Traumatic brain injury (TBI) involves two phases of injury: Primary injury occurs at the moment of impact and includes direct tissue damage from mechanical forces: contusions (coup-contrecoup), diffuse axonal injury (DAI) from rotational acceleration-deceleration shearing white matter tracts, skull fractures, and intracranial hemorrhage (epidural, subdural, subarachnoid, intraparenchymal). Primary injury is irreversible and can only be prevented, not treated. Secondary injury develops hours to days after the initial insult and is the primary target of nursing management. The cascade includes: (1) Cerebral edema from blood-brain barrier disruption and cellular swelling (cytotoxic and vasogenic edema); (2) Increased intracranial pressure (ICP) as brain swelling within the rigid skull compresses brain tissue (Monro-Kellie doctrine: skull contains fixed volume of brain, blood, CSF; increase in one must be compensated by decrease in another); (3) Decreased cerebral perfusion pressure (CPP = MAP - ICP; goal >60 mmHg); (4) Excitotoxicity from glutamate release causing calcium-mediated neuronal death; (5) Inflammation and free radical damage; (6) Cerebral ischemia from vasospasm, microvascular thrombosis, and impaired autoregulation. Cushing's triad (hypertension with widening pulse pressure, bradycardia, irregular respirations) is a LATE and...