Introduction

• Cause: due to exogenous trauma resulting in skull fracture or from gun shot, falling objects such as tree branches, and other weapons.
• Signs: neurological, depression, coma.
• Diagnosis: history, MRI, CT.
• Treatment: symptomatic for brain injury.
• Prognosis: depends on severity of damage.
• See also fibrocartilaginous embolism Fibrocartilaginous embolism , brain trauma Brain: trauma and brainstem contusion Brainstem: contusion.

Pathogenesis

Etiology

• Gun shot.
• Depressed skull fracture, eg RTA.
• Knife or stick injury.

Pathophysiology

• Penetrating wounds to the brain result may result in mechanical disruption of intracranial tissues (primary injury).
• This primary injury may initiate a number of secondary pathophysiological sequelae such as metabolic alterations in neuronal or glial cells; impairment of vascular supply to normal tissue (ischemia); impairment of cerebrovascular autoregulation, hemorrhage (intraparenchymal, intraventricular, extradural or subdural); irritation (seizure generation); obstruction of the ventricular system; edema formation, production of physiologically active products; and finally, increased intracranial pressure (ICP).
• With all penetrating wounds, infection and sequestration of debris are possible.

• The penetrating object or skull initially results in a mechanical injury to the brain.
• The acute (minutes to hours) secondary consequences of this primary injury are multifold:
  • Cerebral edema.
  • Ischemia and hypoxia.
  • Hemorrhage.
  • Increased intracranial pressure → brain-heart syndrome, neurogenic pulmonary edema, respiratory abnormalities.

Timecourse

• More delayed (hours to days) secondary complications primarily center around infection (both bacterial and fungal) and sequestration of debris and foreign material, both of which insite an inflammatory response.

Diagnosis

Treatment

Outcomes