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SUBARRACHNOID HAEMORRHAGE-AN UPDATE

DR. ARDAMAN SINGH Professor Dept. Of MedicineGovt. Medical College Patiala

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SUBARRACHNOID HAEMORRHAGE

• SAH is a neurological emergency

• Hemorrhage in the subarachnoid space

• Less common but an important cause of stroke

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CLASSIFICATION OF STROKE

Stroke

Primary Hemorrhagic (20% of Strokes)

Primary Ischemic (80% of Strokes)

Thrombotic 50%

Embolic 30%

Intracerebral Hemorrhage 15%

Subarachnoid Hemorrhage 5%

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SAH- etiology• Excluding head trauma, the most common cause of SAH is

rupture of a SACCULAR ANEURYSM.

• Other causes include bleeding from a vascular malformation (arteriovenous malformation or dural arterial-venous fistula) and

• Extension into the subarachnoid space from a primary intracerebral hemorrhage.

• Mycotic aneurysms -Most result from infected emboli due to bacterial endocarditis causing septic degeneration of arteries and subsequent dilatation and rupture

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SACCULAR ("BERRY") ANEURYSM• Autopsy and angiography studies have found that

about 2% of adults harbor intracranial aneurysms,• Size- 2 mm. to 2-3 cm• Average size- 7.5mm• Those which rupture are usually 10mm or more but

smaller ones can also get ruptured• Of different shapes and forms- round connected to patrent artery by a narrow stalk some others may be broad based without a stalk –some may have cylindrical form

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Cerebral Aneurysms

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Mechanism of formation of aneurysms

• One theory is – that they result from a developmental defect in the media & elastica

• Other theory says that aneurysmal proscess is initiated by the focal destruction of internal elastic membrane caused by hemodynamic forces acting at bifurcations & branching of arteries

As a result of local weakness in vessel wall intima bulges out covered only by adventetia

• The sac gradually enlarges and subsequently rupture

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• For patients of SAH who arrive alive at hospital, the mortality rate over the next month is about 45%.

• Of those who survive, more than 50% are left

with major neurologic deficits as a result of the

Initial hemorrhage, Cerebral vasospasm with infarction, or Hydrocephalus.

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SACCULAR ("BERRY") ANEURYSM- CONT• If the patient survives but the aneurysm is not

obliterated, the rate of rebleeding is about

• 20% in the first 2 weeks, • 30% in the first month, and about• 3% per year afterwards

• The annual risk of rupture for aneurysms <10 mm in size is 0.1%, and for aneurysms >10 mm in size is 0.5–1%;

• the surgical morbidity rate far exceeds these percentages

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SACCULAR ("BERRY") ANEURYSM- CONT

• GIANT ANEURYSMS, those >2.5 cm in diameter account for 5% of cases. The three most common locations are

-The terminal internal carotid artery, -Middle cerebral artery (MCA) bifurcation, and -Top of the basilar artery.

• Their risk of rupture is ~6% in the first year after identification and may remain high indefinitely.

• They often cause symptoms by compressing the adjacent brain or cranial nerves.

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PATHOPHYSIOLOGY• Saccular aneurysms occur at the bifurcations of the large to

medium-sized intracranial arteries. Rupture is into the subarachnoid space, in the basal cisterns and often into the parenchyma of the adjacent brain.

• Approximately 85% of aneurysms occur in the anterior circulation, mostly on the circle of Willis.

• About 20% of patients have multiple aneurysms, - - many at mirror sites bilaterally.

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PATHOPHYSIOLOGY- cont• Aneurysms are seldom seen in childern on autopsy and so

SAH in childern is rare

• Beyond childhood they gradually increase in size & the frequency of rupture increases between 35-65 yrs of age

• There is increased incidence of polycystic kidneys, fibromuscular dysplasia of extracranial arteries, moyamoya, AV malformations & coarctation of aorta

• Numerous studies have documented familial occurrence of saccular aneurysms, lending support to the idea that genetic factors may play a role in their development

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PATHOPHYSIOLOGY- cont• As an aneurysm develops, it typically forms a neck with a

dome.• . At the site of rupture (most often the dome) the wall

thins, and the tear that allows bleeding is often 0.5 mm long.

