Buckley v Accident Compensation Corporation (Treatment Injury)
Judge held on the balance of probabilities that Marion's cerebral palsy was substantially caused by failure to provide treatment in a timely manner: (1) the pregnancy met clinical indications for being managed as high risk requiring a formal plan, continuous monitoring and consultant oversight, and failure to have...
Source-derived case information.
- Citation
- [2019] NZACC 100
- Parties
- Appellant: Susan Buckley as litigation guardian for Marion Buckley; Respondent: Accident Compensation Corporation
- Court
- District Court
- Jurisdiction
- New Zealand
- Judgment Date
- 20 August 2019
- Procedural Posture
- Accident Compensation Appeal (treatment Injury) / Rehearing in District Court After High Court Remittal
- Outcome
- Appeal allowed; ACC review decision set aside and ACC decision declining cover quashed; appellant awarded cover for treatment injury
- Legal Topics
- Treatment Injury, Causation, Timeliness of Treatment, High Risk Pregnancy Management, Failure to Provide Treatment
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Summary, issues, holding and outcome
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Parties
Susan Buckley as litigation guardian for Marion Buckley
Appellant
Accident Compensation Corporation
Respondent
Procedural Posture
Accident Compensation Appeal (treatment Injury) / Rehearing in District Court After High Court Remittal
Legal Issues
- 1 Whether cerebral palsy was caused by treatment or delay in treatment during labour and delivery
- 2 Whether there was a failure to provide treatment in a timely manner under s33(1)(d) and s32(1)(b)
- 3 Whether any departure from accepted standards caused the injury on the balance of probabilities
Ratio Decidendi
Judge held on the balance of probabilities that Marion's cerebral palsy was substantially caused by failure to provide treatment in a timely manner: (1) the pregnancy met clinical indications for being managed as high risk requiring a formal plan, continuous monitoring and consultant oversight, and failure to have such a plan was an omission that impacted the response to acute bradycardia; (2) there were material delays from the detection of bradycardia (around 10:22) to calling/arrival and to delivery (delivered 10:46), and those delays more than materially contributed to the brain injury; therefore the ACC decision declining cover was quashed and cover awarded.
Court Disposition
Appeal allowed; ACC review decision set aside and ACC decision declining cover quashed; appellant awarded cover for treatment injury
Orders
- Review decision dated 30 January 2012 set aside
- Corporation's decision of 1 December 2010 quashed
Full Case Text
Judgment text and source record
1 paragraphs
IN THE DISTRICT COURT AT WELLINGTON ITE KOTI-A-ROHE KI TE-WHANGANUI-A-TARA [2019] NZACC 100 ACR 217/16 UNDER THE ACCIDENT COMPENSATION ACT 2001 IN THE MATTER OF AN APPEAL UNDER SECTION 149 OF THE ACT BETWEEN SUSAN BUCKLEY AS LITIGATION GUARDIAN FOR MARION BUCKLEY Appellant AND ACCIDENT COMPENSATION CORPORATION Respondent Hearing: 1 March 2019 Appellant's reply submissions completed: 20 June 2019 Appearances: Ms E Bransgrove and Ms B Woodhouse for the appellant Ms A Miller for the respondent Judgment: 20 August 2019 RESERVED JUDGMENT OF JUDGE DENESE HENARE [Treatment Injury ss 32 and 33 Accident Compensation Act 2001] [1] Marion Buckley has cerebral palsy as a result of an hypoxic ischaemic insult to her brain, prior to her delivery on 23 May 2007. [2] The Corporation declined a claim for cover for treatment injury for cerebral palsy. 3] On behalf of Marion, it is claimed there was delay in treatment and her injury could have been mitigated, or avoided entirely, by timely intervention with an available treatment. [4] While it is accepted Marion has suffered a personal injury, the Corporation does not accept the injury was caused by treatment, or delay in treatment. Appeal remitted by consent from the High Court for rehearing in the District Court [5] The appeal was first heard before Her Honour Judge Cunningham in November 2014. In a decision dated 15 April 2015' Judge Cunningham dismissed the appeal, finding that it had not been proved on the balance of probabilities that it was treatment or lack of treatment that caused Marion's injury. [6] The appellant was granted leave to appeal on two questions of law to the High Court.2 [7] By consent of the parties, the appeal was remitted back to the District Court. 3 [8] Justice Williams issued a brief judgment in which he noted: Judge Cunningham did not give reasons that were sufficient for the appellant to understand why the appeal was dismissed. Overall, the reasons given are very brief. [9] Justice Williams made the following orders: [a] The appeal is allowed by consent on the basis that insufficient reasons were given for the findings in the District Court judgment; and [b] The District Court will rehear this proceeding on the basis that the issue for determination is whether the claimant has suffered a treatment injury within the meaning of the Act. [10] By consent, due to Marion's age of 11 years, an order was confirmed at hearing appointing her mother Susan Buckley, litigation guardian in the appeal, within Rule 4.31(1) of the District Court Rules 2014. Buckley v Accident Compensation Corporation [2015] NZACC 84. WN Buckley v Accident Compensation Corporation [2016] NZACC 68. Buckley v Accident Compensation Corporation [2016] NZHC 1500. Agreed Facts [11] This case largely turns on the events during delivery as identified in the agreed facts in the joint memorandum of counsel dated 20 June 2019, as follows: [a] Marion is the second child of Mrs Susan Buckley and was born on 23 May 2007 at Palmerston North Hospital. [b] Mrs Buckley was admitted to the delivery suite with regular contractions at 9.45 am on 23 May 2007. She reported regular contractions since 7.00 am. [c] A CTG was commenced at 10.13 am and was reported as reactive (normal). [d] Mrs Buckley's membranes spontaneously ruptured at 10.20 am and she reported feeling "pushy". Mrs Buckley's cervix was assessed as being fully dilated. Subsequent auscultation of the foetal heart rate by use of sonic aid showed bradycardia was present. The Obstetric Registrar was called. [e] Dr Saleh, Obstetric Registrar, placed a foetal scalp electrode by 10.35 am. This recorded a foetal heart rate of 110-120 bpm with poor variable decelerations. [f] A second midwife, Ms Holmes, paged Dr Grant, Obstetric Consultant at 10.35 am. [g] Dr Grant arrived in the delivery suite at 10.40 am. [h] Following a clinical assessment, a ventouse delivery was performed (with episiotomy) and Marion was born at 10.46 am. A paediatrician was present and gave immediate resuscitation. [i] Marion was born with a true knot in her umbilicus. Her Apgar scores were 3, 6 and 7, and the cord pH was 6.4. She first gasped at 6 minutes of age and breathing was established after ten minutes. The claim and evidence at the first appeal [12] On 11 April 2008 a treatment injury claim was lodged for "birth trauma cerebral palsy." [13] On 8 September 2008 Dr Richardson, Paediatrician reported the personal injury as profound hypoxic ischaemic insult to the brain following the rupture of membranes. As to a causal link between the treatment and the injury he stated: This question is extremely difficult. If Marion's mother - Susan, had undergone an elective caesarean section the week before, or had a plan for caesarean section in early labour, I believe the outcome would have been better. However, there were no indications for such a treatment plan. When the problem arose, this was recognised quickly and a very appropriate management plan was put into effect. Unfortunately, Marion had already suffered a profound hypoxic / ischaemic