Almost one fourth of all deaths attributable to disorders of the nervous system are caused by hemorrhage in the intracranial cavity. When the bleeding occurs primarily within the subarchnoid space rather than in brain parenchyma, the condition is referred to as subarachnoid hemorrhage. It is more a clinical syndrome than a clear pathological entity.

The incidence of subarachnoid hemorrhage varies considerably. The average age of patients with SAH is substantially lower than for other types of stroke, peaking in the sixth decade. Gender, race and region have a marked influence on the incidence of SAH. Women have a 1.6 times higher risk than men, and black people a 2.1 times higher risk than whites. In Finland and Japan, the incidence rates are much higher than in other parts of the world. In Japan the incidence is 25 per 1,00,000 general population and in U.S.A. it is 16 per 1,00,000. The incidence is about 4 per 1,00,000 and is on the increase in India. Considering our population figures, one can imagine the total number of patients in any medical practice.

Risk factors:

Dietary, hereditary, socio-economic factors may have a role in the pathogenesis of this disorder.

Only smoking, hypertension and heavy drinking, and use of oral contraceptives are accepted as significant risk factors which can be modified. The risks are not clear for hormone replacement therapy or an increased level of plasma cholesterol.

An important risk factor is familial predisposition to SAH. Between five and 20% of patients with SAH have a positive family history. First-degree relatives of patients with SAH have a 3- to 7-fold increased risk of being struck by the same disease. In second degree relatives, the incidence of SAH is similar to that found in the general population.

The occurrence of SAH is also associated with specific heritable disorders of connective tissue, but these patients account for only a minority of all patients with SAH. Even though autosomal dominant polycystic kidney disease (ADPKD) is the most common heritable disorder associated with SAH, it is found in only 2% of all patients with SAH. Aortic stenosis and polycystic kidney are the only 2 congenital anomalies with correlation with aneurysms. They may have congenital origin, but they also cause high BP which may be a factor. Other genetically determined disorders include, Ehlers–Danlos disease IV, Marfan's syndrome, Lupus erythematosis, and neurofibromatosis type 1; but these associations are weaker than between ADPKD and aneurysms and these syndromes are seldom found in patients with SAH.

 
Clinical features:

Perhaps nowhere else in medicine, history is so very important.

A sudden, severe headache that is unlike any the patient has experienced previously, is due to subarachnoid hemorrhage until proved otherwise. It may be generalized or localized and associated with nausea or vomiting.

Classically, the headache from aneurismal rupture develops in seconds. However, it is to be noted that even an accurate history does not reliably distinguish between aneurismal rupture and innocuous forms of headache, such as benign vascular headache or a muscle contraction headache. First, only half the patients with aneurysm rupture describe the onset as instantaneous, the other half describe it as coming on in seconds to even a few minutes. Secondly, in the group of patients whose headache came on within a split second, innocuous forms of headache outnumber SAH by 10 to one. If explosive headache is the only symptom, the chance of SAH being the cause is only 10. Also, preceding bouts of similar headaches are recalled in 20% of patients with aneurismal rupture and 15% of patients with innocuous thunderclap headache.

Vomiting occurs in 70% of patients with aneurismal rupture, but also in 43% of patients with innocuous thunderclap headache.

Kerning's sign may appear 6-24 hours later. It does not occur if patients are in deep coma. Mild temperature elevation, photophobia and hypertension are not uncommon.

Dizziness, true vertigo or fatigue may also occur as may memory impairment, confusion or agitation. 1 to 2% of patients with SAH present with an acute confusional state and in most such patients a history of sudden headache is lacking.

Epileptic seizures at the onset of aneurismal SAH occur in 6–16% of patients; however, the majority of patients with de novo epilepsy above age 25 years will have underlying conditions other than SAH, but the diagnosis should be suspected if the postictal headache is unusually severe.

