Habelrih & Ors v Szirt & Ors [2004] NSWSC 54 | Case summary

(b) the plaintiffs' application for mediation. 2 The third defendant consents to the orders sought in each of the motions; the plaintiffs oppose the making of an order for a joint conference of expert witnesses and the first defendant opposes an order for mediation. 3 In this cause the first plaintiff is the mother of the third plaintiff and the second plaintiff is the husband of the first plaintiff and the father of the third plaintiff. The third plaintiff was born at St Margaret's Hospital, and hence the joinder of the second defendant. The first defendant is a specialist obstetrician and gynaecologist who cared for the first plaintiff during her pregnancy and after her admission to the second defendant's hospital on 22 June 1996. The third plaintiff was born at 9.22 pm on that date and was transferred to Prince of Wales Children's Hospital at 3.20 am on 23 June 1996. The events critical to this cause occurred between the time of birth and the time that chest x-rays of the infant first became available. It would seem that the first x-ray was carried out at 11.00 pm on 22 June 1996 and twenty minutes later the result was obtained, demonstrating a right pneumothorax. 4 The case against the second defendant, and hence against the third defendant, its insurer, is significantly broader than the case against the first defendant, but the critical issue in the case against the first defendant is whether he was negligent by delay in calling for a chest x-ray. Professor Colditz, upon whose opinion the plaintiffs rely, is of the view that it was delay in obtaining the chest x-ray which was causative of persistent pulmonary hypertension in the child and this in turn was the cause of the third plaintiff's neurological disability. If the pneumothorax had been treated more quickly, persistent pulmonary hypertension would not have developed. 5 The first defendant denies he delayed in calling for x-rays, but in addition he seeks to meet the plaintiffs' case by medical opinion that the most likely cause of the child's cardiorespiratory illness was primary persistent pulmonary hypertension (primary PPHN), and not secondary persistent pulmonary hypertension (secondary PPHN) due to hypoxia. If the cause of the cardiorespiratory illness was primary PPHN, then the delay in seeking the x-ray would lose its significance; the harm would have been done anyway. 6 The first defendant relies upon the conclusions reached by Dr Evans, supported as they are by Dr McPhee. Professor Colditz and Dr Harbord do not support the diagnosis of primary PPHN. However, Mr McHugh submitted that the appointment of the conference sought was warranted by the possibility that at conference a measure of agreement might well be reached on what he submitted was the carefully reasoned and detailed opinion of Dr Evans which Professor Colditz does not yet appear to have had the opportunity of considering at any length. 7 Mr McHugh submitted that absent a useful conference, the parties face the prospect of a very lengthy and a very costly hearing with lengthy cross examination of expert witnesses in the course of which the cross examiner will obtain for the first time the opinion of the witness being questioned on particular issues. 8 In opposing the proposed conference, Mr Hirsch spoke to detailed written submissions which I have, of course, considered but do not propose to fully record in this brief judgment. Mr Hirsch submitted that the proposed conference cannot bring about the objective which the first defendant seeks, namely to bring about his dismissal from the cause. 9 By way of background, the plaintiffs were prepared to discontinue against the first defendant because expert evidence supported the view that the lack of an expeditious response to the third plaintiff's distress after birth was the responsibility of the hospital and not the first defendant. However the hospital resisted the discontinuance and filed a cross claim against the first defendant, in consequence of which the case against the first defendant remains on foot. The hospital relies upon what allegedly occurred between the first defendant and hospital staff after the birth in seeking to attribute fault to the first defendant in delay in the ordering of the x-rays. Hence, there is a factual issue to be determined as between the first defendant and the third defendant that cannot be resolved by any opinions expressed at the contemplated joint conference. On the other hand of course, that issue would lose relevance if the cardiorespiratory illness was primary PPHN. 10 Mr Hirsch submitted that a consideration of the medical evidence discloses that there has been ample opportunity for the experts to consider the contrary opinions of their peers and that, indeed, such opportunity has been taken. In particular, Mr