• Aneurysm size and site are important in predicting risk of rupture.

Those >7 mm in diameter and Those at the top of the basilar artery and At the origin of the posterior communicating artery

are at greater risk of rupture.

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CLINICAL MANIFESTATIONS-

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CLINICAL MANIFESTATIONS-• Most unruptured intracranial aneurysms are

completely asymptomatic.

• Aneurysms can undergo small ruptures and leaks of blood into the subarachnoid space, so-called SENTINEL BLEEDS.

• SYMPTOMS are usually due to rupture and resultant SAH perse

• Although some present with mass effect on cranial nerves or brain parenchyma.

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CLINICAL MANIFESTATIONS-cont.• With rupture , blood at high pressure gushes in the suarachnoid space

resulting in following three patterns of presentations:

Pt. is stricken with severe headache & vomiting , and falls unconscious immediately

Severe generalized headache occurs suddenly but pt remains lucid with varying degrees of neck stifness

Rarely pt suddenly becomes unconsoius without any preceding complaint. If the bleed is massive pt may die in minute to hrs. So ruptured aneurysm should be considered in the differential diagnosis of

sudden death In these rapidly evolving cases the bleed is so massive that I/c pressure

approaches systemic BP, thus severly compromising the cerebral perfusion

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CLINICAL MANIFESTATIONS-cont.

• In less severe cases , consciousness if lost may be regained in minutes to hrs

• Residual drowsiness, confusion and amnesia

accompanied by severe headache may persist for several days

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CLINICAL MANIFESTATIONS-cont.

• Aneurysmal rupture usually occurs while the pt is active

• In some cases it may occur while straing on stool, sexual intercourse, lifting a heavy weight or some other sustained exertion

• In patients who survive initial rupture the most feared complication is rerupture which may occur at any time from minutes to 2-3 wks

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HEADACHE• In ~45% of cases, severe headache associated

with exertion is the presenting complaint. • The patient often calls the headache "the

worst headache of my life";• However, the most important characteristic

is sudden onset.

• Sudden unexplained headache at any location should raise suspicion of SAH and must be investigated,

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The headache usually generalized, often with neck stiffness, and vomiting is common

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Pain at other sites

• Occipital and posterior cervical pain may signal a posterior inferior cerebellar artery (PICA) or anterior inferior cerebellar artery aneurysm.

• Pain in or behind the eye and in the low temple can occur with an expanding MCA aneurysm

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Loss of consciousness• At the moment of aneurysmal rupture with

major SAH, the ICP suddenly rises.

• This may account for the sudden transient loss of consciousness that occurs in nearly half of patients which may be preceded by headache.

• In 10% of cases, aneurysmal bleeding is severe enough to cause loss of consciousness for several days.

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CLINICAL MANIFESTATIONS- cont. FOCAL NEUROLOGICAL DEFICITS

• Although sudden headache in the absence of focal neurologic symptoms is the hallmark of aneurysmal rupture, FOCAL NEUROLOGIC DEFICITS MAY OCCUR.

• Anterior communicating artery or MCA bifurcation aneurysms may rupture into the adjacent brain or subdural space and form a hematoma large enough to produce mass effect.

The common deficits that result include hemiparesis, aphasia, and abulia (progressive drowsiness or slow mentation)

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Anatomic – clinical corellation of focal neurological Deficits

• Third nerve palsy (ptosis, diplopia,dilatation of pupil & divergent squint) indicates an aneurysm at the junction of post. Comunicating &post. Cerebral arteries

• A sixth nerve palsy may indicate an aneurysm in the cavernous sinus .but uni or bilateral palsy could be because of raised ICP

• Unilateral blindness indicates aneurysm lying anteromedially in the circle of willis usually at the origin of opthalmic artery

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Anatomic – clinical corellation of focal neurological Deficits- cont

• Transient paresis of one or both lower limbs indicates ant comunicating A. aneurysm that has interfered with circulation in ant. Cerebral arteries.