Ophthalmologic findings may be observed in more than one third of patients. Intra ocular hemorrhage in the subhyloid or preretinal space are more characteristic of subarachnoid hemorrhage and occurs in 17% of patients who reach the hospital. III, V & VI nerve Palsies and other focal neurological deficits may develop, depending on the area of brain involved and may be secondary to intraparenchymal bleeding, ischemia, thromboembolism, subdural hematoma or obstruction to CSF pathways.

About one third of patients will have a minor leak referred to as 'sentinel hemorrhage'. Headache is the most common symptom. Other warning signs include impairment of ocular movements, motor or sensory impairment.

Grading of subarachnoid hemorrhage has centered about complaints of headache and the patients level of consciousness.

Cranial nerve palsies are not considered a focal deficit.

Serious systemic diseases such as hypertension, diabetes, chronic pulmonary disease, angiographically evident vasospasm place the patient in the next less favorable grade.

On occasions the history and clinical examination may suggest the cause of SAH.

Causes of  SAH:

85% of SAHs are attributable to saccular aneurysms; 10% are caused by non-aneurysmal SAH and the remaining 5% by a variety of rare conditions.

Saccular ('Berry') aneurysms (85%):

The saccular 'berry' aneurysms and other causes of aneurysms are  discussed elsewhere.
 

Idiopathic non-aneurysmal  perimesencephalic hemorrhage (10%):

This harmless variety is defined only by the characteristic distribution of the extravasated blood on brain CT, in combination with the absence of an aneurysm. The extravasated blood is confined to the cisterns around the midbrain, and the centre of the bleeding is immediately anterior to the midbrain. In some cases, the only evidence of blood is found anterior to the pons. There is no extension of the hemorrhage to the lateral sylvian fissures or to the anterior part of the interhemispheric fissure. Some sedimentation of blood in the posterior horns of the lateral ventricles may occur. There is no frank intraventricular hemorrhage.

Perimesencephalic hemorrhage can occur in any patient over the age of 20 years, but most patients are in their sixth decade. A history of hypertension may be obtained. In one-third of the patients, strenuous activities immediately precede the onset of symptoms, a proportion similar to that found in aneurismal hemorrhage.

Clinically, there is little to distinguish idiopathic perimesencephalic haemorrhage from aneurysmal hemorrhage. The headache onset is more often gradual (minutes rather than seconds) than with aneurysmal hemorrhage, but the predictive value of this feature is poor. Loss of consciousness and focal symptoms are exceptional and then only transient; a seizure at onset virtually rules out the diagnosis. On admission, all patients are, in fact, in perfect clinical condition, apart from their headache. Transient amnesia is found in about one-third and is associated with enlargement of the temporal horns on the initial CT scan. Typically, the early course is uneventful: rebleeds and delayed cerebral ischaemia simply do not occur. Only few have symptoms from this ventricular dilatation and even then an excellent outcome can be anticipated. The period of convalescence is short and almost invariably patients are able to resume their previous work and other activities. Rebleeds after the hospital period have not been documented thus far and the quality of life in the long term is excellent.

A perimesencephalic pattern of hemorrhage may occasionally (in 2.5–5% of cases) be caused by rupture of a posterior fossa aneurysm. The chance of finding an aneurysm is about 5%. In recent years, CTA has been studied as a method to confirm or exclude the presence of an aneurysm in patients with a perimesencephalic pattern of hemorrhage on CT.

Rare causes of SAH (5%):

Trauma:

Trauma may confuse the issue, especially with no external wounds to indicate an accident, with a decreased level of consciousness or with retrograde amnesia, making it impossible to obtain a history. CT may reveal associated contusions, fractures, and unusual locations of subarachnoid blood.

In patients with previous head injury, and particularly with a skull fracture, a dural arteriovenous malformation (AVM) should be suspected, since healing of the fracture may be accompanied by the development of such a malformation.