Hirsch submits that plainly Professor Colditz has considered what Dr Evans has said and disagrees with it. Mr Hirsch has drawn attention to the affidavit of Anna Lee Walsh sworn 6 February 2004 which records what Professor Colditz has to say about the relevant reports of Dr Evans. Further, Mr Hirsch has drawn attention to the earlier affidavit of the same deponent sworn on 21 January 2004 which, in an extremely useful way, has set out the differing views of the various experts on central questions contemplated for the joint conference. Mr Hirsch submitted that what the content of Ms Walsh's two affidavits demonstrates is that the experts upon whom the plaintiffs rely and the experts upon whom the first defendant relies are not at all likely to change their views. Moreover, Professor Colditz would have to come from Brisbane to attend a joint conference and Dr McPhee would have to come from Adelaide. 11 Of course if the parties remain at issue on the matters which the first defendant seeks to address at conference, those same experts would have to come from interstate to give evidence at trial, and this would be likely to involve lengthier absences from their home States than would attendance for a conference. 12 The principles to be applied on an application for a joint conference have been considered by me in Boardman v South Eastern Sydney Area Health Service [2001] NSWSC 930; in Booth v De Francesco [2002] NSWSC 145; and in Spasovic v Sydney Adventist Hospital [2002] NSWSC 164. I must be satisfied of the existence of a reasonable expectation that the appointment of the conference sought by the first defendant could achieve one or more of the objectives expressed in para 2 of Practice Note 121: see Booth at para 24. 13 This involves the necessity of careful consideration of the various medical reports which have been exchanged. 14 The questions which the first defendant wishes to have considered at the proposed conference are defined in Annexure E to the affidavit of Mrs Kearney affirmed 23 January 2004. They are somewhat different from those first posed in an annexure to Mrs Kearney's earlier affidavit of 7 January 2004. The exercise undertaken by Ms Walsh addressed the earlier set of proposed questions, but I do not consider this ought to be determinative of the outcome of the first defendant's notice of motion. As I see it, what is of critical importance is the issue of the origin of the PPHN: was it primary, or secondary due to hypoxia? 15 Professor Colditz opined on 22 May 2002: "I am not sure that there is sufficient detail on the timing of all the clinical details but what is certain is that a chest x'ray was not available until approximately 2255, that is about 1 hour and 10 minutes after transfer of the baby to the nursery and about 1 hour and 15 minutes after Dr Szirt had had Dr Campbell contacted and when Dr Campbell had apparently requested a chest x'ray even before he saw the baby. Dr Campbell was correct in requesting this x'ray and it is reasonable to assume that it could have been done in about the same time frame that it would take Dr Campbell to arrive at the Hospital. It would take only about 5 minutes or less for the x'ray to be taken and a further 5-10 minutes or less for the x'ray film to be available to Dr Campbell. The facts appear to be that Dr Campbell arrived about 45 minutes before the x'ray was available to him. There was either a delay in requesting the x'ray or there was a delay in the radiographer attending the hospital or some unacceptable delay in having the x'ray available. In my opinion this period is the one where the pulmonary hypertension was established and the presence of hypoxia and hypercapnia during this period was prolonged to such a degree that the subsequent course of severe pulmonary hypertension, with all its attendant hazards, was set in place. The response to the pneumothorax appears to have been prompt and all subsequent treatments were both appropriate and established in a standard fashion. ………………. There appears to have been a delay in having a chest x'ray available. Whilst further information on the exact timing of events is required, it appears very likely that this constituted a departure from standard practice. The responsibility for this departure from standard practice may lie with the Hospital or the Radiographer. ……………… Persistent pulmonary hypertension of the newborn was the direct cause of the plaintiff's neurological disabilities." 