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Cerebrovascular diseases include some of the most common and devastating disorders: ischemic stroke, haemorrhagic stroke, and cerebrovascular anomalies such as intracranial aneurysms and arteriovenous malformations (AVMs). Most cerebrovascular diseases are manifest by the abrupt onset of a focal neurologic deficit, as if the patient was “struck by the hand of God” (Smith et al 2008).

Between 5% and 10% of stroke are due to subarachnoid haemorrhage (Aminoff 2007). Subarachnoid haemorrhage typically presents with a sudden severe “thunder clap” headache (often occipital) which lasts for hours or even days, often accompanied by vomiting. There may be loss of consciousness at the onset, so subarachnoid haemorrhage should be considered if a patient is found comatose. Since 1 patient in 8 with a sudden severe headache has had a subarachnoid haemorrhage, clinical vigilance is necessary to avoid a missed diagnosis. All patients with a sudden severe headache require investigation to exclude a subarachnoid haemorrhage (Allen et al 2006).

Forty five percent of patients die with in the first 30 days following subarachnoid haemorrhage, nearly two third die as a result of the initial haemorrhage and most within first two days (Parr et al 1996). Of those who survive more than half are left with major neurologic deficits as a result of the initial haemorrhage, cerebral vasospasm with infraction or hydrocephalus. If the patient survives but the aneurysm is not obliterated the annual rebleed rate is about 3% (Smith et al 2001).

Despite vigorous therapeutic efforts, the mortality rate from subarachnoid haemorrhage remains high. So the major therapeutic emphasis is on preventing the predictable early complications of the rupture which in turn depends upon early diagnosis and prompt therapeutic intervention. A greater understanding of the basic mechanisms and pathology of subarachnoid haemorrhage may lead to more effective prevention and therapeutic strategies. Early diagnosis of subarachnoid haemorrhage requires good knowledge about clinical features and using necessary investigating tools at an earlier and appropriate time.

The aim of writing this review article on subarachnoid haemorrhage is to understand the details of subarachnoid haemorrhage including its pathophysiology, disease presentation, management of such patients and future thinking.

Arteries of the brain (Snell 1997)

The brain is supplied by the two internal carotid and the two vertebral arteries (Fig.1). Four arteries remain within the subarachnoid space and their branches anatomies on the inferior surface of the brain to form the circle of Willis.

Fig.1.The arteries at the base of the brain. The right temporal pole and most of the right hemisphere of the cerebellum have been removed. Verifications in the pattern of these vessels are common. Source: Gray’s anatomy (38th Ed).


Branches of the cerebral portion:

  1. The ophthalmic artery: It supplies the eye and other orbital structures, frontal area of the scalp, the ethmoid and frontal sinus and the dorsum of the nose.
  1. Posterior communicating artery: It is a small vessel, forming part of the circle of Willis.
  1. Choroidal artery: It is a small artery, ends in the choroid plexus also gives off small branches to crus cerebri, the lateral geniculate body, the optic tract, and the internal capsule.
  1. Anterior cerebral artery: It is connected with it opposite anterior cerebral artery by anterior communicating artery; the cortical branches supply all the medial surface of the cerebral cortex as far back as the parieto-occipital sulcus. They also supply a strip of cortex about 1 inch wide on the adjoining lateral surface. A group of central branches supply parts of the lentiform, caudate nuclei and the internal capsule.
  1. Middle cerebral artery: It is the largest branch of the internal carotid; cortical branches supply the entire lateral surface of the hemisphere, except for the narrow strip supplied by the anterior cerebral artery, the occipital pole, and the inferolateral surface of the hemisphere which are supply by the posterior cerebral artery. Central branches supply the lentiform and caudate nuclei and the internal capsule.


The vertebral artery is a branch of the first part of the subclavian artery. It inters the skull through the foramen magnum. At the lower border of the pons, it joins the vessel of the opposite side to form the basilar artery.

Branches of the cranial portion:

  1. Meningial branches
  1. Posterior spinal artery
  1. Anterior spinal artery
  1. Posterior inferior cerebellar artery: It supplies the inferior surface of the vermis. The central nuclei of the cerebellum and the under surface of the cereballar hemisphere, it also supplies the medulla oblongata and the choroid plexus of the fourth ventricle.
  1. Medullary arteries are very small branches that are distributed to the medulla oblongata.


  1. The pontine arteries are numerous small vessels that enter the substances of the pons.
  1. The labyrinthine artery.
  1. The anterior inferior cerebella artery: It supplies the superior surface of the cerebellum. It also supplies the puns, the pineal gland and the superior modularly velum.
  2. The superior cerebella artery: It supplies the superior surface of the cerebellum. It also supplies the pons, the pineal gland, and the superior modularly velum.
  3. Posterior cerebral artery: Cortical branches supply the inferior-lateral and medial surfaces of the temporal lobe and the lateral and medial surfaces of the occipital lobe. Central branches pierce the brain substance and supply parts of the thalamus and the lentiform nucleus and the midbrain, the pineal and the medial geniculations bodies.

subARACHnoid space

This is the space between the subarachnoid and the pie mater, which contains CSF and the larger arteries and veins which traverse the surface of the brain (Fig.2). Arteries and veins are coated by a thin layer of lepto-meninges. The pie and arachnoid mater are connects by collage nous trabecule and sheets. The piamater is reflected from the surface of the brain and pass along with vessels in the brain substance and disappear as the vessels become capillaries (Berry et al 1995).

Wherever the brain and the cranium are not close to each other, there is a wide interval between pia and arachnoid matter and form subarachnoid cisterns, like cerebellomedullary cistern, pontine cistern, interpeduncular cistern, cistern of lateral fossa etc. the interpeduncular cistern contains circle of Willis (Berry et al 1995).

The cerebrospinal fluid subarachnoid space is a modified tissue fluid and amount is about 150 ml. The cerebrospinal fluid gives buoyancy to the brain and protects the nervous tissue from mechanical forces applied to the skull. Inferiorly, the subarachnoid space extends beyond the lower end of the spinal cord and invests the cauda equina. The subarachnoid space ends below at the level of the interval between the second and third sacral vertebrae (Snell 1997).

