. However, even if this had been done it is unlikely to have changed the management. There was no indication to deliver Jia by caesarean section before her sudden bradycardia in the early hours of 20 August 2013. Earlier intervention by way of induction would not have prevented the personal injury - s 32(1)(b) 103. To establish causation for the purposes of s 32(1)(b), the claimant must prove that a sufficient causal link exists between the treatment and the personal injury on the balance of probabilities. 104. In the context of a failure to provide treatment, the Court of Appeal in Adlam v ACC held that this requires the claimant to establish that the clinically indicated alternative treatment would have prevented the injury suffered. 105. ACC submits that, even if the claimant can demonstrate that there has been a failure to treat in not performing an earlier delivery by induction of labour, this alternative treatment would not have prevented her personal injury. This is because, on the evidence of Associate Professor Westgate: (a) the causal mechanism of injury was likely sudden cord occlusion resulting in a sudden bradycardia; and (b) the same events were likely to have occurred if labour occurred sooner, whether spontaneous or by induction. 106. ACC accepts that had the claimant been delivered by caesarean section prior to the occurrence of the bradycardia this alternative treatment would have prevented her personal injury. 107. The exact mechanism of injury in this case is unknown, what is clear is that a bradycardia occurred during labour which has resulted in HIE. 108. ACC anticipates that the claimant will allege that the mechanism of injury in this case was progressive fetal dysfunction, resulting in progressively developing hypoxia when the fetus was unable to cope with the stresses of induced labour, eventually culminating in the bradycardia. 109. ACC submits that the actual mechanism of injury was more likely a sudden cord occlusion resulting in a sudden onset bradycardia. 110. Associate Professor Westgate's view is that the cord became compressed between parts of the fetal body and the uterine wall, and that the cord was more susceptible to this due to the fact that it was hyper coiled. 50 111. Dr Jeanette Mcfarlane performed the placental pathology in this case in which she noted that the claimant had a hyper coiled cord. On the pathology form she recorded a comment that: Hyper coiled cords are thought to be more susceptible to abnormal blood flow and are associated with adverse outcome including fetal distress. 112. Associate Professor Westgate cites studies which have found that an increased numbers of coils in the umbilical cord is associated with fetal growth restriction, abnormal fetal heart rate changes and low birth weight. She notes that in the claimant's case the pathology suggested a "more extreme" degree of coiling. 113. The cord gasses taken at delivery were, as Associate Professor Westgate observes consistent with a sudden prolonged bradycardia due to cord occlusion. The claimant's venous pH was lower than normal for early labour and consistent with a degree of hypoxia, but not consistent with chronic prolonged hypoxia and acidemia (ie not consistent with progressively developing fetal distress). 114. Dr Baird provided an article outlining the causes of sustained fetal bradycardia during labour with his report of 20 September 2017. Associate Professor Westgate observes that of the causes listed in that article: In Mrs Dela Rosa's case there was no evidence of hyperstimulation, maternal hypotension, cord prolapse, abruption, uterine rupture or maternal hypoxia. This leaves sustained cord compression and placental infarction of the causes listed here. 115. Dr Baird's conclusion is that the claimant's bradycardia resulted from reduced placental reserve of the fetus in response to increasing contractions. In response, Associate Professor Westgate states that the CTG results prior to the bradycardia were not abnormal (as would be expected with progressive hypoxia) and therefore the evidence is not consistent with progressive hypoxia caused by contractions but rather a sudden event, in this case, sudden cord occlusion. Conclusion 116. There is no direct evidence from the expert witnesses that induction of labour on an earlier date would have avoided the claimant's personal injury. Professor Stone and Dr Baird refer to missed opportunities to deliver the claimant safely, but do not state that an earlier induction would have been successful in achieving this. 117. Rather, Associate Professor Westgate has observed that, due to the causal mechanism of the claimant's personal injury, it is likely that an earlier induction would have had the same outcome. 118. Most notably, Associate Professor Westgate in her report of 8 April 2016 states that: 51 Had the induction process been commenced one week earlier it is impossible to say with any certainty that the prolonged bradycardia which caused her injuries would have been avoided. 119. ACC submits that even if the claimant can establish a failure in the form of not delivery by induction of labour sooner, she cannot establish that this earlier induction would have avoided her personal injury and therefore under s 32(1)(b) the injury cannot be a treatment injury. Position of the Respondent [127] Counsel refers to Jia requiring significant assistance for basic functions of living. [128] His submissions rely on: Where treatment causes injury the judgment of Adlam v Accident Compensation Corporation ("Adlam") does not require any additional evidence that giving the treatment trespasses medical standards/was contra-indicated. The giving of prostaglandins was at the very least, the proximate physiological cause of her injuries. Her injuries were "caused by treatment" (s 32(1)(b) and s 33(1)(a)) and not "caused wholly or substantially by gradual process disease or infection ($ 26(2) and s 32(2)(a). She should have cover ($ 33(1)(a). [129] In the alternative, he submits (1.4 of his submissions): Where a "failure to provide treatment" causes injury Adlam provides the evidence must establish that treatment 'could and should' have been given, and if given would have likely produced a better outcome. [2007] NZCA 457. 