event and I believe that any delivery plan made at that point would not have achieved a better result, and that any plan that delayed the delivery further would have resulted in Marion's death. In other words, a different (if not indicated prospectively) plan may well have resulted in a normal outcome for Marion. However, under the circumstances, this poor outcome could not have been predicted and the best possible plan was employed from the time the "event" occurred. [Emphasis added] [14] Dr Richardson went on to state: The plan for labour and delivery was not wrong, but a different plan could have led to a normal outcome here. [15] Dr Hill, Obstetrician and Gynaecologist reported on 11 September 2008. He noted ongoing hyperemesis during pregnancy requiring four admissions before 17 weeks. Dr Hill noted Mrs Buckley had "unclassified bleeding" during the third trimester of pregnancy and late onset hypertension and commented: Susan clearly had "unclassified bleeding" during the third trimester of her pregnancy, 60% of these cases being related to marginal sinus rupture. The risks of unclassified bleeding are that this type of bleeding is associated with a higher perinatal mortality rate, which varies from 3.5% to 15.7% (High Risk Pregnancy - Management Options, James, Steer, Weiner and Gonic, Chapter 59, Page 1270). This perinatal rate is higher than that associated with placenta praevia, suggesting some degree of placental dysfunction. I am not sure of the antenatal care structure at Palmerston North Hospital, but I note that a Dr Grant and Dr Ngan Kee were both consultants involved with the care, following the initial admission with a small bleed, Susan was subsequently seen at Antenatal Clinic either by a trainee intern or a house surgeon and I believe that as she was at "high risk" she should have been under the direct care of a consultant obstetrician. Management options of "unclassified bleeding" do depend on gestational age and I do not believe that there was any place for performing a Caesarean section when Susan presented with an antepartum haemorrhage at 32 weeks. There is no written record of this decision having even been contemplated and I am not sure why this is stated in the initial claim. [Emphasis added] [16] Dr Hill noted Mrs Buckley had several scans showing satisfactory foetal growth and it was acceptable for Mrs Buckley to have been managed at home after her bleeding settled on each admission. However, he "accepted that there should be ongoing foetal surveillance". He went on to comment that factors supported his view of "sub-optimal care": Some practitioners advocate induction at 38 weeks, whilst others recommend awaiting the spontaneous onset of labour if foetal growth and welfare are satisfactory and this is the advice from the above-quoted authors. However, I also note the antenatal concerns about her hypertension at 38 weeks at a clinic visit, where her blood pressure was 140/90 and then one week later on 22.5.07 when it was 150/100. There is no record to suggest that induction was even contemplated, but I believe many of my colleagues faced with someone with recurrent unclassified bleeding and late onset hypertension would have considered induction. Susan's rapid labour and late presentation in labour meant that very little could have been done which would likely have changed the outcome, although I note there was a 25 minute delay between the onset of the significant bradycardia and delivery of the baby, and perhaps time was lost when the scalp electrode was applied, rather than expediting delivery. On their own, it is difficult to say whether any of these factors directly contributed to the outcome, but taken as a whole, I believe it would be very difficult to refute allegations of "sub-optimal care" and to that end I believe that this claim should be accepted as Marion is going to require significant help with financial implications, presumably for the rest of her life. [Emphasis added] [17] On causation, Dr Hill stated: It is impossible to know what was the underlying cause of Marion's hypoxic birth ... At 10.22 hours there appears to be the onset if a foetal bradycardia, but there is no further recording until 1034 hours when a fetal scalp electrode had been applied and this shows a significant bradycardia recovering from a lowish level of 85 with poor variability and recurrent decelerations.. . It may well be that this outcome was a completely unpredictable sudden catastrophic event late in late labour, but I do have some concerns regarding Susan's antenatal management. [18] The Corporation obtained a report from Dr Grant, Consultant Obstetrician who attended delivery of Marion. Dr Grant's report dated 24 November 2008, noted that hyperemesis had been a problem in Marion's first pregnancy as well as being present in her second pregnancy. He noted on the morning of delivery (prior to admission to the delivery suite) that Mrs Buckley had regular contractions and 'a bloody show.' He noted the CTG was commenced at 10.15am, but it was not documented why the CTG was discontinued after the last trace at 10.20am. He stated: By the time of my arrival Dr Saleh has already applied a scalp electrode to the foetal head at 10:35. The CTG thereafter shows a foetal heart with minimal variability within it recovering slowly from a foetal deceleration ... Clinical assessment by Dr Saleh and myself indicated that a Ventouse delivery was imminently feasible and this was undertaken. It required only two contractions to facilitate delivery with the assistance of an episiotomy .. . In summary ... Cardiotocographic (CTG) evidence suggests that the baby was well the day prior to her spontaneous onset of labour and the initial CTG taken in delivery suite would also support this given that its appearance is similar to that seen the day before. At some point between 10.20am and 10.35am the baby experienced a profound hypoxic event as evidenced by the dramatic deterioration in the CTG and subsequent cord pH and base excess obtained after delivery. Susan has obviously had a very rapid labour to full dilation. It would appear that upon membrane rupture and associated head descent to the pelvic floor, that the true knot within the umbilical cord tightened thereby restricting oxygen supply to Marion. This resulted in Marion suffering intra-partum asphyxia. [19] The Corporation forwarded Dr Grant's report to Dr Hill for comment. In his second report dated 18 February 2009, Dr Hill reiterated his view that Mrs Buckley had suboptimal antenatal care, and this opinion was reached following a clinical conference with his colleagues, including a British obstetrician and some midwives. He stated: ... everyone felt that Susan should have been under the care of a single obstetrician or a single team with a formal plan made for timing of the delivery, given she had had recurrent small antepartum bleeding. We were also concerned that Susan's CTG tracing had been discontinued, given that she was theoretically 'a high-risk patient', the high risk being based on her recurrent antepartum bleeds and her late onset hypertension. [20] With these reservations, Dr Hill acknowledged: .. . Appropriate actions were taken when the bradycardia was detected, and even if delivery had been expedited without the short delay in placing a scalp electrode, it is unlikely that there would have been any significant difference in the ultimate outcome ... the treatment that Marion's mother received was within reasonable or acceptable standards and strictly legally it would be difficult to establish a case for treatment injury. [Emphasis added] [21] Dr Hill was provided with witness statements and radiology reports and asked for further comment. In a report dated 19 October 2010 he stated the radiology reports did not indicate any