Intracranial hemorrhage
Introduction
- Rare cause of neurological disease → brain dysfunction.
- Cause: trauma (subarachnoid or intracranial hemorrhage), rupture of congenital vascular abnormalities, primary or secondary brain tumors, vasculitis, systemic hypertension, hemorrhagic infarction, impaired coagulation.
- Signs: diverse neurological deficits depending on site and type of hemorrhage.
- Diagnosis: imaging techniques, CSF analysis.
- Prognosis: generally guarded to fair depending on the cause of the hemorrhage.
Presenting signs
- Neurological deficits ranging from mild locomotor abnormalities to loss of consciousness.
Acute presentation
- Coma.
Pathogenesis
Etiology
- Trauma.
- Neoplasia Brain neoplasia (primary or secondary brain tumor).
- Hypertension Hypertension.
- Coagulopathies Hemostatic disorders: acquired.
- Vasculopathy, eg secondary to radiation therapy Radiotherapy, vasculitis.
- Rupture of congenital vascular abnormalities.
- Systemic hypertension.
Predisposing factors
General
- Coagulopathies Hemostatic disorders: acquired.
- Thromboembolic disease Thromboembolism: aorta.
- Hypertension Hypertension.
- Radiation therapy Radiotherapy.
Pathophysiology
- Blood leaks directly into the brain, forming a hematoma within the brain parenchyma, or into the subarachnoid or subdural space, leading to physical disruption of the tissue and pressure on the surrounding brain. This alters CNS volume/pressure relationships, with the possibility of increasing intracranial pressure (ICP) and decreasing cerebral blood flow (CBF).
- As a hematoma develops, ICP may remain constant due to a system of compensation. Within the skull, a change in the volume of one intracranial component (brain tissue, arterial blood, venous blood, CSF) will be balanced by a compensatory change in another.
- Exhaustion of the compensating mechanisms for an intracranial space occupying lesion results in further increases in the volume of the hematoma, producing massive elevations in ICP.
- Due to mechanical autoregulation, CBF remains constant even though cerebral perfusion pressure (CPP) may vary between 40 and 120 mmHg.
- The normal autoregulation of CBF may be impaired following intracranial bleed, causing blood flow to damaged regions to become directly dependent on systemic blood pressure. Such animals may be unable to compensate for reductions in mean arterial pressure, causing decreased CPP in the presence of increased ICP.
In these circumstances, systemic hypotension can result in inadequate perfusion of the brain, which leads to cerebral ischemia and secondary neuronal injury. - Raised intracranial pressure ultimately leads to brain herniation.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Altay U M, Skerritt G C, Hilbe M (2011) Feline cerebrovascular disease: clinical and histopathological findings in 16 cats. JAAHA 47 (2), 89-97 PubMed.
- Garosi L S (2010) Cerebrovascular disease in dogs and cats. Vet Clin North Am Small Anim Pract 40 (1), 65-79 PubMed.
- Acierno M J, Labato M A (2004) Hypertension in dogs and cats. Compendium 26 (5), 336-346 VetMedResource.
Other sources of information
- Garosi L S, Platt S R (2009) Treatment of cerebrovascular disease. In: Bonagura J D & Twedt D C (eds) Current Veterinary Therapy XIV. St Louis, Missouri. Saunders Elsevier. pp 1074-1077.