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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