Fig. 2. Relationships of pia and arachnoid mater to the dura, brain and vessels. (Modified from Alcolado et al 1988 according to Zhang, Inman & Weller 1990).

Source: Grays’ Anatomy (38th Ed).


The circle of Willis lies in the interpeduncular fossa at the base of the brain. It extends from the superior border of the pons to the longitudinal fissure. It is formed by the anastomosis between the two internal carotid arteries and the two vertebral arteries. The anterior communicating, anterior carotid, posterior communicating, posterior cerebral, and basilar arteries all contribute to the circle. The circle of Willis allows blood that enters by either internal carotid or vertebral arteries lobe distributed to any part of both cerebral hemispheres (Snell 1997).

Two types of branches arise from the circle and its major branches; these are arbitrarily divided into cortical and central and they differ from each other in the extent of their anastomosis. The central branches are very numerous and slender; they tend to arise in groups and immediately pierce the surface of the brain to supply its internal parts. The largest collections of these pass through the anterior and posterior perforated substances. They do not anatomies to a significant extent within the brain substance. The cortical branches ramify over the surface of the cortex and anatomies fairly freely on the piameter. They give rise to numerous small branches which enter the cortex at right angles and like central branches, do not anatomies in it. It follows that blockage of an artery on the piameter may produce little if any damage to the brain but damage to branches entering the substances of the brain leads to destruction of brain tissue (Romanes 1986).

The arteries of brain are liberally supplied by sympathetic nerves which run on to them from the carotid and vertebral plexuses. They are extremely sensitive to injury and readily react by passing into prolong spasm. This of itself may be sufficient to cause damage to brain tissue since even the least of neurons can not withstand absolute loss of blood supply for a period exceeding seven minutes (Romans 1986).

Fig. 3. Diagram of the arteries at the base of the brain, showing the constitution of the arterial circle. The arteries constituting this so called arterial ‘circle’ are commonly asymmetrical and sometimes a constituent vessel is missing. AL= anterolateral central branches; AM= anteromedial central branches; PL= poster lateral central branches;

PM= posteromedial central branches. Source: Gray’s Anatomy (38th Ed)


In 85% of cases of spontaneous SAH, the cause is rupture of a cerebral aneurysm—a weakness in the wall of one of the arteries in the brain that becomes enlarged. They tend to be located in the circle of Willis and its branches. While most cases of SAH are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture (Van Gijn et al 2007).

In 15–20% of cases of spontaneous SAH, no aneurysm is detected on the first angiogram (Rinkel et al 1993). About half of these are attributed to non-aneurysmal perimesencephalic haemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e. mesencephalon). In these, the origin of the blood is uncertain (Van Gijn et al 2007).The remainder are due to other disorders affecting the blood vessels (such as arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumors (Van Gijn et al 2007). Cocaine abuse and sickle cell anemia (usually in children) and, rarely, anticoagulant therapy, problems with blood clotting and pituitary apoplexy can also result in SAH (Warrell et al 2003; Rinkel et al 1993).



The incidence and prevalence of unruptured intracranial aneurysms and aneurysmal SAH should be considered separately. Intracranial aneurysms are found on postmortem examination in between 1% and 6% of adults in large autopsy series (Schievink 1997). The frequency of intracranial aneurysm seen during angiography for patients not suspected of harboring an aneurysm is between 0.5% and 1.0%. The overall incidence of SAH from aneurysms is approximately 7-10 per 100,000 people per year (Menghini et al 1998), but this figure includes children, who have a very low incidence of rupture. The mean age of rupture is approximately 50 years. Among adults older than 30 years of age, the incidence of SAH is approximately 40-50 per 100,000 per year, and nearly one half of these individuals die from their SAH. Various reviews have noted a slight female predominance of SAH from aneurysms, with a mean age of haemorrhage of approximately 50 years. Ruptured aneurysms rarely occur in children, and there is a steady increase in the incidence of rupture from 0.3 per 10,000 persons per year between 25 and 34 years of age to 3.7 per 10,000 persons per year for patients 65 years of age or older.

A special category of patients are those who have a family history of aneurysms and SAH. Familial occurrence of intracranial aneurysms is defined by the presence of aneurysms in two or more first to third degree relatives without any known hereditary disease. It is not known whether the pathogenesis of familial intracranial aneurysms differs from that of the general population (Ronkainen et al 1998). In a community-based study from Rochester, MN, the relative risk of SAH among first-degree relatives of patients with the familial form of SAH was four times higher than the general population. Other studies have shown that in patients with familial intracranial aneurysms, there is a lower mean age at the time of rupture compared with SAH in the general population (Ronkainen et al 1998). Screening studies, with MRA, CT angiography, for the presence of aneurysms in this group of patients appears warranted.


Several classifications of aneurysms have been proposed. This was suggested by Weir (1985).

Morphology Saccular



3-6 mm

7-10 mm

11-25 mm

>25 mm(giant)

Location (Roper & Brown 2005)

Approximately 90 to 95 percent of saccular aneurysm lies on the anterior part of the circle of Willis. The four most common sites are

1. The proximal portions of the anterior communicating artery.

2. at the origin of the posterior communicating artery from the stem of the internal carotid,

3. At the first major bifurcation of the middle cerebral artery, and

4. At the bifurcation of the internal carotid into middle and anterior cerebral arteries.

Other sites include the internal carotid artery in the cavernous sinus, at the origin of the ophthalmic artery, the junction of the posterior communicating and posterior cerebral arteries, the bifurcation of the basilar artery, and the origins of the three cerebeller arteries. Aneurysms that rupture in the cavernous sinus may give rise to an arteriovenous fistula.

Fig.4. Common sites of berry aneurysms in the circle of Willis

Source: Robin’s Pathology (6th Ed.)

