What is the pathophysiology of secondary traumatic brain injury (TBI)?

Updated: Feb 01, 2018
  • Author: Percival H Pangilinan, Jr, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Secondary injury may occur hours or even days after the inciting traumatic event. Injury may result from impairment or local declines in cerebral blood flow (CBF) after a TBI. Decreases in CBF are the result of local edema, hemorrhage, or increased intracranial pressure (ICP). As a result of inadequate perfusion, cellular ion pumps may fail, causing a cascade involving intracellular calcium and sodium. Resultant calcium and sodium overload may contribute to cellular destruction. Excessive release of excitatory amino acids, such as glutamate and aspartate, exacerbates failure of the ion pumps. As the cascade continues, cells die, causing free radical formation, proteolysis, and lipid peroxidation. These factors can ultimately cause neuronal death. [21]

The exact role of the inflammatory response in secondary injury is not known. However, it is believed to contribute to cell damage. [21, 22]

Clinical conditions associated with the risk of a decreased CBF are arterial hypotension, hypoxemia, intracranial hemorrhage and malignant brain edema, and hyperthermia. [21]

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