abnormality with the placenta, and he did not think that the medical and nursing team "could or should" have done anything differently regarding any possible infection "as there was no indication to give antibiotics or to have intervened prior to the onset of fetal bradycardia". He commented: As in my first report, I remain critical of some aspects of Susan's antenatal care, in that I believe she should have had more one-to-one consultant supervision of her pregnancy, after she had had recurrent antepartum bleeds, and again at term when she developed hypertension. I personally would have recommended induction of labour when she was found to have had high blood pressure, but that is a matter of debate and I am sure some of my colleagues would have a different opinion. It should however be pointed out that there is no guarantee that the catastrophic fetal bradycardia would not have occurred, even if induction had been undertaken. I would also be critical of the fact that Susan was not seen for more than half an hour after her admission ... with her antenatal history and her hypertension early, and then continuous monitoring would have been appropriate. If it is accepted that there was no need for induction, then the events which unfolded in labour could not have been prevented, and on that basis, there is no issue of failure to treat, as mentioned in my second report. Therefore, this case must be decided on whether or not Susan's antenatal and intrapartum care was of an acceptable standard. Apart from the above-mentioned points, I also personally would not have delayed delivery by putting on a foetal scalp electrode. [22] On 1 December 2010 the Corporation issued a revised decision and declined cover on the basis treatment was not causative of injury. [23] Further evidence was obtained in support of review. Reports were obtained from Associate Professor Westgate, Obstetrician and Gynaecologist and Dr Broadbent, Neonatal Paediatrician. The Corporation obtained an opinion from Dr Welch, Obstetric Medical Advisor. [24] Dr Broadbent's first report dated 22 June 2011 acknowledged the importance of careful monitoring and appropriate action in labour. He opined it was unwise to have advised or allowed Mrs Buckley to go home on the night of 22 May 2007. He stated: It is not defensible to send a woman home who had a high-risk pregnancy because of multiple bleeds and who is coming into labour at term with a significantly elevated blood pressure-and to do so immediately after performing a membrane sweep. [25] Dr Broadbent noted the membrane sweep was an informal attempt to induce labour on 22 May 2007 but noted no record of 'anything regarding the admission to the day assessment unit'. He commented undifferentiated antepartum haemorrhage is relatively common, but "the overall perinatal mortality is reported to be significantly increased when the whole pregnancy and labour are included" and monitoring is advised. He commented predictors of cerebral palsy are hypoxic ischaemic encephalopathy with antepartum bleeding and histologic chorioamnionitis weaker predictors in comparison to hypoxia. He said an umbilical cord knot is not a predictor of cerebral palsy. [26] Dr Broadbent commented on matters leading to ventouse delivery: The response to fetal compromise after membrane rupture was also acceptable. I realise there is criticism regarding the time used while the scalp clip was attached and the CIG allowed to run ... The staff present at the time decided that a short period of monitoring (for 8 minutes as measured on the monitor strip) was necessary to confirm that operative delivery was necessary. Once this was done, the baby was delivered promptly and this undoubtedly prevented a much worse outcome. By the same count, an earlier ventouse delivery even by a few minutes would have led to a better outcome. An advanced practitioner may have been able to handle things in a better manner, but the question is whether the conduct of this delivery meets an adequate standard and in my opinion it does. However, this opinion should be reviewed by an obstetrician. [Emphasis added] [27] Associate Professor Westgate reported on 18 July 2011 and agreed with the obstetric opinions in evidence. She described the pregnancy as "high risk" because Mrs Buckley had a growth restricted baby in her first pregnancy, severe hyperemesis, recurrent bleeding and high blood pressure close to term. Whilst she thought the appropriate investigations were done she 'would have liked to see a management plan for her care and timing of delivery'. She also stated 'I would also have expected some evidence of consultant input or consultation in her antenatal visits'. (28] Associate Professor Westgate opined the CTG recording from 1013 to 1022 showing 5 contractions in 9 minutes did not allow time for re-oxygenation between contractions, and stated: Response to the bradycardia warrants review. Marion was delivered 24 to 25 minutes following loss of the fetal heart rate signal when rupture of the membranes occurred. With the benefit of hindsight it is easy to suggest that delivery could have been quicker had a scalp electrode been applied earlier and had the registrar commenced the ventouse delivery between 1035 and 1040 rather than waiting for Dr Grant to arrive at 1040. I presume the registrar was not confident or experienced enough to perform the delivery themselves. However, the delivery was effected within 12 minutes of the attachment of the fetal scalp electrode. Given the likely duration of the prolonged bradycardia (13 minutes or so), and the fact that the FHR was already in recovery phase, it is impossible to say whether delivering Marion 5 minutes earlier would have definitely resulted in her being born in a better condition or suffering fewer or less significant sequelae. [29] Dr Broadbent provided a supplementary report dated 18 September 2011, in response to Associate Professor Westgate's opinion. As to the timing of the ventouse delivery, he stated "while it is impossible to be definite, on the balance of probabilities the outcome would have been better if the delivery was earlier". [30] Dr Welch reported on 27 October 2011 and agreed with Associate Professor Westgate's view regarding the most probable cause of the bradycardia and concurred that reviews by a number of clinicians have resulted in "essentially similar" findings. [31] Whether earlier delivery would have led to a better outcome, Dr Welch stated: In this case it is very likely that the brain injury has been incurred because of a number of factors coming together. Given the pre-existing histological chorioamnionitis it is difficult to say that delivering Marion a few minutes earlier would have substantially altered the outcome and avoided the injury. [32] At review, evidence was given by Dr Welch, Mrs Buckley and her mother. [33] Mrs Buckley said she suffered a difficult pregnancy including nausea and vomiting early in pregnancy and episodes of bleeding, headaches and high blood pressure right up to the day before she gave birth. She stated whilst Dr Grant was assigned as her obstetrician, she saw him on only five occasions, and at clinic visits she was always seen by the trainee doctors. Mrs Buckley stated she was aware that she was considered a high-risk pregnancy, but she felt she was "certainly never treated like a high-risk patient". [34] Mrs Buckley also raised other concerns about her antenatal care which are the subject of comment from Drs Richardson, Hill, Broadbent and Westgate. Judge Cunningham at para [45] stated: There is broad agreement that she [Mrs Buckley] should have received more oversight and input from a suitably qualified specialist ... Evidence for the second appeal [35] Further evidence for this appeal was filed by the parties following the High Court