====== Hypoxic coma ======

Anoxic [[encephalopathy]] may be due to anoxemic anoxia (drop-in pO2) or anemic anoxia (following exsanguination or [[cardiac arrest]]). [[Myoclonus]] is common.

Vulnerable cells:

1. cerebral gray matter: lesions predominate in 3rd cortical layer (white matter is usually better
preserved due to lower O2 requirements)

2. Ammon’s horn is also vulnerable, especially the Sommer section

3. in the basal ganglia (BG):

a) anoxemic anoxia severely affects globus pallidus

b) anemic anoxia affects the caudate nucleus and putamen

4. in the cerebellum: Purkinje cells, dentate nuclei, and inferior olives are affected


A multivariate analysis yields outcome prognosticators:

This analysis applies only to hypoxic-ischemic coma; and is based retrospectively on 210 patients, most S/P cardiac arrest with many medical complications
((Levy DE, Caronna JJ, Singer BH, et al. Predicting Outcome from Hypoxic-Ischemic Coma. JAMA. 1985; 253:1420–1426)).

More recent studies confirm the poor prognosis of unreactive pupils and lack of motor response to pain
((Zandbergen EGJ, de Haan RJ, Stoutenbeek CP, et al. Systematic Review of Early Prediction of Poor Outcome in Anoxic-Ischemic Coma. Lancet. 1998; 352:1808–1812))
if either of these findings is seen within a few hours after cardiac arrest there is an 80% risk of death or permanent vegetative state, and if present at 3 days, this rate rose to 100%.

Glucocorticoids (steroids) have been shown to have no beneficial effect on survival rate or neurological recovery rate after cardiac arrest
((Jastremski M, Sutton-Tyrell K, Vaagenes P, et al. Glucocorticoid Treatment Does Not Improve Neurological Recovery Following Cardiac Arrest. JAMA. 1989; 262:3427–3430)).