Saccular Aneurysms (Selman et al 2004)

Saccular, or berry, aneurysms are the most common form of aneurysms and are most often responsible for aneurysmal subarachnoid haemorrhage. Saccular aneurysms may arise from defects in the muscular layer of cerebral arteries that occur at vessel bifurcations and from degenerative changes that damage the internal elastic membrane, resulting in weakness of the vessel wall. They usually occur on the first or second order arterial branches of the vessel emanating from the circle of Willis. Evidence suggests that both genetic and environmental factors contribute to the development of saccular aneurysms. The evidence that genetic factors are important comes from the documented association of intracranial aneurysms with heritable connective tissue disorders such as autosomal dominant polycystic kidney disease, Ehlers-Danlos syndrome type IV, neurofibromatosis type 1, and Marfans syndrome. The familial occurrence of intracranial aneurysms also points to a role for genetic factors. In those patients who have a first degree relative with an aneurysmal SAH, the risk of a ruptured aneurysm is four times higher than the risk in the general population. A role for acquired factors in the pathogenesis of saccular aneurysm is suggested by the mean age of 50 for patients with aneurismal SAH, and the increased incidence of haemorrhage occurring with age. Cigarette smoking is a risk factor in all population studies, and a role for systemic hypertension, although not as strong as that of cigarette smoking, in the cause of aneurysm formation appears likely.

Saccular aneurysms may also be caused by infection, trauma, or neoplasm. Mycotic aneurysms results from infected emboli that lodge in the arterial intima or the vasa vasorum and account for approximately 5% of all intracranial aneurysms. They occur most frequently in patients with subacute bacterial endocarditis, congenital heart disease, or a history of intravenous drug use, and are usually located on more distal branches of the cerebral vasculature. Proper management includes appropriate intravenous antibiotic therapy, with surgery in selected cases. Fungal aneurysms, which are much rarer than bacterial, usually are associated with arteritis and thrombosis and have been uniformly fatal.

Traumatic aneurysms are rare but can be caused by either blunt or penetrating head injury. Such aneurysms occur at sites other than bifurcations. Angiograms are not routinely performed following head trauma, and these lesions may not be detected, but they should be considered in patients who suffer delayed deterioration. Early operative repair is recommended because of the high mortality associated with these lesions.

Neoplastic embolization, in rare cases, may produce an aneurysm in patients with choriocarcinoma, atrial myxoma, and undifferentiated carcinoma. In forming an aneurysm, the tumor embolus may remain viable, penetrate the endothelium, grow subintimally, and eventually destroy the arterial wall.

Morphology (girolami et al 1999)

An unruptured berry aneurysm is a thin-walled out pouching at arterial branch points along the circle of Willis or major vessels just beyond. Berry aneurysms measure a few mm to 2 to 3 cm and have a bright red, shiny surface and a thin translucent wall. Demonstration of the site of rupture requires careful dissection and removal of blood in the unfixed brain. Atheromatous plaques, calcification, or thrombotic occlusion of the sac may be found in the wall or lumen of the aneurysm. Brownish discoloration of the adjacent brain and meninges is evidence of prior haemorrhage. The neck of the aneurysm may be their wide or narrow. Rupture usually occurs at the apex of the sac with extravasation of blood into the subarachnoid space, the substances of the brain, or both. The arterial wall adjacent to the neck of the aneurysm often shows some intimal thicking and gradual attenuation of the media as it approaches the neck. At the neck of the aneurysm, the muscular wall and intimal elastic lamina are usually absent or fragmented, and the wall of the sac is made up of thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery.

Fusiform Aneurysms (Selman et al 2004)

Fusiform or dolichoectatic aneurysms are classified separately from saccular aneurysms, although in some patients these types may overlap. The basilar artery is most commonly affected, although these aneurysms also can be seen in the anterior circulation. Only rarely are these lesions associated with SAH. Their presentation is characterized by cranial nerve or brainstem dysfunction secondary to direct compression or by embolization from intraluminal thrombus.

Dissecting Aneurysms (Selman et al 2004)

Dissecting aneurysms result from cystic medial necrosis or a traumatic tear in the endothelium and sub adjacent layers of the artery, allowing the formation of a false lumen. The false lumen may connect with the true lumen distally or may rupture through the remaining external arterial wall. Such aneurysms can occur in any portion of the extra cranial or intracranial arterial circulation. Trauma is a common cause in the neck and anterior circulation, but is a rare cause in the posterior circulation. Connective tissue diseases such as Marfans syndrome and other disorders such as fibromuscular dysplasia predispose to arterial dissections.


At necropsy, subarachnoid haemorrhage is seen as a thin coating of blood in the subarachnoid space over the surface over the surface of the brain and as a rather thicker layer of blood around the ruptured aneurysm. The basal CSF cisterns are often filled with blood which can be visualized by CT scan. If bleeding is focal, it may indicate the location of an aneurysm but false localization may occur if haemorrhage is intraventricular and has leaked through the foramen of Luschka into the pontine cisterna around the basilar artery. Preliminary removal of fresh blood clot from around the circle of Willis may reveal the aneurysm or may facilitate dissection of the aneuryum in the fixed brain. If the blood clot around the aneurysm is allowed to harden by fixation the aneurysm may be difficult to locate or it may be damaged during the removal of the solidified blood clot (Sloam et al 1990).

In many cases of ruptured saccular aneurysm there is significant intraventricular or intracerebral haemorrhage. In a necropsy study of 133 patients with rupture saccular aneurysms ( Sloam et al 1990) intraventricular haemorrhage was observed in 40%, half of which are caused by rupture of an anterior communicating artery aneurysm either through the inferior medial portion of the frontal lobe or through the corpus collosum. Intracerebral haemorrhage was seen in 39% of cases caused by middle cerebral artery aneurysms in half of these (Sheffield & Weller 1980).

SAH can alter mechanisms that control cerebral blood flow and metabolism. Chemical control of blood flow by CO2 is altered in SAH patients (Graham 1990). Auto regulation is commonly lost after SAH. Because the degree of impairment of auto regulation may be different in different regions of the brain, a reduction in cerebral perfusion pressure may cause extreme ischemia in some areas but not others. These changes in the intrinsic control of cerebral blood flow are particularly deleterious because several factors may operate to reduce cerebral blood flow after SAH, including decreased cerebral perfusion pressure from the raised intracranial pressure from the raised intracranial pressure caused by acute hydrocephalus or clot formation (Hiroshima et al 1999).

