Knoester, Bree; Haikerwal, Jyoti --- "The changing landscape of cerebral palsy litigation in Australia" [2023] PrecedentAULA 4; (2023) 174 Precedent 8

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THE CHANGING LANDSCAPE OF CEREBRAL PALSY LITIGATION IN AUSTRALIA

By Bree Knoester and Jyoti Haikerwal

Investigating causation and disentangling any genetic conditions from a potential compensable birth injury is becoming increasingly complex in infant cerebral palsy claims. In particular, where practitioners might once have confidently issued proceedings on the basis of a strong liability report, we may now need to pursue further analysis of causation, the neuroradiology,^[1] and alternative genetic causes of cerebral palsy.

In this article we provide two case studies, where we acted for the infant, which highlight complex causation issues in cases with otherwise strong liability evidence obtained on behalf of infants with cerebral palsy. This article also discusses the emerging role of genetic testing in litigation as well as NDIS-related issues that need to be considered before recommending to families that a claim can be commenced. Lastly, it explores potential compensation for the caregivers of infants with cerebral palsy.

BABY A – A CASE STUDY

Liability

Baby A was born in 2013 and, at birth, was diagnosed as suffering from respiratory distress with meconium aspiration; both respiratory and metabolic acidosis; and pneumothoraxes on both sides.

During labour, the cardiotocograph^[2] (CTG) was significantly abnormal with reduced variability and variable decelerations as well as a prolonged deceleration. Despite the ongoing abnormal CTG, Syntocinon^[3] continued to be administered and Baby A’s mother became increasingly distressed. Twenty-four hours after first presenting at hospital, her baby was born via emergency caesarean.

At the age of one, Baby A had an MRI of his brain. The radiologist considered the findings to show white matter loss^[4] compatible with periventricular leukomalacia – a type of brain injury that can result in cerebral palsy.

The MRI, combined with our review of the CTG findings, gave us confidence that this situation had the hallmarks of a successful medical negligence claim.

Causation investigations

The neuroradiologist who examined Baby A’s MRI was an expert often relied upon in cerebral palsy litigation cases. However, we wanted to supplement that evidence with that of our own neuroradiologist so sought an opinion from a peer – who we expected to reach the same conclusion.

That was not the case. The second neuroradiologist considered the white matter loss to simply represent non-myelination of key parts of the brain. Myelination is a process by which the brain produces the myelin that wraps around the brain’s axons – which appear white on an MRI – and provides an insulation-like protective coating. When a brain is fully myelinated, those white areas then appear black. As such, white areas can simply be parts of the brain that are non-myelinated or, in some cases, they can represent injury. Complete myelination of the brain takes around two years.

The question for us then became whether the white matter features on the MRI represented injury or simply areas of the brain that had not yet myelinated.

We had strong evidence in terms of breach and that labour should not have been permitted to progress for as long as it did. It was also clear that Baby A had cerebral palsy and would require lifelong supports. However, we were confronted with a situation where two neuroradiologists disagreed as to whether the negligent management of the birth caused an injury to Baby A. Given the impact a successful claim would have on Baby A and their family, we sought a third opinion from another neuroradiologist.

The third neuroradiologist requested that Baby A, now nine years old, undergo a further MRI to ascertain if the white matter on the earlier MRI was an injury or non-myelination.

The new MRI revealed that Baby A had a small brain mass size. We learned that this can both arise from a birth injury and/or a pre-existing or unrelated condition. The third neuroradiologist compared Baby A’s brain mass size against a database of similarly aged children to see if Baby A had a clinical microcephaly,^[5] and concluded that:

1. Baby A had a primary microcephaly and this existed from birth, which is less consistent with a hypoxic injury^[6] where there is microscopic damage and the brain shrinks over time; and

2. there was no clear radiological evidence of a cerebral injury – put another way, the white matter loss seen in the earlier MRI was only areas of the brain that had not yet myelinated.

The third neuroradiologist did accept that one can have both an essentially normal MRI and a brain injury at birth resulting in cerebral palsy. However, it would be very difficult to establish the necessary relationship between the birth injury and the cerebral palsy in the absence of major radiological changes such as damage to the basal ganglia.