52 . In terms of Adlam this requires evidence 'there has been some departure from a standard' in terms of a failure to act "some indication not require a standard of negligence". [130] In the alternative, in his submissions Counsel states: i. Where a "failure to provide treatment" causes injury (s 33(1)(d)), Adlam provides that the evidence must establish that treatment "could and should" have been given, and, if given, would have likely produced a better outcome. [131] This is supported, Counsel submits, with reference to Adlam, which states: [61] In the result, we consider the relevant provisions properly construed mean that in order for there to be treatment injury as a result of a failure to provide treatment it is necessary to show that an alternative treatment that would have prevented the injury suffered could and should have been given having regard to the clinical indications at the time of the alleged failure. [132] Counsel relies on the evidence of Dr Ngan-Kee's report. 2.3 In his report dated 8 December 2013, consultant obstetrician Dr Ngan- Kee said: Unfortunately Ms Dela Rosa appeared to have reduced placental function at 41 weeks gestation that was reflected by the oligohydramnios. Placental reserve is likely to have been severely reduced, and most likely the prostaglandin increased uterine tone precipitating the fetal bradycardia ... [Emphasis added] 2.4 In his report dated 15 January 2015, Dr Ngan-Kee said: The subsequent bradycardia was likely, in my opinion, to have been due to reduced placental reserve and the fetus's response to increasing contractions following the administration of prostaglandins. This is a variable and unpredictable outcome that is an accepted risk of using prostaglandins for induction of labour. [Emphasis added] [133] He also refers to Associate Professor Westgate's evidence in answer to the question "Do you consider the use of Prostaglandin gel contributed to or caused the ultimate outcome?" [134] This answer is set out in full in paragraph [66] above (counsel does not refer to the final paragraph). 53 [135] Counsel refers also to Professor Stone's report of 1 February 2017 in response to Associate Professor Westgate where he says: I am not entirely certain that cord occlusion alone was the mechanism because we all know (including Dr Westgate) that in cord prolapse if the baby who is otherwise healthy is delivered within 20-30 minutes, the outcome is good. Thus I am arguing, that whether or not cord occlusion here is a mechanism, it was occurring on the background of a fetus who had reduced uteroplacental reserve I emphasise that this is difficult territory for ACC to be in, but under the definitions of treatment, she was having medical care and as Dr Westgate has noted she had Prostaglandins which she states contributed to the events. The scenario is not uncommon and could potentially occur in many post-term or even term deliveries with reduced placental reserves. However, I am arguing for elements of the outcome to have been avoidable by treatments and thus I believe this is a treatment injury. [Emphasis added] [136] Counsel then refers at 2.7 to Associate Professor Westgate's report of 18 October 2017 where he states she "recapitulated": We know in retrospect that it was very likely that Jia would get into trouble once she began to experience uterine contractions for two reasons. The first, and most common, relates to her small placenta. During a uterine contraction there is a temporary reduction in oxygen supply to the fetus. Most fetuses have more than enough oxygen to compensate for this so contractions doe no cause problems for them. But in a fetus with a small placenta, with one infarct, like Jia had, this is not going to be the case. Therefore, Jia was likely to experience problems in a spontaneous labour, or an induced labour, whether the induction was on the weekend of 17/18 August 2013 or on 19 August 2013. [137] This part of her report is set out in more detail at paragraph [118] where she discussed the application of hindsight and the impact of the problems with the placenta which only came to light later. [138] Counsel at 2.8 of his submissions then refers to Dr Baird's email of 27 October 2017: [Question: Even if we accept H.A/Prof Westgate's postulate that the bradycardia related to a cord problem, does it remain correct to say that the labour (and the rupture of the maternal membranes) was caused by the giving of induction productions on the day (irrespective of what may have happen[ed] naturally alters)?] It is correct to say that the giving of induction products [not the usual way for clinicians to describe Prostaglandins but accurate nonetheless] was the cause of the onset of the labour. There is nothing to suggest that the labour had begun prior to the insertion of the Prostaglandins. 54 [139] Counsel concludes at 2.9 of his submissions that this implies nothing less than a direct relationship between treatment caused (prostaglandin administration) and injury event (fetal bradycardia). [140] In his submissions Counsel submits: 2.11 Clearly, the evidence incorporates a dispute about the exact physiology of the bradycardia. H.A/Prof. Westgate, postulates that the bradycardia "may" have been related to umbilical cord compression secondary to the artificiality induced uterine activity. Conversely, Dr Ngan-Kee, Dr Baird and Prof. Stone say that the bradycardia reflects fetal inability to compensate for the brief hypoxic episodes associated with induced uterine contractions (Prof. Stone leaving open the possibility of cord compression playing a role). [141] He refers to the decision of the High Court in Treloar v Treloar as to the meaning of "wholly or substantially" where Justice McGechan states: ... the word 'substantially' is not to be taken by itself. It is to be taken in the context of the phrase 'wholly or substantially', and in the wider context of the purpose of the matrimonial property legislation as a whole. The phrase 'wholly or substantially' gives the first interpretative clue. It is a gradation. The word 'wholly' of course requires the entirety: the word "substantially' then is used in the sense of some reduction downwards from that entirety. The word 'substantially' is not used in a context envisageing a building upwards from nothing; or in an objective comparative way. the use envisages marginal departure away from entirety". [142] Counsel continues: 2.13 Clearly, either the reduced placental reserves per se or some cord pathology (or a combination of those pre-clinical factors) were contributory to the outcome. However, the evidence is that the treatment set in motion the physiology that caused injury. The underlying factors are only relevant to the extent that they rendered Jia vulnerable to the risks of treatment. They cannot be regarded as the whole or substantial cause on a plain language basis. 