Diagnosis and management of subarachnoid hemorrhage

Review Article Diagnosis and Management of Subarachnoid Hemorrhage Address correspondence to Dr Jose I Suarez, Baylor College of Medicine, One Baylor Plaza, NB:302, Houston, TX 77030, jisuarez@bcm.edu Relationship Disclosure: Dr Suarez reports no disclosure Unlabeled Use of Products/Investigational Use Disclosure: Dr Suarez reports no disclosure * 2015, American Academy of Neurology Jose I Suarez, MD, FNCS, FANA ABSTRACT Purpose of Review: The purpose of this article is to present the epidemiology, clinical presentation, and management of patients with subarachnoid hemorrhage (SAH) SAH is a neurologic emergency that carries high morbidity and mortality Patients with SAH are at risk for several significant neurologic complications, including hydrocephalus, cerebral edema, delayed cerebral ischemia, rebleeding, seizures, and neuroendocrine abnormalities that lead to impaired body regulation of sodium, water, and glucose Recent Findings: The incidence of SAH has remained stable, but mortality of hospitalized patients has significantly declined over the past decades Many common therapies for SAH have created controversy, and various recent neuroprotective clinical trials have produced negative results However, the publication of two consensus guidelines by the American Heart Association/American Stroke Association and the Neurocritical Care Society have provided a clarification for what should constitute best practice for patients with SAH The most important of those recommendations include the following: admission of patients to high-volume centers (defined as more than 35 patients with SAH per year) under the management of a specialized and multidisciplinary team; early identification and management of the bleeding source; evaluation and treatment decision for unsecured aneurysms by a multidisciplinary team made up of cerebrovascular neurosurgeons, endovascular practitioners, and neurointensivists; management of patients in the neurocritical care unit with oral nimodipine, blood pressure control, euvolemia, and frequent monitoring for neurologic and systemic complications; and delayed cerebral ischemia secondary to cerebral vasospasm should be treated with induced hypertension and endovascular therapies once confirmed Summary: SAH is a devastating neurologic disease Management of patients with SAH should adhere to currently available treatment guidelines Several aspects of SAH management remain controversial and need further studies to clarify their role in improving patient outcome Continuum (Minneap Minn) 2015;21(5):1263–1287 INTRODUCTION Nontraumatic subarachnoid hemorrhage (SAH) represents about 3% of all strokes in the United States.1 The worldwide incidence of SAH ranges from to 16 per 100,000 people and has not changed in the past decades.2 Most epidemiologic studies have shown Continuum (Minneap Minn) 2015;21(5):1263–1287 that women are more likely to have SAH compared to men (1.24:1.0) and that minority groups (particularly African American and Hispanic populations) are more frequently affected compared to white Americans.1,2 The incidence of SAH increases with age, with a typical mean age of onset of 50 years or www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1263 Subarachnoid Hemorrhage KEY POINTS h Subarachnoid hemorrhage is more frequent in women than men and more frequent in minority populations compared to white Americans h Case-fatality rates of hospitalized patients with subarachnoid hemorrhage have decreased with the advent of neurocritical care, endovascular therapy, and more refined microsurgical techniques h The most important points in the management of patients with subarachnoid hemorrhage are prompt evaluation and diagnosis, immediate transfer to appropriate centers, expeditious diagnosis and treatment of the bleeding source, and overall good neurocritical care adhering to available treatment guidelines 1264 older.2 In about 80% of SAH cases, a ruptured cerebral aneurysm is found However, neuroimaging techniques may show no source of bleeding in 15% of SAH cases or show other abnormalities (eg, arteriovenous malformation, vasculitis) in the remaining 5% of cases SAH causes significant morbidity and mortality Mortality rates vary widely among studies, ranging from 8% to 67% (median of 30% in the United States), with the caveat that most of these studies did not account fully for prehospital deaths, which have been estimated to be between 10% and 15%.3 However, there has been a significant decrease in case-fatality rates of SAH across the globe,3 which has been attributed to improved survival of hospitalized patients and is most likely owing to changes in management of patients with SAH, including neurocritical care, endovascular therapy, and more refined microsurgical techniques Nevertheless, it is important to emphasize that despite the decrease in case-fatality rates, about half of survivors experience