The third neuroradiologist ultimately agreed with the second that the radiology did not confirm an injury caused by the circumstances of the birth, however negligent it was.

A further complication arose when Baby A underwent genetic testing. The genetic testing reported a chromosomal mutation at 7q22.11. Further investigation revealed that there are recognised mutations close to chromosome 7q22.11, which are associated with primary microencephaly. In other words, it was thought that this chromosomal mutation may be causative of Baby A’s microencephaly. This gave further weight to the conclusion that Baby A’s microencephaly was genetic, not an indication of a birth injury.

Ultimately, despite the strong evidence in respect of liability, we could not recommend that the claim on behalf of Baby A be pursued given the unsupportive causation evidence.

BABY B – A CASE STUDY

Liability

In the case of Baby B’s birth, labour was induced and the CTG was abnormal. There were significant fetal heart rate (FHR) abnormalities and profound variable decelerations. Reduced FHR variability persisted initially for 70 minutes and then for four hours, which was an abnormal sign.

The changes in variability did not prompt any specific action; our obstetric expert advised us that arrangements for a caesarean section should have been made when the second protracted episode of reduced FHR variability occurred. By this time there had been episodes of protracted FHR deceleration lasting five minutes and variable decelerations, as well as repeated reports of an abnormal CTG conveyed to a senior doctor.

Armed with a strong report indicating a breach of duty by the hospital, we moved forward with the claim. An MRI taken of Baby B one month after the birth showed hyper-intense white matter with a differential diagnosis of infection or ischemia.^[7] Infection was investigated and none was present. We thought the MRI further strengthened our case, with ischemia posited as the only other alternative injury once infection was excluded.

Noting what we considered to be very strong evidence on breach, we anticipated that the defendant would seek the opinion of a neuroradiologist and we should do this pre-emptively.

Causation investigations

Our neuroradiological expert disagreed that the MRI demonstrated periventricular white matter changes that suggested the possibility of an ischaemic injury. Given the MRI was taken only four weeks after the birth, he considered the white areas to simply be non-myelination. Our expert reviewed the images of the basal ganglia, which is most often affected by a hypoxic ischaemic insult, and considered its appearance normal.

However, he considered two parts of the brain, the pons and the medulla, extremely unusual and the specific findings on the MRI of these parts rare.

A further MRI demonstrated that there was a V-shape in the rear of the pons resulting in a split or midline cleft. The medulla also had a midline posterior cleft, creating a butterfly shape. Furthermore, there was a brain stem malformation: the brain stem was markedly dysplastic. Ocular misalignment was also visible. Images of the spine demonstrated a pronounced thoracolumbar dextroscoliosis.

Our expert considered the brain and spinal images consistent with a condition called horizontal gaze palsy with progressive scoliosis and Moebius syndrome. A genetics review was recommended.

When we then examined the antenatal imaging taken during the pregnancy and prior to the delivery, we could see that the brain stem and pons defects were already present.

The question then was: could there be both a birth-induced injury as well as a genetically caused condition? And if so, could those two conditions be disentangled?

Genetics investigations also confirmed that Baby B had an inherited microdeletion, which can be the cause of developmental delays. It also revealed two variants in the gene ROBO3 and confirmed the diagnosis of familial horizontal gaze palsy with progressive scoliosis. Each of Baby B’s parents was carrying one of the variants identified in Baby B and she therefore did not have a working copy of the gene. However, the genetic condition was not typically associated with neurological or cognitive disabilities. So, putting aside the two genetic conditions at play, could the birth have been the cause of Baby A’s cerebral palsy?

Our expert said that the most recent MRI did not demonstrate anything supportive of a hypoxic ischaemic injury. He accepted that there can be an undetectable hypoxic insult on an MRI and, in that scenario, diagnosis is based on presentation and symptoms. However, in this case, he thought it would be almost impossible to separate the disabilities that arise from microdeletion and the significantly abnormal brain stem, pons and medulla, from any disability that may arise from a radiologically undetectable hypoxic insult.

