Intracranial hemorrhage in Cats (Felis) | Vetlexicon
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Intracranial hemorrhage

ISSN 2398-2950

Contributor(s) :


  • 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.



Predisposing factors



  • 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.


Presenting problems

Client history

Clinical signs

  • Hemorrhage should be suspected in any animal with an acute onset of an intracraninal abnormality.
  • Neurological deficits usually refer to a focal anatomical diagnosis and depend on the neurolocalization of the vascular insult (telecephalon, thalamus, midbrain, pons, medulla, cerebellum).
  • Neurological signs are largely related to elevated ICP, which gives rise to non-specific signs of forebrain, brainstem or cerebellar disturbance.
  • Cranial nerve deficits Cranial nerve neuropathy, eg facial weakness Facial nerve neuropathy, menace deficits, altered pupillary light reflex or other pupillary abnormalities and reduced facial sensation.
  • Vestibular eye movements poor or absent.
  • Hemiparesis.
  • Decerebrate rigidity.
  • Tetraparesis.
  • Irregular respiration, may become progressively more shallow if brain herniation progresses.
  • Stupor, coma.
  • Alterations in contour of skull, suggestive of fractures.
  • Circling, ataxia, proprioceptive defects .
  • Unilateral signs with deficits contralateral to side of lesion.
    Neurological signs (conduct neurological examination ) depend on site of bleed, the extent of ischemia and the size of subsequent clot.

Diagnostic investigation



  • Computed tomography Computed tomography: brain:
    • Exquisitely sensitive for detection of acute hemorrhage.
    • Acute hemorrhage is evident as a hyperdensity on CT due to hyperattenutation of X-rays by the globin portion of blood. The attenuation decreases until the hematoma is isodense at about 1 month after the onset. The periphery of the hematoma contrast enhances from 6 days to 6 weeks after the onset due to re-vascularization.
  • Magnetic resonance imaging Magnetic resonance imaging: brain signal intensity of intracranial hemorrhage is also influenced by several intrinsic (time from ictus, size and location of hemorrhage) and extrinsic (pulse sequence and field strength) factors.
  • The causes of these intrinsic and extrinsic variations in hematoma intensity are difficult to evaluate with clinical studies since it is frequently impossible precisely to ascertain the interval between hemorrhage and MR imaging.
  • Gradient echo sequences have been proven to be the most accurate of all the MR pulse sequences, and more accurate than computed tomography, in predicting the extent of hemorrhage on pathologic examination in a dog model. Compared to other sequences, gradient echo scans demonstrate readily detectable hypointensity regardless of the time from ictus, the source and location of hemorrhage, or the field strength. Hypointensities on gradient echo images is however not specific for hemorrhage and may also be seen with calcification, air, iron, foreign bodies and melanin.


  • CSF analysis  Cerebrospinal fluid: sampling:
    • Xanthochromia (hemosiderin and hemoglobin).
    • Red blood cells - present if there is bleeding into ventricles/subarachnoid space, however difficult to distinguish from a traumatic tap Cerebrospinal fluid: cytology.
    • Contra-indicated if underlying coagulopathy or evidence of raised intracranial pressure (brain hernation on MR or CT imaging).

Contrast radiography

  • Contrast venography may show deviation of vascular pattern due to space occupying lesion.

Ancillary diagnostic test

Confirmation of diagnosis

Discriminatory diagnostic features

  • Clinical signs.

Definitive diagnostic features

  • Computed tomography.
  • Magnetic resonance imaging.

Gross autopsy findings

  • Intracranial hemorrhage.

Differential diagnosis

  • Brain neoplasia (primary or metastatic).
  • Head trauma.
  • Infectious or non-infectious meningo-encephalitis.
  • Metabolic encephalopathy.
  • Neurotoxicity.


Initial symptomatic treatment

  • Most important consideration is maintenance of cerebral perfusion by treatment of hypotension and elevated intracranial pressure (ICP) as well as treating the underlying cause if one is identified.
  • Initial approach should focus on extracranial stabilization.
  • Stabilization of the patient:
    • Airway protection.
    • Avoid hypoxia.
    • Correction of hypoventilation (immediate intubation and ventilation should be considered if PaCO2 cannot be maintained within acceptable range and not exceed 40 mmHg).
    • Correction of tissue perfusion (goal is rapid restoration of blood pressure such that cerebral perfusion pressure is maintained at >70 mmHg).
    • Correct systemic hypertension if at a high risk of end-stage organ damage (systolic blood pressure >180 mmHg) and/or cats with severe ocular manifestation of hypertension such as retinal detachment or intraocular hemorrhage.

Standard treatment

  • Once initial assessment and extracranial stabilization have occurred, medical intervention to address intracranial issues should be considered, with main focus being on decreasing ICP Intracranial pressure measurement.
  • Three principles can be applied:
    • Reducing cerebral edema associated with intracranial hemorrhage (osmotic diuretic such as mannitol Mannitol 0.25-0.5  g/Kg over 10-20 mins up to q4-8h.
    • Optimising cerebral blood volume (temporary hyperventilation by reducing PaCO2).
    • Eliminating the space-occupying mass (surgical evacuation of hematoma in cats with large subarachnoid hematoma and deteriorating neurological status despite medical management).


  • Vital parameters (oxygen levels, fluid balance, blood pressure, body temperature).
  • Neurological status.

Subsequent management


  • Nursing care.




  • Depend overall on initial severity of the neurological deficit, initial response to supportive care and severity of underlying cause if one has been identified.

Further Reading


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.