Pituitary apoplexy:

The initial features are a sudden and severe headache, with or without nausea, vomiting, neck stiffness or a depressed level of consciousness. A combination of visual and oculomotor deficits should raise the suspicion of a pituitary apoplexy. Usually, the underlying adenoma has insidiously manifested itself before the dramatic occurrence of the hemorrhage by a dull retro-orbital pain, fatigue, a gradual decrease of visual acuity or a constriction of the temporal fields.

The precipitating event of arterial hemorrhage occurring in a pituitary tumor is thought to be tissue necrosis, involving one of the hypophyseal arteries. Several contributing factors may precipitate hemorrhagic infarction of a pituitary tumor, such as pregnancy, raised intracranial pressure, anticoagulant treatment, cerebral angiography or the administration of gonadotrophin-releasing hormone.

Intracranial AVMs:

Subarachnoid bleeding at the convexity of the brain may occur from superficial cerebral AVMs, but only in <5% of all ruptured AVMs is the extravasation only in the subarachnoid space, without intracerebral hematoma. Saccular aneurysms form on feeding arteries of 10–20% of AVMs, presumably because of the greatly increased flow and the attendant strain on the arterial wall. If bleeding occurs in these cases, it is more often from the aneurysm than from the malformation. In those cases the site of the aneurysms is different from the classical sites of saccular aneurysms on the circle of Willis and again the hemorrhage is more often into the brain itself than into the subarachnoid space.

The risk of hemorrhage from dural AVMs depends on the pattern of venous drainage. Patients with direct cortical venous drainage have a relatively high risk, which is further increased if a venous ectasia is present. Patients with drainage into a main sinus have a low risk of hemorrhage and if no reflux occurs into the smaller sinuses or cortical veins, it is negligible. After a first rupture, rebleeding may occur.

Arterial dissection:

Dissection, in general, tends to be recognized more often in the carotid than in the vertebral artery, but SAH from a dissected artery occurs mostly in the vertebral artery.

Neurological deficits that may accompany SAH from vertebral artery dissection are palsies of the ninth and tenth cranial nerves, by subadventitial dissection, or Wallenberg's syndrome. Rebleeds occur in between 30 and 70% of cases. The interval can be as short as a few hours or as long as a few weeks. The second episode is fatal in approximately half of the patients.

Dissection of the intracranial portion of the internal carotid artery or one of its branches as a cause of SAH is much less common than with the vertebral artery. Reported cases have affected the terminal portion of the internal carotid artery, the middle cerebral artery.

Drug abuse:  

The source of SAH in drug abusers without an aneurysm is unknown, although vasculitis has been suggested. In patients with SAH related to the use of cocaine, 70% have an underlying aneurysm. CT may simulate SAH due to saccular aneurysm.

Coagulopathies:

Anticoagulant drugs are seldom the sole cause for SAH. Severe coagulopathy other than by anticoagulant drugs, e.g. congenital deficiency of factor VII, is also a rare cause of SAH. If aneurysmal hemorrhage occurs in a patient on anticoagulants, the outcome is relatively poor.

Thirty per cent of patients with sickle cell disease and SAH are children. CT scans in these children show blood in the superficial cortical sulci; angiograms show no aneurysm, but often show multiple distal branch occlusions and a leptomeningeal collateral circulation. The SAH is attributed to rupture of these collaterals. The outcome is poor. Most adult patients in whom sickle cell disease underlies SAH have a ruptured aneurysm at the base of the brain.

Superficial siderosis of the CNS:  

There is no sudden headache. The clinical syndrome is almost invariably characterized by sensorineural deafness (95%), furthermore by cerebellar ataxia (88%) and pyramidal signs (76%). Possible other features include dementia, bladder disturbance and anosmia. Men are more often affected than women (3:1). This condition is characterized by iron overload of the pial membranes, through chronic oozing of blood from any source in the subarachnoid space. Other causes of chronic bleeding include a CSF cavity lesion or cervical root lesion, a vascular tumor or any other vascular abnormality. 

