IPHREHAB : Intracranial Hemorrhage

IPHREHAB

Intracranial Hemorrhage
This is the common, well-known “spontaneous” brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries.Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema.
Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually  caused by arterial bleeding.


The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues . Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death.

1. Intracerebral Hemorrhage

Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic.It has been given its own name, “apoplexy”.

Clinical Picture

• With smaller hemorrhages, the clinical picture conforms more closely to the usual temporal profile of a stroke, i.e, an abrupt onset of symptoms that evolve gradually and steadily over minutes, hours, or a day or two, depending on the size of the ruptured artery and the speed of bleeding. 
• Headache and vomiting are cardinal features.Very small hemorrhages in “silent” regions of the brain may escape clinical detection.
• Clinical features vary with the site of hemorrhage.
• Deep cerebral hemorrhage  The two most common sites of hypertensive hemorrhage are the putamen and the thalamus, which are separated by the posterior limb of the internal capsule. This segment of the internal capsule is traversed by descending motor fibers and ascending sensory fibers, including the optic radiations.
• Lobar hemorrhage  Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temporal, and occipital lobes. Symptoms and signs vary according to the location.
• Pontine hemorrhage  With bleeding into the pons, coma occurs within seconds to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eye movements are absent or impaired, but vertical eye movements may be preserved.
• Cerebellar hemorrhage  The distinctive symptoms of cerebellar hemorrhage (headache, dizziness, vomiting, and the inability to stand or walk) begin suddenly, within minutes after onset of bleeding.

Laboratory Findings  

Among laboratory methods for the diagnosis of intracerebral hemorrhage, the CT scan occupies the foremost position. In CT scans, fresh blood is visualized as a white mass as soon as it is shed. The mass effect and the surrounding extruded serum and edema are hypodense.

By MRI, either in T1-or-T2 weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding.

In general, lumbar puncture is ill advised, for it may precipitate or aggravate an impending shift of central structures and herniation. The white cell count in the peripheral blood may rise transiently to 15,000 per cubic millimeter, a higher figure than in thrombosis.

Differential Diagnosis: 

Putaminal, thalamic, and lobar hypertensive hemorrhages may be difficult to distinguish from cerebral infarctions. To some extent, the presence of severe headache, nausea and vomiting, and impairment of consciousness are useful clues that a hemorrhage may have occurred; the CT scan  identifies the underlying disorder definitively.

CT scan or MRI is the most useful diagnostic procedure, since hematomas can be quickly and accurately localized.