by blood products or adhesions or by a reduction of CSF absorption at the arachnoid granulations [114]. The former occurs as an acute complication; the latter tends to occur two weeks after or later and is more likely to be associated with shunt dependence. The clinical presentation of hydrocephalus in this setting is progressive deterioration in level of consciousness, accompanied by ventricular dilation on head CT scan. Ocular signs of elevated ICP (miosis, downward eye deviation, or restricted upgaze) occur in many but not all patients [115]. Spontaneous improvement occurs in approximately 30 percent of patients with acute hydrocephalus and impaired consciousness, usually within 24 hours [22,116]. In the remainder, acute hydrocephalus is associated with increased morbidity and mortality secondary to rebleeding and cerebral infarction [117]. https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 12/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate Factors associated with an increased risk for hydrocephalus include older age, intraventricular hemorrhage, posterior circulation aneurysms, treatment with antifibrinolytic agents, and a low Glasgow Coma Scale score on presentation [118,119]. The incidence had also been reported to be increased in patients with hyponatremia or a history of hypertension. Management of elevated ICP CSF diversion Immediate CSF diversion with an external ventricular drain (EVD) or lumbar drainage is indicated for patients who have a deteriorating level of consciousness and evidence of elevated ICP and/or hydrocephalus [117]. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Removal of CSF'.) EVD placement is always indicated if the hydrocephalus is deemed noncommunicating (ie, from obstruction of CSF flow, typically at the level of the aqueduct). EVD placement ( figure 1) can improve the clinical grade of patients presenting with SAH [3]. Lumbar drainage is an alternative for patients with communicating hydrocephalus but is contraindicated with obstructive hydrocephalus or intraparenchymal hematoma [2]. There is controversy regarding the preferred mode of CSF drainage through an EVD [120]. Some experts recommend a rapid weaning of the EVD after the aneurysm is secured, or within 48 hours of EVD placement, for patients who are neurologically stable [22,121]. Other experts prefer to avoid weaning the EVD during the first week or longer after the onset of SAH, a time when the risk of vasospasm reaches its peak. An intermittent CSF drainage with rapid EVD wean approach has been associated with fewer ventriculoperitoneal (VP) shunt placements, fewer complications, and shorter length of stay compared with a continuous CSF drainage with gradual EVD wean approach [122]. However, premature EVD wean resulting in increased ICP could exacerbate cerebral hypoperfusion, a particularly hazardous problem if the patient is also having vasospasm [123]. In one study, the number of failed clamping trials (ie, clamping the EVD catheter and stopping external drainage of CSF to determine if EVD removal can be tolerated) increased the likelihood that the patient would require a shunt [124]. Thus, more research is necessary to define the optimal strategy for CSF drainage and EVD wean in patients with aneurysmal SAH. EVD placement may be complicated by infection (eg, ventriculitis/meningitis), particularly when drainage is continued for more than three days [116,125], and bleeding (eg, hemorrhage along the catheter tract), with a risk of approximately 8 percent for each [126]. There are few high-quality data to guide optimal EVD placement and management to minimize these risks [121]. https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 13/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate Osmotic therapy and diuresis Patients without a ventriculostomy can be managed medically with osmotic therapy and diuresis. Hyperventilation is generally avoided because it may precipitate or exacerbate vasospasm. The use of hypertonic saline has been evaluated in patients with elevated ICP related to traumatic brain injury and appears to lower ICP and may improve cerebral perfusion. A small observational study in 16 patients with poor-grade SAH suggests that it may also be useful in this setting, but further study is required [127]. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Osmotic therapy and diuresis'.) Hemicraniectomy In some cases, decompressive craniectomy may be needed for ICP control in the setting of intracerebral hemorrhage and/or severe cerebral edema. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Decompressive craniectomy'.) Shunt-dependent hydrocephalus The need for long-term CSF diversion is assessed in the subacute period by attempts at weaning ventricular drainage hydrocephalus [1,22]. Some patients who had EVD removed in the hospital after passing a clamping trial may subsequently require placement of a ventricular shunt to treat delayed recurrence of symptomatic hydrocephalus that develops after hospital discharge [128,129]. In a systematic analysis including 23 studies and more than 22,000 patients with SAH, 22 percent developed shunt-dependent hydrocephalus [130]. Notable predictors of developing shunt dependency included acute hydrocephalus at presentation, poor clinical grade (elevated Hunt and Hess score) at admission, vasospasm, intraventricular bleeding, and female gender. Shunt rates were similar between patients undergoing surgical clipping and endovascular coiling [1,22,128,129,131,132]. Other studies have reported similar results [128,133,134]. Hyponatremia Hyponatremia develops in up to 30 percent of patients with SAH [1,3,135] and is probably mediated by hypothalamic injury [22]. The water retention that leads to hyponatremia following SAH may result from either the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) or from cerebral salt wasting. These are physiologically distinct: Patients with SIADH are euvolemic. In other settings, therapy of asymptomatic hyponatremia in SIADH usually consists of water restriction, but fluid restriction is not desirable in patients with SAH as it increases the risk of intravascular volume contraction and consequently vasospasm-related ischemic injury. Thus, hyponatremia in patients with SAH is treated with hypertonic saline. (See "Treatment of hyponatremia: Syndrome of https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 14/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat", section on 'Subarachnoid hemorrhage'.) Cerebral salt wasting is caused by excessive secretion of natriuretic peptides that diminish central sympathetic activity. It is characterized by volume depletion, which leads to the release of antidiuretic hormone (ADH). Cerebral salt wasting can be treated with fluid administration using infusions of isotonic saline if serum sodium is normal but may require infusions of hypertonic saline and fludrocortisone to counteract diuresis and natriuresis when these conditions impede maintenance of euvolemia. Restoration of euvolemia will suppress the release of ADH. (See "Cerebral salt wasting".) SIADH and cerebral salt wasting can be difficult to differentiate since the laboratory findings are similar in both, including hyponatremia (<134 mEq/L), low serum osmolality (<274 mosmol/kg), high urine sodium (>40 mEq/L), and high urine osmolality (>100 mosmol/kg) [22]. The major distinguishing feature is intravascular volume status; patients with SIADH are euvolemic or even hypervolemic, while patients with cerebral salt wasting are hypovolemic. A protocol for managing hyponatremia using 3 percent sodium chloride (NaCl) solutions in patients with SAH is presented in the table ( table 8). Seizures Acute seizures occur in 6 to 18 percent of patients with SAH [3]. Risk factors include thick subarachnoid clot, intracerebral hemorrhage, delayed infarction, and aneurysm in the middle cerebral artery. Seizures that occur prior to aneurysm treatment are often a sign of early rebleeding [22]. (See 'Neurologic morbidity' below.) Patients with acute seizures after SAH are treated with antiseizure medications to prevent recurrence. Agents with favorable side effect profile, such as levetiracetam, are typically used. It is advisable to avoid phenytoin because its use has been associated with worse cognitive outcomes in patients with aneurysmal SAH [21]. (See "Initial treatment of epilepsy in adults".) Antiseizure medications are usually continued for a few months in patients who have experienced an acute seizure following SAH, although there are no strict guidelines. While acute seizures are a risk factor for developing epilepsy, most patients do not require long-term antiseizure medications. (See 'Neurologic morbidity' below.) Generalized convulsive status epilepticus is unusual after SAH, occurring in 0.2 percent of patients in one study [136]. However, with increased use of continuous electroencephalography (EEG) monitoring, nonconvulsive status epilepticus and subclinical seizures have been