• Hemiperesis or aphasia suggests aneurysm at the first bifurcation of middle cerebral artery

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The side of aneurysmal rupture may be indicated by

• monocular pain• unilateral preponderace of headache or• unilateral preretinal(subhyaloid)

hemorrhage (Terson Syndrome)

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D/D- SAH to be differentiated from• THUNDERCLAP HEADACHE is a variant of

migraine that simulates a SAH.

• Headache of explosive onset may also be caused be ingestion of sympathomimetic drugs or ingestion of tyramine containg foods in a pt. who is taking MAO inhibitors

• Sudden severe hadahe may also be a symptom of phaeochromocytoma

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D/D• Other conditions which may present as severe

headache need to be differentiated, like:-

Cerebral venous thrombosis, Diffuse vasospasm (call-flemming syndrome), Pituatry apoplexy, Hypertensive encephalopathy, Intracranial or extracranial arterial dissection

• CSF examination assumes great importance in differentiating these conditions from SAH

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D/D

• Before concluding that a patient with sudden, severe headache has thunderclap migraine or any other type of severe headache,

a definitive workup for aneurysm is always required in the form of CT scan, Lumbar puncture, and if the diagnosis still remains doubtful, then cerebral angiography

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DELAYED NEUROLOGIC DEFICITS

• There are four major causes of delayed neurologic deficits:

1. RERUPTURE/REBLEED, 2.HYDROCEPHALUS 3.VASOSPASM 4.HYPONATREMIA.

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1.RERUPTURE/REBLEED.

• This is the tendency for the hemorrhage to recur from the same site in more than one third of patients, often catastrophically

• The incidence of rerupture of an untreated aneurysm in the first month following SAH is ~30%, with the peak in the first 7 days.

• The cause of recurrence is not clearly understood but appears to be related to naturally ocuring mechanisms of clot lysis at the initial site of rupture

• Rerupture is associated with a 60% mortality and poor outcome.

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2.HYDROCEPHALUS• Acute hydrocephalus can cause stupor and

coma and can be mitigated by placement of an external ventricular drain.

• More often, subacute hydrocephalus may develop over a few days or weeks and causes progressive drowsiness or slowed mentation (abulia) with incontinence.. It may clear spontaneously or require temporary ventricular drainage.

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Hydrocephalus-cont.

• Chronic hydrocephalus may develop weeks to months after SAH and present as normal pressure hydrocephalus (NPH) manifested by gait difficulty, incontinence, or impaired mentation.

Subtle signs may be a lack of initiative in

conversation or a failure to recover independence

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3.VASOSPASM• Causes symptomatic ischemia and infarction in ~30% of

patients and is the major cause of delayed morbidity and death.

• Signs of ischemia appear 4–14 days after the hemorrhage, most often at 7 days.

• The severity and distribution of vasospasm determine

whether infarction will occur.

• Vasospasm is believed to result from direct effects of clotted blood and its breakdown products on the arteries within the subarachnoid space.

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VASOSPASM- cont.• Spasm of major arteries produces focal symptoms

referable to the appropriate vascular territory.

• All of these focal symptoms may present abruptly, fluctuate, or develop over a few days.

• In most cases, focal spasm is preceded by a decline in mental status.

• Patient may develop fluctuating hemiperisis or aphasia

• Severe cerebral edema in patients with infarction from vasospasm may increase the ICP enough to reduce cerebral perfusion pressure.