decision. [36] The hospital records relating to delivery on 23 May 2007 were filed in the supplementary bundle of documents. Some of these notes are referred to in the agreed facts memorandum filed by counsel. [37] Professor Gunn, Physician and Paediatrician is an international authority on neuro-pathophysiology. He is Head of Department of Physiology at Auckland University. In a report dated 23 May 2017 Professor Gunn opined this "is a clear case of acute onset of asphyxia in labour leading to acute brain injury." However, as to timing, Professor Gunn stated that delay in delivery was causative of injury. He agreed with Professor Broadbent that an earlier ventouse delivery 'even by a few minutes would have led to a better outcome.' [38] In response to a question "assuming a decision to delivery time of 5-6 minutes, is it likely that Marion would have avoided or suffered a less severe injury if she had been delivered at 1036?" Dr Gunn stated: I understand this to mean delivery as soon as the scalp electrodes were placed and confirmed resolving bradycardia after - 13 min of asphyxia ... In Marion's case ... variable deceleration continued from 10:35 to 10:46 ... Thus, we can be confident that fetal oxygenation had not been completely restored ... i.e. that intermittent asphyxia continued to occur ... it is highly probable that these continuing shorter periods of asphyxia for even 10 minutes contributed to augmenting damage in an already damaged brain. ... It is highly likely that delivery at 10:36 would have materially reduced the severity of brain injury. I therefore strongly agree with Associate Professor R Broadbent's conclusions that this further delayed worsened outcome for Marion [sic]. Finally, could the ventouse delivery have been performed earlier? ... My understanding as a non-obstetrician is that non-reassuring fetal heart pattern is an indication for careful further monitoring. In this context, removing the CTG does not seem optimal care. Had the CTG been continued, then it may have been possible to document bradycardia earlier, and so undertake the ventouse several [sic] before the scalp electrode was applied, that is to say before 10:36 reducing the period of sustained asphyxia by several minutes. If so, this would unequivocally materially reduced injury. [Emphasis added] [39] The Corporation obtained opinion from Dr Tait, Chief Medical Officer Capital and Coast DHB, Obstetrician. In a report dated 4 July 2017 Dr Tait noted regarding the use of CTG and a scalp electrode, that: Mrs Buckley was admitted to Delivery Suite at 09:45. A CTG was commenced at 10:15, which would be normal practice. The CTG ran until 10:21. The CTG during that time was within normal limits. Mrs Buckley ruptured her membranes and felt 'pushy'. The CTG was discontinued, presumably while a vaginal examination was performed. The foetal heart was then monitored with intermittent auscultation. Ideally the CTG would have been continued but they may have had difficulty getting a good trace. A scalp electrode is used during labour when abdominal CTG is not giving a good or accurate recording. In my opinion using a scalp electrode was appropriate. The previous CTG was normal, a bradycardia was noted and the most accurate way of determining the foetal heart rate is with a scalp electrode. [40] Dr Tait described the steps required to perform a ventouse delivery which "will be performed by a suitably credentialed registrar or O & G specialist". He commented that: A ventouse delivery was appropriate in this case. The other alternative was a forceps delivery but the method would depend on the obstetricians' preference. The registrar was called at 10:30, scalp electrode applied at 10:35, decision made to expedite delivery and baby Buckley was delivered at 10:46 ... In my opinion the delivery was performed in a timely manner. ... [41] Finally, Dr Tait concluded that: ... Once the bradycardia had occurred I believe that the treatment offered was within normal parameters of obstetric care. One can wonder whether the scalp electrode application delayed delivery it is difficult to believe that it would have altered the outcome. The decision making and treatment was within a reasonable or acceptable standard of obstetric care. The sudden profound bradycardia at the onset of the second stage is the most likely cause of Miss Buckley's injury. The reasons for this are unclear but are likely to be due to cord occlusion, possibly a true knot in the cord. The event was not predictable and in my opinion there was nothing that could have prevented the bradycardia. I also believe that once the event had occurred there was no delay in treatment. [42] Information was obtained from MidCentral DHB in January and April 2017. On specialist staffing in the delivery suite, the DHB representative commented: There were no specialist staff on site in the delivery suite at that time. That was standard practice in NZ in 2007 ... In 2007 both consultant specialist and registrar were available on call, and would respond from whatever clinical setting they were engaged in at the time of the call. The time taken to respond would depend on the location of the staff at the time of the call. ... [43] As to ventouse delivery, the DHB advised that: All specialist obstetricians are credentialed to undertake a Ventouse delivery with episiotomy. Credentialed in this context means having been formally confirmed as having the necessary knowledge, skills and capability to undertake the activity. . . . A number of factors would influence the time taken to undertake a Ventouse delivery - including the clinical and patient safety imperatives. [44] In response to this new information, the Corporation obtained further comment from Dr Tait. In a letter dated 27 October 2017 he advised that: If one looks at the timeline again the registrar was called at 10:30. The consultant Dr Grant was paged at 10:35 and was present in the delivery room at 10:40. The new information does not change my opinion that the obstetric staff responded in a timely manner and that the appropriate actions were taken, also in a timely manner. [Emphasis added] [45] Whether a registrar is a specialist obstetrician able to perform a ventouse delivery, Dr Tait advised that: Registrars are not specialist obstetricians. Whether or not a registrar could perform a ventouse delivery would depend on the stage of their training. It is uncertain, looking at the notes, who actually performed the ventouse delivery, whether it was the registrar or the specialist. Having said that, if the registrar could not perform the procedure, the specialist still arrived within a timely manner to expedite delivery. It would be expected that the registrar would contact the specialist prior to commencing a ventouse delivery and that while waiting for the specialist to arrive would have prepared the patient in the lithotomy position. [46] Dr Tait concluded that: ... in my opinion it would have been difficult to deliver Baby Buckley any quicker. Even with a specialist in the delivery suite there is no evidence that Baby Buckley would have been delivered that much quicker, when you take into account the time taken to assess the situation and ensure that the ventouse delivery was done safely. [Emphasis added] Requirements for a Treatment Injury 47] Treatment injury is defined in s 32 of the Act. The relevant parts of s 32 provide: 32 Treatment injury (1) Treatment injury means personal injury that is- (a) suffered by a person- (i) seeking treatment from 1 or more registered health professionals; or ii receiving treatment from, or at the direction of, 1 or more registered health professionals; or iff referred to in subsection (7); and (b) caused by treatment; and ( c ) not a necessary part, or ordinary consequence, of the treatment, taking