PT  - JOURNAL ARTICLE
AU  - J E Constantinou
AU  - J Gillis
AU  - R A Ouvrier
AU  - P M Rahilly
TI  - Hypoxic-ischaemic encephalopathy after near miss sudden infant death syndrome.
AID  - 10.1136/adc.64.5.703
DP  - 1989 May 01
TA  - Archives of Disease in Childhood
PG  - 703--708
VI  - 64
IP  - 5
4099  - http://adc.bmj.com/content/64/5/703.short
4100  - http://adc.bmj.com/content/64/5/703.full
SO  - Arch Dis Child1989 May 01; 64
AB  - Between 1982 and 1985, 14 infants aged 3-26 weeks presented with severe hypoxic episodes as a result of the 'near miss' sudden infant death syndrome (SIDS). They all had metabolic acidosis, cardiovascular instability, acute renal failure, ischaemic colitis, or acute neurological dysfunction. Investigation of the cause excluded infection and trauma, or a primary metabolic, pulmonary, cardiac, or seizure disorder. Seven infants were deeply comatose on admission, never regained consciousness, and died within 60 hours. A characteristic evolution of hypoxic-ischaemic encephalopathy not previously clearly described after near miss SIDS was seen in the seven who lived. Five of the seven were conscious within one hour of resuscitation and showed a striking interval of near normality before neurological deterioration that was characterised by status epilepticus, deep coma, and brain stem dysfunction from 36-96 hours after the event. A biphasic course was not apparent in the remaining two, each of whom was comatose on admission, though refractory seizures did develop. Computed tomograms of the brain more than a week after the event showed cortical infarction or cerebral atrophy. Six of the survivors, followed up from 16-55 months, have serious residual deficits including spastic quadriplegia, delayed development, cortical blindness, or infantile spasms.