recognized as a potential contributor to prolonged impairment of consciousness in patients after SAH. In one series, subclinical seizures were documented by continuous recording in 7 https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 15/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate percent of patients after SAH [137,138]. Even when documented, the clinical correlates of nonconvulsive seizures can be subtle and nonspecific and may be limited to changes in heart rate, blood pressure, and/or ICP [139]. The management of status epilepticus is discussed separately. (See "Convulsive status epilepticus in adults: Classification, clinical features, and diagnosis".) Nonconvulsive status epilepticus (NCSE) and subclinical seizures are increasingly recognized as a potential contributor to prolonged impairment of consciousness in patients after SAH. Diagnosis of NCSE and subclinical seizures requires a high index of suspicion as patients with NCSE are often those with poor neurologic grade and other neurologic complications of SAH, making it difficult to detect subclinical seizures; continuous EEG monitoring is often required. NCSE is associated with worse outcomes after SAH [139]. The diagnosis and management of NCSE is discussed separately. (See "Nonconvulsive status epilepticus: Classification, clinical features, and diagnosis".) Anemia Anemia is common after SAH, occurring in 18 percent of patients during their hospital stay in one report [140]. Most studies suggest that anemia is associated with worse outcomes, while higher hemoglobin levels are associated with fewer cerebral infarctions and improved outcomes [141-144]. A goal hemoglobin for transfusion has not been defined in patients with SAH [3]; some experts recommend a target above 8 to 10 g/dL [4] and one randomized trial found that a higher transfusion goal (11.5 g/dL versus 10 g/dL) appeared to be safe [145]. Yet, red blood cell transfusion has been independently associated with worse outcomes in observational studies of patients with SAH, particularly among patients without delayed cerebral ischemia [146,147]. Therefore, larger randomized trials are necessary to determine the optimal transfusion strategy in SAH [148]. Cardiopulmonary complications Pulmonary edema and cardiac arrhythmias complicate 23 and 35 percent of SAH cases respectively [149]. (See "Complications of stroke: An overview", section on 'Cardiac complications' and "Complications of stroke: An overview", section on 'Pulmonary complications'.) A number of cardiac changes occur after SAH, including electrocardiography (ECG) changes, structural changes on echocardiography, and acute troponin elevations. These appear to be more common and more severe in those with more severe SAH [150,151]. Occasionally, focus on these findings can result in misdiagnosis. ECG abnormalities The most frequent ECG abnormalities are ST segment depression, QT interval prolongation, deep symmetric T-wave inversions, and prominent U waves [152]. Life-threatening rhythm disturbances such as torsades de pointes have also been https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 16/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate described, as well as atrial fibrillation and flutter. ST-T wave abnormalities along with bradycardia and relative tachycardia were found in one large series to be independently associated with mortality [153]. Another study reported an association between QT prolongation and angiographic vasospasm [154]. The ECG changes are predominantly reflective of ischemic changes in the subendocardium of the left ventricle. The development of actual myocardial injury (in as many as 20 percent of patients) can be established by elevations of creatine kinase-MB (CK-MB) or serum troponin I (>0.1 mcg/L), which is a specific and more sensitive marker of myocardial necrosis [151,155]. Patients with elevated troponin I concentrations are more likely to have ECG abnormalities and clinical evidence of left ventricular dysfunction. Subendocardial ischemia is an independent predictor of poor outcome in patients with SAH and must be managed aggressively (although without the use of aspirin) [150]. (See "Troponin testing: Clinical use" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".) Left ventricular dysfunction Echocardiographic abnormalities may be found in approximately 21 percent of patients with acute SAH [156]. A wide spectrum of regional left ventricular wall motion abnormalities can occur with SAH; these are typically but not always reversible [151,157,158]. Heart failure and pulmonary edema can result [159]. Some patients develop a pattern of transient apical left ventricular dysfunction that mimics myocardial infarction (but in the absence of significant coronary artery disease), a condition known as takotsubo cardiomyopathy, or transient left ventricular apical ballooning syndrome [158,160]. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".) Troponin release Acute troponin elevation after SAH appears to be associated with increased risk of cardiopulmonary and cerebrovascular complications [150,161]. Elevated peak troponin levels have been associated with an increased risk of left ventricular dysfunction, pulmonary edema, and hypotension requiring pressors as well as with increased mortality and worse functional outcome [150]. (See "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome", section on 'Acute stroke'.) Other complications Hyperglycemia has been associated with a poor outcome after SAH in many studies [162- 166]. One study found that the use of an aggressive hyperglycemia management protocol appeared to improve glycemic control and neurologic outcomes; however, the use of a historical control group limits the validity of this study [167]. No blood glucose targets have https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 17/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate been specifically identified for intervention. The 2012 American Stroke Association guidelines suggest careful glucose management with strict avoidance of hypoglycemia [3]. Fever of infectious and noninfectious origin is a common complication of SAH, particularly in those with a higher neurologic grade, and is associated with a poor prognosis [168,169]. Body temperature should be monitored and infection should be ruled out or treated. We treat fever with antipyretics and cooling blankets. While high-quality evidence of benefit with this approach is lacking, one nonrandomized study found that the use of external cooling devices in patients with fever after SAH was associated with improved outcomes [170]. Hypothalamic-pituitary dysfunction is common after SAH, but the clinical implications and appropriate treatment is uncertain [171]. Routine administration of glucocorticoids is not recommended after SAH but may be considered in patients who are unresponsive to vasopressor therapy for vasospasm [4]. PROGNOSIS Outcome after treatment of aneurysmal SAH is affected by potential brain injury from the SAH and subsequent complications as well as by risks related to neurosurgery. (See "Treatment of cerebral aneurysms".) Mortality Early mortality SAH is associated with a high early mortality rate [172]. Population-based studies found that 18 to 24 percent of patients with SAH died suddenly prior to even being evaluated in a hospital [173,174]. Among patients who reach the hospital alive, much of the subsequent early mortality is caused by the common complications of aneurysmal SAH related to initial bleeding, rebleeding, vasospasm and delayed cerebral ischemia, hydrocephalus, increased intracranial pressure, seizures, and cardiac complications [175- 177]. While early mortality due to SAH remains high, it is decreasing over time [174,178-184]. Historical case-fatality rates for SAH reached 50 percent [185], but they have declined to approximately 30 percent from 1988 to 2010 [178]. In a Finnish study of patients hospitalized with SAH, the 30-day case-fatality rate declined an average of nearly 2 percent each year between 1998 and 2017 with an overall rate of 20 percent during the study period [174]. Improved diagnostic accuracy over time and therapeutic advances in https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 18/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate neurocritical care are plausible but unproven reasons for the reduction in mortality [22,184]. Long-term mortality Survivors of aneurysmal SAH have an increased mortality rate compared with the general population (standardized mortality ratio [SMR] 1.6) [186-190]. In a Swiss national registry of 1787 patients with SAH, the one-year mortality rate was 22 percent [191]. In the International Subarachnoid Aneurysm Trial (ISAT), the risk of death at five years was lower in the endovascular therapy group than in the surgical group [186]. In one cohort study, the excess mortality risk appeared to be attributed to cerebrovascular events [189]. The risk of nonfatal vascular events (eg, stroke, myocardial infarction) was also increased (relative risk [RR] 1.5) in survivors of aneurysmal SAH [188]. Neurologic morbidity Long-term complications of SAH include neurocognitive dysfunction, epilepsy, and other focal neurologic deficits. In one registry, more than 10 percent of patients with SAH remained moderately or severely disabled [191]. Several studies suggest that SAH survivors have high rates of memory and neurocognitive impairment [3,192-198]. The largest prospective evaluation of neuropsychological function evaluated 873 survivors of SAH [196]. At three months after aneurysmal clipping, global impairment was present in approximately 20 percent of all survivors and in 16 percent of those with excellent preoperative condition. Detailed neuropsychological testing of patients after surgically treated SAH has commonly shown cognitive deficits, even among patients making an otherwise good neurologic recovery [199]. The importance of these neuropsychological deficits to long-term morbidity is controversial, but they are often permanent [58,200]. The location of the aneurysm responsible for SAH does not appear to influence cognitive outcome [192], but the occurrence of vasospasm, delayed cerebral infarction, and other complications does [58,201]. Treatment modality does not compellingly influence outcome. In the ISAT, the proportions of survivors who reached independent status were similar in those treated with endovascular therapy versus surgical clipping [186]. However, among the group that was not otherwise disabled (modified Rankin Scale [mRS] >2), the proportion of those with cognitive impairment at 12 months was higher in those treated surgically than with endovascular coiling [193]. By contrast, in a follow-up study of the ISAT, health-related quality of life was higher after endovascular coiling compared with neurosurgical clipping, which contributed to the quality-adjusted life years gained over a 10-year period [202]. Depression, anxiety, and sleep disturbances are also common and contribute to decreased quality of life; these may be more amenable to treatment [195,197,203]. https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 19/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate The incidence of late epilepsy after SAH is unclear. In a retrospective report of 472 patients with aneurysmal SAH who had undergone surgical clipping of the aneurysm between 1994 and 2000 and were followed for at least 12 months, late epilepsy occurred in 23 (5 percent) [204]. Patients presenting with a poor grade had a higher incidence of epilepsy (9.6 and 12.5 percent of those grades 3 and 4, respectively), as did those with associated cerebral infarction or subdural hematoma. In the ISAT, 25 of 612 patients (4 percent) had a diagnosis of epilepsy at a 12-month assessment; the rate was lower in patients treated with endovascular coiling as compared with surgical clipping [193]. Patients who have had acute seizures after SAH are somewhat more likely to develop epilepsy than those who do not. The management of epilepsy is discussed separately. (See "Initial treatment of epilepsy in adults" and "Overview of the management of epilepsy in adults".) Anosmia may complicate SAH. Studies suggest that this is a more frequent complication in patients who undergo aneurysm clipping (one in three patients) than in those who undergo endovascular coiling (one in six patients) and that recovery is more likely in patients who also have endovascular therapy [205,206]. Intraventricular hemorrhage is a risk factor for this complication. Anosmia is a less frequent complication of nonaneurysmal perimesencephalic hemorrhage [207]. Aneurysm recurrence and late rebleeding Patients who survive aneurysmal SAH have a small but enduring risk of recurrent SAH, which can occur despite successful endovascular or surgical treatment of the ruptured aneurysm. Recurrent SAH may result from recurrence of the treated aneurysm, rupture of another pre-existing aneurysm in a patient with multiple aneurysms, and de novo aneurysm formation. The risk of these events and recommendations for monitoring and treatment are discussed separately. (See "Late recurrence of subarachnoid hemorrhage and intracranial aneurysms".) Predictive factors The most important predictive factors for acute prognosis after SAH include [19,26,57,78]: Level of consciousness and neurologic grade on admission Patient age (inverse correlation) Amount of blood on initial head computed tomography scan (inverse correlation) Other studies have noted that hypoxemia, hyperglycemia, renal insufficiency, fever, and anemia are also common after SAH and are associated with poor outcomes [149,162,208-210]. Correction of these physiologic derangements in patients with SAH is suggested [16], although no studies have confirmed the benefit of such treatments. Seizures at the onset of SAH appear https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 20/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate to be an independent risk factor for late seizures (epilepsy) and a predictor of poor outcome [139,211,212]. Screening of family members First-degree relatives of patients with SAH have a two- to fivefold increased risk of SAH compared with the general population [213,214]. It may be reasonable to screen some family members for the presence of cerebral aneurysm. The risk is much higher when there are two or more first-degree family members with ruptured aneurysms [214]. This issue is discussed in detail separately. (See "Screening for intracranial aneurysm".) SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topics (see "Patient education: Hemorrhagic stroke (The Basics)" and "Patient education: Subarachnoid hemorrhage (The Basics)") Beyond the Basics topics (see "Patient education: Stroke symptoms and diagnosis (Beyond the Basics)" and "Patient education: Hemorrhagic stroke treatment (Beyond the Basics)") SUMMARY AND RECOMMENDATIONS https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 21/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate Acute care Patients with aneurysmal subarachnoid hemorrhage (SAH) should be admitted to an intensive care setting for constant hemodynamic, cardiac, and neurologic monitoring. Additional initial measures to reduce the risk of neurologic and systemic complications include: Blood pressure should be titrated to a target systolic blood pressure (SBP) <160 mmHg or mean arterial pressure (MAP) <110 mmHg for most patients with SAH. (See 'Blood pressure control' above.) All antithrombotic agents should be discontinued and anticoagulation reversed until the aneurysm is repaired by surgery or coiling. (See 'Antithrombotic reversal' above.) The use of antiseizure medications for seizure prophylaxis after SAH is controversial. Antiseizure prophylaxis prior to aneurysm repair may be reasonable for some patients with poor neurologic grade, unsecured aneurysm, and associated intracerebral hemorrhage. (See 'Seizure prophylaxis' above.) Euvolemia should be maintained and monitored by documentation of fluid input and output to decrease the risk of ischemic complications. (See 'Euvolemia maintenance' above.) Nimodipine 60 mg every four hours is administered for 21 days to improve outcomes for patients aneurysmal SAH. (See 'Nimodipine' above.) Other general measures for all patients with acute aneurysmal SAH include includes bedrest, analgesia for pain control, and venous thromboembolism prophylaxis. Hypoxemia, hyperglycemia, and fever should be prevented and promptly treated. (See 'Acute care' above.) Treatment of aneurysm Aneurysm repair with surgical clipping or endovascular coiling is the only effective treatment to prevent rebleeding and should be performed as early as feasible, preferably within 24 hours, and immediately if rebleeding does occur. (See 'Aneurysm treatment' above and "Treatment of cerebral aneurysms".) Early complications Medical and neurologic complications are common after SAH. In addition to rebleeding, major concerns include vasospasm and delayed cerebral ischemia, elevated intracranial pressure (ICP) related to hydrocephalus or other causes, hyponatremia, and seizures. (See 'Early complications' above.) Vasospasm and delayed cerebral ischemia Following treatment of the aneurysms, neurologic deterioration due to vasospasm may be treated with hemodynamic https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 22/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate augmentation via induced hypertension, balloon angioplasty, and/or intra-arterial administration of vasodilators. (See 'Vasospasm and delayed cerebral ischemia' above.) Elevated intracranial pressure Immediate CSF diversion with an external ventricular drain (EVD) is indicated for patients who have a deteriorating level of consciousness and evidence of elevated ICP and/or hydrocephalus. Additional options for some patients include osmotic diuresis and hemicraniectomy. (See 'Elevated intracranial pressure' above.) Seizures Seizures