2.14 This fact profile dove-tails with the s 33(1)(a) example given by the Court of Appeal in Adlam: [43] Suppose a drug is administered which, as a result of an unanticipated allergic reaction causes injury. It is clear that there has been treatment injury. The injury was plainly not the ordinary consequence of the treatment, which would never have been administered had the consequence been anticipated. (1988) 5 NZFLR 209. 55 2.15 Because of the underlying factors, Jia was (rhetorically) "allergic" to induction treatment given. The treatment caused injury (at least in part). Therefore, there is a treatment injury. Section 33(1) (d) - Failure to Treat [143] Counsel again refers to paragraph [61] of Adlam which states: [61] In the result, we consider the relevant provisions properly construed mean that in order for there to be treatment injury as a result of a failure to provide treatment it is necessary to show that an alternative treatment that would have prevented the injury suffered could and should have been given having regard to the clinical indications at the time of the alleged failure. [144] In respect to Failure to Treat not requiring a negligence finding to make out a "failure to treat" in s 33(1)(d) terms, Counsel refers further to Adlam: [65] As is always the case, it is necessary to focus on the words Parliament has actually used. It will be apparent from our reasoning that we have discerned a legislative policy that, while not requiring a finding of negligence, still operates on the basis that a treatment injury will only have occurred where there has been some departure from a standard and that departure has caused a personal injury . . . [69] He [Professor Todd] goes on to suggest that the now replaced concepts of medical mishap and medical error "implicitly remain highly relevant", and potentially "cover the ground". We consider these observations go further than justified by the treatment injury provisions of the Act. A distinction can be drawn between finding that a different treatment course should have been followed and establishing there was negligence. While both conclusions would often happily co-exist, the negligence finding is not one required by the Act. More importantly, we consider an approach focused on negligence reasoning runs the risk of failing to meet the legislative purpose ... [Counsel's Emphasis] [145] Counsel submits: 3.3. It follows that Adam does not require a "failure to observe a standard of care that could be reasonably expected in the circumstances8 Accordingly, it is submitted the clinical indications for an alternate course need not be absolute in a medical sense. [146] Counsel also discusses determining a "Failure to Treat" permits the use of hindsight. Negligence as codified in s 33(1) of the Accident Compensation Act (1 April 2002 to 30 June 2005). 56 He refers to [63] of Adlam that states: [63] ... with respect to the additional material on which reliance was placed in this Court, while we accept that they indicate an intention to remove the previously applicable hindsight exclusion we do not accept that is conclusive for the interpretative exercise we are required to undertake. [147] Counsel submits: 3.8 It follows that the necessary implication is that the Parliament approved the use of hindsight reasoning, which is in keeping with the intention to harmonise treatment with the "no-fault" ethic of the scheme generally and removal of the need to find negligence. [148] In his submissions Counsel states, what is required is: 3.9 This is ostensibly the first case to be decided post-Adlam, and tasks the Court to decide regarding what normative standard of should be applied to the evidence (i.e. what "should" means in s 33(1)(d) terms). Two comments can be made with some surety: i. A "failure to treat" means something more than a failure simplicitor; and if. a "failure to treat" means something less than "failure to observe a standard of care that could be reasonably expected in the circumstances". 3.10 It is submitted that the Court does not need to satisfy itself that there were indications in an absolute medical sense for a s 33(1)(d) to be engaged although that finding is eminently available on the evidence). Rather, it will be sufficient to identify some observable clinical indications capable of reasonably triggering a treatment that that would, on the balance of probabilities, have been preventative. If the Court adopts a standard of absolute indication agitated for by the Corporation, the law goes full- circle to negligence and the intent of the 2005 amendment is fully subverted. [149] In support of the position of "Failure to Treat", Counsel refers to the reports of Professor Stone and Dr Baird as "mutually corroborative" arising from the progressing lack of placental reserve and refers to: . The midwife setting a EDD "for no reason. . 6 August 2016 noted reduction of amniotic fluid - referral to National Women's Hospital the following day. . Reduction in amniotic fluid not collated with EDD. 57 . Clinic 13 August 2013 "no valid assessment of amniotic fluid. CTG did not produce a trace "reassuring" - referral on 16 August 2013". 16 March 2013 No ultrasound scan available. Dr Baird (after identification he was the attending clinician on that date) stated: "... I failed to do a full assessment" ... "I must take some responsibility for the delay in the birth of Jia". . National Women's Hospital protocol. Clinic 19 August 2013 "saw doctor" and "no measurable pocket of liquor". Induction arranged. Uterine contraction following administration of induction products, stress response and sent sudden bradycardia at 0301. [150] Counsel states: 3.12. In the round, Prof. Stone notes that the care was fragmented, which compromised full assessment and a synthesis of the clinical data as a coherent whole. A salient example of the fragmentation is that, at a critical juncture, Dr Baird provided an assessment to a patient he did not know, in circumstances where he was not even rostered onto obstetric services. [151] In 3.14 of his submissions counsel refers to various parts of Professor Stone's report from Tab 24, pages 6 and 7 of his report. In particular counsel emphasises Professor Stone's statement that: There would appear to have been opportunities to offer a different care plan which would almost certainly have led to a different outcome. The care provided to Joanna Dela Rosa was clearly planned by specialists and as serial post term assessments continues and the labour was finally induced there clearly was an intervention based on their clinical judgement. Thus, the patient underwent treatment, from which there was a poor outcome. [152] Counsel also refers to Dr Baird's evidence - where he refers to what "should" have occurred at the 16 August review, Dr Baird also takes issue in the menstrual date/EDD date being different was of importance. 