Canis ISSN: 2398-2942

Brain: penetration wound

Contributor(s): Rodney Bagley

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

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Bagley R S (1996) Pathophysiologic sequelae of intracranial disease. Vet Clin North Am 26 (4), 711-734 PubMed.
  • Bagley R S, Baszler T V, Harrington M L, Pluhar G E, Moore M P, Keegan R D & Greene S A (1995) Clinical effects of longitudinal division of the corpus callosum in dogs. Vet Surg 24 (2), 122-127 PubMed.
  • Dewey C W, Budsberg S C & Oliver Jr J E (1993) Principles of head trauma management in dogs and cats - Part II. Comp Contin Ed 15 (2), 177-193 VetMedResource.
  • Pal J, Brown R & Fleiszer D (1989) The value of the Glasgow coma scale and injury severity score - Predicting outcome in multiple trauma patients with head injury. J Trauma 29 (6), 746-748 PubMed.
  • Hall E D (1985) High-dose glucocorticoid treatment improves neurological recovery in head-injured mice. J Neurosurg 62 (6), 882-887 PubMed.
  • Tornheim P A, Liwnicz B H, Hirsch C S, Brown D L & McLaurin R L (1983) Acute responses to blunt head trauma. Experimental model and gross pathology. J Neurosurg 59 (3), 431-438 PubMed.

Other sources of information

  • Wheeler S J (1995) In:Manual of Small Animal Neurology.West Sussex: BSAVA.
  • Bagley R S (1994)Pathophysiological effects of central nervous system tumor.In:Proceedings of the Twelth Annual Veterinary Medical forum. Washington DC, May 1994. pp 928-930.
  • Kornegay J N (1993)Pathogenesis of diseases of the central nervous system.In:Textbook of Small Animal Surgery. 2nd edn. Slatter D (ed). Philadelphia: W B Saunders. pp 1022-1037.
  • Chrisman C L (1991)Problems in Small Animal Neurology.2nd edn. Philadelphia: Lea & Febiger.
  • Shores A (1989)Craniocerebral trauma.In: Kirk RW (ed)Current Veterinary Therapy. 10th edn. Philadelphia: W B Saunders. pp 847-853.


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