The high iron content of the pial membranes causes a characteristic signal on MRI scanning.

Spinal causes:

10% of the spinal AVMs present with SAH. In >50% of these patients, the first hemorrhage occurs before the age of 20 years. There may be a sudden and excruciating pain in the lower part of the neck, or pain radiating from the neck to the shoulders or arms. In the absence of such symptoms, the true origin of the hemorrhage emerges only when spinal cord dysfunction develops, after a delay that may be as short as a few hours or as long as a few years.  A history of even quite minor neck trauma or of sudden, unusual head movements before the onset of headache may provide a clue to the diagnosis of vertebral artery dissection as a cause of SAH.

Rebleeds may occur, even repeatedly. If a spinal origin of the hemorrhage is suspected, MRI are the first line of investigation, because spinal angiography is impractical without localizing signs or symptoms. Saccular aneurysms of spinal arteries are extremely rare, with recorded incidents in 12 patients. As with AVMs of the spinal cord, the clinical features of spinal SAH may be accompanied by those of a transverse lesion of the cord, either partial or complete.

Investigations:

CT scan of the brain (plain) confirms the bleed and suggests the site and probable cause of bleed. 

It is the procedure of choice because of the characteristically hyperdense appearance of extravasated blood in the basal cisterns. The pattern of hemorrhage often suggests the location of any underlying aneurysm, although with variable degrees of certainty. A false-positive diagnosis of SAH on CT is possible in the presence of generalized brain edema, with or without brain death, which causes venous congestion in the subarachnoid space and in this way may mimic SAH.  CT studies, currently, are negative in 2% of patients with SAH.

CT angiography (CTA) is based on the technique of spiral CT. It can easily be obtained immediately along with routine non-contrast CT upon which the diagnosis is first made. It is minimally invasive because it does not require intra-arterial catheterization. Compared with MRA, it involves radiation and it requires injection of iodine-based contrast, but is much simpler to perform, especially in ill patients. In addition, maximum intensity projection (MIP) images derived from CTA can be rotated and studied on a computer screen at every conceivable angle, which is a great advantage over the limited views with conventional angiography.

MRI scan with FLAIR (fluid attenuated inversion recovery) techniques demonstrates SAH in the acute phase as reliably as CT, but MRI is impracticable because the facilities are less readily available than CT scanners, and restless patients cannot be studied unless anesthesia is given. After a few days (up to 40), however, MRI is increasingly superior to CT in detecting extravasated blood. This makes MRI a unique method for identifying the site of the hemorrhage in patients with a negative CT scan but a positive lumbar puncture, such as those who are not referred until 1 or 2 weeks after symptom onset.

MR angiography (MRA) is safe, but less suitable in the acute stage, because in the acute stage patients are often restless or need extensive monitoring. A recent review of studies suggest a sensitivity in the range of 69–100% for detecting at least one aneurysm per patient. For the detection of all aneurysms the sensitivity is 70–97%, with specificity in the range 75–100%. Despite its limitations, MRA is a feasible tool for detecting aneurysms in relatives of patients with SAH.

Transcranial Doppler (TCD) can be combined with echo imaging (duplex technique) and with colour coding (transcranial colour-coded duplex sonography). It  helps in dynamic assessment of the functional status of the circle of Wills and complement angiography. A recent modification of color Doppler called Color Doppler Energy or Power Doppler offers greater sensitivity to flowing blood than standard color flow imaging. The sensitivity of power Doppler increases further by using an ultrasonic contrast agent, but even then the sensitivity is only 55% with a corresponding 83% specificity. Another drawback of this technique is that 15% of patients have no adequate bone window, which prevents adequate insonation. Also, the technique is highly dependent on the skills of the operator.

Somato sensory evoked potential (SSEP) pre operatively, intra operatively and post operatively gives good indication of brain ischemia.

