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Secondary injury refers to the ongoing cellular damage that occurs after the initial traumatic brain injury (TBI). This damage is not caused by the direct force of the impact but by a complex series of biochemical reactions and molecular changes that are set in motion by the primary injury. These events can lead to brain swelling (edema), inflammation, and a self-perpetuating cycle of cell death that extends the damage over days or even weeks.

Key components of the secondary injury cascade include lack of oxygen (anoxia), low blood oxygen (hypoxemia), low blood pressure (hypotension), anemia, bleeding in the brain (hemorrhage), and increased pressure within the skull (intracranial pressure). This increased pressure can compress brain tissue, leading to further damage and potentially herniation of brain structures. The process can involve both necrosis (unprogrammed cell death) and apoptosis (programmed cell death).1

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2 Britannica Sources
  1. traumatic brain injury
  2. crush injury

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