into account all the circumstances of the treatment, including- i) the person's underlying health condition at the time of the treatment; and (ii) the clinical knowledge at the time of the treatment. (2) Treatment injury does not include the following kinds of personal injury: (a) personal injury that is wholly or substantially caused by a person's underlying health condition: ( b ) personal injury that is solely attributable to a resource allocation decision: (c) personal injury that is a result of a person unreasonably withholding or delaying their consent to undergo treatment. (3) The fact that the treatment did not achieve a desired result does not, of itself, constitute treatment injury. [48] Also relevant is s 33, which sets out the meaning of treatment for the purpose of s 32: 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: 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: (e) [49] In Adlam, the Court of Appeal considered the treatment injury provisions in a case where a baby was born with cerebral palsy. The Court of Appeal discussed that failure to provide treatment in a timely manner incorporated a standard. The Court noted that: [51] ... the reference to provision of treatment in a "timely manner" of itself necessarily incorporates a standard. It involves a judgement that something was not done as soon as it should have been done. This must turn on some standard that can be referred to in order to make the judgement. It is inherently unlikely in our view that "failure" in this context was intended to connote only the simple idea that the appropriate treatment was not given earlier; to say in this context that something was not done in a timely manner involves a judgement that it should have been done earlier. . . . 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 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 [50] At [65] the Court of Appeal found that the legislative scheme operated "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." The Court of Appeal concluded, on the question before it, that a failure to treat cannot Adlam v Accident Compensation Corporation [2007] NZCA 457. occur in circumstances where there are no indications for a different treatment course at [76]. [51] The High Court's decision in Adlams (upheld by the Court of Appeal) includes statements of principle: [36] The phrase "failure to provide treatment" used in s 33(1)(d) to my mind is strongly coloured by notions of departure from a standard, which are imported by the word "failure"... [38] These definitions as I see it impart, by implication at least, the need for some form of trigger (such as an omission to do something that could or should have been done in the circumstances) to occur before the "falling short", the failure "to achieve" the "leaving undone", or the "omission to do" occurs. 39] And, the ACC's interpretation here in my view is also consistent with these definitions and the context of the provision whereby s 32(1)(c) requires that treatment injury not be a necessary part or ordinary consequence of the treatment, taking into account the clinical knowledge at the time of treatment. The Court of Appeal in McEnteer v Accident Compensation Corporation has held that s 32(1)(c) requires an analysis that is rooted in the facts of particular cases, requiring expert opinion reflecting what actually occurred. [52] Causation is in issue and the principles established by the Court of Appeal in Ambrose guide understanding of causation: [69] We agree that the question of causation is one for the courts to decide and that it could in some cases be decided in favour of a plaintiff even where the medical evidence is only prepared to acknowledge a possible connection. We refer to Dais v Accident Compensation Corporation DC WN 178/2002 5 August 2003, Smith v State Insurance Ltd at 959 and Estate of Albert Francis McQueen v Accident Compensation Corporation DC HM 190/2005 28 June 2005. [70] Finally on this topic, we note that the generous and unniggardly approach advocated in Harrild v Director of Proceedings [2003] 3 NZLR 289 at [19] (CA) per Elias CJ, at [39] per Keith J and at [130] per McGrath J was used by the High Court in this case to modify the causation test. This, in our opinion, is not an appropriate application of the principle, given the plain words of the 998 Act and the rejection of the increased risk test in Atkinson. The generous and unniggardly approach referred to in Harrild may, however, support the drawing of "robust" inferences in individual cases. It must, however, always be borne in mind that there must be sufficient material pointing to proof of causation on the balance of probabilities for a court to draw even a robust inference on causation. Risk of causation does not suffice. Accident Compensation Corporation v Adlam [2016] NZHC 1487. Accident Compensation Corporation v Ambros [2008] 1 NZLR 340 (CA). The case for the appellant [53] Ms Bransgrove submitted Marion is entitled to cover for injury caused by a failure to provide treatment in a timely manner in ss 32(1) (b) and 33(1)(d) terms. [54] Ms Bransgrove submitted there were clinical indications in the pregnancy causing it to be high risk. Consequences and standards flowed from this status which were not done and should have been done. There should have been close oversight by a single consultant obstetrician and a formal plan made for labour and delivery. Following admission, Mrs Buckley and her baby were put in a dire situation with no obstetrician present, and this resulted in delay between onset of bradycardia and delivery. [55] Ms Bransgrove submitted the following factors were also causative of failure to provide treatment in a timely manner: [i] An emergency delivery was necessary when bradycardia was identified by the midwife at 10.22 am; [ii] The appropriate or standard treatment path in such cases is to perform delivery without delay; [iii] There was a delay in performing the emergency delivery having been carried out 18 minutes later at 10.40 am-10.46 am which was a departure from the standard treatment path that should have been taken; [iv] Marion's injuries would have been materially less severe or avoided entirely, if delivery had been performed without delay. The case for the Corporation 56] Ms Miller submitted there is no credible evidence to support a failure to provide treatment in a timely manner, rather the evidence supports the view that treatment was provided within expected standards and within expected timeframes. [57] Ms Miller submitted that treatment is not causative of Marion's personal injury, rather it has been caused by non-injury related factors: [i] Relying on the evidence of Associate Professor Westgate, there was a knot in the umbilicus that is not usually detected on scan; [ii] There was a post-delivery histological finding of infection or inflammation that "could be expected to adversely affect the ability of the fetus to cope with labour" in Associate Professor Westgate's view. Dr Welch opined there was no clinical evidence of infection requiring treatment. Dr Broadbent opined there is "no expectation the diagnosis should be made before delivery;" [ifi] There was rapid labour, with frequent uterine activity over a short period of time which affected the ability of the baby to reoxygenate between contractions. [58] On this basis, Ms Miller submitted it cannot reasonably be argued the health professionals could or should have done anything differently prior to Marion's birth. This submission was made both in respect to the management of the pregnancy in the antenatal period of care and in respect to labour and delivery. [59] Ms Miller submitted that apart from Professor Gunn, the specialists conclude the steps taken to expedite delivery were within appropriate