Showing posts with label HEMORRHAGE. Show all posts
Showing posts with label HEMORRHAGE. Show all posts

Monday, 9 January 2012

IPHREHAB: Spontaneous Subarachnoid Hemorrhage


IPHREHAB

Spontaneous Subarachnoid Hemorrhage

This is the fourth most frequent cerebrovascular disorder following atherothrombosis, embolism, and primary intracerebral hemorrhage. Saccular aneurysms are also called berry” aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure.
Aneurysms are multiple in 20 percent of patients

In childhood , rupture of saccular aneurysms is rare, and they are seldom found at routine postmortem examination; beyond childhood, they gradually increase in frequency to reach their peak incidence between 35 and 65 years of age.
Approximately 90 to 95 percent of saccular aneurysms lie on the anterior part of the circle of Willis.

Clinical picture
  • Prior to rupture, saccular aneurysms are usually asymptomatic. Exceptionally, if sufficiently large to compress pain-sensitive structures, they may cause localized cranial pain.
  • The presence of a partial oculomotor palsy with dilated pupil may be indicative of an aneurysm of the posterior communicating-- internal carotid junction.
  • With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space(where the circle of Willis lies).
  • Rupture of the aneurysm usually occurs while the patient is active rather than during sleep , and in some instances sexual intercourse, straining at stool, lifting heavy objects, or other sustaining exertion precipitates the ictus. In patients who survive the initial rupture, the most feared complication is rerupture, an event that may occur at any time from minutes up to 2 or 3 weeks later.
  • In less severe cases, consciousness, if lost , may be regained within a few minutes or hours, but a residual of drowsiness, confusion, and amnesia accompanied by  severe headache and stiff neck persists for several days.
  • Since the hemorrhage is confined to the subarachnoid space, there are few or no focal neurologic signs.
  • AVM is another most common cause for SAH
  • Convulsive seizures, usually brief and generalized.
  • Vasospasm  Delayed hemiplegia or other focal deficit usually appears 3 to 12 days after rupture and rarely before or after this period. These delayed accidents and the focal narrowing of a large artery or arteries, seen on angiography, are refered to as vasospasm.
  • Hydrocephalus  If a large amount of blood ruptures into the ventricular system or floods the basal subarachnoid space, The patient then may become confused or unconscious as a result of acute hydrocephalus. A subacute hydrocephalus due to blockage of the CSF pathways by blood may appear after 2 to 4 weeks.

Laboratory Findings  
A CT scan will detect blood locally or diffusely in the subarachnoid spaces or within the brain or ventricular system in more than 90 percent of cases and in practically all cases in which the hemorrhage has been severe enough to cause momentary or persistent loss of consciousness.
In all other cases a lumbar puncture should be undertaken when the clinical features suggest a subarachnoid hemorrhage. Usually the CSF is grossly bloody within 30 min of the hemorrhage, with RBC counts up to 1 million per cubic millimeter or even higher.
Carotid and vertebral angiography is the only certain means of demonstrating an aneurysm and does so in some 85 percent of patients in whom the correct diagnosis of spontaneous subarachnoid hemorrhage is made on clinical grounds.
MRI and MRA detect most aneurysms of the basal vessels but are as yet of insufficient sensitivity to replace conventional angiography. Even when MRA or “ CT angiography  “ demonstrates the aneurysm, the surgeon usually requires the kind of anatomic definition that can only be obtained by conventional angiography. 

Establish the diagnosis
If there is a typical history, marked neck stiffness and no focal neurological deficit, lumbar puncture is still the best way to make the diagnosis, revealing uniformly blood-stained CSF. 
If the history is typical with marked neck stiffness, but the patient remains in coma or shows a marked focal neurological deficit, a CT scan is a safer way to establish the diagnosis (revealing blood in the subarachnoid space),since lumbar puncture may lead to worse condition in this group of patients (whose coma or focal neurological deficit may indicate the presence of an associated intracerebral blood clot).

