Aneurysmal Subarachnoid Hemorrhage

1. Introduction

Subarachnoid hemorrhage (SAH) is a devastating disease and is associated with high mortality and poor outcomes among survivors, management by multidisciplinary team is associated with improved outcomes; however, intensive care management presents big challenge. Most of spontaneous SAH is due to the rupture of saccular aneurysm, the prevalence of intracranial saccular aneurysm by radiographic and autopsy series is 5%, about 20–30% of patients have several aneurysms [1].

Aneurysmal SAH (aSAH) occurs at a rate of 2–16 per 100,000 population, mostly occurring between 40 and 60 years of age; however, young children and elderly can be affected. The incidence of SAH is higher in women than men, which may be due to hormonal status. African Americans are at a higher risk of SAH than Caucasian Americans. Mortality rate is about 60% within first 6 months [2, 3].

2. Circle of Willis

The circle of Willis is an anastomotic structure. It is formed when the internal carotid artery enters the cranial cavity bilaterally and divides into the anterior cerebral artery and middle cerebral artery, and the anterior cerebral arteries are then united by an anterior communicating artery. These anastomoses form the anterior half of the circle (anterior circulation). Posteriorly, the basilar artery branches to give left and right posterior cerebral artery (posterior circulation). Posterior cerebral arteries join the internal carotid system anteriorly to complete the circle via posterior communicating arteries. Figure 1 shows the common sites of cerebral aneurysm [4, 5].

3. Etiology

Subarachnoid hemorrhage is defined as bleeding into the space between the arachnoid and pia mater of the meninges enclosing the brain (subarachnoid space). The most common reason for spontaneous (non‐traumatic) SAH is the rupture of a cerebral aneurysm (85%) [5].

In about 15% of non‐traumatic SAH, no bleeding cause is identified by digital subtraction angiography (DSA). In these scenarios, differentiation between perimesencephalic and non‐perimesencephalic location of the SAH is very important to determine further therapeutic approach [3].

Perimesencephalic SAH (PMSAH) is defined by the absence of an aneurysmatic bleeding and the classic presence of blood within the perimesencephalic and prepontine cisterns [3].

Computed topography angiogram (CTA) and magnetic resonance angiography (MRA) have high sensitivity of excluding aneurysmal bleedings in PMSAH.

PMSAH has less complication and better prognosis than aneurysmal SAH.

Non‐perimesencephalic is SAH without bleeding source in the baseline DSA, the chance of positive findings in a follow‐up angiography fluctuated between 5 and 35%, that is why DSA should be repeated not before 3 weeks after the initial bleeding if there are no other therapeutic indications [3].

Non‐traumatic SAH can be caused by various other non‐aneurysmatic causes (Table 1), and the management of these cases must be performed according to the underlying cause [3].

4. Risk factors

Most spontaneous SAHs result from the rupture of intracranial aneurysms; therefore, risk factors for aneurysm formation overlap with risk factors for SAH.

1. Cigarette smoking: It is associated with 11‐fold increased risk of SAH. Worldwide, it is the most important preventable risk factor, which has been proved in numerous cohort (relative risk, RR, of current smoking, 2.2) and case‐control studies (odds ratio, OR, 3.1); cigarette smoking also hastened aneurysm growth rate [2, 3].

2. Hypertension: It is a major risk factor for SAH and possibly for aneurysm formation and fatal aneurysm rupture. Treatment of hypertension may reduce the risk of aneurysmal SAH [6].

3. Alcohol abuse: Excessive alcohol abuse raises the possibility for SAH independent of cigarette smoking, age, and history of hypertension [3].

4. Genetic risk: The risk of SAH increases seven folds in first‐degree relatives of patient; in addition, number of rare inherited conditions (Autosomal dominant polycystic kidney, Ehler‐Danlos syndrome) are associated with cerebral aneurysm and SAH [2, 6].