Lumbar puncture is an indispensable step in the exclusion of SAH in patients with a convincing history and negative brain imaging. At least 6 and preferably 12 hrs should have elapsed between the onset of headache and the spinal tap, for sufficient lysis and formation of bilirubin and oxyhemoglobin, the pigments that give the CSF a yellow tinge after centrifugation (xanthochromia). Xanthochromia is a critical feature in the distinction from a traumatic tap, and are invariably detectable until at least 2 weeks later. The `three tube test' (a decrease in red cells in consecutive tubes) is notoriously unreliable, and a false-positive diagnosis of SAH can be almost as invalidating as a missed one. Spinning down the blood-stained CSF should be done immediately; otherwise oxyhemoglobin will form in vitro. If the supernatant appears crystal-clear, the specimen should be stored in darkness until the absence of blood pigments is confirmed by. Although the sensitivity and specificity of spectrophotometry have not yet been confirmed in patients with suspected SAH and a negative CT scan, it is the best technique currently available.

There is no scientifically sound method to distinguish reliably between blood caused by a traumatic tap from blood that was already present. Even the smoothest puncture can end in a vein.

Cerebral  angiography is still the gold standard for detecting aneurysms; but this procedure can be time consuming and it is not an innocuous procedure with a complication rate (transient or permanent) of 1.8%. At any rate, the aneurysm may re-rupture during the procedure, as occurs in 1–2% of cases overall. The rupture rate in the 6 hrs period following angiography has been estimated at 5%, which is higher than the expected rate.

Given the risk of a later rebleed, it is in patients with an aneurysmal pattern of hemorrhage on CT that repeat angiography seems to be most clearly indicated. The combined yield of a second angiogram is about 17%. If a second angiogram again fails to demonstrate the suspected aneurysm, perhaps a third angiogram may be positive, after an interval of several months.

There is no doubt that catheter angiography is on its way out for the pre-treatment assessment of cerebral aneurysms, as the techniques of CTA and MRA are still improving and as neurosurgeons and interventional radiologists are growing familiar with them.

Management:

The initial management is medical.

The aim is to preserve residual brain function and prevent neurological and systemic complications.

Bed rest, adequate analgesics  and sedation and careful attention to fluid and electrolyte balance are mainstay in medical management. 40% of them may have respiratory abnormalities during initial bleed, and assisted ventilation for an hour or so helps.

Intracerebral hematomas (ICH) occur in up to 30% of patients with ruptured aneurysms. Immediate evacuation of the hematoma should be seriously considered with simultaneous clipping of the aneurysm if it can be identified, often with the aneurysm having been demonstrated only by MR angiography or CT angiography. An acute subdural hematoma, which is usually associated with recurrent aneurysmal rupture but can also occur with the initial hemorrhage, may be life threatening; immediate surgical evacuation may be required.

Rebleeding is one of the most devastating complication of initial hemorrhage with a maximum incidence between 5th - 9th day. The total risk of rebleeding without medical or surgical intervention in the 4 weeks after the first day can be estimated to be 35–40%. Between 4 weeks and 6 months after the hemorrhage, the risk of rebleeding gradually decreases from the initial level of 1–2% a day to a constant level of 3% a year. Female gender, advancing age, poor neurological grade, poor medical condition, moderate to severe (170 - 240 mm Hg) systolic hypertension are some of the predisposing factors.

In the first few hours after admission for the initial hemorrhage, up to 15% of patients have a sudden episode of clinical deterioration that suggests early rebleeding. At present it is virtually impossible to prevent this from happening, but surgical or endovascular intervention can prevent recurrent hemorrhages occurring later.

Use of Antifibrinolytic agents such as Epsilon Amino Caproic Acid is not widely accepted these days as studies show no change in final outcome. Although the risk of rebleeding was significantly reduced by antifibrinolytic therapy, but this was offset by a similar increase of the risk of secondary cerebral ischemia.

Vasospasm is another dreaded complication with an incidence of about 35%, and has been blamed for delayed cerebral ischemia. It develops between 4-14 days with a peak incidence between 6th-8th day and lasts for up to 2 weeks.