58 [153] Counsel refers to the Contra evidence of Associate Professor Westgate in paragraphs 3.17-3.22 of his submissions as to the reasons why the evidence of Professor Stone and Dr Baird should be preferred. [154] This is essentially because: Associate Professor Westgate's view is not that a progressive decrease in liquor volume (oligohydramnios) determines "progressive placental retrograde" and that she "artificially" confines herself to an analysis of each clinical encounter, while the opinions of Professor Stone and Dr Baird looked at each situation in the context of the clinical course as a whole. Associate Professor Westgate is inconsistent in the matter of the lack of liquor in the scans being indicative of need of induction or otherwise. Counsel is of the view this suggests Associate Professor Westgate recognised earlier induction as an option. In respect to the discrepancy between EDD based on the menstrual data/on reliance on the scan her preference for the scan is not justified. Counsel submits Associate Professor Westgate is searching for a level of normative departure that is not required by the Act (i.e. close to negligence). [155] Counsel states: 3.22 At no fault of her own, the conclusion demonstrates why Associate Professor Westgate's evidence is conceptually unsuited to determining the question before the Court. It indexes the analysis against the norms of clinical medicine and the contingencies which govern practice. Weighting factors such as "resources constraints" and "hindsight bias" might be appropriate in a negligence action or a disciplinary proceeding but tends to situate the central concern of the evidence at real distance from a "failure to provide treatment" inquiry in s 33(1)(d) terms. 59 [156] In Conclusions, counsel states: 3.23 ... it is submitted that there were indications of a different treatment course, and that treatment course would have been likely to change Jia's outcome. Whether or not failure to act on those indications amounted to a "failure to observe a standard of care that could be reasonably expected in the circumstances" is irrelevant. At bare minimum there were signs hat meant the clinicians involved should have reasonably taken a different course. It follows that a failure to treat in s 33(1)(d) terms is made out. [157] Counsel refers to Professor Stone's report. Under the heading, "Additional Ground: Failure to Perform Earlier Caesarean", Counsel states "However, he also said the following about the indications of a caesarean immediately prior to the index event": It could not really be accepted that: during the labour the CTG would have been regarded by most specialists as satisfactory, for over 1 hour 20 minutes between 0025-0145 hours the baseline variability was abnormal and after review intravenous fluids were given to the mother. [for complete quote, see paragraph [71] above.] [158] Counsel also refer to Dr Baird who states: ... a CTG showed a baseline of 160-165 which is at the upper boarder of normality and the depths of the pools of liquor were 1.9 and 2.3, at the lower end of the normal range. Whilst it is possible to tick these off as "normal", a health baby at this stage would have much more fluid. Although Professor Westgate is an expert in fetal GTGs, there are grey areas where the interpretation can be difficult and what used to be called "non-reassuring", should lead to further assessment. The CTG during the induction of labour showed diminished variability and a bachycardia at times which I would have called "non-reassuring". [159] Counsel notes that Associate Professor Westgate responded. Discussion and Conclusion [160] The Adlam decision in the Court of Appeal arose from the Gendall J High Court decision in Accident Compensation Corporation v Adlam' which allowed an appeal overturning the District Court 's decision. 9 [2016] NZHC 1487 [2016] 3 NZLR 497. 60 [161] I find that Counsel for the respondent has attempted to dilute the wording of the answer in his submissions. The Court is not applying the wording of s 33(1) prior to the amendment in 2005. It is requiring certainty as set out in their wording of [61] (see para [143 above) and stating in [62]: [62] Taken as a whole the provisions indicate a legislative intent to limit cover for persons who suffer injury while undergoing treatment, rather than providing cover for all those who suffer. The injury said to be a treatment injury must be the consequence of a departure from appropriate treatment choices and treatment actions. The drafting could have simply provided for cover for all injury suffered while a person undergoes treatment. But that course was not taken. Rather, boundaries were set out that have the effect of limiting the availability of cover for injury during treatment. A failure in the sense of omitting to take a step required by an objective standard is necessary. [Emphasis added] [162] I find Counsel also goes on to blur the issue of "hindsight" by referring only to the last sentence of paragraph [63] (see para 146 above). [163] The Court of Appeal make it clear this is not an interpretative exercise they are required to undertake: [63] We are not persuaded there is necessarily any inconsistency between these conclusions and the various policy considerations on which Mr de Groot relied. For example, we do not consider the Hansard extracts to which he referred justify the claims made about the intent of the legislature in passing the 2005 amendment. It may accurately be said, as the Minister claimed, that a consequence of the amendment was that ACC was no longer obliged to make findings of fault, but that is not the same thing as saying that ACC does not have to be satisfied that an alternative course was available that should have been pursued. Similarly, with respect to the additional materials on which reliance was placed in this Court, while we accept that they indicate an intention to remove the previously applicable hindsight exclusion we do not accept that is conclusive for the interpretative exercise we are required to undertake. [164] Mr de Groot choses to make an unsupported assumption that this implies "Parliament approved the use of hindsight reasoning" [165] I find there is no basis for this assertion whatsoever and would seem to be a gratuitous comment without foundation and is not the intent of para [63] above. 