RC was born on 22 September 1999 in good condition, having Apgar scores of 8 at 1 minute and 8 at 5 minutes. In early October 1999 he was diagnosed at Harefield Hospital with a transposition of the great arteries and a small ventriculo-septal defect (VSD).
On 4 October 1999 surgery was performed to undertake anatomical correction of RC’s great vessels. He was on cardiac bypass for 128 minutes and circulatory arrest was 9 minutes. The procedure was complicated by bleeding but the operation was successful.
Post-operatively RC required ventilation and became unwell. There was a period of persistently severe alkalosis and hypocarbia (incorrect pH of the blood due to carbon dioxide levels which were too low) from about 20.30 on 4 October 1999. Blood gases were performed as they should have been and the ventilator settings were adjusted accordingly but on each occasion the adjustment were inadequate. RC’s blood gases only became normal when peritoneal dialysis commenced.
RC developed seizures however a cranial ultrasound performed on 11 October 1999 was reported as normal. He was discharged home on 22 November 1999. An ultrasound scan performed on 24 August 2000 showed significant hydrocephalus (abnormal collection of cerebro-spinal fluid (CSF) in the ventricles of the brain). A ventricular peritoneal shunt was inserted on the 6th September 2000. On 9 June 2008, RC underwent an MRI scan of his head, which showed marked enlargement of the supratentorial ventricles and extensive reduction in the volume of cerebral white matter. RC suffers from a right-sided hemiplegia and cerebral palsy with delayed milestones, behavioural problems and epilepsy as a result of brain damage.
The case advanced on RC’s behalf was that after the operation on 4 October he was over ventilated, leading to hypocarbia, cerebral vascular constriction and resulting cerebral hypoxia. As a consequence he sustained brain damage. The damage to brain cells led to the release of large amounts of protein into the CSF, which blocked its re-absorption thereby giving rise to hydrocephalus.
The Defendant denied that in 1999 hypocarbia was a recognised cause of brain damage and denied that it was a breach of duty to have allowed RC to become hypocarbic. Moreover, the Defendant alleged that it was more probable that brain damage was consequent upon his congenital heart condition, which had (a) given rise to low oxygen levels before the operation of the 4th (b) had required the RC to undergo a serious operation with bypass time of 128 minutes and an induced circulatory arrest of 9 minutes and (c) had led to a period of significant hypoperfusion following the operation. These, the Defendant argued, were the inevitable consequences of the heart defect itself and the need to correct the defect in the neonatal period.
One of the problems facing us was that there is a significant body of medical literature which suggests that 50% of infants with congenital heart disease have evidence of neurological injury on MRI prior to surgery. However the neonatologists helpfully agreed at the joint meeting that RC’s brain damage probably occurred in the peri-operative period. We came to the conclusion that there was no sufficient evidence to enable the Defendant to argue successfully that the RC had sustained a specific injury giving rise to the damage sustained before 4 October. However we considered that it would be difficult to argue that RC’s heart disease would have had no impact on cognitive development absent the event that gave rise to the specific injury.
The cardiac surgeons agreed that there was no evidence to suggest that anything untoward had happened during the surgery which probably caused brain damage, however, they also agreed that cerebral damage occurrs in up to 25% of neonates undergoing such surgery and that such damage occurred without there being a recognised adverse event. We considered that the perfusion problems experienced by RC before the operation, taken together with the fact that the procedure itself could cause some further damage, meant that it was unlikely the Court would regard RC as wholly neurologically unscathed by his heart disease.
The causation experts considered that post-operatively RC was hypocarbic, had a low cardiac output and was hyperoxic (excess oxygen in his blood). The Defendant’s expert contended that the low cardiac output following the operation (and which it was agreed could not have been prevented) contributed to the RC’s brain injury. Our causation experts accepted that a period of hypotension on 8 October had the potential to be associated with brain damaging ischemia but on balance it had not caused or contributed to brain damage. Our experts considered that it was probable that hypocarbia following the operation caused brain damage. The Defendant’s experts agreed that it was possible but argued (a) that it was not possible to say that damage had actually occurred and (b) that it was improbable that the hypocarbia was the sole cause of the damage given all of the other factors that operated to make cerebral perfusion vulnerable. Our paediatric intensivist agreed that in a term infant rather than a premature one, the risk of damage due to hypocarbia was less relevant.
We concluded that it was probable that the Court would accept that post-operative hypocarbia made a material contribution to the damage sustained by RC. However, there was some risk that the Court would accept that on the facts of this case it was not possible to say that hypocarbia had probably caused the damage sustained.
A further problem was that the paediatric intensivists agreed that there was a period of non-negligent (unavoidable) hypocarbia before the negligent hypocarbia. The neonatologists disagreed as to how long the period was before the failure to reverse the hypocarbia became a breach of duty. The difference between them was 3½ hours and it would have been open to the Defendant to say that in such circumstances apportionment of damage was possible and should be carried out. If that exercise had been carried out then the period of hypocarbia from 20.30 until 01.00 hours would have been non-negligent and the period from 01.00 hours until 04.00 hours negligent.
That would have opened the interesting question of whether the damage was indivisible and incapable of apportionment as in Bailey v MOD  EWCA Civ 883 or whether the Court would be entitled on a broad basis to apportion the damage as in Holtby v Brigham & Cowan (Hull) Ltd  EWCA Civ 111.
A Joint Settlement meeting was held on the 30th September 2011. We considered that a discount to reflect the risks of litigation was inevitable for the reasons given above. The Defendant offered to settle the case on a 50:50 basis. That offer was rejected. After further negotiation the Defendant offered to accept two-thirds of the liability. That offer was also rejected. Eventually settlement was reached on the basis that the Defendant would pay 70% of the full value of the claim and this was approved by the Court in October 2011. The claim will now be quantified. While RC is seriously disabled his life expectancy is to about 75 years and the full value of the claim will be in the region of £8,000,000. This will comprise a lump sum for accommodation, equipment, treatment etc and periodical payments for life for care.
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