16 Dr Williams, the second specialist who the plaintiffs want to attend any conference that may be ordered, has furnished several reports. On 24 April 2002, Dr Williams wrote: "Although there may have been some hypoxia prior to delivery, I do not believe that this was the cause of cerebral injury. I believe that foetal distress set the scene for meconium intrapartum aspiration and postpartum respiratory failure with pneumothoraces and severe pulmonary hypertension of the newborn. Because the pneumothoraces were not diagnosed or treated early, the hypoxia was not corrected. Richard suffered the primary hypoxic ischaemic insult to the brain in the first 45 minutes after birth. …………… Because there was evidence of a complicated labour, the paediatrician should have been present at birth. He would have diagnosed that Richard had respiratory difficulty. The respiratory difficulty was, initially, mild and he would have been transferred to the special care nursery. He would have been kept warm and he would have been appropriately oxygenated in a headbox. The pneumothoraces would have been detected early with a chest x-ray and there would have been early drainage. His hypotension and hypoglycaemia would have been corrected with intravenous fluids. He would have been intubated early to prevent further hypoxic ischaemic insults. On the balance of probability, had appropriate resuscitative measures been instituted from birth, then Richard would not have suffered the hypoxia that contributed to his current neurological disabilities." 17 In a supplementary report commenting on what Professor Colditz had written, Dr Williams wrote, on 15 August 2002: "It is more likely than not that adequate attention to the early treatment of the respiratory distress would have averted the severe pulmonary hypertension and all its sequelae, which includes the plaintiff's disability." 18 It was Dr Evans who first expressed the opinion that the third plaintiff had primary PPHN. In his report of 2 April 2003 Dr Evans wrote: "30. Primary PPHN is not a well understood condition but the problem is almost certainly intrinsic to the relaxing mechanism in the blood vessels in the lungs. The cause of this is not known. The characteristics of primary PPHN are: • The problem is not predicted or predictable from the pregnancy or labour. • The deterioration is early after birth, often very rapid and characterised by cyanosis and varying degrees of respiratory distress. • Resuscitation can be very difficult because there is no blood flowing through the lungs to pick up the oxygen, so improvement in oxygenation is slow." 19 Dr Evans went on to consider the x-rays: "• The chest xray shows clear lung fields or minimal opacification. • The pulmonary artery pressure on echocardiogram is often well above systemic pressure. • When ventilated, they have very wide fluctuations in PaO2 but will usually have low PaCO2. • They often show a brisk improvement to inhaled nitric oxide (personal experience). • Because the cause of this condition is now known, with echocardiography accurate diagnosis is difficult. These babies often get mislabelled with a wide range of diagnostic possibilities. This is relevant to the wide range of opinions as to the diagnosis in the expert reports on Richard's case." 20 Dr Evans then considered the question as to whether the PPHN was secondary or primary: "31. It is the assumption of the Plaintiff's experts that Richard's PPHN was secondary to his period of postnatal hypoxia. While such a period of hypoxia can precipitate PPHN, usually this is quickly reversible with oxygen and or ventilation unless the hypoxia has been critical (eg. associated with bradycardia and acidosis, neither of which were recorded in Richard). As will be discussed below, there is no evidence that Richard's hypoxia at St Margaret's Hospital was critical. It can be seen from the above listed characteristics, that Richard's course was much more consistent with primary PPHN. In other words the problem causing his respiratory distress, hypoxia and complicated intensive care course was intrinsic (in a way medical science cannot yet explain) to the relaxation mechanism of his pulmonary blood vessels. He had: • An early and rapid deterioration. • He was very slow to improve oxygenation with resuscitation. • There is no formal report that I could find on his initial xray but opacification of the lung fields is not mentioned. • He responded well to inhaled nitric oxide. • When ventilated at SCH, he had low PaCO2's and widely fluctuating PaO2. 