61 [166] The Court of Appeal endorsed the High Court's position in respect to the first question, i.e. that the High Court was correct to find that a failure to treat cannot occur where there are no indications for a different treatment course. [167] Given the second question was not answered and the Court of Appeal indicated it was unsafe to answer the other 3 questions in the form they were in, the position must be that the view of the High Court in this matter prevails. [168] Accordingly, in respect to the question of whether a treatment injury occurred where with the benefit of hindsight a different course of treatment would have yielded a better result, the High Court in respect to the discussion on this issue states by way of introduction: 10 [33] ... Shortly, I will turn to consider the two questions at issue in this appeal as outlined at [8] above. But before I do so, it is useful to record certain remarks made by Judge Powell in his District Court decision to grant leave for the present appeal. Although what he had to say is not in any way binding on this Court, nevertheless, those comments in his decision are worth repeating here: "Having considered Judge Mclean's decision carefully, I agree with the parties there are clearly arguable questions of law capable of bona fide and serious argument with regard to his Honour's interpretation of s 33(1)(d) of the Act and how it otherwise interfaces with the definition of Treatment Injury contained in s 32 of the Act. Given the application is now by consent it is not necessary to go into any great detail but I note in particular that his Honour's suggestion that irrespective of any clinical indication requiring earlier intervention a treatment injury could be determined objectively through hindsight is a radical interpretation of the legislation and is arguably in conflict with s 32(1)(c)(ii). Such an interpretation would also appear to obviate the need for any causal link between the injury and the treatment actually received by a claimant and is also arguably inconsistent with earlier case law with regard to the interpretation of both s 32 and 33 of the Act." [169] Gendall J goes on to state: [58] However, I do find persuasive the submission advanced by Mr Butler for ACC that a hindsight analysis would effectively turn the ACC scheme into a system under which perfect treatment outcomes were guaranteed for patients. The effect of that would obviously result in a significant extension of cover, (possibly to include for example all kinds of illnesses that much later proved to have undiagnosed consequences) with correspondingly significant impacts on the scheme itself. 10 Accident Compensation Corporation v Adlam [2016] NZHC 1487 62 [170] In his decision, Gendall J, refers to the Court of Appeal decision of McEnteer v Accident Compensation Corporation" and states: [61] ... The Court of Appeal held that reference to circumstances and underlying health must be based on actuality and not supposition. It is artificial to predict what medical professionals might reasonably anticipate to be a necessary part or ordinary consequence of a treatment beyond what actually emerges during the course of treatment. The claimant's approach would result in an "abstracted expectation of the 'average outcome' or 'norm"". The Court of Appeal held further: "[19] Mr Gorringe's argument introduces undesirable complexity and uncertainty because it is based on a hypothetical treatment of the patient, not on the treatment that was actually required in light of what emerged during the course of treatment. This seems to us to open much scope for dispute, for no discernable [sic] reason. It is difficult to see why Parliament would wish to adopt such an approach, and we would not attribute such an intention to Parliament without clear language. [20] We consider that s 32(1)(c) requires an analysis that is rooted in the facts of the particular case- what was the injury suffered? Was it suffered in the course of the treatment undertaken? Was the injury a necessary part or ordinary consequence of that treatment? The third question, in particular requires expert opinion, but not expert opinion in the abstract; rather, it requires expert opinion reflecting what actually occurred." [171] The "alternative treatment" in this case was not specified by either Counsel. The respondent however, appears to divide events between: [a] Failure to provide treatment, where there has been some departure from standard, (para 65) prior to Mrs Dela Rosa's admission to the hospital on 19 August 2013 for induction; and [b] Failure to provide treatment, where there had been some departure from the standard post her admission on 19 August 2013. Prior to admission [172] In respect to the events prior to admission, the position of the appellant is examined in a very careful analysis of the evidence of Associate Professor Westgate 11 [2010] NZCA 126; [2010] NZAR 301 at [20]. 63 who discussed, in her three reports, the summary of each of the clinical events up to, and including, the mother's admission for induction. [173] The evidence of Professor Stone also transverses these events. Although at page 9 of Professor Stone's report, he indicates (and accepts to some extent the recovered scan) was satisfactory he is of the view that at that date the "information available was non-reassuring and the findings were indicative of progressive placental dysfunction". He does not however indicate any alternative treatment at that time that would have prevented the hypoxic ischemic encephalopathy and could have and should have been given. [174] Dr Baird's evidence I find is unreliable, created speculatively on a hindsight basis, and highly critical of the events of 16 August until he realised, he was in fact the specialist on that occasion. [175] It is noted at 3.25 of the respondent's submission he relies on Dr Baird's submission (see para [158] above) but the event Dr Baird is referring to was his own consultation with Ms Dela Rosa. [176] It is noted he was referred to by name in Associate Professor Westgate's report of 8 April 2016 on at least two occasions, and received a copy of this report. His report effectively relates to unsubstantiated criticism of most of the medical professionals including the Women's Assessment Unit and staff. [177] Dr Baird's report is presented as that of an 'expert witness', although no CV is attached. As such Rule 9.34 of the District Court Rules 2014 state that he must be provided with a copy of the Code of Conduct set out in the High Court Rules, and have read the Code of Conduct and agreed to comply with it. It is clear this has not occurred. Schedule 4 of r 9.43 of the High Court Rules 2016 state: 64 An expert witness has an overriding duty to assist the court impartially on relevant matters within the expert's area of expertise. 