5. Use of sympathomimetic drugs such as (cocaine) [6].

6. Female sex: This is believed to be due to estrogen deficiency (estrogen replacement therapy reduces the risk), so it is higher in postmenopausal women than premenopausal ones [3, 6].

7. Antithrombotic therapy: It increases the severity of the hemorrhage, there are no data to prove whether antithrombotic therapy increases the risk of aneurysmal rupture or not [3, 6].

8. Inflammation seems to play a vital role in the pathogenesis and growth of intracranial aneurysms. Prominent mediators include the nuclear factor k - light-chain enhancer of activated B cells (NF‐κB), tumor necrosis factor, macrophages, and reactive oxygen species. Although there are no controlled studies in humans, 3‐hydroxy‐3‐methylglutaryl coenzyme A reductase inhibitors (statins) and calcium channel blockers could impede aneurysm formation by the inhibition of NF‐κB and other pathways [6, 7].

9. Aneurysm size of 7 mm increases risk of rupture and subsequent SAH [6].

10. Aneurysm morphology such as bottleneck shape and the ratio of size of aneurysm to parent vessels are associated with rupture of aneurysm [6].

11. The risk of SAH increases in symptomatic patient with large unruptured cerebral aneurysm especially if it is located either on posterior communicating artery or on the vertebrobasilar system [6].

5. Pathophysiology

Smoking, chronic hypertension, and alcohol abuse lead to weakened arterial tunica media. Chronic exposure to intravascular shear stress leads to pouching of the weakened wall, especially in the vicinity of bifurcations where turbulent flow is prominent.

The aneurysmal rupture is directly proportional to the size of the aneurysm, which is rising from 0.05% in aneurysms less than 10 mm to 6% for those greater than 25 mm.

More than 80% of cerebral aneurysm arises from the anterior carotid circulation (anterior and posterior communicating and middle cerebral arteries), with only 10–20% arising from the posterior vertebrobasilar circulation [1, 2].

Subsequent to aneurysmal rupture, blood spreads quickly within cerebrospinal fluid (CSF), rapidly increasing intracranial pressure (ICP), this sudden increase in the ICP leads to severe headache, cerebral edema, and hydrocephalus. Bleeding usually lasts for a few seconds; however, re‐bleeding is common and occurs within the first 24 h. The presence of blood and breakdown products of hemoglobin in the subarachnoid space is responsible for meningeal irritation, meningism, and vasospasm [2].

6. Clinical manifestation

Headache is the hallmark of aSAH in awake patient who describes it “as worst headache in their life,” this headache has a sudden onset and immediately reaches maximal intensity (thunderclap headache). Sentinel headache is also reported by 10–43% of patients, which is minor headache, and it is symptoms of minor hemorrhage (sentinel bleed or warning leak). Most of these minor hemorrhages occur within 2–8 weeks before major hemorrhage [6, 8].

The headache may be associated with nausea and/or vomiting, stiff neck, photophobia, brief loss of consciousness, or focal neurological deficits (including cranial nerve palsies).

Seizures occur in about 26% of patients within the first 24 h of SAH, most of the time before medical care is accessed. It is common in presence of intracerebral hemorrhage, in hypertensive patients, and patient with middle cerebral or anterior communicating artery aneurysms [6].

7. Diagnosis

8. Grading of SAH

Hard work has been made for the development of scales to clinically grade patients with SAH, to assess the severity of initial injury, to guide treatment decision, to provide prognostic information regarding outcome, and to standardize patient evaluation for scientific study purposes. Since 1933, more than 40 grading systems have been proposed for patients with cerebral aneurysm. Currently, the most commonly used SAH grading scales are the Hunt and Hess scale, Fisher scale, Glasgow Coma Scale (GCS), and the World Federation of Neurological Surgeons (WFNS) scale [10].