Treatment 
  • This is influenced by the neurologic and general medical state of the patient as well as by the location and morphology of the aneurysm.
  • The general medical management in the acute stage includes the following , in all or part: 
  • bed rest
  • fluid administration to maintain above-normal circulating volume and central venous – pressure
  • use of elastic stockings and stool softeners
  • administration of beta-blockers
  • calcium channel blockers
Treatment 
  • intravenous nitroprusside
  • or other medication to reduce greatly elevated blood  pressure and then maintain systolic blood pressure at 150 mmHg or less;
  • and pain-relieving medication for headache ( this alone will often reduce the hypertension ).
  • The prevention of systemic venous thrombosis is critical, usually accomplished by the use of cyclically inflated whole-leg compression boots.
Treatment 
  • The use of anticonvulsants is controversial; many neurosurgeons administer them early, with a view of preventing a seizure-induced risk of rebleeding.
  • Calcium channel blockers are being used extensively to reduce the incidence of stroke from vasospasm. Nimodipine 50 mg, administered intravenus, is currently favored.
  • Notable advances in the techniques for the obliteration of aneurysms, particularly the operating microscope, and the management of circulatory volume have significantly improved the outcome of patients with ruptured aneurysms.
  • Both the risk of rerupture of the aneurysm and some of the secondary problems that arise because of the massive amount of blood in the subarachnoid space can be obviated by early obliteration of the aneurysm.
  • lumbar puncture is carried out for diagnostic purposes if the CT scan is inconclusive; thereafter this procedure is performed only for the relief of intractable headache, to detect recurrence of bleeding, or to measure the intracranial pressure prior to surgery. 
  • Advice from specialist neurosurgical units should be sought. Patients who have withstood their first bleed well are submitted to carotid and vertebral angiography within a few days to establish whether or not an operable aneurysm is present. Patients who do not recover from their first bleed well, patients with inoperable aneurysms should be nursed in bed for a few weeks and then mobilized over a further few weeks, being encouraged to return to full normal activities at about 3-4 months.
  • Prevent re-bleeding

Rehabilition
Since the incidence of significant damage to the brain is high  in patients surviving subarachnoid haemorrhage, many will not be able to return to normal activities.
They will need support from relatives,  nurses, physiotherapists, speech therapists, occupational therapists, social workers and specialist units in rehabilitation.

Course and prognosis
 Patients with the typical clinical picture of spontaneous subarachnoid hemorrhage in whom an aneurysm or arteriorvenous malformation cannot be demonstrated angiographically have a distinctly better prognosis than those in whom the  lesion is visualized.
 Vasospasm and rebleeding were the leasing causes of morbidity and mortality in addition to the initial bleed. In respect to rebleeding , Aoyagi and Hayakawa found that this occurred within 2 weeks in 20 percent of patients, with a peak incidence in the 24 h after the initial bleed.


IPHREHAB : INTRACEREBRAL HEMORRHAGE & TREATMENT

IPHREHAB


INTRACEREBRAL HEMORRHAGE & TREATMENT
The management of patients with large intracerebral hemorrhages and coma includes the maintenance of adequate ventilation, use of controlled hyperventilation to a Pco2 of 25 to 30 mmHg, monitoring of intracranial pressure (ICP) in some cases and its control by the use of tissue-dehydrating agents such as mannitol (osmolality kept at 295 to 305 mosmol/L and Na at 145 to 150 meq), and  limiting intravenous infusions to normal saline.


Rapid reduction in blood pressure, in the hope of reducing further bleeding , is not recommended, since it risks compromising cerebral perfusion in cases of raised intracranial pressure. On the other hand, sustained mean blood pressure  of greater than 110mmHg may exaggerate cerebral edema and risk extension of the clot. It is at approximately this level of acute hypertension that the use of beta-blocking drugs(esmolol, labetalol) or angiotensin-converting enzyme inhibitory drugs is recommended.


In contrast to cerebral hemorrhage, the surgical evacuation of cerebellar hematomas is a generally accepted treatment and is a more urgent matter because of the proximity of the mass to brainstem and the risk of abrupt progression to coma and respiratory failure.




Course and Prognosis
The immediate prognosis for large and medium-size cerebral clots is grave; some 30 to 35 percent of patients die in 1 to 30 days.
Either the hemorrhage extends into the ventricular system or intracranial pressure is elevated to levels that preclude normal perfusion of the brain.
Sometimes the hemorrhage itself seeps into vital centers such as the hypothalamus or midbrain.


A volume of 30 ml or less, calculated from the CT scan, predicted a generally favorable outcome.
In patients with clots of 60 ml or larger and an initial Glasgow Coma Scale score of 8 or less, the mortality was 90 percent. As remarked earlier, it is the location of the clinical effects.



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.