Felis ISSN 2398-2950

Head: trauma

Introduction

• Cause: road traffic accident/hit by car, falls, kicks and gunshot injuries.
• Signs: head trauma may be evident from visible wounds or from a dysfunction of one of the organs in the head, eg the brain, nose or tongue. Acute onset of neurological signs related to area of brain injury.
• Treatment: emergency care should be given to establish an airway and to ensure that breathing and circulation are adequate. Decrease intracranial pressure; remove compressive lesions such as hematomas and depressed fractures; treat cerebral edema; treat seizures if they occur.
• Eye trauma may need urgent treatment to maximize the chances of retaining sight.
• Prognosis: guarded - depends on neurological status at presentation, response to emergency treatment, as well as presence of concurrent systemic injuries.

Pathogenesis

Etiology

• Road traffic accident/hit by car.
• Fight with another cat or bitten by dog.
• Other causes are falls and non-accidental injury (gunshot injury, kicks).

Predisposing factors

General

• Un-neutered male cats more prone to wandering.

Pathophysiology

• The 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.
  • Increased intracranial pressure (ICP).

Intracranial pressure after head trauma

• Increases in intracranial pressure Intracranial pressure measurement are often responsible for clinical decline in many animals after head trauma.
• After head trauma, the volume of the brain tissue compartment increases usually due to edema or hemorrhage.
• As the brain tissue compartment increases, the cerebrospinal fluid and the blood compartments must decrease or intracranial pressure will increase (compensation).
• Once the ability for compensation is exhausted, a further small increase in intracranial volume will result in dramatic elevations of ICP, with the immediate onset of clinical signs.

Timecourse

• Minutes to hours.

Diagnosis

Treatment

Outcomes