32. Further support for an intrinsic primary pathology for his PPHN is provided by the persistent nature of the pulmonary hypertension. Each time the Nitric Oxide was weaned his pulmonary pressure would rise and the oxygenation would deteriorate. This was elegantly demonstrated on echocardiography by Dr Cooper on the 27th June. Richard had persisting clinical evidence of pulmonary hypertension (loud second heart sound and tricuspid incompetence murmur) even on his readmission at 6 weeks of age. It would be important to obtain the results of any cardiovascular assessment by Dr Cooper during this recovery phase. I was the principle investigator in a study that described the serial echocardiographic findings in a cohort of term babies with high oxygen requirements. The results emphasised the importance of distinguishing between primary and secondary PPHN, the characteristics of which were consistent with what I've described above. However, one of the babies in this cohort with primary PPHN had a persistent course very similar to Richard. Each time we weaned the therapy, the pulmonary artery pressures would rise dramatically to above systemic blood pressure with deterioration in oxygenation. Just like Richard, eventually we were able to wean therapy but residual pulmonary hypertension and lung problems secondary to needing high inspired oxygen (high oxygen concentrations damage the lung) persisted. This persistence emphasises the intrinsic nature of the problem. Nitric Oxide is a symptomatic treatment, it controls but does not cure the problem. When it is weaned, the problem re-emerges until spontaneous improvement of the function of the pulmonary blood vessels occurs. 33. It can be seen above that poor response to resuscitation is a feature of primary PPHN. When a baby fails to improve colour in response to positive pressure ventilation, the instinctive (and correct) response of the resuscitator is to increase the pressure. I would speculate that this is what may have happened to Richard, so the pneumothorax may have occurred in the period immediately preceding the xray. The delay in getting a chest xray while unfortunate (but not inconsistent with a standard of care in a smaller private hospital), probably made little difference to the subsequent clinical course. In summary, it is likely that what happened at St Margaret's Hospital was the initial manifestation of his pathology not the cause of it." 21 Dr Evans wrote a further report of 18 July 2003, but it is unnecessary for me to refer to it for present purposes. 22 When Dr McPhee had considered Dr Evans report from which the above extracts have been taken, he wrote, on 2 January 2004: "There is general agreement in the various reports that Richard Habelrih's neonatal cardiorespiratory difficulties were dominated by persistent pulmonary hypertension of the newborn (PPHN). As discussed in Dr Evans' report, this condition can arise as a primary condition, in which a fundamental and prenatally determined problem in pulmonary vasodilatory capacity is postulated, or as a secondary or reactive condition. In the latter situation, the PPHN is usually precipitated and/or aggravated by neonatal respiratory problems of which meconium aspiration syndrome is the commonest. Dr Evans is an acknowledged expert in the area of neonatal cardiopulmonary transition and, in my opinion, his assessment of the serial echocardiography studies performed at the Sydney Children's Hospital make a compelling case for a diagnosis of primary PPHN. Thus, elevated pulmonary vascular pressures were seen well beyond the newborn period, and were still high at 12 weeks of age (see discussion in item #32 in Dr Evans' report of 2.4.2003, and items #1-3 and #7 in his report of 18.7.2003). Both Professor Colditz and I felt that an element of meconium aspiration syndrome was implicated in the pathogenesis of Richard's neonatal cardiorespiratory problems, as did both Dr Campbell and the neonatal team at the Sydney Children's Hospital. In this regard I note that although Dr Campbell did not specifically describe the X-rays performed at St Margaret's, he summarised babe's problems in the clinical record as being due to meconium aspiration. Also, the paediatric resident (Dr Lukic) referred to the (? initial) X-ray as showing a 'a right pneumothorax' and 'meconium aspiration'. Unfortunately, the X-rays performed at St Margaret's were not available for review. The X-rays performed at the Sydney Children's Hospital were available to myself, though not apparently to Dr Evans or Professor Colditz; their opinions of these films would be of interest. In my opinion (see p3 of my report), these films did show some patchy parenchymal opacities, consistent with meconium aspiration syndrome. The radiographic features are not those however of severe meconium aspiration syndrome, which typically involves widespread diffuse parenchymal involvement with patchy areas of atelectasis and hyperinflation/air trapping. ……………….. I believe that Dr Evans makes a strong case for primary pulmonary hypertension as the dominant factor, implying that a fundamental and prenatally determined derangement in pulmonary vasoreactivity was involved. It should be noted that this doesn't exclude a contribution of meconium aspiration syndrome and/or the pneumothoraces, but these were likely less significant elements in Richard Habelrih's deranged cardiopulmonary transition. Finally, if primary pulmonary hypertension is accepted as the dominant factor in Richard's neonatal problems, then it must also be acknowledged that this condition is particularly difficult to treat and not 'preventable' by current treatment strategies." 