Neither the amount of subarachnoid blood nor the angiographically demonstrated arterial narrowing can predict the severity. The narrowing in distal branches can escape a transcranial doppler study.

It is manifested by decreased by level of consciousness and fever followed by focal symptoms and signs. The deficits may remain unchanged, resolve within a few days or progress to cause permanent disability or death. Satisfactory treatment is not available. 

Blood volume expansion and arterial hypertension is being recommended by some, not supported by any valid study. The HHH therapy involves, attention to patients fluid balance to keep hematocrit at around 35% and hemoglobin at 10 -12 mg/dl and maintenance of the systolic blood pressure at 150 -180 mmHg.

Calcium Entry blockers (Nimodipine), it is claimed, is effective in high doses. Lately, nimodipine 60mg orally every 4th hourly for 3 weeks is widely recommended. It is uncertain whether nimodipine acts through neuroprotection, through reducing the frequency of vasospasm, or both. Other calcium antogonists (Nicardipine and AT877) definitely reduce the frequency of vasospasm, but the effect on overall outcome remains unproved. Other strategies to combat the vasospasm, such as, use of calcitonin-gene-related peptide (a potent vasodilatator), and lysis of the intra-cisternal blood clot with intrathecally administered recombinant tissue plasminogen activator, are still under trial.

Prophylactic transluminal balloon angioplasty, and intra-arterial infusion of papaverine, following super-selective catheterization have been advocated by some.

Acute non communicating hydrocephalus is of grave prognostic significance and has an incidence of about 20% and often requires ventriculostomy. Gradual obtundation within 24 hrs of hemorrhage, sometimes accompanied by slow pupillary responses to light and downward deviation of the eyes, is fairly characteristic of acute hydrocephalus. The role of early drainage is not well established.

Chronic and sub acute hydrocephalus occurs in 15-20% may require surgical intervention in only 5 to 10 % of patients.

Management of Blood pressure is an issue in patients with stroke including SAH. Studies suggest that hypertension after SAH is a compensatory phenomenon, at least to some extent, and that it should not be interfered with. It is better to reserve antihypertensive drugs (other than those the patients were on already) for patients with extreme elevations of blood pressure as well as evidence of rapidly progressive end organ deterioration, diagnosed from either clinical signs, such as, left ventricular failure.

Fluid and electrolyte abnormalities are common and have been attributed to the hypothalamic disturbance. Most commonly there is hyponatremia which may be associated with inappropriate hypersecretion of ADH and in some due to the so called 'Cerebral salt wasting syndrome' which appears to be the commoner cause.  SIHADH requires fluid restriction and 'Cerebral salt wasting syndrome' requires fluid replacement. Diabetes insipidus may result from failure of ADH release and has a grave prognosis. Treatment may require vasopressin.

Neuroprotectors: Recently nimodipine and vitamin E are widely used as brain protectors.

N'-propylenedinicotinamide (nicaraven), and Tirilazad are claimed to have some neuroprotection. Use of aspirin and other antiplatelet agents have not shown to improve the outcome. Studies continue.

Other complications include cardiac abnormalities, respiratory problems, gastro intestinal hemorrhage associated with Cushings ulcers and they need close monitoring and treatment.

Surgical clipping:

The aim of surgery is to prevent rebleed and preserve residual brain function. Ideally it is clipping of the neck of aneurysms.

Many centers in Japan carry out surgery as an emergency procedure. But most prefer to do it when the patient's condition is stable. There is a swing towards early surgery lately. Ideally patients should be in Grade I condition i.e., with no headache and stable blood pressure. At times a hematoma may require evacuation, irrespective of the grade, and obviously clipping is carried out along with evacuation.

Various studies suggest that there is no difference in outcome between early (<3 days), and late clipping. The surgical clipping is avoided between day 7 and 10 after the initial hemorrhage. This disadvantageous period for performing the operation in the second week after SAH coincides with the peak time of cerebral ischaemia and of cerebral vasospasm.