standards and there was no delay in treatment. [60] Ms Miller submitted the Corporation does not rely on the exclusion provision, s 32(2)(b) of the Act. Issue [61] The agreed issue in the appeal is whether Marion's personal injury (cerebral palsy) was caused by treatment, or any delay in treatment, during labour and delivery. Discussion 62] In Adlam, the Court held that s 33(1)(d) incorporates a standard, that something was not done as soon as it should have been done. The Court stated it is not a question that the appropriate treatment was not given earlier. It involves a judgment that it should have been done earlier. Further, the causal element "depends on what is clinically indicated: a course of action that is not clinically indicated could not be said to be available." [63] I am satisfied there were clinical indications for a course of action in this case which were not done and should have been done. This course of action does not amount to a plan of action developed with hindsight bias. The main clinical indicator requiring a formal plan for the pregnancy and birth was known at the outset of the second pregnancy due to complications including hyperemesis and placental difficulties identified in the first pregnancy. Mrs Buckley was referred by her GP to an obstetrician because she was assessed as high risk. [64] Given her high-risk status, specialists agree that a formal management plan should have been developed to provide close obstetric specialist oversight and ongoing foetal surveillance at all stages. Notwithstanding the sudden onset of bradycardia that could not have been predicted, there were clinical indications in the pregnancy that required continuous close monitoring pursuant to a formal plan for labour and delivery. The evidence too shows standards relating to high- risk pregnancy that were not met. [65] I conclude on balance, when all the circumstances of this case are taken together, that Marion has suffered a personal injury that was caused by treatment. [66] I turn to consider the evidence. High risk pregnancy [67] Judge Cunningham noted the agreement of specialists that Mrs Buckley should have received close oversight and input from a suitably qualified specialist. Dr Hill stated that his view Mrs Buckley received suboptimal antenatal care was made after a clinical conference with his colleagues, including a British obstetrician and midwives he consulted. He said there was consensus Mrs Buckley should have been under the care of a single obstetrician or a single team with a formal plan for delivery. [68] I observe there is no evidence from Dr Grant which discusses the pregnancy as high risk. Dr Grant said there was no clinical guideline as to what should be done if a woman presents with vaginal bleeding in pregnancy. Dr Grant went on to note that each time Mrs Buckley's complaint was taken seriously and investigated appropriately. [69] Reviewing the hospital records for this appeal, there is no note flagged that Mrs Buckley's pregnancy is high risk. Yet consequences flowed from having high risk pregnancy at the Palmerston North hospital. There was a standard. Mr Tait reported in 2007, high risk pregnancy is an indicator for continuous use of CTG. Mr Tait said ideally the CTG 'would have been continued' and speculated it was discontinued because a good trace might not have been achieved. [70] Ms Miller submitted this is not a case of applying an ideal standard or gold standard. I observe the CTG was stopped when giving normal reading, and it is unclear why it was stopped. It is the case there was a standard for continuous CTG use for high risk pregnancies, and this standard was not observed. [71] Associate Professor Westgate noted high risk pregnancy for Mrs Buckley included both a previous history of a growth restricted baby as well as severe hyperemesis, "recurrent AP" and high blood pressure close to term. Associate Professor Westgate agreed with Dr Hill and Dr Broadbent that she would have wanted to see "a management plan for care and the timing of delivery, given her [Mrs Buckley's] high risk pregnancy". These specialists agreed high risk pregnancy had significance for what should have been done, specifically the pregnancy required continuous monitoring by a single obstetrician and ongoing foetal surveillance. [72] Dr Welch reflected how the missed opportunity of lack of a management plan caused or added to Marion's injury. Dr Welch did not discuss high risk pregnancy. In commenting on what was appropriate, Dr Welch considered the treatment given, and responses made were adequate. Dr Richardson considered "when the problem arose" an appropriate management plan was put into effect. This is an approach that is event responsive, rather than a management plan providing prospectively for eventualities taking into account the known clinical indications and the predictors for risk. In his further comments, Dr Richardson said a different plan could have led to a normal outcome, though he thought the health professionals managed the situation well. [73] Dr Hill expressed concerns about Mrs Buckley's treatment in reference to the medical literature about high risk pregnancy-management options. Dr Hill discussed the evidence that unclassified bleeding during the third trimester of pregnancy raised risk of rupture, is associated with higher perinatal mortality and in association with placenta praevia, suggests "some degree of placental dysfunction". This risk required assessment as against previous placental dysfunction occurring in the first pregnancy. Dr Broadbent considered Mrs Buckley's bleeding fell within the category of undifferentiated antepartum haemorrhage bleeding and occurs in 2-5% of pregnancies. He said whilst there is no risk at the time, the overall perinatal mortality is reported to be significantly increased when the whole pregnancy and labour are included. He said close monitoring in labour is advised. Dr Broadbent said the strongest predictor of cerebral palsy is hypoxia, and bleeding and histologic choriamnionitis are weaker predictors. It is apparent medical science acknowledges the overall circumstances of unclassified or undifferentiated bleeding as predictor of possible risk. This is another clear reason for close obstetric monitoring in a formal plan for labour and delivery. [74] The issue of early induction is noted by specialists to be controversial. Associate Professor Westgate's opinion that the case for "induction was very strong" is compelling given her awareness of the full clinical picture of both pregnancies. Dr Hill noted early induction was neither contemplated nor discussed. [75] Dr Broadbent criticised Mrs Buckley's discharge from hospital on 22 May 2007 saying, "it is not defensible to send a woman home who had a high risk pregnancy." He thought a decision to admit safer, though he could not say a better outcome was probable. Dr Broadbent noted the relevant consideration at the time was elevated blood pressure. He considered if there had been admission at that ... .. stage, signs of foetal compromise could have been detected. Whilst CTG was then reported as normal, and bleeding settled Mrs Buckley was sent home. The decision to have sent Mrs Buckley home is also to be viewed in context of the standard for continuous CTG use for high risk pregnancy. This was not explained by Mr Tait. [76] A management plan that took account of the clinical indications of high risk pregnancy together with possible risk factors would have constituted the measure for action. The hospital records note on the morning of admission Mrs Buckley "had bloody show". Dr Grant noted this in terms of no membrane rupture at the time, otherwise its significance is left unexplained. [77] The specialist opinion of requirement for a plan for close monitoring and oversight for