Blood in the subarachnoid space triggers a pathological process that results in a spasm of the vessels of the major branches of the circle of Willis. Increased plasma platelet activating factor and ant phospholipids may contribute to the pathogenesis of cerebral vasospasm after SAH (Endo et al 1995). In Japan, there is a study at Tokayama, to evaluate the usefulness of measuring anti-phospholipids’ antibodies (APLS) for the occurrence of symptomatic vasospasm and the outcome after SAH. They explained the association of ant phospholipids with worse outcome; APLS were detected between 7 and 13 days after SAH. The mechanism of transient APLS is unclear but it is more likely to occur in the severer grade patients. The reduction in platelet count, the increased platelet factor 4 concentrations was also observed in APLS-positive patients with symptomatic vasospasm (Endo et al 1995).

Delayed cerebral vasospasm that occurs after SAH seems to be associated with both impaired dilator and increased constrictor mechanisms in cerebral arteries. Mechanisms contributing arteries after SAH have been intensively investigated in recent years. Nitric oxide is produced by the endothelium and is an important regulator of cerebral vascular tone by tonic ally maintaining the vasculature in a dilated state. Endothelial injury after SAH may interfere with Nitric oxide (NO) production and lead to vasoconstriction and impaired responses to endothelium vasodilators (Sobeys et al 1998).

Inactivation of NO by Oxyhaemoglobin or superoxide from erythrocytes may also occur in the subarachnoid space after SAH. Nitric oxide stimulates activity of soluble guanylate cyclase in vascular in vascular muscle leading generation of cGMP and relaxation. Subarachnoid haemorrhage appears to cause impaired activity of soluble granylate cyclase, resulting in reduced basal levels of CGMPin cerebral arteries to nitric oxide. Endothelin (ET) is a potent, long lasting vasoconstrictor that may contribute to the spasm of cerebral arteries after SAH. Endothelin is present in increased levels in the cerebrospinal fluid of SAH patients. Pharmacological inhibition of ET synthesis or ET receptors has been reported to attenuate cerebral vasospasm. Production of and vasoconstriction by Endothelin may be due, in part, to the decreased activity of Nitric oxide and formation of CGMP (Sobey et al 1998).

Protine kinase C (PKC) is an important enzyme involved in the contraction of vascular muscle in response to several agonists, including ET, activity of the PKC appears to be increased in the cerebral arteries after SAH indicating that PKC may be critical in the development of cerebral vasospasm. Recent evidence suggests that PKC activation may occur in cerebral arteries after SAH as a result of decreased negative feedback influence of NO/CGMP. Cerebral arteries are depolarize after SAH, possibly due to decreased activity of potassium channels may be due to several mechanisms, including impaired activity of Nitric oxide (and/or CGMP) or increased activity of PKC. Thus endothelial damage and reduced activity of Nitric oxide may contribute cerebral vascular dysfunction after SAH (Sobey et al 1998).

Because cerebral blood flow is inversely proportional to the fourth power of the radius, small changes in vessel caliber can have profound effects. If regional flow falls below the critical thresholds for membrane integrity, ischemic edema formation and infraction can occur. Focal regions of edema can further impair local blood flow despite on overall normal intracranial pressure. AVP (Arginine vasopressin) plays an important role in the development of antidiuersis and disturbance of the brain water and electrolyte imbalance after SAH (Laszi et al 1995).


Unruptured Aneurysms

Most unruptured intracranial aneurysms are completely asymptomatic. Aneurysms may demonstrate evidence of their presence or of growth, before rupture, in other ways besides headache. Premonitory manifestations depend on the location of the aneurysm and include diplopic, visual field deficits, or facial pain (Weir 1994).


Because aneurysms can produce catastrophic haemorrhage before they reach a size that would produce neurological deficits, the lack of clinical findings should not preclude further diagnostic evaluation. The physical findings in patients with unruptured aneurysms are determined in part by the size and location of the aneurysm, although few aneurysms can be diagnosed with confidence on the basis of clinical presentation alone. Thus aneurysms arising from the anterior communicating artery can produce visual field defects, endocrine dysfunction, or localized frontal headache. Aneurysms of the internal carotid artery can produce coulometer paresis, visual field deficits, impaired visual acuity, endocrine dysfunction, and localized facial pain. Aneurysms of the internal carotid artery in the cavernous sinus can produce a cavernous sinus syndrome when they reach a sufficient size. Those of the middle cerebral artery can produce aphasia, focal arm weakness, or paresthesias. Basilar bifurcation aneurysm can be associated with oculomotor paresis, although the clinical features of posterior circulation aneurysms seldom permit diagnosis before they rupture (Selman et al 2004).

Ruptured saccular aneurysms

With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space (usually in relation to the circle of Willis), and the resulting clinical events assume one of the three patterns:

(1) The patient is stricken with an excruciating generalized headache and vomiting and falls unconscious almost immediately;

(2) Headache develops in the same manner but the patient remains relatively lucid- the most common syndrome;

(3) Rarely consciousness is lost quickly without any preceding complaint. Decelerate rigidity and brief clinic jerking of the limbs may occur at the onset of the haemorrhage, in association with unconsciousness. If the haemorrhage is massive, death may ensue in a matter of minutes or hours, so that ruptured aneurysm must be considered in the differential diagnosis of sudden death. A considerable proportion of such patients probably never reach a hospital. Persistent deep coma is accompanied by irregular respirations, attacks of extensor rigidity, and finally respiratory arrest and circulatory collapse. In these rapidly fatal cases, the subarachnoid blood has greatly increased the intracranial pressure to a level that approaches arterial pressure and caused a marked reduction in cerebral perfusion. In some instances the haemorrhage has dissected intracerebrally and entered the ventricular system (Roper & Brown 2005).

