Choudhury v South Central Ambulance Service & Anor

In a clinical negligence claim, proof that treatment generally improves outcomes does not establish causation in an individual case. Statistical and epidemiological evidence must be assessed against the particular facts, the nature of the evidence and any relevant control or comparison group. An observational study comparing different treatments cannot, without more, establish what would have happened without treatment or with delayed treatment. The claimant must prove on the balance of probabilities that the breach caused the injury claimed. Where the evidence leaves material variables unresolved and supports no more than an increased chance of a better outcome, the causation test is not satisfied.

The claimant suffered a basilar artery thrombosis, followed by a serious collapse and later locked-in syndrome. He brought negligence claims against an ambulance service and a hospital trust. Both defendants admitted significant breaches, including delay in hospital admission, diagnostic delay and delay in administering aspirin.

The claimant accepted that the initial collapse had caused permanent brain damage. He claimed damages for the additional disability resulting from his later deterioration in hospital. The central issue was whether, if aspirin and appropriate stroke care had been provided between 06:00 on 16 March 2010 and 02:30 on 17 March, he would probably have avoided the further deterioration and locked-in syndrome.

1. Causation. The claimant failed to prove, on the balance of probabilities, that earlier aspirin and good stroke care would have prevented the recurrent stroke, further deterioration or locked-in syndrome. The claim therefore failed on causation.
2. The court accepted that the initial collapse at about 04:30 on 16 March had caused serious and irreversible brain damage. Had the later deterioration not occurred, the most likely outcome would have been an mRS score of 3, even after rehabilitation. The claimant’s injury was therefore the difference between that condition and his actual locked-in state.
3. The court found that the later deterioration was most probably caused by recurrent embolism and further basilar artery occlusion. The lumbar puncture had no causative effect. The evidence did not establish significant dehydration, hypoxia or other intervening factor sufficient to explain the deterioration.
4. The observational BASICS study compared different treatment strategies for acute basilar artery occlusion. It did not compare aspirin with no treatment or delayed treatment. Without a control group, it could not establish what proportion of patients would have achieved a similar outcome without aspirin. Its broad mild-to-moderate category also included patients whose conditions differed materially from the claimant’s.
5. The randomised CAST and IST trials provided relevant evidence concerning aspirin against placebo, although their direct applicability to basilar artery thrombosis was limited. The evidence indicated only a modest reduction in recurrent stroke and did not demonstrate a greater-than-even chance that aspirin would have prevented this claimant’s deterioration.
6. Consistently with Sienkiewicz v Greif [2011] UKSC 10, the significance of statistical and epidemiological evidence depended on the nature of that evidence and the particular facts. The claimant’s reliance on unpublished research and studies involving TIA or minor stroke did not cure the evidential deficiencies.
7. The court found for the defendants on causation and invited submissions on the appropriate order and directions.

Not stated in the judgment.