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.
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 imagingMagnetic 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.
Infectious or non-infectious meningo-encephalitis.
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:
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.
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).
Depend overall on initial severity of the neurological deficit, initial response to supportive care and severity of underlying cause if one has been identified.