2 An expert witness is not an advocate for the party who engages the witness. In his report, he states, "With the benefit of hindsight, which is unavoidable in this review of care", where he is critical of every step and states that he can say that some aspects of care were less than optimal. I accordingly place little weight on Dr Baird's evidence given his failure to even recall he was part of the medical team involved. [178] I find Associate Professor Westgate's comments in her reports reasoned and persuasive and I accept Counsel for the appellant's comments in this respect. [179] Associate Professor Westgate, as noted, has gone through all of the medical events, even located the missing scan report and provided same to Professor Stone. [180] In her report of 28 April 2017, she responds at length to the Question 1 (see para [75] above), including a response to Professor Stone's comments and citing research where appropriate. [181] I find that Associate Professor Westgate also provides careful responses to the Question as to whether or not the outcome of this case was predictable in a post term pregnancy with reduced amniotic fluid and the questions as to whether the EDD date based on menstrual date rather than the "agreed" rate had any direct relevance. [182] Accordingly, I find no reliable evidence, other than speculation, that there was an indication there had been a departure from the proper standard of care and treatment available to the mother and fetus in the events leading up to her admission. Subsequent to Admission [183] Professor Stone was more forthcoming in his views subsequent to the induction which eventually commenced on 19 August. 65 [184] Counsel for the respondent states Professor Stone's position is that induction should have been earlier, but this is not articulated. [185] Professor Stone records the events at page 5 of his report. He states that between 2010 to 2050 hours "there appears to be accelerations of the fetal heart with maternal contractions and some commentators have concluded this is a stress response in the fetus". [186] He states following this "the CTG is difficult to categorise ... but from 0025 the baseline is generally abnormal with reduced variability ... intravenous fluids around 0145 ... from 0150 to 0220 the CTG appears to be within normal parameters" ... and "The clinical notes show moderate meconium stained liquor on gown.". [187] He noted "the CIG remained within normal parameters until 0257 when the variability reduced and shortly thereafter was followed by a terminal bradycardia ... an emergency caesarean was arranged ...". [188] As noted (see para [152] above), Professor Stone states that "There would appear to have been opportunities to offer a different care plan which would almost certainly have led to a different outcome." However, although he is critical of the post-induction treatment, particularly the low amniotic fluid being a risk factor Professor Stone does not identify specifically what alternative treatment should have been used. 189] Associate Professor Westgate's view is that even if labour had proceeded naturally, the same difficulties may well have arisen. This is not something that Professor Stone specifically challenges. He suggests other specialists may follow a different course but does not identify when or how. 66 [190] Professor Stone accepts Associate Professor Westgate's explanation in respect to fetal behaviour (awake/sleep cycles), and although he refers to the issue of "standard of care" he questions to whom it should apply. [191] Associate Professor Westgate in her report of 28 April 2017 goes carefully through all the factors raised by Professor Stone. [192] In particular she disputes that the concern was the low normal liquor volumes on the scan at 39 weeks, and states other than this the scan was normal, the BPPs done then and on 16 August 2013 were normal, fetal movements were good and the scan on 16 August reported a greater volume of liquor than the scan at 39 weeks 2 days. [193] Associate Professor Westgate states "I struggle to find any evidence of a progressive fetal dysfunction" (p 5 of her report). [194] She again reviews the medical events to establish on the treatment timeline whether a different treatment path was available and should have been followed and other issues raised. She confirms (BofD Tab 26): [a] The CTG of 13 August 2013 fulfilled the criteria for normal CTGs; [b] In respect to a reassessment of fetal growth suggested by Professor Stone she states, "I have never seen a low fundal height measure during a normal growth scan as far as fetal assessment of growth goes" [c] In respect to whether there was any indication at any point in the post induction CTG that a caesarean section should have been performed prior to the unexpected bradycardia she disagrees with Professor Stone's view and states: Firstly, the topograph pattern does not show the usual smooth shape e of increased pressure which accompanies uterine contractions. The increases in pressure recorded are irregular in timing and quite spiky and are much more likely to be due to maternal movement and contractions. This is partially noticeable between 2035 and 2100. Secondly, in the presence of accelerance 67 with contractions is not described as a feature of concern in the ADHB or RANZCOC fetal monitoring guidelines, nor in any other guidelines I'm not aware of. There is no evidence to support such a claim, nor does Professor Stone provide any references in support of his suggestions that the ability to mount a sympathetic nervous system response to uterine activity indicates a fetus at risk. [195] Associate Professor Westgate also provides explanation for the variability of the CTGs, including Mrs Dela Rosa going to the bathroom so the CTG was temporarily removed, and the marked reduction in fetal movements being the evidence of fetal 'sleep' state. [196] In respect to the presence of meconium during labour as an indication a caesarean should have been performed sooner, she also provides explanation of gestational age and race differences and there is no evidence before me that challenges her view. [197] Associate Professor Westgate also disagrees with the term "terminal fetal bradycardia" and refers to "sudden unexpected bradycardia" with a proceeding normal FHR. She refers to the literature to show "this was a well reported phenomena in cases with poor outcome" She also refers to her previous report that discrepancy in the arterial and venous cord gases indicate the sudden onset tachycardia as the cause of the asphyxia ...". Conclusion [198] There are a number of areas of agreement in the reports of Professor Stone and Associate Professor Westgate. [199] In respect to whether there was "failure to treat" either pre or post induction I accept Associate Professor Westgate's thorough analysis, in terms of the individual steps as recorded. 