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4.HYPONATREMIA• Hyponatremia. Hyponatremia may be profound and can develop

quickly in the first 2 weeks following SAH. There is both natriuresis and volume depletion with SAH, so that patients become both hyponatremic and hypovolemic.

• Both atrial natriuretic peptide (ANP)and brain natriuretic peptide (BNP) have a role in producing this "cerebral salt-wasting syndrome.“

• There may some role of antidiuretic hormone also, causing water retention

• Typically it clears over the course of 1–2 weeks and, in the setting of SAH, should not be treated with free-water restriction as this may increase the risk of stroke.

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SYSTEMIC CHANGES ASSOCIATED WITH SAH• ECG changes suggestive of subendicardial or myocardial ischemia• Elevation of troponis/CPK (MB) levels• In some patients cardiac dysfunction may be severe enough to cause

fall in EF % and heart failure

• There is evidence that structural myocardial lesions produced by circulating catecholamines and excessive discharge of sympathetic neurons may occur after SAH, causing these ECG changes and a reversible

cardiomyopathy sufficient to cause shock or congestive heart failure. • Hyponatremia• D. Insipidus• Albuminuria,• Glycosuria• leukocytosis

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INVESTIGATIONS

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NON CONTRAST CT SCAN.• CT Scan is Initial investigative procedure

• The extent and location of subarachnoid blood on noncontrast CT scan help

locate the underlying aneurysm, identify the cause of any neurologic deficit, and predict delayed vasospasm. A high incidence of symptomatic vasospasm in the MCA and

ACA has been found when early CT scans show subarachnoid clots >5 x 3 mm in the basal cisterns or layers of blood >1 mm thick in the cerebral fissures.

• CT scans less reliably predict vasospasm in the vertebral, basilar, or posterior cerebral arteries.

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More than 95% of cases have enough blood to be visualized on a high-quality NONCONTRAST CT SCAN obtained

within 72 h.

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IMAGING STUDIES-cont. Exact site of offending aneurysm can be inferred from

the location of main clot in CT scan• Collection of blood in the anterior inter-hemispheric

fissure indicates rupture of an ant. Communicating artery

• Blood in sylvian fissure – middle cerebral artery• Blood in ant. Perimesencephalic cistern- post.

Communicating artery or distal basilar artery aneurysm • MRI can also detect blood in the proton density

sequence

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Lab investigations-cont • If the scan fails to establish the diagnosis of SAH and no mass

lesion or obstructive hydrocephalus is found, • Then a lumbar puncture should be performed to establish the

presence of subarachnoid blood.• Usually CSF becomes grossly bloody within 30 minutes of bleed

with RBC counts upto 1 million/c mm or more

• Lysis of the red blood cells and subsequent conversion of hemoglobin to bilirubin stains the spinal fluid yellow within 6–12 h.

• This xanthochromic spinal fluid peaks in intensity at 48 h and lasts for 1–4 weeks, depending on the amount of subarachnoid blood

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Angiography

• Once the diagnosis of hemorrhage from a ruptured saccular aneurysm is suspected, four-vessel conventional x-ray angiography (both carotids and both vertebrals) is generally performed

• to localize and define the anatomic details of the offending aneurysm and

• to determine if other unruptured aneurysms exist).

• CT angiography is an alternative method for locating the aneurysm and may be sufficient to plan definitive therapy.

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Angiography-cont.• in 5-10% pts with aneurysmal bleed , there may

not be any evidence of aneurysmal rupture on angiography.

It may be because

in some cases obliteration of lesion occursIn some lesions were somewhat more benign

• Pts without evidence of an offending aneurysm or an arteriovenous malformationhave a better prognosis

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Angiography-cont.

• Perimesencephalic hemorrhage also caries a better prognosis

In this cisterns surrounding midbrain & upper pons gets filled up with blood

Mild headache, no vasospasm Usually no aneurysm is found at the expected

site i.e. at the top of basillary artery

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Lab Inv. – cont.

