Cerebral hypoxia pathophysiology
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Overview
The brain consumes significant amount of the energy compared to its size and weight. Cellular injury can begin within minutes, and permanent brain injury will follow if prompt intervention does not occur.
Pathophysiology
- The brain depends on a constant energy supply provided by glucose and oxygen but is unable to store energy. With the cessation of blood flow, intracellular production of adenosine triphosphate is diminished. This results in dysfunction of energy-dependent ion channels, which contributes to intracellular sodium accumulation and cytotoxic edema. Ongoing ischemia results in the release of glutamate, an excitatory neurotransmitter, which promotes calcium influx through N-methyl-D-aspartate (NMDA) receptors. Calcium influx exacerbates neuronal injury by activating lytic enzymes, precipitating free radical formation, and interfering with mitochondrial function. This process, known as excitotoxicity, can ultimately lead to cell death. [6][7]
Histopathology
- The mechanisms that lead to delayed cell death following hypoxic-ischemic injury in the brain are complex. Ischemic cell death occurs via two different pathways: necrosis and apoptosis. During hypoxia-ischemia of the brain, acute energy failure leads to loss of ion homeostasis where intracellular sodium and calcium accumulate creating osmotic swelling which, can lead to cell lysis.[8]
- This process releases glutamate and free radicals which are cytotoxic and exacerbate the injury. A secondary phase of neuronal death can occur hours later. Moderate global ischemia leads to infarcts in watershed areas (e.g., the area lying between regions fed by the anterior and middle cerebral artery).
- These infarcts can damage the highly vulnerable areas such as pyramidal neurons of the hippocampus (CA1 region), pyramidal neurons of the cerebral cortex (layers 3, 5, and 6) which leads to laminar necrosis, the death of neurons in the basal ganglia (caudate nucleus and putamen), and the Purkinje cell layer of the cerebellum.[9]
- The cells of these areas are high in metabolic demand and contain a high concentration of excitatory neurotransmitter receptors.
- Other histologic findings include a shrunken eosinophilic neuron (anoxic neuron) and a red neuron which represents neuronal cells that die because of hypoxia.
Pathophysiology
