Download - Sub-Arachnoid Hemorrhage
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Sub-Arachnoid Hemorrhage
-Dr. Raajit Chanana
Introduction
SAH : fourth most frequent cerebrovascular disorder-following atherothrombosis, embolism and primary intracerebral hemorrhage.
CAUSE: Excluding head trauma, the most common cause of SAH is rupture of saccular aneurysm.
INCIDENCE incidence of SAH increase with age,occuring most commonly between 40 and 60 years of age,but it can occur from childhood to old age
is ~1.6 times higher in women than in men.
Risk factors for Aneurysmal SAH
Hypertension
Smoking
Heavy alcohol
Sympathomimetic drugs-cocaine &phenlypropanolamine
Certain genetic syndromes ADPKD Type IV Ehlers-Danlos syndrome
Familial intracranial aneurysms
Increased incidence of fibromuscular dysplasia of extracranial arteries, moyamoya disease, AV malformation of the brain , COA among persons with saccular aneurysms
Saccular/berry aneurysm
About 2% of adults harbor intracranial aneurysms.
Small thin walled blisters protruding from arteries of circle of willis or its main branches.
Rupture causes filling of the subarachnoid space with blood under high pressure.
~90-95% of saccular aneurysms lie on the anterior part of circle of willis.
4 most common sites are-
Proximal portions of the anterior communicating arteries
At the origin of the posterior communicating artery from the stem of the internal carotid
At the first major bifurcation of MCA
Bifurcation of the ICA into MCA and ACA
Pathophysiology
results from development defects in the media and elastica of the arteries.
Aneurysmal process initiation-> by focal destruction of the internal elastic membrane,which is produced by hemodynamic forces at the apices of bifurcation.
As a result of local weakness in the vessel wall,the intima bulges outward, covered only by adventitia, the sac then gradually enlarges and finally ruptures.
At the site of rupture (mostly the dome), the wall thins and the tear that allows bleeding is often =7mm, at the top of the basilar artery and at the origin of the posterior communicating artery are at the greatest risk of rupture.
The annual risk of rupture for aneurysms 10mm is 0.5 to 1%.
GIANT CEREBRAL ANEURYSMS
Congenital anomalies
>2.5 cm in diameter
Located on carotid,basilar, anterior or middle cerebral artery.
Compress adjacent structures eg those in the cavernous sinus, optic nerve or lower cranial nerves
There are several other type of aneurysms- mycotic, fusiform, diffuse and globular
Mycotic : caused by a septic embolus that weakens the wall of the vesselin which it lodges.
Clinical syndrome
One of the three
Excruciating generalized headache and vomiting and falls unconscious almost immediately.
Severe generalized headache but the patients remain relatively lucid,
Consciousness is lost so quickly ,that there is no preceding complaint.
Rupture usually occurs while the patient is active.
Sentinel headache
Symptoms consistent with a minor hemorrhage before a major rupture-sentinel headache or warning leak.
Occur within 2-8weeks before overt SAH.
Headache often is unrelated to hemorrhage and is attributable to migraine.
thunderclap headache: may be a variant of migraine, pituatory apoplexy, hypertensive encephalopathy, intracranial hypotension.
As the hemorrhage is localized to subarachnoid space, there are few if any local signs.
Convulsive seizure occur in 10 to 25 % of cases.
Anatomic-clinical correlation
Third nerve palsy: indicates an aneurysm at the junction of posterior communicating artery and internal carotid artery.
Transient paresis of one or both of lower limbs :suggests an anterior communicating aneurysm that has interfered with the circulation in the anterior cerebral arteries.
Hemiparesis or aphasia :points to an aneurysm at the first major bifurcation of MCA.
U/L blindness : indicates an aneurysm lying anteromedially in the circle of willis
Delayed neurological deficits
Rerupture
Hydrocephalus
Vasospasm
Hyponatremia
Lab findings
CT scan- will detect blood locally or diffusely in the subarachnoid space or within the brain or ventricular system in more than 90% of cases. first 24 hrs : sensitivity of CT for SAH is 98%.
LP-when SAH is suspected but not apparent on imaging studies.
The diagnosis of ruptured saccular aneurysm is excluded if blood is not present in the CSF, provided the spinal fluid is examined more than 30 min after the event.
RBC counts upto 1million/mm3
Xanthochromia
Bilirubin
4 vessel angiography- B/L external carotid and vertebral arteries-to localize and define the anatomic details of aneurysm. Selective cerebral angiography is currently the standard for diagnosing cerebral aneurysm as the cause of SAH
MRA/CTA
Systemic changes associated with SAH
ECG-symmetrical large peaked T waves-cerebral T waves,prolonged ORS interval, increased QT intervalsuggesting subendocardial or myocardial ischemia
Minor elevation in cardiac enzymes
Some cases -reversible cardiomyopathy
Leukocytosis -15,000-18,000cells/mm3
Treatment
Emergency evaluation and pre-op care history examination clinical grading
CAB
Medical measures to prevent rebleeding Blood pressure should be monitored and controlled to balance the risk of stroke,hypertension rebleeding and maintainence of CPP.
to reduce BP nicardipine, labetalol and esmolol used because of there safety profile and short action
bed rest
Early treatment with short course of anti fibrinolytic and prophylaxis against hypovolemia and vasospasm may be reasonable but further research is needed.
Surgical and endovascular
methods
Endovascular approach with electrolytically detachable platinum coilsAneurysm is packed with coils.Coils induce thrombosis.
surgical clipping
Management of cerebral vasospasm after SAH
It is the delayed narrowing of the large capacitance arteries at the base of the brain after SAH.
Angiographic vasospasm:seen in 30-70% of patients with a typical onset 3-5days after the hemorrhage,maximum narrowing at 5-14 days and a gradual resolution over 2 to 4 weeks
The development of new focal deficit, unexplained by hydrocephalus or rebleeding is the first objective sign of symptomatic vasospasm
The goal of management is to reduce the threat of ischemic neuronal damage by controlling ICP, decreasing the metabolic rate of oxygen use, and improving CBF.
Volume expansion prevent hypotension, augments cardiac output and reduces blood viscosity by reducing the hematocrit.
This method is called triple H therapyhypertensionhemodilutionhypervolemic
Nimodipine improves outcome py preventing ischemic injury rather than reducing the risk of vasospasm
Cerebral angioplasty and/or selective intraarterial vasodilator therapy may be reasonable after, together with or in place of Triple H therapy.
Treatment of hyponatremia
CAUSE: Due to natriursis and volume depletion.
Hypovolemic and hyponatremic
Clears over 1 to 2 weeks
Should not be treated with free water clearance as it increases the risk of stroke
Management of hydrocephalus
Acute