Showing posts with label DIFFERENTIAL.DIAGNOSIS. Show all posts
Showing posts with label DIFFERENTIAL.DIAGNOSIS. Show all posts

Monday, 9 January 2012

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.



IPHREHAB : DIFFERENTIAL DIAGNOSIS AND TREATMENT CEREBRAL THROMBOSIS AND TIAs

IPHREHAB

DIFFERENTIAL DIAGNOSIS CEREBRAL THROMBOSIS AND TIA


Differential Diagnosis
Vascular disorders are mistaken for ischaemic stroke include intracerebral hemorrhage, subdural or epidural hematoma , and subarachnoid hemorrhage from rupture of an aneurysm or vascular malformation. These condition can often be distinguished by a history of trauma or of excruciating headache at onset, a more marked depression of consciousness, or by the presence of neck stiffness on examination. They can be excluded  by CT scan or MRI.


Differential Diagnosis: Other structural brain lesion such as tumor or abscess can also produce focal cerebral symptoms of acute onset. Brain abscess is suggested by concurrent fever, and both abscess and tumor can usually be diagnosed by CT scan or MRI. Metabolic disturbances, particularly hypoglycemia and hyperosmolar nonketotic hyperglycemia, may present in stroke like fashion. The serum glucose level should therefore be determined in all patients with apparent stroke.

Treatment of Cerebral Thrombosis and Transient Ischemic Attacks
The current treatment of it may be divided into four parts:
Management in the acute phase
Measures to restore the circulation and arrest the pathologic process
    1. Thrombolytic agents ( t-PA only for completed stroke,w/in 3~6hrs ) 2.Anticoagulant drugs ( Heparin, LMWH & warfarin)
    3. Antiplatelet drugs ( Aspirin  or  Clopidogrel, Dipyridamole or   Ticlopidine )
    4.Difibrase
    5. Neuroprotective agents: barbiturates, opioid  antagonist naloxone,Manitol

Treatment
Treatment of cerebral edema and raised intracranial pressure
Acute surgical revascularization 
Surgery for symptomatic carotid stenosis, Carotid endarterectomy, intralumenal stents, extracranial-intracranial bypass
Physical therapy and rehabilitation.
Measures to prevent further strokes and progression of vascular disease.
  • Since the primary objective in the treatment  of  atherothrombotic disease is prevention , efforts to control the risk factors must continue. 
  • Aspirin
  • Hypotensive agents
  • Oversedation should be avoided
  • Systemic hypotension, severe anemia should be treated promptly
  • Particular care should be taken to maintain the systemic blood pressure, oxygenation  and intracranial  blood flow during surgical procedures, especially in elderly patient.
Course and Prognosis
When the patient is seen early in the cerebral thrombosis, it is difficult to give an accurate prognosis.
As for the eventual or long-term prognosis of the neurologic deficit , there are many possibilities.
It must be mentioned that having had one thrombotic stroke, the patient is at risk in the ensuing months and years of having a stroke at the same or another site, especially if there is hypertension or diabetes mellitus.