On balance, he considered the likely cause of Baby B’s significant developmental delays to be horizontal gaze palsy with progressive scoliosis as a result of a mutation in ROBO3, not an injury caused at birth. In light of this opinion, we did not have the sufficient evidence required to recommend a claim be commenced on behalf of Baby B.

WHAT HAVE WE LEARNED FROM BABY A AND BABY B?

Investigating these cases raised the importance of requesting, understanding and analysing genetic and radiological evidence as well as the need to understand the impact of any chromosomal abnormalities on the clinical picture.

It also highlighted that the fields of radiology and genetics play large roles in cerebral palsy litigation. Plaintiff lawyers must pre-emptively investigate these areas, knowing that even in light of the strongest breach evidence defendant lawyers will investigate questions of causation.

GENETIC TESTING AND THE FUTURE OF CLAIMS

Causation is often the most fiercely fought part of a cerebral palsy case. Now that there is greater knowledge about genetic variants and mutations that can contribute to the diagnosis of cerebral palsy, investigating a claim often requires delving deeper into whether there is a genetic cause. This means that genetic testing for the purposes of litigation is a real consideration when bringing a claim.

Australian courts have considered applications where a defendant has sought an order for genetic testing of the plaintiff.^[8]

For example, in Pederson v Northern NSW Local Health District,^[9] the defendant sought an order to take a saliva sample from the plaintiff for the purpose of genetic analysis. In this case, the plaintiff alleged that his development of Autistic Syndrome Disorder was due to the hypoxia ischemia encephalopathy that he suffered at the time of his birth. The defendant admitted failures in the care given during the birth that led to the hypoxic episode. Both parties filed evidence on the issue of causation. In particular, the defendant’s evidence was that the diagnosis could be due to chromosomal abnormalities rather than the negligent treatment. The defendant submitted that the proposed saliva testing would be important evidence for the Court when deciding whether the diagnosis was negligent treatment or due to genetic causes. Ultimately, Campbell J decided that ‘the interests of justice are best served by making the orders sought by the defendant’.^[10]

Australian courts allowing orders for genetic testing is consistent with international approaches. For example, in 2021 the Superior Court of Justice of Ontario in Canada considered whether it was appropriate to make an order for a plaintiff to undergo genetic testing.^[11] This matter involved a plaintiff who was born in 2014 and was diagnosed with cerebral palsy. A claim was commenced in which it was alleged that the defendant failed to recognise signs of fetal distress and order an emergency caesarean section. During the course of the proceedings, the defendant sought orders to collect a blood sample from the plaintiff and their biological parents for genetic testing. The Court granted these orders on the basis that, on the current expert evidence, there was a reasonable possibility that there was a genetic cause of the condition.

The consensus from both Australian and international courts appears to be that unless there is an exceptional reason for the plaintiff not to undergo genetic analysis, the court will make an order for the testing to occur.

NDIS CONSIDERATIONS

Since the introduction of the National Disability Insurance Scheme (NDIS) in 2013, most infants with cerebral palsy receive NDIS benefits which, mostly, pay for future occupational therapy needs.

The introduction and use of the NDIS affects a claim for compensation and, in turn, a claim for compensation affects an NDIS package.^[12] In particular, if compensation is achieved and the NDIS is involved, statutory obligations include:

• repaying the value of the services received in the past; and

• reducing the value of the future NDIS package proportionally to the amount the plaintiff receives.

The likely reduction of a funding package in the future can be a difficult consideration for families when weighing up the impact of NDIS funding against an offer of compensation.

Prior to the establishment of the NDIS, a case with evidentiary challenges, such as the baby A and baby B case studies described above, may have resolved for a reduced sum to provide the plaintiff with funds to assist with their treatment and supports. However, since the introduction of the NDIS, plaintiffs, families and lawyers are understandably reluctant to pursue a claim with evidentiary risks that may result in a discounted offer of settlement. This is because, irrespective of the sum received, if compensation is provided for past and future treatment, the plaintiff will be required to repay the NDIS for all services provided up to that date and future funding packages will be affected.