68 In addition, in respect to her detailed analysis of the pre-induction issue of oligohydramnios it is accepted this is a risk factor, but that it was monitored, and the induction procedure with the various clinicians responsible for Jia compiled with the AD HB Guideline for induction in post-date pregnancies. [200] It is noted by Associate Professor Westgate page 6 of her second report: The maximum liquor pool depth was also at a level at which induction was recommended and there were no other clinical indications (such as reduced fetal movements) to indicate that induction should have been offered. [201] In respect to post induction "failure" neither Professor Stone or Dr Baird specifically indicate an alternative procedure which should have occurred. [202] Professor Stone concurs with Associate Professor Westgate that the CTG from 0150 to 0220 was within normal parameters until 0257, which I find supports Associate Professor Westgate's opinion that a cord becoming 'kinked' has considerable merit and is supported by the subsequent report of the Perinatal and Paediatric Pathologist of 20 August 2013, and the research material referred to. [203] Professor Stone acknowledges the possibility of cord occlusion, although his view is that in cord prolapse, if the baby who is otherwise healthy is delivered with 20-30 minutes, the outcome is good. [204] Associate Professor Westgate however notes that this is in cases where the cord comes down through the cervix before the baby and she states (see para [93] above) "... cord occlusion in utero is not analogous to a cord prolapse because in a cord prolapse the degree of cord occlusion varies from case to case." [205] Dr Mcfarlane, in addition, the day after the birth, confirms in her report the difficulties with the placenta and concludes: The placental weight (285g) lies below the third centile, and the disc contains a large infarct (dead tissue due to inadequate blood supply to affected cord). The umbilical cord shows increased cooling. Hypercoiled cords are thought to be more susceptible to minimalised blood flow and associated with adverse outcome including fetal distress. 69 [206] Accordingly, I do not find grounds for a treatment failure pursuant to s 33(1)(d) of the Act have been established. Injury caused by Treatment Given s 33(1)(a) [207] The position of the respondent is that the use of Prostaglandins to assist in inducing Mrs Dela Rosa initiated the uterine contraction and membrane rupture which caused "the injury mechanisms postulated to manifest". [208] Counsel for the appellant states at 2.11 of his submissions: In that regard, the underlying factors are accommodated by ss 26(2) and s 32(2)(a) which provide that cover is only excluded where injuries are caused "wholly or substantially" by non-treatment factors. [209] Counsel continues: Clearly, either the reduced placental reserves per se or some cord pathology (or a combination of these pre-clinical factors) were contributing to the outcome. However, the evidence is that the treatment set in motion the physiology that caused injury. The underlying factors are of relevance to the extent that they rendered Jia vulnerable to the risk of treatment. They cannot be regarded as the whole or substantial cause on a plain language basis. [210] Counsel states that this fact profile dove-tails with the s 33(1)(a) example given by the Court of Appeal in Adlam: [43] Suppose a drug is administered which, as a result of an unanticipated allergy reaction causes injury. It is clear that there has been treatment injury. The injury was plainly not the original consequence of the treatment, which would never have been administered had the consequence been anticipated. [211] Counsel for the appellant relies on the evidence of Dr Ngan-Kee (report 8 December 2013): Unfortunately Ms Dela Rosa appeared to have reduced placental function at 41 weeks gestation that was reflected by the oligohydramnios. Placental reserve is likely to have been severely reduced, and most likely the Prostaglandins increased uterine tone precipitating the fetal bradycardia ... [Emphasis added] [212] Counsel also refers to Dr Ngan-Kee's report of 15 January 2015: The subsequent bradycardia was likely, in my opinion, to have been due to reduced placental reserve and the fetus's response to increasing contractions 70 following the administration of Prostaglandins. This is a variable and unpredictable outcome that is an accepted risk of using Prostaglandins for induction of labour. [Emphasis added ] [213] Counsel refers to part of Associate Professor Westgate's report of 8 April 2016 (set out in para [65] above). [214] Counsel refers to Professor Stone's statement: ... I emphasise that this is difficult territory for ACC to be in, but under the definitions of treatment, shew as having medical care and as Dr Westgate has noted she had prostaglandins which she states contributed to the events. The scenario is not uncommon and could potentially occur in many post-term or even term deliveries with reduced placental reserve. However, I am arguing for elements of the outcome to have been avoidable by treatments and thus I believe this is a treatment injury. \ [Emphasis added by Counsel] [215] Counsel also refers to Associate Professor Westgate further report of 18 October 2017 and Dr Baird's report of 27 October. [216] The position of Counsel for the respondent is that the administration of Prostaglandin gel constitutes the giving of treatment for the purposes of s 32(1)(b). However, the Prostaglandin gel contributed to the events only by virtue of the fact that induction was required to progress labour. It is inserted to "soften and open" the cervix to assist delivery. Earlier "sweeping" or a balloon catheter insertion had not been possible. [217] Counsel submits is not established on the balance of probabilities that the administration of the prostaglandin gel caused the personal injury for the purpose of s 32(1)(b) and only contributed to events by the fact that it induced the natural progress of labour. [218] As stated by Associate Professor Westgate "It is likely the same events would have occurred with spontaneous onset of labour". 