Abstract
This action arose from events in the 40 hours following the Claimant's birth at Basildon Hospital at 23:55 on 2 June 1990. Billy suffers from cerebral palsy, severe motor and intellectual deficit and has epilepsy. The experts agreed that his condition was caused by periventricular leucomalacia (PVL), namely damage to the white matter of the brain which usually occurs between 26 and 34 weeks of gestation, although it can develop subsequently in pregnancy and even post birth.
It was alleged on behalf of Billy that: (1) there was failure to monitor his blood sugar level with sufficient accuracy; (2) care given between birth and 10:00 on 3 June was negligent; (3) inadequate management occurred in the special care baby unit (SCBU); and (4) management from 12:00 on 4 June was negligent. It was further maintained that negligent treatment had caused the PVL.
Billy's mother, Mrs Knight, had become diabetic at the age of 13 years. The Defendants accepted that, as a consequence, Billy was at high risk of brain damage and would therefore require careful monitoring. Babies born to diabetic mothers can develop low levels of blood sugar and are at risk of hypoglycaemia (a deficiency of glucose in the bloodstream) unless given appropriate amounts of glucose. This danger is compounded by the fact that hypoglycaemia can be symptomless.
Both sides agreed that a hypoxic-ischaemic event occurred shortly before Billy's birth, which led to a decision to deliver him by emergency Caesarian section. The Defendants argued that it was this event alone which caused his condition, whereas the Claimant's experts considered that failure to monitor or treat the hypoglycaemia caused PVL.
The Claimant's experts also argued that a blood sugar level of 2.2 mmol/L was appropriate, whereas the clinicians involved in Billy's treatment, supported by expert paediatrician Dr Kovar, stated that a reading of 2.0 was their target. Judge Mitchell held that this was reasonable for 1990.
The circumstances immediately post birth
The Apgar scores after birth were reasonable and Billy was fed at 01:00. However at 04:10 a blood sugar level test (‘BM stix’) resulted in a reading of 0. The paediatric SHO was informed, and advised 20 ml of formula feed and two-hourly blood glucose tests.
The treating midwife and other clinicians gave evidence as to the unreliability of the BM stix test. A sample of blood is taken and put onto a stick, which is then placed under a tap and the resultant colour checked against a chart. It was the midwife's experience that the test often underestimated the true level. There was no laboratory on site to undertake more reliable tests.
At 06:00, Billy was fed but the blood glucose reading was absent from the notes, probably because it was on the feed chart which had vanished.
On change of shift at 08:00, a second midwife recorded ‘BM stix remains down’. She did not record the actual reading, but said that it was likely to have been between 1.0 and 2.0 mmol/L. She maintained that if the level had been 0 she would definitely have documented it.
Professor Levene, on behalf of the Claimant, was very uncomfortable about the standard of care during this period, particularly in view of the fact that the blood sugar rarely reached a safe level. He considered that Billy had been hypoglycaemic for an unknown period between birth and 04:10. He thought that Billy should have been sent to SCBU at 06:00 and a drip set up. However, Dr Kovar for the Defendants felt that the hospital staff should not be criticized because they had aimed to keep the reading at 2.0, even though they had failed to achieve that level.
Held: on a balance of probabilities, the readings between 06:00 and 10:00 were between 1.0 and 2.0. Dr Kovar had observed that many of the symptoms of hypoglycaemia were non-specific, so a diagnosis had to be made on the basis of best judgment. His evidence was to be accepted. While there were certain reservations about the treatment during this period, the Claimant had not established negligence.
Transfer to SCBU
Judge Mitchell accepted that this took place at approximately 09:30. At 10:00, Billy was fed and the BM stix reading was 1.0. At 11:00, 10% glucose was commenced at 8 mls per hour. At 12:00 Billy was fed again and the BM stix reading had increased to 2.0. Intravenous glucose was reduced to 2 mls per hour.