Ruptured of the aneurysm usually occurs while the patient is active rather during sleep, and in a few instances during sexual intercourse, straining at stool, lifting heavy objects, or other sustained exertion. Momentary valsalva maneuvers, as in coughing or sneezing, have generally not caused aneurismal rupture. 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 (Ropper & Brown 2005).

In less severe cases, consciousness, if lost, may be regained within a few minutes or hours, but a residuum of drowsiness, confusion, and amnesia accompanied by severe headache and stiff neck persists for several days. It is not uncommon for the drowsiness and confusion to last 10 days or longer. Since the haemorrhage is confined to the subarachnoid space, there are few if any focal neurologic signs. That is to say, gross lateralizing signs in the form of hemiplegia, hem paresis, homonymous hemianopia, or aphasia are absent in the majority of cases. On occasion, a jet of blood emanating from an aneurysm may rupture into the adjacent brain or clot in the insular cistern and produce a hemiparesis or other focal syndrome. There may also be a focal syndrome from acute or delayed ischemia in the territory of the aneurysm-bearing artery. Usually this occurs several days after a large subarachnoid haemorrhage. The pathogenesis of such manifestations is not fully understood, but a transitory fall in pressure in the circulation distal to the aneurysm is postulated in early cases and vasospasm is responsible for the later focal signs. Transient deficits are not common, but they do constitute reliable indicators of the site of the ruptured aneurysm (Ropper & Brown 2005).

Convulsive seizures, usually brief and generalized, occur in 10 to 25 percent of cases according to Hart et al (but far less often in our experience) in relation to acute bleeding or rebreeding. These early seizures do not correlate with the location of the aneurysm and do not appear to alter the prognosis (Ropper & Brown 2005).

In most patients the neurologic manifestations do not point to the exact sight of the aneurysm, but it can often be inferred from the location of the main clot on CT scan. A collection of blood in the anterior interhemispheric fissure indicates rupture of an anterior communicating artery aneurysm; in the sylvian fissure, a middle cerebral artery aneurysm; in the anterior perimesencephalic cistern, a posterior communicating or distal basilar artery aneurysm; and so on. In some instances clinical signs provide clues to its localization, as follows:

· Third nerve palsy (ptosis, diplopia, dilation of pupil, and divergent strabismus), as stated above, usually indicates an aneurysm at the junction of the posterior communicating artery and the internal carotid artery- the third nerve passes immediately lateral to this point;

· Transient paresis of one or both of the lower limbs at the onset of the haemorrhage suggests an anterior communicating aneurysm that has interfered with the circulation in the anterior cerebral arteries;

· Hemi paresis or aphasia points to an aneurysm at the first major bifurcation of the middle cerebral artery;

· Unilateral blindness indicates an aneurysm lying anteromedially in the circle of Willis (at the origin of the ophthalmic artery or at the bifurcation of the internal carotid artery);

· A state of retained consciousness with akinetic mutism or abulia (sometimes associated with paraparesis) favors a location on the anterior communicating artery, with ischemia of or haemorrhages into one or both of the frontal lobes or hypothalamus (with or without acute hydrocephalus);

· The side on which the aneurysm lies may be indicated by a unilateral preponderance of headache or preretinal haemorrhages, the occurrence of monocular pain, or, rarely, lateralization of an intracranial sound heard at the time of rupture of the aneurysm. Sixth nerve palsy, unilateral or bilateral, is usually attributable to raised intracranial pressure and is seldom of localizing value.

In summary, the clinical sequence of sudden severe headache, vomiting, collapse, relative preservation of consciousness with few or no lateralizing signs, and neck stiffness is diagnostic of subarachniod haemorrhages due to a ruptured secular aneyrysm.

The initial clinical manifestations of SAH can be graded using the Hunt-Hess or World Federation of Neurosurgical Societies classification schemes. For ruptured aneurysms, prognosis for good outcomes falls as the grade increases. For example it is unusual for a Hunt-Hess grade 1 patient to die if the aneurysm is treated, but the mortality for grade 4 and 5 patients may be high as 80%.

Table: Grading Scales for Subarachnoid Haemorrhage (Hemphill & Smith 2008)

Grade Hunt-Hess Scale World Federation of Neurosurgical societies (WFNS) Scale
1 Mild headache, normal mental status, no cranial nerve or motor findings Glasgow Coma Scale score 15, no motor deficits
2 Severe headache, normal mental status, may have cranial nerve deficit GCS 13-14, no motor deficits
3 Somnolent, confused, may have cranial nerve or mild motor deficit GCS 13-14, with motor deficits
4 Stupor, moderate to severe motor deficit, may have intermittent reflex posturing GCS 7-12, with or without motor deficits
5 Coma, reflex posturing or flaccid GCS 3-6, with or without motor deficits


The laboratory evaluation of patients suspected of having a rupture aneurismal SAH uses a combination of CT scan, magnetic resonance imaging, lumber puncture and angiography.

CT Scan

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 (if within 48 hours of bleed) and in practically all cases in which the haemorrhage has been severe enough to cause momentary or persistent loss of consciousness. This should therefore be the initial investigative procedure. The sooner the CT scan is performed in relation to the suspected haemorrhage the greater the likelihood of visualizing blood.

The blood may appear as a subtle shadow along the tentorium or in the sylvian or adjacent fissures. A large collection of subarachnoid blood or a hematoma in brain tissue or within the sylvian fissure indicates the adjacent location of the aneurysm and the likely region of subsequent vasospasm, as already noted. A high incidence of symptomatic vasospasm in the middle and anterior cerebral arteries has been found when early CT scan shows sudarachnoid clots larger than 5*3 mm in the basal cisterns or layers of blood more than 1 mm thick in the cerebral fissures. CT scan less reliably predicts vasospasm in the vertebral, basilar, or posterior cerebral arteries .Also, coexistent hydrocephalus will be demonstrable. If the CT scan documents subarachnoid blood with certainty, a spinal tap is not necessary.

