Adult hypoxic and ischemic lesions

Published on 19/03/2015 by admin

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Last modified 19/03/2015

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Adult hypoxic and ischemic lesions


Although ‘hypoxia’ (reduction in oxygen supply or impairment of its utilization) and ‘ischemia’ (reduction in blood supply) are often used interchangeably, and the term ‘hypoxic-ischemic encephalopathy’ is utilized widely in everyday practice, these conditions can have different etiologies, pathophysiologic mechanisms and clinical, as well as morphologic, sequelae in the CNS.


Blood flow to the CNS may be entirely normal or even somewhat increased. The CNS is relatively resistant to pure hypoxia, but hypoxia

exacerbates the damage produced by ischemia. In practice, many causes of stagnant or hypoxemic hypoxia (e.g. cardiac arrest and carbon monoxide poisoning, respectively) also depress cardiac output, resulting in combined hypoxic/global ischemic brain injury.

Global brain ischemia

This occurs with a pronounced decrease in cerebral perfusion pressure (CPP) to a level below the threshold required for optimal vascular autoregulation. Reduced systemic blood pressure or raised intracranial pressure produces such a deleterious reduction in CPP. Cardiac pathologies (producing arrest, dysrhythmia, or tamponade) or traumatic hemorrhage dominate the causes of reduced systemic blood pressure, but these are very varied. Severe head injury is a leading cause of raised intracranial pressure. Resulting brain damage is accentuated in watershed/borderzone regions, the boundaries between vascular territories, especially in the depths of sulci.

Local brain ischemia

This usually results from arterial stenosis and/or mural thrombosis, atheroemboli, or thromboembolic arterial occlusion, any resulting infarct being within the perfusion territory of an affected artery.


Adult and infant brains react differently to hypoxia and ischemia. In general, infant brains are more resistant than those of adults; hypoxic-ischemic lesions have a different distribution in infants and adults reflecting an age-related differential (selective) vulnerability to such insults (Fig. 8.1). Because of the brain’s immense metabolic demands, after the onset of ischemia levels of brain glycogen, glucose, ATP and phosphocreatine plummet and are often depleted within 10 min of the acute event. After 15 min of cardiac arrest, up to 95% of the brain may be damaged. Primary respiratory arrest (e.g. due to aspiration, anaphylaxis, or airway trauma) may cause transient brain dysfunction, but less severe damage than ischemia. Optimal brain function and respiration are dependent upon the availability of glucose; however, the neuropathology of hypoglycemic brain injury differs from that due to hypoxia-ischemia.


Despite the relatively straightforward clinical stratification of syndromes that result from prolonged brain hypoxia, the macroscopic and microscopic features associated with hypoxic/ischemic insults can be very variable, and matching clinical history to neuropathology can be imprecise.

Lesions may be considered as either acute/subacute or chronic.


NECROTIC: Nuclear pyknosis

Brightly eosinophilic cytoplasm (‘red neurons’) plus loss of Nissl substance.

APOPTOTIC: Apoptotic bodies/Nucleosomal segmentation

The relative importance of apoptosis in AIE/HIE is debated; ultrastructural evidence suggests it is of minimal significance, though some apoptotic pathways may be activated in the course of necrotic cell death.

AUTOPHAGIC: Condensed cytoplasm

Large cytoplasmic vacuoles.