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Post-Anoxic Encephalopathy...

Although post-anoxemic encephalopathy is considered to be the most precise term semantically, both anoxic encephalopathy and hypoxic encephalopathy, which is perhaps the most commonly used term, are also used. All three terms are regarded as acceptable for referring to the serious neuro-Anoxic)logical lesions caused by the oxygen and circulatory deficits that result in cessation of the aerobic metabolic processes required to maintain cerebral neuronal functioning.

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Articles of Interest

Anoxic Encephalopathy

Anoxic encephalopathy, or hypoxicischemic brain injury, is a process that begins with the cessation of cerebral blood flow to brain tissue, which most commonly results from poisoning (for example carbon monoxide or drug overdose), vascular injury or insult, or cardiac arrest. Many patients who suffer anoxic brain injury expire without regaining full consciousness and many patients have significantly poor neurologic outcomes. However, some advances are beginning to demonstrate preservation of brain tissue, and there is a focus on identifying patients with the prospect of improving neurologic morbidity and mortality.

Delayed toxic–hypoxic encephalopathy

The syndrome of delayed toxic–hypoxic encephalopathy is triggered by a sedating toxin that precipitates a period of cerebral hypoxaemia. The syndrome is rare and has a classic biphasic course with a seemingly complete recovery from the first episode of coma followed by a dramatic deterioration.

Five Minutes... To Avoid Anoxic Brain Injury

If something dire goes wrong during anesthesia and surgery and the flow of oxygen to the brain is cut off, an anesthesia practitioner has about five minutes to diagnose the cause of the problem and treat it. Some brain cells start dying within five minutes after the oxygen supply disappears, and brain hypoxia can rapidly cause severe brain damage or death.

Hypoxic Brain Injury

aka hypoxic encephalopathy; the terms anoxic or ischaemic may also be used.

Neuroprognostication after cardiac arrest

Patients often sustain severe neurologic injury during cardiac arrest. As the heart ceases to pump oxyhemoglobin, tissues with higher metabolic rates are more at risk of developing irreversible hypoxic injury. The brain, particularly the cortex, deep gray nuclei and cerebellum, have very high metabolic demand and are thus prone to sustain injury during periods of cardiac arrest. In these cases, the decision to provide ongoing support often hinges on whether the patient might regain meaningful consciousness. Prognostication is extraordinarily important. Excessively pessimistic prognostication could lead to a premature withdrawal of care in a patient with the potential to recover. However, overly optimistic prognostication may lead to ongoing support for days or weeks in a hopeless situation.

Neuroprotective Treatment of Postanoxic Encephalopathy: A Review of Clinical Evidence

Promising results from animal studies on neuroprotective treatments in postanoxic encephalopathy could not be extrapolated to patients after cardiac arrest. This lack of extrapolation is related to overestimation of pre-clinical evidence, and critical disparities between animal models and patients.

Post-Hypoxic Myoclonus

Post-hypoxic myoclonus (PHM) refers to myoclonus occurring after hypoxic brain injury resulting from a cardiac arrest, characterised by abrupt, irregular contractions of muscles that may be focal or generalised.

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StatPearls

Anoxic encephalopathy, or hypoxic-ischemic brain injury, is a process that begins with the cessation of cerebral blood flow to brain tissue, which most commonly results from poisoning, as is the case, for example, with carbon monoxide poisoning or drug overdose, vascular injury, or insult, or cardiac arrest.