labour and delivery includes the requirement for close oversight by a consultant obstetrician at the time of Mrs Buckley's admission on 23 May 2007 in late labour for delivery. [78] Applying the Adlam test, there were indications that identified this pregnancy as high risk such that a different treatment plan could and should have been prepared. This is supported by the observable indications in pregnancy for close oversight by a single consultant obstetrician. The absence of a formal plan for labour and delivery providing prospectively for specialist treatment in context of a high-risk pregnancy in this case, indicates a "falling short" or omission which had causal consequence for immediate delivery upon sudden onset of bradycardia. Delay in treatment [79] There is no doubt the sentinel event in the second stage of labour is the sudden onset of bradycardia, that is the sudden fall in foetal heart rate. [80] At the outset, I find the evidence of the physician assists understanding of the neuro-pathophysiology in the case and find no reason not to accept it. It provides a valuable context to the events that unfolded, and it is broadly corroborated by the evidence of Dr Broadbent. Professor Gunn's evidence is that profound bradycardia is triggered when there is near complete asphyxia. In these circumstances, the bradycardia will start to cause the first, mild neuronal loss from eight minutes onwards. It then takes a further four to five minutes to prevent the extent of brain injury that led to subsequent cerebral palsy. [81] What does this mean for delivery? Professor Gunn stated delivery up to eight minutes from the detection of bradycardia would have been needed to prevent any neural injury. Further, delivery up to 12 to 13 minutes from the start of bradycardia would have been needed to prevent the severity of brain injury leading to cerebral palsy. [82] Ms Miller submitted specialists agree the steps taken to expedite delivery were within the appropriate standards. Ms Miller submitted the focus on timeframes looks like an argument for loss of chance, an argument rejected in Ambros. [83] Ms Bransgrove submitted delay in treatment arises from a failure to deliver when bradycardia was detected. The delay in delivery caused identifiable added injury for Marion. The question then is whether there was delay in treatment. [84] The time when the bradycardia was detected is in issue. [85] Ms Miller submitted it is unclear when the bradycardia was first detected. Ms Miller submitted that what occurred at 10.22 am was the rupture of the membranes. Ms Miller referred to the clinical records and Dr Grant's evidence that 'sometime between the end of the CTG at 10.20 and 10.35 there was a profound hypoxic event. Ms Miller submitted there was bradycardia sometime after the trace ended and sometime before the registrar was called at 10.30. [86] The relevance of this evidence relates to the indication for immediate delivery. I accept looking at the clinical records that the time of detection is not altogether clear. However, I am mindful of the pitfalls of a lay interpretation on this point. [87] I refer to the evidence as follows: (i) Dr Richardson: "10:20 hours the membranes ruptured and the foetal heart rate could not be detected."" (ii) Dr Hill: "At 10:22 hours there appears to be the onset of a foetal bradycardia." (ifi) Dr Westgate: "Thus it appears that the sudden bradycardia persisted from around 1022 or soon thereafter and the fetal heart rate probably did not ise above 100bpm until 1035, a period close to 13 minutes." (iv) Treatment Injury Advice: "There seems to be agreement between doctors Westlake (sic) and Broadbent that Marion's brain injury most likely incurred around 1022 on 23/05/2007. This is the time when a bradycardia developed for the first time following the spontaneous rupture of the membranes (SRM) during labour." (v) Dr Welch: 10.22 on 23/05/2007. This is the time the bradycardia developed. (vi) Professor Gunn: "There was a very sudden fall in fetal heart rate by auscultation at ~ 10.22." [88] I observe too Judge Cunningham's view of the evidence that: However, what all the medical specialists agree on is that there was a sudden onset of profound and prolonged fetal bradycardia at around the time Mrs Buckley's membranes ruptured at 10.22. [89] I accept Ms Miller's submission it is unclear why the experts point to 10.22. However, the consensus of the experts is the bradycardia occurred around 10.22. [90] Ms Miller submitted it is not accepted there was continuous hypoxia from the time bradycardia was identified to the point of delivery. Reviewing the evidence, the medical specialists agree the bradycardia was both profound and prolonged, at least 13 minutes with some recovery from 10.35 am but still unprovoked decelerations, the effect of which was consistent with causing the brain insult to Marion. In the opinions of Dr Grant, Associate Professor Westgate, Mr Tait and Professor Gunn immediate delivery was therefore necessary. They stated: (i) Dr Grant: The CTG thereafter shows a foetal heart with minimal variability within it recovering slowly from a foetal deceleration. The baseline rises from a commencing point of 90 bpm to finally reaching approximately 160 bpm. Minimal variability is noted within the trace, with unprovoked decelerations present. (ii) Dr Westgate: Thus it appears that the sudden bradycardia persisted from around 1022 or soon thereafter and the fetal heart rate probably did not rise above 100bpm until 1035, a period of close to 13 minutes. This duration of profound hypoxia in a term baby would be enough to account for the condition of Marion at her delivery. (ifi) Mr Tait: The sudden profound bradycardia at the onset of the second stage[when the membranes ruptured] is the most likely cause of Miss Buckley's injury. (iv) Professor Gunn: In Marion's case, not only was recovery slow, but, critically, variable decelerations continued from 10:35 to 10:46. Falls in FHR indicate a near complete reduction in gas exchange with severe fall in fetal oxygenation. Thus, we can be confident that fetal oxygenation had not been completely restored and moreover that it continued to fall to very low levels intermittently, i.e. that intermittent asphyxia continued to occur. Given the effect of repeated episodes of even brief (1 minute) periods of asphyxia to cause progressively worse hypotension and cumulative injury to the brain, it is highly probable that these continuing shorter periods of asphyxia for even 10 minutes contributed to augmenting damage in an already damaged brain. [91] It is apparent that without continuous monitoring of the foetal heart rate due to CTG recording of five minutes, there is difficulty achieving certainty. But medical certainty is not required. The clinical picture shows that despite variable decelerations, intermittent hypoxia continued to occur and it was sufficiently severe and causative of injury. The appropriate standard treatment path was to deliver immediately. [92] It is apparent the medical professionals present before 10.40am did not perform the ventouse delivery immediately on detection of bradycardia. Mr Tait confirmed that registrars are not specialist obstetricians. Mr Tait said ventouse delivery depended on registrar training. The specialist obstetrician credentialed to undertake a ventouse delivery did not arrive until 10.40 am. Whilst Mr Tait opined the delivery was carried out in a timely manner regardless of the registrar's ability to perform a ventouse delivery, Associate Professor Westgate considered the duration of profound hypoxia between 10.22 am and 10.35 am would have been a sufficient period to account for the condition of Marion at her delivery. [93] There is some ambiguity regarding the time the registrar and consultant