In all other cases, where subarachnoid haemorrhage is suspected but not apparent on imaging studies or computed tomography is unavailable but the patient is oriented and obeying commands, a lumber puncture should be undertaken. Lumber puncture should not be performed in patients with papilloedema or focal neurological signs (Duffy 1982). Usually the CSF becomes grossly bloody within 30 min of the haemorrhage, with red blood cell counts up to 1 million/mm3 or even higher. With a relatively mild haemorrhage, there may be only a few thousand cells, but it is unlikely that a severe headache syndrome from subarachnoid haemorrhage would be associated with less than a several hundred cells. It is also probably not possible for an aneurysm to rupture entirely into the brain tissue without some leakage of blood into the subarachnoid fluid. In other words, the diagnosis of ruptured saccular aneurysm (by lumber puncture) is essentially excluded if blood is not present in the CSF. Xanthochromia is found after centrifugation if several hours or more have elapsed from the moment of the ictus. In a patient who reports a headache that is consistent with subarachnoid haemorrhage but the occurrence was several days earlier, the CT scan may be normal and xanthrochromia the only diagnostic finding. Also helpful after several days is the MRI taken with the FLAIR sequence, with will demonstrate blood.

Fig. 5. CT scan of the brain showing subarachnoid haemorrhage as a white area in the center

MRI Scan

Not routinely used, but in patients with multiple aneurysms, MRI performed several days after the bleed may provide greater sensitivity than CT in detecting small areas of subarachnoid clots and help determine the particular lesion responsible (Yadav et al 1998).


A rupture of intracerebral haemorrhages due to hypertension, into the subarachnoid space or the ventricles may be difficult to distinguish from a subarachnoid haemorrhage occurring in a hypertensive patient and invading one cerebral hemisphere. When the diagnosis of subarachnoid haemorrhages has been confirmed by CT scan or examination of cerebral fluid, therefore, it is necessary to exclude a ruptured aneurysm or a bleeding angioma as its cause. This may call for angiography, which raises the question of whether this should be done in every case, and if so when ( Yadav et al 1998).

There is a difference of opinion about this, some surgeons recommending that carotid angiography should be performed in every case of subarachnoid haemorrhages as soon as the diagnosis is made while others are more selective. The rational answer seems to be that if there is possibility that a life saving operation may be carried out as the result of information yielded by angiography, angiography should be performed. If on the hand this is not the case because it is thought that the patient is too ill to stand operation or that either angiography or the operation is fraught with greater risks than expected treatment. As may be the case particularly in patients over the age of 60 with evident atheroma, angiography should be postponed. There is no doubt, however, that surgery carried out sufficient early may save lives which would otherwise be lost (Pathirana et al 1994).

Angiography is usually carried out at the earliest convenience, although in patients in poor clinical condition, the clinician may prefer to delay investigation until improvement has occurred. If a patient deteriorates from the mass effect of an intracranial hematoma, then emergency angiography is required prior to any decompressive operation.

Four vessels angiography is usually performed in all patients. Anterior-posterior, lateral and oblique views are requires for each vessel.

Carotid angiography may show not only the site, size and shape of the aneurysm but also whether as sometimes happens there is an associated spasm of important arteries which may be contributing to the clinical picture (Lindsay et al 1997).

Magnetic resonance angiography

Magnetic resonance angiography is a useful non-invasive technique for demonstrating intracranial aneurysms but the resolution is still insufficient to ensure that small aneurysms are not missed.

MRA is less sensitive than conventional arteriography to visualize anomalies (Anzalone 1995). MRA is not sensitive enough to serve as a screening procedure after SAH. It can be used however to detect unruptured aneurysms in selected patients (Burst 1995).

Negative angiography

Angiography fails to reveal a source of the subarachnoid haemorrhages in approximately 20% of patients. In the presence of arterial spasm, reduction in flow may prevent the demonstration of an aneurysm and repeat angiography may be required at a later date (Jose et al 1996).Four vessels angiography confirms the presence of an AVM and delineates the feeding and draining vessels. Reasonably small AVMs are difficult to detect and only early venous filling may draw attention to their presence. In the presence of a hematoma, angiography should be delayed until the hematoma resolves, otherwise local pressure may mask demonstration of AVM. If the angiogram is subsequently negative, then MRI is required to exclude the presence of a cavernous malformation (Lindsay et al 1997).

Transcranial droppler ultrasound assessment of proximal middle, anterior and posterior cerebral and basilar artery flow is helpful in detecting the onset of vasospasm, even prior to symptoms and following its course and response to therapy (Donald et al 2001).Skull radiographs sometimes reveal calcification in the AVM or increased vascular markings in the overlying bone (Brust 1995).

Associated Systemic Changes

Acute subarachnoid haemorrhages are associated with several characteristic responses in the systemic circulation, water balance, and cardiac function. The ECG changes include symmetrically large peaked T waves and other alterations suggesting subendocardial ischemia. Also there is a tendency to develop hyponatremia; this abnormality and its relationship to intravascular volume depletion play a key role in treatment. Albuminuria and glycosuria may be present for a few days. Rarely, diabetes insipid us occurs in the acute stages, but water retention or a natriuresis is more frequent. There may be a leukocytosis of 15,000 to 18,000 cells per cubic millimeter, but the sedimentation rate is usually normal (Ropper & Brown 2005).

Complications of aneurysmal SAH(Mohr et al 2004)

Intracranial complications:

  1. Recurrent haemorrhages.
  2. Vasospasm- induced ischemic stroke.
  3. Hydrocephalus.
  4. Seizures.
  5. Brain edema.

Extra cranial complications:

  1. Systemic
    1. Arterial hypotension or hypertension
    2. Electrolyte disturbances (hyponatremia, hypernatremia, hypokalemia)
    3. Cardiac (myocardial infraction, arrhythmia, congestive heart failure)
  1. Pulmonary (neurogenic pulmonary edema, adult respiratory distress syndrome, atelectasis, pneumonia)
  2. Gastrointestinal bleeding.
  1. Sepsis
  2. Renal or hepatic dysfunction
  3. Venous thromboembolism

7. Bleeding disorders, including thrombocytopenia

Vasospasm (Ropper & Brown 2005)

Delayed hemiplegia and other focal deficits usually appear 3 to 12 days after rupture and rarely before or after this period. These delayed syndromes and the focal narrowing of a large artery or arteries, seen on angiography, are referred to as vasospasm. Fisher and coworkers (1975) have shown that spasm is most frequent in arteries surrounded by the largest collections of clotted subarachnoid blood. The vasospasm appears to be a direct effect of blood or some blood product, possibly hem tin or a platelet product, on the adventitia of the artery. Areas of ischemic infraction in the territory of the vessel bearing the aneurysm, without thrombosis or other changes in the vessel, is the usual finding in such cases. These ischemic lesions are often multiple and occur with great frequency, according to Hijdra and associates (1986).