8.4. Fisher scale

In 1980, the Fisher scale was projected to predict cerebral vasospasm after SAH (Figure 2), the scale quantifies the amount of blood seen on CT scan (Table 5). It was developed when imaging technology had roughly one‐tenth of the resolution currently available. Subarachnoid clot less than 1 mm in true thickness is uncommon, as is the finding of no blood on admission CT scan, therefore, grades 1 and 2 were actually be quite uncommon [3, 10].

Group	Blood on CT scan
I	No subarachnoid detected.
II	Diffuse or thin vertical layer <1 mm thick.
III	Localized subarachnoid clot and/or vertical layer >1 mm thick.
IV	Intraventricular or intra-parenchymal clot with diffuse or no SAH.

Table 5.

Fisher grade scale.

9. Complications associated with SAH

Complications of subarachnoid hemorrhage can be divided into CNS and systemic compli cations.

9.2. Systemic complications associated with SAH

The high morbidity and mortality associated with SAH is not only due to neurological complications, non‐neurological complications also play a major role in increasing mortality and morbidity rates [16].

9.2.1. Cardiac complications

Cardiac complications occur in about 50% of patients with SAH; it ranges from mild elevation in cardiac enzymes and electrocardiogram (ECG) changes to obvious clinical and echocardiographic pathology. Cardiac damage markers are associated with an increased mortality and poor outcome and DCI [16].

9.2.1.1. Pathophysiology

9.2.1.1.1. Mild myocardial injury

This is presented by mild elevation in serum cardiac troponin I (not reaching diagnostic threshold of MI). This elevation occurs in 20–68% of patients with SAH. The degree of neurological injury, as graded by the Hunt‐Hess scale, is an independent predictor of myocardial injury in SAH patients. Serum troponin is a powerful predictor for cardiac and pulmonary complications, such as hypotension requiring vasopressor, left ventricular (LV) dysfunction, pulmonary edema, and DCI, especially in patient presenting with a high grade on WFNS.

Serum troponin is a more specific and sensitive indicator of myocardial injury than creatinine kinase‐MB; therefore, serum troponin levels and trends must be monitored through serial measurements particularly in SAH patients with past history of cardiovascular disease [16].

9.2.1.1.2. Cardiomyopathy

Neurogenic stunned myocardium (NSM) is the most severe form of myocardial injury in SAH, it occurs in 20–30% of patients with SAH. The elevated level of sympathetic tone leads to calcium overload with reduced sensitization of contractile filaments to this cation, eventually causing myocardial depression. It is characterized by subendocardial contraction band necrosis.

Echocardiography shows abnormal LV contractility and abnormal wall motion, which are reversible but sometimes leads to cardiogenic shock [16].

CK‐MB levels, female gender, and poor neurological grade are predictors of LV dysfunction.

Severe LV dysfunction decreases cardiac output (CO) and mean arterial pressure leading to reduction in cerebral blood flow (CBF). Furthermore, LV dysfunction may be associated with cerebral vasospasm and significant decrease in cerebral perfusion pressure therefore, optimal heart function is critical to prevent progression of neurological dysfunction and to promote recovery in patients with SAH [2, 6, 16–18].

The use of inotropes such as dobutamine or milrinone may be required to optimize cardiac output (CO). In severe LV dysfunction, implementation of intra‐aortic balloon pump may be required [2, 6, 16, 18].

9.2.1.1.3. ECG findings

It is common in SAH patients, particularly in the first 3 days of presentation, nearly 50–100% of SAH patients will show different forms of ECG changes such as ST segments changes, T wave changes, QTc prolongation, and Prominent U wave (Table 6) [16, 17].

ECG abnormality	Reported incidence (%)
ST‐segment changes	15–51
Inverted or isoelectric T waves	12–92
QTc prolongation	11–66
Prominent U waves	4–47
Sinus bradycardia	16
Sinus tachycardia	8.5

Table 6.

ECG changes after subarachnoid hemorrhage [17].

Around 4–8% of SAH patients will have malignant arrhythmias such as ventricular tachycardia (VT), torsade de pointe, and asystole [16, 18].