It was alleged that the blood glucose levels were only just within an acceptable range when the infusion was reduced. However, the Defendants argued that by 12:00, Billy was tolerating oral feeds and was no longer vomiting. He had shown no symptoms of hypoglycaemia at any point prior to 12:00. Accordingly, the decision to reduce the infusion was reasonable.
At 17:30, the following record was made: ‘baby lying prone small amount of blood from nose and went dusky’. On another sheet, the word ‘fitting’ was added in a different hand. The Defendants argued that the second writing was that of Nurse Bennett, who did not come on duty until 22:00 and was a comment made after the event by someone who did not witness it. Dr Kovar, for the Health Authority, considered that this was an episode of gastric reflux aspiration, i.e. that Billy had aspirated his stomach contents.
Held: the evidence of Dr Kovar, which had been supported by another Defence expert, Dr Hawdon, was to be accepted. The Claimant had therefore not demonstrated that medical staff had been negligent during this period.
Events after 12:00 on 4 June 1990
At 06:00 on 4 June, the BM stix had been recorded at 3.0 mmol/L; at 10:00 the reading was 2.5; and at midday 2.0. At that point, intravenous dextrose was increased to 15 mls per hour. It was clear from the contemporary note, from a doctor who had not been traced because he had returned to Africa, that this was done because Billy was not tolerating oral feed and his blood sugar level was falling.
Dr Hameed, the paediatric registrar, considered that he was now dealing with symptomatic hypoglycaemia. At 14:20, it was recorded on the fitting chart: ‘eyes rolled, limbs shook 10 seconds’. Further fits were recorded at 15:00 and 15:30. The blood sugar level was down to 1.0. Dr Hameed considered this to be an emergency and ordered phenobarbitone, glycogen and hydrocortisone, and had Billy transferred to the High Dependency Unit. Interestingly, a laboratory test on a blood sample taken at 15:00 produced a glucose level of no less than 5.2.
Professor Lucas for the Claimant, described by the judge as ‘perhaps the world's leading expert of his field’, considered that this reading must have been incorrect and that the reading of 1.0 could not have referred to the period described in the notes. However, Judge Mitchell observed that his evidence on this point ‘has almost crossed into the realms of speculation rather that of hard opinion’. In the Judge's view, there was no good reason to reject the laboratory reading.
Held: it could not be said that the standard of care given by the doctors and midwives fell below that which was reasonable in all the circumstances. The Claimant had failed to prove his case.
Causation
While this was arguably academic in view of his finding on negligence, Judge Mitchell decided to deal with the subject at some length because of the degree of attention paid to it by both sides during trial.
In essence, the Claimant had to prove that hypoglycaemia could cause PVL, and secondly that it did so in his case. There was no doubt that this was a developing area of medical knowledge, and the Claimant's Leading Counsel acknowledged that there were limited data concerning an association between PVL and hypoglycaemia. Nonetheless, he invited the court to take a bold approach.
Judge Mitchell then considered at some length a number of academic articles on the subject, but concluded that these were not probative. He observed: ‘it seems to me that the evidence … demonstrates just what a struggle it is for the Claimant to establish on a balance of probabilities that hypoglycaemia does cause end stage PVL’. Very experienced neuroradiologists, namely Drs Anslow and Kendall, had given evidence for the respective sides. Dr Kendall was of the view that the type of damage shown on the MRI scan was not caused by hypoglycaemia. Dr Anslow said in evidence in chief that he did not think one could be as positive as that. These experts were both very impressive witnesses, but Dr Anslow's view did not support the proposition that there was a connection between hypoglycaemia and PVL on a balance of probabilities.
The burden of proof was on the Claimant, and he had failed to prove his contention on causation. There was a series of missing links in the causal chain which meant that the Defendants succeeded on causation as well.
Peter Andrews QC and Michael Harrison (instructed by Field Fisher Waterhouse) appeared for the Claimant. Michael de Navarro QC and Roger Harris (instructed by Brachers) appeared for the Health Authority.