Post anoxic brain damage

Signs & symptoms:

Clinical features of anoxic-ischemic and hypoxemic encephalopathy can be divided into the acute and subacute-chronic phases. After cardiac arrest, patients with severe hypotension or asphyxia are often comatose. Since hypothermia (body temperature lowered to 32-34 degrees Celsius for 24 hours) has been shown to be neuro-protective (lessening both morbidity and mortality)1,2, in the acute phase, patients are deeply sedated and pharmacologically paralyzed to facilitate this therapy. During this time, neurological assessment is limited to the pupillary reactions. After normothermia is restored, the examination is directed at establishing a prognosis and to check for treatable complications such as seizures and brain swelling. Generalized, axial myoclonus (bilaterally synchronous jerks involving face, diaphragm and proximal limbs), occurring either just before or after hypothermia, is usually but not invariably an unfavorable prognostic sign (indicating severe disability with dependency at 6 months).3 Other indications of an unfavorable prognosis include absent pupillary and/or corneal reflexes by Day 3.4 In patients treated with hypothermia recovery of the motor response can be delayed until at least Day 6.5 In patients not treated with hypothermia no better than extensor (decerebrate) posturing was associated with a poor outcome. Those patients who have lost brainstem reflexes can be tested further to determine if they meet the criteria for brain death. 4

Subacute and Long-Term Outcomes: Patients who have been resuscitated from cardiac arrest and are not brain dead have a range of neurological outcomes ranging from the vegetative state to complete recovery of neurological function. Between these two extremes are various levels of disability, e.g., the minimally conscious state and dementia; problems with executive functions and memory occur in half the patients treated with hypothermia after cardiac arrest.6 The same may apply to patients who have suffered severe hypotension or asphyxia. A complication of severe hypotension is “watershed infarction” due to ischemic infarction in the region of the terminal branches of the anterior, middle and posterior cerebral arteries. In addition to biparietal lobe damage, such patients may have bibrachial paralysis (the “man in the barrel syndrome”). In patients with asphyxia alone (without hypotension), a rare cause of brain damage (as the PaO2 must fall below 30 mm Hg), the encephalopathy is more global as with cardiac arrest patients.