significant chronic reductions in health-related quality of life.4,5 For example, a large proportion of survivors not return to their previous level of employment, social independence and interactions, or personal or family relationships even years after the event This reduction in health-related quality of life may be due to a combination of factors, including impaired physical functioning, cognitive deficits (particularly executive function and memory), mood and emotional symptoms (eg, anxiety, depression, and posttraumatic stress disorder), and personality changes Several risk factors for SAH have been identified (Table 1-1).2,6Y10 Whether any of these factors plays a predominant role in an individual patient remains unclear Genetic and environmental factors also can increase the risk of SAH, and some of these factors can interact For instance, the size at which cerebral aneurysms rupture may be smaller for those patients with concomitant hypertension and cigarette smoking than for those with either factor alone SAH remains one of the top neurologic emergencies, and neurologists must familiarize themselves with this devastating disease This review discusses the main features of diagnosis and management of SAH The main areas of emphasis when caring for patients with SAH should include the following: prompt evaluation and diagnosis,11 immediate transfer to appropriate centers,2,12 expeditious diagnosis and treatment of the bleeding source,13,14 and overall good neurocritical care adhering to available treatment guidelines.2,12 CLINICAL PRESENTATION SAH typically presents with sudden and severe headache (usually described as ‘‘the worst headache ever’’) accompanied by nausea, vomiting, photophobia, neck pain, and loss of consciousness (Case 1-1A).15 Physical examination should include determination of level of consciousness, funduscopic evaluation, determination of meningeal signs, and presence of focal neurologic deficits (Table 1-2) The latter are present in about 10% of patients with SAH and are associated with worse prognosis when due to the presence of thick subarachnoid clot or parenchymal hemorrhage Transient elevation in the intracranial pressure (ICP) causes nausea, vomiting, and syncope However, more sustained and severe increases in ICP can lead to coma and brain death Terson syndrome (vitreous hemorrhage associated with SAH) can present in up to 40% of patients with SAH.16,17 The sudden spike in ICP is thought to lead to preretinal hemorrhages, which are associated with more severe SAH and increased mortality Some patients with SAH can have a more atypical presentation.11,15 Occasionally, patients may present with seizures, www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 TABLE 1-1 Risk Factors for Subarachnoid Hemorrhage b Nonmodifiable Risk Factors Age Female sex Prior history of aneurysmal subarachnoid hemorrhage Family history of subarachnoid hemorrhage History of aneurysm in first-degree relatives (especially in two or more relatives) b Modifiable Risk Factors Hypertension Cigarette smoking Heavy alcohol use Sympathomimetic drug use (eg, cocaine) b Other Certain genetic disorders (eg, autosomal dominant polycystic kidney disease, type IV Ehlers-Danlos syndrome) Anterior circulation aneurysms are more likely to rupture in patients who are younger than 55 years of age Posterior circulation aneurysms are more likely to rupture in men Significant financial or legal problems within the past 30 days Cerebral aneurysms of more than mm in diameter Case 1-1A A 45-year-old right-handed woman presented to a primary stroke center with sudden onset of severe headache accompanied by nausea, vomiting, and syncope, which developed hour prior to presentation while she was moving furniture at her house She had a past history of heavy smoking and cocaine use Upon arrival to the emergency department, her blood pressure was 180/100 mm Hg, heart rate was 105 beats per minute, arterial oxygen saturation (SaO2) was 97% on room air, and her temperature was 36.5-C (97.7-F) Her examination revealed a Glasgow Coma Scale score of 15, normal cranial nerves, and no motor or sensory deficits Her World Federation of Neurological Surgeons Scale (WFNSS) score was and her modified Fisher Scale score was She reported neck pain throughout the interview She was treated with mg of IV morphine sulfate and 10 mg of IV labetalol without much response She was then started on a nicardipine drip to maintain a systolic blood pressure less than 160 mm Hg A noncontrast head CT showed a subarachnoid hemorrhage (SAH) with predominance in the anterior interhemispheric fissure (Figure 1-1A) The patient was immediately transferred by helicopter to a comprehensive stroke center for further care Digital subtraction angiography (DSA) revealed an irregular, multilobed, and wide-neck anterior communicating artery aneurysm (Figure 1-1B and 1-1C) After discussion among the neuroradiologist, the cerebrovascular