Related Experiment Videos
Hypoxic-ischaemic encephalopathy after near miss sudden infant death syndrome
J E Constantinou1, J Gillis, R A Ouvrier
1Department of Neurology, Royal Alexandra Hospital for Children, Sydney, Australia.
Insights
Near-miss sudden infant death syndrome (SIDS) can cause severe hypoxic episodes and neurological damage in infants. Survivors often experience long-term deficits, including developmental delays and cerebral palsy.
Area of Science:
- Neonatology
- Pediatric Neurology
- Critical Care Medicine
Background:
- Sudden infant death syndrome (SIDS) remains a significant concern in infant mortality.
- Near-miss SIDS events present unique challenges in understanding infant resuscitation and outcomes.
Purpose of the Study:
- To describe the clinical course and neurological outcomes of infants experiencing severe hypoxic episodes due to near-miss SIDS.
- To characterize the evolution of hypoxic-ischaemic encephalopathy in this vulnerable population.
Main Methods:
- Retrospective analysis of 14 infants (3-26 weeks) with severe hypoxic episodes from near-miss SIDS between 1982-1985.
- Clinical assessment, laboratory investigations, and neuroimaging (CT scans) were utilized.
Main Results:
- All infants presented with metabolic acidosis, cardiovascular instability, acute renal failure, ischemic colitis, or neurological dysfunction.
- Seven infants died within 60 hours; the seven survivors displayed a characteristic biphasic hypoxic-ischaemic encephalopathy.
- Long-term follow-up revealed significant neurological deficits in six survivors, including spastic quadriplegia and cortical blindness.
Conclusions:
- Near-miss SIDS can lead to severe hypoxic-ischaemic encephalopathy with a distinct neurological progression.
- Infants surviving near-miss SIDS are at high risk for significant long-term neurological impairments, necessitating specialized care and follow-up.
Abstract:
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.