obstetrician were called. Counsel did not agree the time in the agreed facts memorandum. Ms Bransgrove referred to the evidence of midwife Buckley-Taine that at 10.20 there was attempted FHR with sonic aid and the registrar called. Ms Bransgrove submitted Dr Grant's evidence is the foetal heart rate was attempted to be heard using sonic aid and bradycardia present. At this point both the registrar and himself were called. For these reasons Ms Bransgrove submitted the evidence shows medical intervention was called immediately after 10:22 am. [94] Ms Miller countered the calls were made at 10:30 am. Accepting Ms Miller's submission is correct, it follows there was a period of eight minutes from the detection of the bradycardia at 10:22 am to the call for medical intervention at 10:30 am. [95] Given Professor Gunn's evidence of an eight-minute window where brain damage can be avoided, there was a delay of eight minutes between the detection of the bradycardia at 10.22 am and 10.30 am when the registrar arrived at the delivery suite. [96] The DHB Guidelines provide that in an obstetric emergency, which includes a baby in significant distress, the midwife must call the obstetric registrar and obstetric specialist immediately. On this basis, a period of eight minutes passed before making the call. Dr Broadbent noted if there is significant bradycardia especially in a high-risk pregnancy, 'one should proceed to immediate delivery'. Dr Broadbent stated the staff present at the time decided a period of eight minutes was necessary to confirm that operative delivery was necessary. Once this was done, the baby was delivered promptly, and this prevented a much worse outcome. However, he went on to say that an earlier delivery would have led to a better outcome. Whatever the reason for delay in calling for medical intervention, the DHB guidelines are clear a midwife must call the obstetric registrar and obstetric specialist immediately. Not doing so amounted to a departure from a standard. [97] The question then is whether the delay is significant enough to cause, or at least contribute to, Marion's injury. [98] If delivery had been performed immediately on arrival of the obstetric registrar, within a time known to be feasible, Marion's injuries would have been materially less severe than those that eventuated. [99] It is agreed that profound bradycardia was present at this point: (a) The registrar arrived at the delivery suite at 10:30 am. (b) He took five minutes to apply the scalp electrodes at 10:35 am. (c) The registrar monitored the foetal heart rate for five minutes, from 10:35 am to 10:40 am [100] There is no evidence the period of observation by the registrar was done deliberately. Ms Bransgrove submitted the registrar's actions caused some delay. [101] I turn to consider the evidence: (i) Dr Broadbent: It was not helpful for the baby to remain undelivered during this time, as it simply gave time for more contractions and more foetal compromise: "The knot in the cord tightened each time the head descended with a contraction and blood flow stopped or slowed, causing damage to the baby" (ii) Associate Professor Westgate: The delivery could have been quicker had the scalp electrode been applied earlier and had the Registrar commenced the ventouse delivery between 10:35am and 10:40am, rather than waiting for Dr Grant to arrive. (iii) Dr Hill: The placement of the foetal scalp electrode delayed delivery. [102] There is no dispute that Dr Grant's attendance was delayed. He was in theatre when called and arrived 10 minutes after the registrar, at 10:40 am. At that stage, Marion had been deprived of oxygen for 18 minutes. In Professor Gunn's opinion if an obstetric consultant had attended immediately and effected delivery within a time known to be feasible, no injury would have eventuated. [103] The reason for Dr Grant's delay is not relevant to the enquiry under s 33(1)(d). The critical point is that Dr Grant was delayed in arriving at the delivery suite when called. Immediate medical attention was required, and this standard was not met in a non-negligent sense. If Dr Grant had not been delayed, he would have arrived at the delivery suite by 10:29 am at the latest, and Marion would have been born with less severe injury. If he had arrived more promptly, injury would have been avoided altogether. [104] Ms Miller submitted the evidence shows that treatment was provided within expected standards, and there was nothing that could or should have been done differently. [105] Ms Bransgrove submitted that earlier intervention would have made Marion's brain damage materially less severe. If no delay, the delivery time would have been before 10:36 am, the point at which delivery would have materially mitigated progression of evolving injury. [106] Professor Broadbent's evidence is that ventouse delivery, even by a few minutes would have led to a better outcome. Professor Broadbent went on to say while impossible to be definite, on the balance of probabilities, the outcome would have been better if the delivery was earlier. The evidence of Professor Gunn is that delivery at 10:36 would have materially reduced the severity of brain injury. [107] Ms Miller referred to Mr Tait's evidence that decision making and treatment was within a reasonable or acceptable standard of obstetric care. However, the Adlam test is whether there were observable indications that a different treatment could and should have been undertaken. [108] Since I find treatment is causative of injury, there is no need to assess the role played by non injury factors. In any event, I observe Dr Richardson, Dr Broadbent and Associate Professor Westgate broadly agree the factors of cord knot and histologic infection whilst relevant to delivery, are not relevant to the outcome for Marion. [109] I conclude in all the circumstances the weight of the evidence shows that failure to treat in a timely manner has made a more than material contribution to Marion's injury. [110] Relying on the evidence of Dr Richardson, Dr Hill and Associate Professor Westgate, the outcome for Marion is the exact opposite of any plan for management of a pregnancy and delivery. These specialists agree the injury was neither a necessary part nor an ordinary consequence of treatment. Decision [111] On balance, I conclude on the facts that Marion's injury was substantially caused by a failure to provide treatment in a timely manner. 112] This conclusion is reached first on drawing causal elements together to find it was an omission or falling short not to provide for a formal plan for labour and delivery in context of high risk pregnancy that required close and continuing oversight by an obstetrician, including the provision for attendance of an obstetrician on admission of Mrs Buckley on 23 May 2007. The absence of such plan had significance for the time taken to respond to the hypoxia and bradycardia and in turn for immediate delivery. Secondly, the factual circumstances show multiple delays and departure from the standard treatment path that should have been taken to perform delivery immediately on indication of sudden onset of bradycardia. If delivery had been performed immediately and without delay, Marion's injury would have been materially less severe or avoided. Result [113] Accordingly, Marion is entitled to cover for a treatment injury. [114] The review decision dated 30 January 2012 is set aside and the Corporation's decision of 1 December 2010 is quashed. [115] In my opinion, this is a case of high complexity and the appellant is entitled to costs on a 3B Band basis under the District Court Rules 2014. perese o cherare Judge Denese Henare District Court Judge Solicitors: John Miller Law, Wellington, for the appellant Claro Law, Wellington, for the respondent ACR 217-16-Buckley