neurosurgeon, and neurointensivists, the patient underwent surgical clipping of the unsecured aneurysm Following surgery, the patient was transferred to the neurocritical care unit, where she received oral nimodipine, pain control, IV levetiracetam (seizure prophylaxis for days), and fluids to maintain euvolemia Nicardipine was discontinued, and she maintained her systolic blood pressure between 140 and 160 mm Hg spontaneously Her neurologic examination remained unchanged and she was mobilized out of bed Continued on page 1266 Continuum (Minneap Minn) 2015;21(5):1263–1287 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1265 Subarachnoid Hemorrhage Continued from page 1265 Initial imaging studies of the patient in Case 1-1 A, Nonenhanced head CT shows diffuse subarachnoid hemorrhage with predominance in anterior interhemispheric fissure without cerebral edema or significant hydrocephalus B, A two-dimensional digital subtraction angiogram shows an anterior communicating artery aneurysm on a lateral view (arrow) C, A three-dimensional rotational digital subtraction angiogram reveals that the anterior communicating artery aneurysm is irregular and trilobed and has a wide neck (arrow) FIGURE 1-1 Comment This case delineates the initial management of a patient with SAH The key issues to consider include early identification, transfer to a high-volume center, admission to a specialized neurocritical care unit, identification and treatment of the bleeding source, and multidisciplinary discussion to undertake best treatment for an unsecured aneurysm In addition, this patient underwent blood pressure control prior to aneurysm treatment to prevent rebleeding, and received oral nimodipine, which has been shown to improve long-term outcomes in patients with SAH 1266 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 TABLE 1-2 Focal Physical Findings in Patients With Subarachnoid Hemorrhage Findings Likely Cause Third nerve palsy Usually posterior communicating aneurysm; also posterior cerebral artery and superior cerebellar artery aneurysms Sixth nerve palsy Elevated intracranial pressure (false localizing sign) Combination of hemiparesis and aphasia or visuospatial neglect Middle cerebral artery aneurysm, thick subarachnoid clots, or parenchymal hematomas Bilateral leg weakness and abulia Anterior communicating artery aneurysm Ophthalmoplegia Internal carotid artery aneurysm impinging upon the cavernous sinus Unilateral visual loss or bitemporal hemianopia Internal carotid artery aneurysm compressing optic nerve or optic chiasm Impaired level of consciousness and impaired upward gaze Pressure on the dorsal midbrain due to hydrocephalus Brainstem signs Brainstem compression by basilar artery aneurysm Neck stiffness Meningeal irritation by the presence of subarachnoid blood Retinal and subhyaloid hemorrhages Sudden increase of intracranial pressure Preretinal hemorrhages (Terson syndrome) Vitreous hemorrhage due to severe elevations of intracranial pressure acute encephalopathy, and concomitant subdural hematoma and head trauma, making the underlying diagnosis of SAH more elusive A minority of patients may have a warning ‘‘sentinel’’ headache days to weeks before an aneurysmal SAH, which is thought to represent a small aneurysmal leak.18,19 Regrettably, this piece of information is only obtained retrospectively as most of the time the headache is transient and head CT scanning is unrevealing in about 50% of cases DIAGNOSIS Head CT Scan The most appropriate initial diagnostic test for patients suspected of having SAH is a noncontrast head CT scan (Figure 1-2) (Case 1-1A).15 The sensitivity of a CT scan has been reported to be 98% to 100% for the detection of subarachnoid blood within 12 hours of symptom onset when compared to lumbar puncture However, the sensitivity of a CT scan decreases to 93% at Continuum (Minneap Minn) 2015;21(5):1263–1287 24 hours and 50% at days.20,21 The characteristic appearance of extravasated blood in the basal subarachnoid cisterns is hyperdense (Figure 1-1A) Other locations include the sylvian fissures; interhemispheric fissure; interpeduncular fossa; and suprasellar, ambient, and quadrigeminal cisterns CT also can detect intracerebral hemorrhage, intraventricular hemorrhage, and hydrocephalus Although MRI may be as sensitive as CT scan in the first days of SAH presentation, it is rarely performed in this scenario because of logistical issues.22,23 MRI with hemosiderin-sensitive sequences (gradient echo and susceptibility-weighted imaging) or with fluid-attenuated inversion recovery (FLAIR) sequences is more sensitive than CT scan when performed several days after the onset of SAH KEY POINTS h In some instances, diagnosis of subarachnoid hemorrhage can be elusive owing to atypical findings on presentation such as seizures at onset, acute encephalopathy, and concomitant subdural hematoma and head trauma h The sensitivity of CT for detection of subarachnoid blood may