This is a new and additional burden for plaintiffs, families and lawyers. All must be confident that a claim will be successful and will result in full or close to full payment of damages to offset NDIS obligations.

CARING FOR THE CARERS

Psychiatric claims

Most infant cerebral palsy cases are brought on the basis of alleged negligent treatment at the time of birth. In these circumstances, it is also likely that the birthing person suffered a traumatic birthing experience and may be suffering from a psychological injury.

Often, the birthing person is also the caregiver and litigation guardian for the plaintiff. In these circumstances, plaintiff lawyers may get an insight into their life and the impact of the traumatic birthing experience. A nervous shock claim for the psychological injuries of the birthing person may be viable, along with a claim for the infant.

For example, if we look back to the case of Baby A, during the investigation process we noticed that Baby A’s mother, and litigation guardian, was struggling with her mental health. When we spoke with her about this further, she disclosed that she was experiencing flashbacks and nightmares of the birth. We realised that she was suffering from psychological injuries due to the medical treatment during the birth, which we had established was negligent. We sought instructions to commence a claim on her behalf and were successful in getting her compensation for her psychological injuries.

Can parents be paid for their gratuitous care?

Practitioners are also encouraged to consider the gratuitous care provided to the infant by their caregivers, who are often their parents.

In some cases involving infant cerebral palsy injuries, the infant has full-time carers engaged through private companies or the NDIS to help them on a daily basis. However, in other circumstances, the parents may take on the role of full-time carer.

When the past out-of-pocket expenses are calculated, a claim for the past gratuitous care provided is often considered. If the claim settles and an allowance is made for the past gratuitous care, it is worthwhile exploring whether some of the funds can be paid to the parents in recognition of any past gratuitous care they have provided.

Similarly, when a claim for future out-of-pocket expenses is settled, compensation is often awarded for the cost of future care. However, sometimes a parent is the person with the best skills and training to continue to perform full-time carer duties, rather than engaging a commercial company. In this situation, consideration should be given to whether some of the funds can be paid to the parent as the carer, as a financial payment would be made to a commercial carer.

CONCLUSION

Families must now consider the prospect of being involved in lengthy litigation when bringing a claim, as well as the possibility of their child undergoing genetic testing and neuroradiological investigation for the purposes of the legal proceedings.

Cerebral palsy cases are likely to continue to become more complex as medical expertise develops, particularly given the ramifications that a settlement can have on any NDIS benefits. Legal practitioners need to remain proactive when briefing experts and ensure they are up to date with the most recent advancements in genetic testing and technology. It is vital to ensure that the issue of causation is thoroughly explored – even in cases where there is strong evidence of the mismanagement of labour.

Bree Knoester is the Founder and Principal of Brave Legal specialising in medical negligence, dust diseases and workers compensation injury claims. PHONE [phone] EMAIL [e-mail].

Jyoti Haikerwal is an Associate at Brave Legal specialising in medical negligence claims. PHONE [phone] EMAIL [e-mail].

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^[1] A subspecialty of diagnostic radiology that focuses on diagnosing abnormalities of the central and peripheral nervous systems, spine, head and neck.

^[2] A monitoring device placed on the mother’s abdomen to measure fetal heart rate and uterine contractions.

^[3] A drug given to encourage uterine contractions.

^[4] White matter loss can represent damaged brain tissue caused by reduced blood flow to the tissue – which can occur when a baby is deprived of oxygen in utero.

^[5] Small brain.

^[6] Brain injuries that arise due to a reduced oxygen supply to the brain.

^[7] Restriction in blood supply to a tissue or organ causing a shortage of oxygen to that part of the body.

^[8] S Vallance and M Brain, ‘The appropriateness of genetic testing in cerebral palsy cases’, Precedent, No. 133, 2016.

^[9] [2020] NSWSC 741.

^[10] Ibid, [19].

^[11] Klinck v Dorsay [2021] ONSC 6285.

^[12] National Disability Insurance Scheme Act 2013 (Cth).