23 Professor Colditz was asked to consider Dr Evans' opinion and annexed to the affidavit of Ms Walsh sworn 6 February 2004 is a note (but not a formal report) from Professor Colditz in which he expresses his disagreement with Dr Evans: "Dr Evans has accurately reported the clinical events. If I were to summarise his agreement, it is that the plaintiff was destined to have persistent pulmonary hypertension of the newborn (PPHN), a condition he refers to as primary PPHN. As a consequence of this the management afforded the plaintiff has very little relevance to the outcome. I am in fundamental disagreement with this proposal. My view is that there is no particular evidence that the plaintiff was pre-destined to PPHN, but rather that the PPHN is likely to have been caused by environmental factors after birth, namely the period of hypoxia that occurred in the hour or so after birth. Management during this time is likely to have been critical as to whether PPHN would develop. I believe we are in agreement with the fact that once this serious condition had unfolded that the brain damage occurred during the course of its management in the first week. Of course I would be willing to expand on my opinions summarised above. My opinions expressed in my earlier reports I stand by and they have been in no way modified by these two reports of Dr Evans. I await your instructions on whether you wish me to proceed to expound in detail my opinions particularly in relation to Dr Evans' two reports." 24 There is no report from Dr Williams addressing Dr Evans' views about primary PPHN. 25 Whilst a joint conference will not generally be ordered where there is "a clear, firm and considered divergence of opinion between the experts" (see Booth (supra) at para 30), as Professor Colditz acknowledged in his note above set out, his reasons for disagreement are not expressed. I observe that Professor Colditz has made no comment on the significance of the echocardiography by Dr Cooper (see para 32 of Dr Evans' report). Nor is it clear what "the early and aggressive treatment" was that Professor Colditz had in mind (see p 2 of his report of 26 June 2002) to halt the progress of the PPHN, once diagnosis by x-ray was achieved. Dr Evans' reasons for his conclusion that the PPHN was primary have been exposed in the extract from his report of 2 April 2003 recorded earlier, and Dr McPhee has commented that Dr Evans' "assessment of the serial electrocardiography studies performed (at SCH) make[s] a compelling case for a diagnosis of primary PPHN." 26 I do not here intend to be indicating a preference for any particular medical opinion that has been expressed in this case, and, indeed, I make it clear that I entertain no preference. Plainly it would be altogether premature and inappropriate for me to do so. However, a close reading of the medical reports leads me to conclude that a conference between the experts in this case could well prove to be useful in at least narrowing what are presently many and complex medical issues for trial. I consider the possible utility test posed in the earlier cases would here be satisfied by a conference directed to addressing the questions posed in Annexure E to the affidavit of Mrs Kearney affirmed on 23 January 2004. 27 I propose therefore to order that there be convened a joint conference of expert witnesses, which Professor Coldtiz, Dr Williams, Dr McPhee and Dr Evans should attend. The plaintiffs should be given the opportunity of input into the form of the questions to be posed should any variation of those questions be sought. I will give liberty to apply for this purpose. 28 The first defendant seeks the appointment of an independent person to act as chairperson of the conference (see Practice Note 121 para 18). I am persuaded by Mr McHugh's submissions that the appointment of an independent chairperson would be desirable in this case. 29 In seeking an order for mediation, Mr Hirsch submitted that a mediation should be appointed forthwith, and that any outcome of the joint conference which I have decided should take place would be irrelevant to the mediation. It was submitted that the outcome of the conference would not influence the first defendant's attitude to mediation, because of the first defendant's opposition to mediation. 30 I do not accept that submission. In my opinion, the plaintiffs' application for an order for mediation would be better considered when all the parties have the advantage of knowing the content of the experts' reports. I propose therefore to adjourn the hearing of the plaintiff's motion concerning mediation to a date to be arranged with my associate.

Habelrih & Ors v Szirt & Ors

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