Management of arrhythmias in SAH patients depends upon the type of arrhythmia and classification, clinical significance, and the patient's condition. As a first step, it is vital to assure satisfactory oxygenation and correct electrolyte abnormalities and metabolic disturbance.

The use of beta‐blockers to treat cardiac tachyarrhythmia in SAH should be balanced against hypotension and decrease in cerebral blood flow (CBF). A new study concluded that the presence of arrhythmias is associated with poor outcome; in spite of this, no correlation was found between severity of cardiac arrhythmia and the site or the extent of intracranial hemorrhage on CT scan, neurological condition, or the location of ruptured malformation [6, 16, 18].

9.2.2. Electrolyte disturbance

The SAH is associated with different forms of electrolyte disturbances, such as hyponatremia, hypokalemia, hypocalcaemia, and hypomagnesaemia [6].

9.2.2.1. Hyponatremia

Hyponatremia is the most common clinically significant electrolyte derangement associated with SAH. It has an incidence ranging from 35 to 56 %, its diagnostic and therapeutic dilemma needs to be sorted to improve outcome of SAH patient [2, 16, 19].

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of hyponatremia; other causes are acute cortisol insufficiency, cerebral salt wasting syndrome (CSW), extreme fluid therapy, and/or diuretic therapy.

Kao et al. stated that 34.5% of severe hyponatremia were secondary to SIADH, whereas 23% were considered to be due to CSW. Noteworthy, the patients recruited in this study had more severe SAH than in the comparative studies, and the inclusion criterion was a plasma Na <130 mEq/L [19].

Irrespective of the cause, hyponatremia in SAH patients increases hospital stay, risk of vasospasm, and mortality rate.

The incidence of hyponatremia is associated with the location of aneurysmal rupture. Hyponatremia mostly occurs after rupture of anterior communicating artery (AComA). It was seen in 52.4% of patients with AComA; it may be because the hypothalamus is supplied by branch from AComA [19].

9.2.2.2. Causes of hyponatremia

SIADH is considered the most common cause of severe hyponatremia in SAH; it is secondary to excessive secretion of antidiuretic hormone as a result of stimulation of hypothalamus with traumatic or ischemic factor, causing increased water reabsorption in the distal convoluted tubule of the kidney, resulting in dilatational hyponatremia and fluid retention [19].

In CSW, the increase in urinary sodium excretion and urine output are due to abnormal release of atrial and brain natriuretic hormones, causing reduction in circulating blood volume, as well as extracellular fluid. Cerebral salt wasting syndrome can be treated with hypertonic saline solution which increases cerebral blood flow, brain tissue oxygen, and PH in patient with SAH [19].

Clinically, it is very difficult to differentiate between SIADH and CSW syndrome, due to significant overlapping clinical findings between both syndromes: both syndromes are associated with brain lesions; have normal thyroid, adrenal, and kidney functions are hyponatremic and hypouricemic and have concentrated urines, high urinary sodium over 40 mEq/L, and high fractional excretion (FE) of urate. The only clinical difference is the state of their extracellular volume (ECV): being hypervolemic or euvolemic in SIADH and hypovolemic in CSW (Table 7) [20].

	SIADH	CSW
Plasma volume	↑ or ↔	↓↓
Water balance	↑ or ↔	Negative
Signs and symptoms of dehydration	Absent	Present
Central venous pressure	↑ or ↔	↓↓
Salt balance	Variable	Negative
Hematocrit	↔	↑ or ↔
Serum osmolality	↓↓	↓↓
Urine sodium	↑	↑↑
Urine volume	↓or ↔	↑↑
Plasma BUN/creatinine	↓↓	↑ or ↔
Treatment	Fluid restriction, hypertonic saline, furosemide, demeclocycline	Normal saline, hypertonic saline, fludrocortisone

Table 7.

Difference between SIADH and CSW [21].