should be treated promptly and antiseizure medications are usually discontinued in a few months following SAH unless seizures recur. If prophylactic antiseizure medications were administered acutely, therapy may be discontinued after the aneurysm is secured. (See 'Seizures' above and 'Seizure prophylaxis' above.) Hyponatremia Hyponatremia after SAH is usually due to syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and rarely due to cerebral salt wasting. A protocol for managing hyponatremia in this setting is presented in the table ( table 8). (See 'Hyponatremia' above.) Prognosis Mortality within the first 30 days after SAH approaches 30 percent and is attributed largely to the effects of initial and recurrent bleeding. Long-term complications of SAH include neurocognitive dysfunction, epilepsy, other focal neurologic deficits, and late rebleeding from aneurysm recurrence. (See 'Prognosis' above and "Late recurrence of subarachnoid hemorrhage and intracranial aneurysms".) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Suarez JI. Diagnosis and Management of Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2015; 21:1263. 2. Lawton MT, Vates GE. Subarachnoid Hemorrhage. N Engl J Med 2017; 377:257. 3. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke 2012; 43:1711. 4. Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference. Neurocrit Care 2011; 15:211. https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 23/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate 5. Cross DT 3rd, Tirschwell DL, Clark MA, et al. Mortality rates after subarachnoid hemorrhage: variations according to hospital case volume in 18 states. J Neurosurg 2003; 99:810. 6. Bardach NS, Zhao S, Gress DR, et al. Association between subarachnoid hemorrhage outcomes and number of cases treated at California hospitals. Stroke 2002; 33:1851. 7. Varelas PN, Schultz L, Conti M, et al. The impact of a neuro-intensivist on patients with stroke admitted to a neurosciences intensive care unit. Neurocrit Care 2008; 9:293. 8. Josephson SA, Douglas VC, Lawton MT, et al. Improvement in intensive care unit outcomes in patients with subarachnoid hemorrhage after initiation of neurointensivist co- management. J Neurosurg 2010; 112:626. 9. McNeill L, English SW, Borg N, et al. Effects of institutional caseload of subarachnoid hemorrhage on mortality: a secondary analysis of administrative data. Stroke 2013; 44:647. 10. Schmidt JM, Ko SB, Helbok R, et al. Cerebral perfusion pressure thresholds for brain tissue hypoxia and metabolic crisis after poor-grade subarachnoid hemorrhage. Stroke 2011; 42:1351. 11. Wijdicks EF, Vermeulen M, Murray GD, et al. The effects of treating hypertension following aneurysmal subarachnoid hemorrhage. Clin Neurol Neurosurg 1990; 92:111. 12. van Gijn J. Subarachnoid haemorrhage. Lancet 1992; 339:653. 13. Frontera JA, Lewin JJ 3rd, Rabinstein AA, et al. Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage: A Statement for Healthcare Professionals from the Neurocritical Care Society and Society of Critical Care Medicine. Neurocrit Care 2016; 24:6. 14. Germans MR, Dronkers WJ, Baharoglu MI, et al. Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2022; 11:CD001245. 15. Post R, Germans MR, Tjerkstra MA, et al. Ultra-early tranexamic acid after subarachnoid haemorrhage (ULTRA): a randomised controlled trial. Lancet 2021; 397:112. 16. Suarez JI, Tarr RW, Selman WR. Aneurysmal subarachnoid hemorrhage. N Engl J Med 2006; 354:387. 17. Naval NS, Stevens RD, Mirski MA, Bhardwaj A. Controversies in the management of aneurysmal subarachnoid hemorrhage. Crit Care Med 2006; 34:511. 18. Marigold R, G nther A, Tiwari D, Kwan J. Antiepileptic drugs for the primary and secondary prevention of seizures after subarachnoid haemorrhage. Cochrane Database Syst Rev 2013; :CD008710. 19. Hijdra A, van Gijn J, Nagelkerke NJ, et al. Prediction of delayed cerebral ischemia, rebleeding, and outcome after aneurysmal subarachnoid hemorrhage. Stroke 1988; 19:1250. https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 24/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate 20. Ruptured cerebral aneurysms: Perioperative management. In: Concepts in Neurosurgery, R atcheson RA, Wirth FP (Eds), Williams & Wilkins, Baltimore 1994. Vol 6. 21. Naidech AM, Kreiter KT, Janjua N, et al. Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage. Stroke 2005; 36:583. 22. Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn) 2018; 24:1623. 