After a few days, arteries in chronic spasm undergo a series of morphologic changes. The smooth muscle cells of the media become necrotic, and the adventitia is infiltrated with neutrophilic leukocytes, mast cells, and red blood corpuscles, some of which have migrated to a subendothelial position (Chyatte and Sundt). These changes are caused by products of hemolyzed blood seeping inward from the pia-arachnoid into the muscular is of the artery.

The clinical features of cerebral vasospasm depend on the affected blood vessel but typically include a fluctuating hemiparesis or aphasia and increasing confusion that must be distinguished from the effects of hydrocephalus. In the past, an arteriogram was required to verify the diagnosis, although it is not often performed now because of the slight associated risk of worsening vascular spasm and the ease with which the condition can be visualized with MRA and spiral CT techniques. Tran cranial Doppler measurements are an indirect and easier way of following, by observations of blood flow velocity, the caliber of the main vessels at the base of the brain. Almost all patients have a greatly increased velocity of blood flow in the affected vessel that can be detected by this method in the days after haemorrhages. However, progressive elevation of flow velocity in any vessel (especially if over 175 cm/s) suggests that focal vasospasm is occurring. There is a reasonable correlation between these findings and the radiographic appearance of vasospasm, but the clinical manifestations of ischemia depend on additional factors such as collateral blood supply and the cerebral perfusion pressure .

Recurrent Haemorrhage

Recurrent haemorrhage is a feared complication of SAH because it is a leading cause of death or neurologic morbidity during the first 2 weeks after SAH (Roos et al 2000; Hillman et al 1998). The cumulative rate of rebreeding during the first 2 weeks after SAH is approximately 15% to 20% (Torner et al 1981). Turner and colleagues (1981) found that the period of greatest risk for rebleeding is the first 24 hours after the ictus; the risk peaked at approximately 4% during that time.

Several clinical features identify those patients at the highest risk for early rebleeding. The most important is the level of consciousness at admission; patient admitted in coma at the greatest risk. Rebreeding is also more common among older people, women, and people whose systolic blood pressure exceeds 170 mm Hg. The results of the baseline CT do not predict recurrent haemorrhage.

A recurrent haemorrhage usually causes a sudden headache and a rapid change in neurologic condition, including a drop in consciousness. Extensor spasm s and posturing are important early signs. A “convulsion” that occurs immediately after SAH also can mark a recurrent haemorrhages (Hart et al 1981). However, rebreeding in a comatose patient may be overlooked. It may be manifested only by a sudden change in respiratory pattern or vital signs. Recurrent haemorrhages should be sought whenever a patient experiences a new headache or worsens neurologically (Mohr et al 2004).

The differential diagnosis of rebreeding are vasospasm-induced brain ischemia, sub acute hydrocephalus, seizure, electrolyte imbalance, hypotension, hypoxia, medication effects, systemic complication etc. The diagnosis of rebreeding should not be solely on clinical features, because this approach leads to over diagnosis. Recurrent haemorrhages can be proved most easily by the detection of additional blood on CT scans (Mohr et al 2004).


Hydrocephalus is a common complication of SAH, resulting from the massive collections of blood that fill the ventricles, block the aqueduct of sylvius, or obstruct the fourth ventricle. Blood can fill the subarachnoid cisterns or coat the arachnoid villa (Mohr et al 2004).

Sheehan and associates (1999) reported that hydrocephalus developed in approximately one fourth of their patients during the acute treatment period. Hydrocephalus is more common among patients who, upon admission, have severe neurologic impairments or CT evidence of ventricular dilation or intraventricular haemorrhages. In addition, women, patients with preexisting hypertension, and patients with a history of alcohol abuse have higher rates of hydrocephalus (Sheehan et al 1999).

The hydrocephalus after SAH may be classified according to its time of appearance as (1) acute- appearing within 12 hours after aneurysmal rupture, (2) sub acute- developing a few days after the ictus, or (3) delayed- noted as ventricular dilation week to years later. Acute hydrocephalus is an important cause of increased intracranial pressure and coma. Sub acute hydrocephalus is a cause of a gradual decline in consciousness that can occur approximately 7 to 10 days after SAH. In this situation, intracranial pressure may be modestly elevated. Delayed hydrocephalus often manifests as a sub acute dementia, gait apraxia, and bladder incontinence. In the setting, intracranial pressure often fluctuates and may not be consistently elevated (Mohr et al 2004).

Approximately 16% to 34% of patients have CT findings consistent with acute hydrocephalus. Some patients with ventricular enlargement may be asymptotic, but most have decreased consciousness. Symptoms of acute hydrocephalus in addition to decline in alertness are bilateral motor signs, mitosis, and downward deviation of the eyes. Acute hydrocephalus predicts increased mortality and morbidity and is correlated with subsequent development of vasospasm and ischemic stroke (Mohr et al 2004).


