Anoxic Encephalopathy
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Contents |
Etiology
- cardiac arrest
- respiratory failure
- catastrophic stroke
- poisoning
Pathology
- hippocampal pyramidal neurons selectively vulnerable [4]
- CA1 region most vulnerable [5]
- cererbellar Purkinje cells selectively vulnerable [4]
- diffusely affects neocortex [2,4]
- thalamus consistently injured [2]
- neurons of the nucleus accumbens relatively spared [3]
- in neonatal anoxia, periventricular white matter is also selectively vulnerable [4]
- calcium channels and excitatory glutamate receptors are implicated in hypoxic/ anoxic brain damage [4]
- hypoglycemia & ATP deficiency implicated
Clinical-manifestations
- progression through the Glascow coma scale within seconds to minutes
- 98% of patients with Glascow coma scale < 5 remain die or remain comatose after 2 weeks
- other signs/symptoms* associated with poor prognosis
- absent corneal reflexes
- absent pupillary reaction to light
- absent withdrawal to pain
- absent motor responses
- * 24 hours after onset
Laboratory
- markedly elevated neuron-specific enolase (> 33 ug/L) or serum S-100 associated with poor prognosis
Radiology
- CT or MRI for the evaluation of stroke or head trauma if indicated
- PET scan may play a role in the future
Management
- specific measures for specific etiology
- supportive care
- induced hypothermia may improve morbidity & mortality if insult is removed
More General Terms
References
- UpToDate 14.2 [1]
- Adams JH et al, The neuropathology of the vegetative state after an acute brain insult. Brain 2000, 123:1327 PMID: [2]
- Huang KW and Zhao Y Selective sparing of human nucleus accumbens in aging and anoxia. Can J Neurol Sci 1995, 22:290 PMID: [3]
- Cervos-Navarro J and Deimer NH, Selective vulnerability in brain hypoxia. Crit Rev Neurobiol 1991, 6:149 PMID: [4]
- Ng T et al, Changes in the hippocampus and the cerbellum resulting from hypoxic insults: frequency and distribution. Acta Neuropathol (Berl) 1989, 78:438 PMID: [5]