• Close monitoring (daily or twice daily) of electrolytes is important because hyponatremia can occur precipitously during the first 2 weeks following SAH

• An asymptomatic troponin elevation is common.

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ECG Changes

• The electrocardiogram (ECG) frequently shows ST-segment and T-wave changes similar to those associated with cardiac ischemia.

• Prolonged QRS complex, increased QT interval, and prominent "peaked" or deeply inverted symmetric T waves are usually secondary to the intracranial hemorrhage ( cerebral T waves).

• Serious ventricular dysrhythmias are unusual

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ECHO

• Echocardiography reveals a pattern of regional wall motion abnormalities that follow the distribution of sympathetic nerves rather than the major coronary arteries

• The sympathetic nerves themselves appear to be injured by direct toxicity from the excessive catecholamine release.

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TREATMENT The medical management of SAH focuses on • Protecting the airway, • Managing blood pressure• Preventing rebleeding prior to treatment, • Managing vasospasm, • Treating hydrocephalus, • Treating hyponatremia, and • Preventing pulmonary embolus.

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Treatment- cont• Because rebleeding is common, all patients who are not candidates for

early aneurysm repair are put on bed rest in a quiet room and are given stool softeners to prevent straining.

• If Headache or neck pain is severe, mild sedation and analgesia are

prescribed. • Extreme sedation is avoided because it can obscure changes in

neurologic status.

• Adequate hydration is necessary to avoid a decrease in blood volume predisposing to brain ischemia.

So adequate amount of fluid is administered so as to maintain above

normal circulating blood volume & central venous pressure

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Managing raised ICP

• Intracranial hypertension following aneurysmal rupture occurs secondary to

subarachnoid blood, parenchymal hematoma, acute hydrocephalus, or loss of vascular autoregulation.Perilesional edema if infarct occurs

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Managing raised ICP- cont.• Patients who are stuporous should undergo

emergent ventriculostomy to measure ICP and to treat high ICP in order to prevent cerebral ischemia.

• Medical therapies designed to combat raised ICP e.g., mild hyperventilation, mannitol, and sedation can also be used as needed. (Mannitol dose-25-100gm q4h)

• High ICP refractory to treatment is a poor prognostic sign

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MANAGING BP• Prior to definitive treatment of the ruptured aneurysm,

care is required to maintain adequate cerebral perfusion pressure

while avoiding excessive elevation/fall of arterial pressure.

• If the patient is alert, it is reasonable to lower the blood pressure to <150 systolic using nicardipine, labetolol, or esmolol.

• If the patient has a depressed level of consciousness, then ICP(Intracranial pressure) should be measured and the cerebral perfusion pressure targeted to 60–70 mmHg.

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Managing Seizure Activity• Seizures are uncommon at the onset of aneurysmal

rupture.

• The quivering, jerking, and extensor posturing that often accompany loss of consciousness with SAH are probably related to

the sharp rise in ICP or, perhaps, acute generalized vasospasm rather than seizure.

• Use of anti-seizure drugs is controvercial. However, phenytoin is often given as prophylactic

therapy since a seizure may promote rebleeding.

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MANAGING VASOSPASM

• Vasospasm remains the leading cause of morbidity and mortality following aneurysmal SAH.

• Treatment with the calcium channel antagonist nimodipine (60 mg PO every 4 h) improves outcome, perhaps by preventing ischemic injury

• Nimodipine can cause significant hypotension in some patients, which may worsen cerebral ischemia in patients with vasospasm

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Managing Hydrocephalus

• Acute hydrocephalus can cause stupor or coma.

• It may clear spontaneously or require temporary external ventricular drainage.

• When chronic hydrocephalus develops, permanent ventricular shunting is the treatment of choice.

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Role of Steroids

• Glucocorticoids may help reduce the head and neck ache caused by the irritative effect of the subarachnoid blood.