71 Discussion [219] Mrs Dela Rosa was admitted for an induction in the evening of 19 August 2013. [220] It is accepted that in terms of Auckland District Health Board protocol, there was some risk and this was why induction was to proceed. [221] It is clear, as referred to by Dr Ngan Kee, that following the results of the Bishop's score of only 2, and the patient's consent obtained, in order to proceed with the induction, prostaglandins were required to be administered. The CTG done after the prostaglandins were administrated was normal. [222] As noted, Associate Professor Westgate has made it clear that the only alternative method is placement of a catheter balloon through the cervix, with the inflation of the balloon however in Mrs Dela Rosa's case her cervix was closed and insertion of a balloon not possible (page 7 of report 18 October 2017). Certainly, no alternative means of progressing her labour has been identified by any other medical expert. [223] Associate Professor Westgate also provides evidence that a review of the CTG shows the prostaglandin did not cause uterine hyperstimulation - an over stimulation of contractions, which can result in reduced oxygenation to a fetus. She states "Thus, it was not the prostaglandins per se which caused the problem, but the onset of contractions and spontaneous rupture of the membranes" and "in real time, there was no clear indication on that delivery by caesarean section was required at any time before the sudden bradycardia occurred". [224] She confirms Ms Dela Rosa reported normal fetal movements and the CTGs on Monday 19 August 2013 were all normal". [225] Accordingly, in respect to an injury caused by treatment, I do not find, on the balance of probabilities, that the treatment received by Ms Dela Rosa, including the administration of prostaglandin gel is treatment that caused Jia's condition. 72 The Review Decision [226] I note that the decision the respondent is endeavouring to uphold is the decision of the Reviewer, Ms Gay, issued 23 December 2015. [227] Present Counsel was also acting for Ms Dela Rosa in that hearing and the review decision states, in respect to Mr de Groot's written submissions: Reduced placental reserve was clearly a factor involved in Jia's inability to tolerate induction. However, this was an underlying factor predisposing Jia to injury, rather than a causative factor in the sense of's 32(2)(a). [228] In addition, the Reviewer also refers, and relies on Mr de Groot's submissions in the District Court decision in Adlam (since overturned in the High Court and upheld in the Court of Appeal). [229] However, the High Court decision and the Court of Appeal decision in Adlam change the landscape and now form an integral part of reaching any conclusion as to failure to treat, and requires that a claimant (in this case the respondent) must show alternative treatment would have prevented the injury suffered and could and should have been given. [230] However, the respondent's position falls well short of this. In addition, in respect to the Reviewer's decision, this was not the test that was applied. [231] Accordingly, Counsel for the respondent's statement, that this "dove-tails with [43] of Adlam, where the drug administered resulted in an unanticipated reaction causing injury" is incorrect. I find it has not been established that the use of prostaglandin gel produced any adverse or unexpected effects. [232] Accordingly, I find that the bradycardia which resulted in Hypoxic Ischemic Encephalopathy (HIE) and basal ganglia was not a treatment injury and has not been shown to have occurred either wholly or substantially because of an underlying health condition. 73 [233] I accept the submission of Counsel for the appellant that the evidence does not support the assertion that the Prostaglandin gel had a causal relationship to the claimant's personal injury, either on its own, or linked in some way suggested by Counsel for the respondent, with reduced placental reserves per se or some cord pathology. [234] I accept Associate Professor Westgate's opinion that Jia was likely to have experienced problems in a spontaneous labour or an induced labour. [235] I accept the submissions of Counsel for the appellant that under s 33(2)(g) of the Act, an injury can only be a treatment injury, if it is demonstrated on the balance of probabilities it was not caused wholly or substantially by her underlying condition. [236] The fact that the umbilical cord was hypercoiled rendered her susceptible to sudden cord occlusion during labour and it is noted in the Paediatric Pathologist's report it is often associated with adverse outcomes. [237] In this particular circumstance, this was the probable cause for the sudden bradycardia and resulting HIE, and alines with Associate Professor Westgate's wording of "sudden unexpected bradycardia" occurring, was sudden cord occlusion. Medical Evidence [238] Overall, I find that both Associate Professor Westgate and Professor Stone have presented their views in terms of their observations and analysis of the presentation of Ms Dela Rosa at the time of the various events in terms of expert witnesses in terms of R 9.43 of the High Court Rules 2016. [239] I have express some disquiet as to the "expert" evidence of Dr Baird and his views based on 'hindsight' [240] I find Associate Professor Westgate has expertise in this area and interpretation of CTG of particular importance, combined with Dr Ngan Kee's report as specialist at the time of the induction process. 74 [241] Although both Associate Professor Westgate and Professor Stone identify some shortcomings in the matters leading up to Mrs Dela Rosa's admission, these are more of form than identifying where there could be process improvement, rather than identifying error or any basis for alternative treatment. [242] The evidence of the expert witnesses has been a major feature of this decision, and I have taken into account their qualifications and experience in their fields, their opinions and their analysis. [243] In this, I prefer the reports of Associate Professor Westgate who has provided detail and research supporting her statements. Orders [244] The appeal is granted. [245] The decision of the Reviewer is quashed and the decision of the Corporation, declining this application for cover is reinstated. [246] There is no issue as to costs. Judge J H Walker District Court Judge 75