ECV assessment by usual clinical criteria is very difficult, not accurate to any degree [20].

Determination fractional excretion (FE) of urate is very helpful to differentiate between these syndromes, FEurate, normal 4–11%, has been constantly increased to >11% in both syndromes and has a distinctive relationship to serum sodium in both syndromes. In SIADH, correction of hyponatremia will normalize FEurate to 4–11% but in CSW syndrome FEurate consistently > 11% event after correction of hyponatremia (Figure 3).

This algorithm is useful only with normal glomerular filtration rate GFR, because FEurate can exceed normal values in patients with reduced glomerular filtration rate (GFR) [20].

Cortisol deficiency is one of the important causes of hyponatremia, which has not been well investigated in SAH patients because routine examination of adrenocorticotropic hormone (ACTH)/cortisol dynamic is not part of SAH work up [19].

Klose et al. and Parenti et al. investigated pituitary function post‐SAH and found that between 7.1 and 12% of patients are cortisol‐deficient at the time of presentation with SAH [20].

9.2.2.3. Treatment of hyponatremia

Patients with SAH should be closely monitored in an intensive care unit, preferably neurointensive care for at least 2–3 weeks post‐SAH, to allow for close monitoring of signs and symptoms of delayed cerebral ischemia (DCI), cerebral vasospasm, as well as fluid and electrolyte balance on daily basis, which can help treating doctors in early detection and efficient management of hyponatremia. A daily follow‐up of electrolyte is ideal and should be routine. If patients require intravenous hypertonic saline, sodium level should be checked every 4 h.

Urgent investigations of sodium level are mandatory if there are changes in mental status, massive fluctuation of fluid balance, and/or polyuria.

Rapid correction of hyponatremia can cause central myelinolysis and should be avoided, but insufficient correction of hyponatremia can result in brain edema, convulsion, and death [17, 20–22].

Fluid restriction to correct hyponatremia is associated with increased risk of cerebral vasospasm [19, 23].

Audibert et al. looked at the endocrinological response to severe SAH and found alterations in plasma level of numerous hormones such as aldosterone, renin, ADH, angiotensin, ANP, and BNP. However, these changes are noted during the first 12 days post‐SAH. It is not practical to correctly and promptly get hormone levels, because their profile fluctuates frequently.

The expertise recommended that assessing bedside sodium and fluid balance is the best valuable and economical technique for avoiding hyponatremia in patients with SAH [17].

Traditionally, patients with SAH are maintained on sodium chloride‐based fluids (i.e., 0.9% saline) for baseline and fluid replacement requirements, to avoid cerebral edema due to fluid shifts across a damaged blood‐brain barrier [19].

The recent guidelines of the Neurocritical Care Society for the management of patients with SAH suggested avoiding large amounts of free water intake and fluid restriction to treat hyponatremia [19].

In addition, the guidelines of the American Heart Association recommend that volume contraction be replaced with isotonic fluids (Class IIa, Level B evidence) and that large volumes of hypotonic fluids should be avoided in patients with SAH. The guidelines, however, did not make recommendations on the composition of baseline fluid administration in SAH patients [17].

Recently, Lehmann et al. suggested balanced crystalloids and colloid solutions (those with electrolyte compositions similar to plasma) in SAH patients, which do not cause frequent hyponatremia or hypo‐osmolality, also prevent electrolyte imbalance such as hyperchloremia, hyper osmolality, and extreme positive fluid balances associated with saline‐based intravenous fluids [19, 24].

Fluid restriction to less than 500 mL/day is the treatment of choice in SIADH, although such approach may not be feasible in SAH, because fluid restriction can cause cerebral vasospasm and subsequently cerebral infarction. What's more, most of these patients are not fully conscious and require enteral feeding which results in a daily fluid intake of 1–2 L [19, 25].