Rarely surgeons fail to define the neck and are forced to wrap the aneurysm to promote thrombosis. Various materials such as gauge, acrylic are used. Such measures are becoming more and more uncommon in this microsurgical era.

Giant aneurysm (more than 2 cm) remains a problem. More often than not, clipping is impossible. Proximal or Hunterian ligation and trapping the aneurysm with proximal and distal occlusion of the parent vessel are obvious options. The results depend on adequate collateral circulation. It has been claimed that a EC - IC bypass to look after the distal circulation will make these procedures safe. Despite varying success rates, trapping procedures remain main stay of treatment of giant aneurysm. Development of interventional neuroradiology hopefully will solve this problem.

Occasionally we come across a surfacing AVM which has caused the SAH and they may be excised. The problem of rebleed is not such an emergency, as in an aneurysm.

Interventional radiology:

Endovascular procedures are increasingly employed these days. Comparisons between endovascular and surgical clipping is still being debated. In a recent small study, there is no difference in outcome at 3 months between the surgical group and the endovascular group.

Rerupture of aneurysms may occur even months after apparently successful coiling and the long-term rates of rebleeding after endovascular coiling still need to be established. A recent study showed rebleeding rates of 0.8% in the first year, 0.6% in the second year and 2.4% in the third year, with no rebleeding in subsequent years.

Surgical clipping is not always definitive either; in a retrospective review of post clipping angiograms, 8% of patients showed aneurysms with a residual lumen or aneurysms that were previously undetected.

SAH due to Unknown causes:

If angiography is negative, it is essential to take account of the pattern of hemorrhage on the initial CT scan. If this pattern is perimesencephalic, the diagnosis of nonaneurysmal hemorrhage is established and no repeated studies are needed given the absence of rebleeds and the invariably good outcome. Such patients need no longer be on an intensive or medium care unit and can be transferred to a regular ward. Patients with a perimesencephalic hemorrhage can usually be discharged home after a few days and should be reassured that no complications will ensue and that they can take up their lives without any restrictions.

Patients with an aneurysmal pattern of hemorrhage on CT, but a negative angiography, can still develop secondary ischemia and have a 10% risk of rebleeds. These patients should therefore remain on the intensive or medium care unit. The substantial risk of rebleeding in patients with an aneurysmal pattern of hemorrhage indicates that, at least in some patients, an aneurysm escapes radiological detection. Apart from technical reasons, such as insufficient use of oblique projections, this phenomenon may have several explanations. Narrowing of blood vessels by vasospasm has been invoked in some cases. Thrombosis of the neck of the aneurysm or of the entire sac is another possible reason. Obliteration of the aneurysm by pressure of an adjacent hematoma may also prevent visualization, particularly with aneurysms of the anterior communicating artery.

Conclusion:

Only half a century ago the exact diagnosis in cases of spontaneous subarachnoid hemorrhage was rarely established during the patient's life time. At present with persistent efforts the lesions responsible can be identified in the vast majority of cases. Reports indicated that 15% of the patients with subarachnoid hemorrhage don't live long enough to reach the hospital and about 43% of those hospitalized die within  one month after the event. 42% of such cases are due to rebleed.

Of patients who survive the hemorrhage, approximately one-third remain dependent. Recovery to an independent state does not necessarily mean that outcome is good. Various studies suggest that  all in all, only a small minority of all patients with SAH have a truly good outcome. The relatively young age at which SAH occurs and the poor outcome together explain why the loss of years of potential life before age 65 years from SAH is comparable to that of ischemic stroke.

No gains are to be made, however, by a passive approach in managing the patient with recent subarachnoid hemorrhage. The severity of this illness and its tendency to recur and produce death and disability justify an aggressive attempt by the neurosurgeon to establish a prompt and accurate diagnosis and treatment.