Table 1. Factors Predicting Less Favorable Outcome after Subarachnoid Haemorrhage (Mohr et al 2004)

Clinical factors
  1. Admitting level of consciousness( coma)
  2. Interval from subarachnoid haemorrhages(<3 days)
  3. Age(>65years)
  4. Prior unrecognized haemorrhage or warning leak
  5. Presence of local neurologic signs on admission
  6. Presence of severe co morbid disease or extra neural organ involvement
Diagnostic results
  1. Hyponatremia or hypovolemia
  2. Abnormal CT scan

Local, thick, or diffuse collection of subarachnoid blood

Intracerebral or intraventricular blood

  1. Mass effect
  2. Hydrocephalus
  3. Evidence of rebreeding detected by sequential CT scan
  4. Vasospasm detected by arteriography or by transcranial Doppler ultrasonography
  5. Aneurysm located on anterior cerebral or vertebrobasilar arteries
  6. Size of aneurysm(>10mm)


The patient with recent SAH is critically ill and should be evaluated and treated urgently (May berg et al 1994; Wijdicks 1995). He or she should be transported rapidly to a medical center that has the expertise to treat a patient with a ruptured aneurysm. Acute, potentially life-threatening complications should be anticipated. Personnel should assess the patient quickly and should measure vital signs and assess neurologic status frequently. The heart rate and rhythm should be monitored. The airway, breathing, and circulation should be supported, and if necessary, supplemental oxygen, end tracheal intubation, or ventilatory assistance should be given (Wijdicks 1995). Intravenous access is established to expedite emergency administration of medications. Normal saline can be given at a slow rate to maintain patency of the intravenous line. Unfortunately, the urgent approach to acute management of SAH is often suboptimal in emergency departments (Thomson et al 2000). Each institution should develop a protocol for the management of SAH in the emergency department, including plans for both acute treatment and urgent evaluation.

The initial evaluation should include CT scan, chest radiograph, electrocardiogram, and blood studies. CT can demonstrate subarachnoid blood and a number of other acute intracranial complications. When CT shows intracranial bleeding, a lumber puncture can be avoided. The findings of CT that is performed within 24 hours after onset of symptoms with the use of third-generation scanners are normal in approximately 2% to 7% of cases (Zouaoui 1997). If the CT findings are normal, a cerebrospinal fluid specimen should be obtained.

Patients should be admitted to a unit that has monitoring equipment and is staffed by neurologically trained nurses. Acute care can be divided into general supportive efforts and therapies aimed at preventing or controlling specific complications (May berg et al 1994; Wijdicks 1995). For the first 24 hours, blood pressure, vital signs, and neurologic status should be assessed hourly. Thereafter, examinations can be spaced further apart in stable patients. Cardiac monitoring and, if necessary, continuous intra-arterial or noninvasive blood pressure monitoring are extended for at least 24 to 48 hours after admission.

Forced bed rest is a traditional part of management. Visitors and external stimuli are restricted. Passive range-of-motion exercises and frequent turning are performed. A water mattress or an alternating- pressure pneumatic bed can reduce the risk of pressure sores and atelectasis. Patients are assisted with self-care activities, such as bathing and eating. Black and associates (1986) showed that external pneumatic calf compression stocking and devices reduce the incidence of deep vein thrombosis. The use of heparin as a prophylaxis against deep venous thrombosis is generally avoided until the ruptured aneurysm is treated.

Gentle pulmonary suctioning and nursing care are important for avoiding pneumonia. The value of absolute bed rest in preventing rebreeding was tested by the cooperative study of Intracranial Aneurysms and Subarachnoid Haemorrhage; the cumulative rate of rebreeding was 25% during the first 14 days after SAH (Nishioka 1981). In general, the prognosis of patients treated only with absolute bed rest now represents the natural history of SAH.

Because intravenously administered medications are often needed, a slow infusion of saline is continued. Alert patients are usually given a soft, high-fiber diet supplemented by stool softeners (Wijdicks 1995). Caffeinated beverages are avoided. Stupor us and comatose patients are not fed during the acute treatment period. If a seriously ill person is stable several days after SAH and the airway is secured, nasogastric feedings can be instituted.

Symptomatic treatment

Patients with SAH are often confused or agitated as a result of brain injury, hydrocephalus, or increased intracranial pressure. Pain or nausea can also lead to irritability. Agitation raises the risk of rebreeding and aggravates increased intracranial pressure. Control of pain or nausea can calm an upset patient. Regular administration of diazepam or Phenobarbital may be useful in providing sedation for agitated patients.

The headache of SAH is intense, and patients should receive ample doses of analgesics (May berg et al 1994; Wijdicks 1995). Most alert patients require a medication such as codeine, meperidine, or morphine. The agent is usually administered parent rally. These medications can be combined with acetaminophen, hydrolyzing hydrochloride, or promethazine. Some patients have photophobia; a quiet, dark environment can help relieve some of these conditions, which otherwise might worsen the head pain. Sedation and sleep might also help control pain. Aspirin affects platelet aggregation and prolongs the bleeding time; there is concern that aspirin might potentiate rebreeding.

Severe nausea and vomiting are common and important complaints, particularly during the first 24 hours after SAH. Nauseated patients should receive an antiemetic, such as ondansetron, trimethobenzamide, or prochlorperazine, to control these complaints.


Approximately 25% of patients have seizures, most of which occur within the first 24 hours (Hart et al 1981; Rhoney et al 2000; Sundaram et al 1986). Rhoney and colleagues (2000) reported that seizures were most common among patients with thick cisternal clots. Most seizures happen before the patient reaches the hospital. Hart and associates (1981) noted that 63% of the seizures happened at the time of aneurismal rupture. However, some of these ‘seizures’ may not be truly epileptic phenomena but may represent transient decelerate posturing secondary to increased intracranial pressure (Hart et al 1981; Fisher 1975).

Although seizures occurring after hospitalization are uncommon, they can be associated with recurrent haemorrhages. Physicians prescribe anticonvulsants to patients who have experienced a seizure as part of SAH, but the prophylactic use of these agents in treatment of patients who have not had a seizure is controversial. The rationale for prophylactic of anticonvulsants is that a seizure is a dangerous event in a person with a recent SAH. Because of the low rate of seizures after admission, however, Hart and associates (1981) and sundaram and chow (1986) question the necessity for routine prescription of anticonvulsants to patients with recent SAH. However, regular use of phenytion or another parent rally administered anticonvulsant is recommended to reduce the likelihood of seizures. No trial has tested the value of anticonvulsants in management of patients with recent SAH. Pending such a trail, the decision to prescribe these medications is individualized. If a patient has had or is having convulsions, intravenous doses of anticonvulsants are given.


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