23. Hoff R, Rinkel G, Verweij B, et al. Blood volume measurement to guide fluid therapy after aneurysmal subarachnoid hemorrhage: a prospective controlled study. Stroke 2009; 40:2575. 24. Hasan D, Vermeulen M, Wijdicks EF, et al. Effect of fluid intake and antihypertensive treatment on cerebral ischemia after subarachnoid hemorrhage. Stroke 1989; 20:1511. 25. Ciccone A, Celani MG, Chiaramonte R, et al. Continuous versus intermittent physiological monitoring for acute stroke. Cochrane Database Syst Rev 2013; :CD008444. 26. Steiner T, Juvela S, Unterberg A, et al. European Stroke Organization guidelines for the management of intracranial aneurysms and subarachnoid haemorrhage. Cerebrovasc Dis 2013; 35:93. 27. Sloan MA, Alexandrov AV, Tegeler CH, et al. Assessment: transcranial Doppler ultrasonography: report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2004; 62:1468. 28. Krejza J, Kochanowicz J, Mariak Z, et al. Middle cerebral artery spasm after subarachnoid hemorrhage: detection with transcranial color-coded duplex US. Radiology 2005; 236:621. 29. Staals JM, Edsen T, Romner B, Olsen NV. Transcranial Doppler velocimetry in aneurysmal subarachnoid haemorrhage: intra- and interobserver agreement and relation to angiographic vasospasm and mortality. Br J Anaesth 2013; 110:577. 30. van der Schaaf I, Wermer MJ, van der Graaf Y, et al. Prognostic value of cerebral perfusion- computed tomography in the acute stage after subarachnoid hemorrhage for the development of delayed cerebral ischemia. Stroke 2006; 37:409. 31. van der Schaaf I, Wermer MJ, van der Graaf Y, et al. CT after subarachnoid hemorrhage: relation of cerebral perfusion to delayed cerebral ischemia. Neurology 2006; 66:1533. 32. Pham M, Johnson A, Bartsch AJ, et al. CT perfusion predicts secondary cerebral infarction after aneurysmal subarachnoid hemorrhage. Neurology 2007; 69:762. 33. Etminan N, Beseoglu K, Heiroth HJ, et al. Early perfusion computerized tomography imaging as a radiographic surrogate for delayed cerebral ischemia and functional outcome after subarachnoid hemorrhage. Stroke 2013; 44:1260. https://www.uptodate.com/contents/aneurysmal-subarachnoid-hemorrhage-treatment-and-prognosis/print 25/49 7/7/23, 11:27 AM Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate 34. Vatter H, G resir E, Berkefeld J, et al. Perfusion-diffusion mismatch in MRI to indicate endovascular treatment of cerebral vasospasm after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2011; 82:876. 35. Francoeur CL, Mayer SA. Management of delayed cerebral ischemia after subarachnoid hemorrhage. Crit Care 2016; 20:277. 36. Hellingman CA, van den Bergh WM, Beijer IS, et al. Risk of rebleeding after treatment of acute hydrocephalus in patients with aneurysmal subarachnoid hemorrhage. Stroke 2007; 38:96. 37. Allen GS, Ahn HS, Preziosi TJ, et al. Cerebral arterial spasm a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983; 308:619. 38. Philippon J, Grob R, Dagreou F, et al. Prevention of vasospasm in subarachnoid haemorrhage. A controlled study with nimodipine. Acta Neurochir (Wien) 1986; 82:110. 39. Petruk KC, West M, Mohr G, et al. Nimodipine treatment in poor-grade aneurysm patients. Results of a multicenter double-blind placebo-controlled trial. J Neurosurg 1988; 68:505. 40. Pickard JD, Murray GD, Illingworth R, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 1989; 298:636. 41. Barker FG 2nd, Ogilvy CS. Efficacy of prophylactic nimodipine for delayed ischemic deficit after subarachnoid hemorrhage: a metaanalysis. J Neurosurg 1996; 84:405. 42. Feigin VL, Rinkel GJ, Algra A, et al. Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology 1998; 50:876. 43. Mee E, Dorrance D, Lowe D, Neil-Dwyer G. Controlled study of nimodipine in aneurysm patients treated early after subarachnoid hemorrhage. Neurosurgery 1988; 22:484. 44. Ohman J, Heiskanen O. Effect of nimodipine on the outcome of patients after aneurysmal subarachnoid hemorrhage and surgery. J Neurosurg 1988; 69:683. 45. Harders A, Kakarieka A, Braakman R. Traumatic subarachnoid hemorrhage and its treatment with nimodipine. German tSAH Study Group. J Neurosurg 1996; 85:82. 46. Dayyani M, Sadeghirad B, Grotta JC, et al. Prophylactic Therapies for Morbidity and Mortality After Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Network Meta- Analysis of Randomized Trials. Stroke 2022; 53:1993. 47. Dorhout Mees SM, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2007; :CD000277. 48. Helbok R, Kurtz P, Vibbert M, et al. Early neurological deterioration after subarachnoid