Therapeutic options for water restriction include hypertonic saline solutions and albumin [19]. Hypertonic saline (2–3% solution) not only increases plasma sodium concentration efficiently and rapidly but also increases the risk of pulmonary edema and heart failure and neurological complications secondary to the increase in blood volume [19].

Fludrocortisone causes sodium retention, but it is associated with fluid overload and limited evidence of its effectiveness [19].

Vasopressin receptor antagonists such as conivaptan have been projected and trialed in small studies but have not become routine therapy, because harmful effect secondary to the rapid increase in plasma sodium (4–6 mEq/L) [19, 26].

Acute cortisol deficiency is typically corrected with administration of parenteral hydrocortisone, but the beneficial effect of hydrocortisone is still uncertain and further studies are required, because it is not clear whether corticosteroid therapy is effective in management of acute relative adrenal insufficiency after SAH

[19, 27].

Overall, the management of hyponatremia in SAH patients necessitates additional investigation of treatment options that avoid fluid restriction, and further studies will help standardize ideal care.

9.2.3. Fever

Fever is one of the common medical complications of SAH and occurs in 70% of SAH patients. Fever may be due hypothalamic effect of the hemorrhage; it is associated with the severity of the injury, amount of hemorrhage, and development of vasospasm. Effective fever management may improve functional outcome. Paracetamol is the treatment of choice for fever. Active cooling is very effective but adverse effects of shivering may offset its benefit [6, 17].

It is worth noting that the infectious cause such as pneumonia needs to be excluded [17].

9.2.4. Anemia

Anemia is very common and is associated with poor outcome, due to compromising brain oxygen delivery. Correction of anemia and high hemoglobin value improve outcome after SAH. Current guidance recommends to keep hemoglobin concentration between 8 and 10 g/dL [17].

9.2.5. Thrombocytopenia and deep venous thrombosis (DVT)

Heparin‐induced thrombocytopenia (HIT) is directly associated with the number of angiographic procedures have been performed. Patients with heparin‐induced thrombocytopenia type II seems to be at high risk of thrombotic complications, vasospasm, and poor outcome.

Currently, it is uncertain whether there is practical means of avoiding HIT (as it is essential in angiographic procedures); however, it is vital to know this complication to avoid further heparin exposure and to use non‐heparin substitute under the supervision of a hematologist.

DVT is relatively recurrent event after SAH, especially in immobilized patients [3, 6].

Table 8 and Figure 4 summarize the incidence rate of non‐neurological complications.

Complications	Incidence (%)
Fever	54
Anemia	36
Hyperglycemia	30
Hypertension	27
Hypernatremia	22
Pneumonia	20
Hypotension	18
Pulmonary edema	14
Hyponatremia	14
Life‐threatening arrhythmia	8
Myocardial ischemia	6

Table 8.

Non‐neurological complications of subarachnoid hemorrhage [17].

10. Surgical and endovascular methods for treatment of ruptured cerebral aneurysms

Ruptured aneurysms can be cured by microsurgical clipping or endovascular coiling.

Microsurgical clipping requires craniotomy to prevent re‐bleeding of the aneurysm via insertion of a clip through its neck, thus isolating the aneurysm from circulation. This technique conveys a 98% certainty of elimination of the risk of rupture [29].

Endovascular coiling is the blocking of an aneurysm by an endovascular approach with electrically detachable platinum coils device which induces secondary thrombosis of the aneurysm [6]. The first published prospective randomized outcome study of surgical versus endovascular coiling, concluded that endovascular treatment results in clinical outcomes equal to that of surgical clipping.

Koivisto and co‐worker (2000) published first prospective randomized outcome study of surgical versus endovascular coiling, they concluded that endovascular treatment results in clinical outcomes equal to that of surgical clipping [30].