• There is no good evidence that they reduce cerebral edema, are neuroprotective, or reduce vascular injury, and

• Their routine use therefore is not recommended

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INTERVENTIONAL MANAGEMENT

• Early aneurysm repair prevents rerupture/rebleeding and allows the safe application of techniques to

improve blood flow (e.g., induced hypertension and hypervolemia) should symptomatic vasospasm develop. • An aneurysm can be "clipped" by a

neurosurgeon or "coiled" by an endovascular surgeon.

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Hunt - Hess scale is helpful in assessing the patient before

deciding for intervntional management

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HUNT-HESS SCALE• GRADE1:• Mild headache, normal mental status, no cranial nerve or motor

findings –(GCS* score 15, no motor deficits)• GRADE 2: Severe headache, normal mental status, may have cranial nerve

deficit –(GCS score 13–14, no motor deficits) • GRADE 3: Somnolent, confused, may have cranial nerve or mild motor

DEFICIT- (GCS SCORE 13–14, WITH MOTOR DEFICITS) • GRADE 4 : Stupor, moderate to severe motor deficit, may have intermittent

reflex posturing- (GCS score 7–12, with or without motor deficits) • GRADE 5: Coma, reflex posturing or flaccid (GCS score 3–6, with or without

motor deficits)

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Management based on HH scale

Grades 1 & 2• Current approach is to go for intervention within 24 hrs This will prevent rebleed and will allow measures to be

taken to improve cerebral circulation

• Grade 3 patients- if their condition allows , they too would be benefitted by the procedure

• Grade4- the outcome is generally poor but some times by putting a ventricular drain and improving the grade, pt are sometimes taken for intervention

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SURGICAL REPAIR

•Involves placing a metal clip across the aneurysm neck, thereby immediately eliminating the risk of rebleeding.

•This approach requires craniotomy and brain retraction, which is associated with neurologic morbidity.

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Endovascular techniques involve placing platinum coils, or other embolic material, within the aneurysm via a catheter that is passed from the femoral artery.

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. Endovascular techniques-CONT

• The aneurysm is packed tightly to enhance thrombosis and over time is walled-off from the circulation

• The benefit of endovascular therapy is durable. • However, some aneurysms have a morphology that

is not amenable to endovascular treatment. • Thus, surgery remains an important treatment

option• But for aneurysms which are not approachable by

surgery, endovascular technique would become the only choice

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INTERNATIONAL SUBARACHNOID ANEURYSM TRIAL (ISAT)

• The only prospective randomized trial of surgery versus endovascular treatment for ruptured aneurysm, the International Subarachnoid Aneurysm Trial (ISAT), was terminated early when 24% of patients treated with endovascular therapy were dead or dependent at 1 year compared to 31% treated with surgery, a significant 23% relative reduction.

• After 5 years, risk of death was lower in the coiling group,

• Although the proportion of survivors who were independent was the same in both groups

• Risk of rebleeding was low, but more common in the coiling group

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TO SUM-UP• SAH is a neurolgical emergency• It is less common but an important cause of stroke(5%)• saccular/berry aneurysmal rupture is the commonest cause of SAH • Most common presenttion is an excruciating headache which needs

to be differentiated from other causes of severe headache including thunderclap migrane

• CT scan is very helpful in making a dianosis and differentiating it from other headaches of severe intensity

• If CT is negative but there s strong suspecion of SAH then one should go for CSF examination

• If othe CT scan & CSF are inconclusive then cerebral angiography is the last resort

• Complications include rerupture, hydrocephalus, vasospasm and hyponatremia

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• Management icludes – bed rest, maintaing a clear airway, managing BP, giving adequate amount of fluids, monitoring hyponatremia preventing vasospasm and instituting measures to lower ICP

• one third of patients are prone to develop rebleed which can be effectively taken care of by interventional modalities i.e. surgical (clipping)/ endovascular technique (coiling)

• Randomzed trial (ISAT) has shown coiling to superior to clipping

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