The International Subarachnoid Aneurysm Trial (ISAT) is the first multicenter prospective randomized trial comparing the two options; the included 2143 patients with ruptured intracranial aneurysms were randomly assigned to clipping (1070) or coiling (1073). Primary outcomes included death or dependent living, and secondary outcomes included risk of seizures and risk of re‐bleeding. Initially, 1‐year outcomes concluded a fall in death and disability from 31% in the clipping arm to 24% in the endovascular arm, this difference was mainly driven by a reduction in the rate of disability among survivors (16% in the endovascular arm and 22% in the clipping arm) [6, 29, 30].

The risk of epilepsy and significant cognitive decline was also reduced in the endovascular group, but the occurrence of late re‐bleeding was increased in endovascular group (2.9% after endovascular repair vs. 0.9% after open surgery) and only 58% of coiled aneurysms were completely obliterated compared with 81% of clipped aneurysms [6].

Although these results have affected the approach to patients with intracranial aneurysm in neurosurgical centers across the world, the study has been criticized due to the lack of generalizability, for example, posterior circulation aneurysms, which account for 8% of patients admitted with subarachnoid hemorrhage and up to 48% of ruptured aneurysms managed by endovascular coiling at some centers, made up only 2.7% of the ISAT study population [30].

Tahir et al. [29] concluded no significant difference in the clinical outcome of coiling and clipping of ruptured intracranial aneurysms; however, clipping is more cost effective than coiling.

Clipping is recommended for middle cerebral artery aneurysms (difficult to treat with endovascular technique) and patients presenting with an intraparenchymal hematoma >50 mL (high occurrence of critical outcome). Endovascular coiling is the preferred technique for patients presenting with vasospasm, elderly, poor clinical grade, and posterior cerebral aneurysms [6].

11. Time of surgical intervention

The most important strategy to reduce the risk of aneurysm rupture is early aneurysm repair, although evidence for best time of intervention is limited, it is uncertain whether ultra‐ early treatment (before 24 h) is better than aneurysm repair within 72 h (early). Recently published data analysis suggested that the surgical intervention can be done safely within 72 h after SAH. The American Heart Association/American Stroke Association recommend that “surgical clipping or endovascular coiling of the ruptured aneurysm should be performed as early as feasible in the majority of patients to reduce the rate of re‐bleeding after SAH” (Class 1B). This recommendation is supported by the European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage, which indicated that “aneurysm should be treated as early as logistically and technically possible to reduce the risk of re‐bleeding; if possible it should be aimed to intervene at least within 72 hours after onset of first symptoms.” There is ongoing study that only recruiting SAH with poor grade may help answer the question of whether intervention within 72 h (early intervention) is associated with better outcome compared with intervention within 4–7 days [12].

12. Prognosis and outcome

In spite of improvement in interventional and medical treatment of SAH, rupture of an aneurysm is still associated with significant high mortality rates (about 33%) and sever disability (17%). In last decades, mortality rates decreased by 17%, and the chance to recover to independent state has increased by 1.5% per year. Severity of initial bleeding plays a vital role in the determination of mortality rate and functional outcome [3].

Age is another important factor: mortality rate increased three times if the patient was older than 80 years. Aneurysm size, site, history of hypertension, high systolic pressure, history of alcohol consumption, cigarette smoking are all important factors associated with poor outcome regardless the severity of SAH [3].

Complications such as re‐bleeding, DCI, hydrocephalus, hyperglycemia, metabolic disturbances, cardiopulmonary complications, prolonged bed rest are associated with increased probability of poor outcome.

Small studies suggest that increased catecholamine levels in cerebrospinal fluid (CSF) are associated with early mortality or disability. Serum S100 is another marker of poor outcome after SAH [3].

13. Conclusion

Aneurysmal SAH is a devastating neurovascular disease associated with very high mortality and morbidity despite improvement in interventional and medical treatment due to multiple neurological and systemic complications, especially re‐bleeding and DCI secondary to vasospasm. Age, smoking, alcohol consumption, hypertension, site and size of aneurysm are important factors associated with poor outcome. SAH needs multidisciplinary specialized care, best provided in high‐volume centers to improve outcome.