be 98% to 100% when obtained within 12 hours of onset of symptoms, compared to lumbar puncture Lumbar Puncture A lumbar puncture is recommended in any patient with suspected SAH and negative or equivocal results on head CT www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1267 Subarachnoid Hemorrhage FIGURE 1-2 Diagnostic algorithm for subarachnoid hemorrhage CT = computed tomography 15 Reprinted with permission from Suarez JI, et al, N Eng J Med NEJMra052732 KEY POINT h The diagnosis of subarachnoid hemorrhage is supported by the finding of xanthochromia in CSF 1268 B 2006 Massachusetts Medical Society www.nejm.org/doi/full/10.1056/ scan (Figure 1-2) CSF should be collected four consecutive tubes, and red blood cell count should be determined in tubes one and four.11,15 The diagnosis of SAH is supported by the following: elevated opening pressure, elevated red blood cell count that does not significantly decrease from tube one to tube four, and especially xanthochromia The latter, which indicates red blood cell breakdown, can be determined by visual inspection or by spectrophotometry Xanthochromia takes about 12 hours to develop after SAH, and spectropho- tometry seems to be more sensitive than visual inspection However, most hospitals in the United States use visual inspection, and no well-conducted clinical studies exist that allow clinicians to know with certainty what the falsenegative rate for xanthochromia is at various time intervals from SAH onset.24 Identification of Bleeding Source All patients with a diagnostic CT scan or with either equivocal or diagnostic lumbar puncture must undergo further imaging with CT angiography (CTA) or cerebral www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 digital subtraction angiography (DSA) (Figure 1-1).11,15 The latter has traditionally been considered the ‘‘gold standard’’ to elucidate the source of bleeding in SAH (particularly aneurysmal), but CTA has become widely available and is being commonly performed as firstline vascular imaging or even in lieu of DSA in some centers CTA has a sensitivity and specificity ranging from 90% to 97% and 93% to 100%, respectively, depending on technique (16-detector rows versus 64-detector rows, slice thickness, and data processing algorithms) and the reader’s experience.25,26 CTA may not be reliable for the detection of smaller (ie, less than mm) or distal aneurysms The decision to perform CTA or DSA will vary depending on resource availability and institutional practices However, loss of consciousness at the onset of SAH may be a strong predictor for the detection of ruptured cerebral aneurysm on subsequent DSA.27 Thus, in those patients with a negative CTA, this presentation should still prompt a DSA In the author’s institution, a combination of two-dimensional and threedimensional DSA are performed as the standard diagnostic testing for aneurysm detection in all SAH cases Patients with a negative DSA should have a repeat study to 14 days after initial presentation, and if negative, MRI should be performed to uncover a possible vascular malformation of the brain, brainstem, or spinal cord.15,23 Misdiagnosis Misdiagnosis of SAH is still common because the classic findings may occur inconsistently or patients may present with atypical findings Misdiagnosis is associated with significantly increased mortality and disability (up to fourfold) in those patients presenting without neurologic deficits at their initial hospital visit Fortunately, the frequency of SAH misdiagnosis has decreased from more than 60% in the early 1980s to less than Continuum (Minneap Minn) 2015;21(5):1263–1287 15% more recently.28,29 Nevertheless, it is important to emphasize that practitioners should have a high level of suspicion for any patient presenting with new-onset headache and understand the possible pitfalls in the diagnosis of SAH (Table 1-3) A recent study reported 100% sensitivity to detect SAH in patients older than 40 years of age using clinical decision-making rules that include any of the following factors: neck pain or stiffness, witnessed loss of consciousness, and symptom onset during exertion plus thunderclap headache and pain on neck flexion.30 Perimesencephalic Subarachnoid Hemorrhage As previously mentioned, in about 15% of patients with SAH, imaging studies fail to demonstrate the source of bleeding Approximately 38% of these patients have nonaneurysmal perimesencephalic SAH.31 Most patients with nonaneurysmal perimesencephalic SAH (about 54%) are male and have a low risk of complications and better outcomes than patients with aneurysmal SAH A correct diagnosis is important because of the catastrophic consequences of missing a ruptured cerebral aneurysm Nonaneurysmal perimesencephalic SAH is confirmed in the presence of a negative CTA or DSA in patients with the following head CT scan pattern32: center of hemorrhage located immediately anterior to the midbrain, with or without extension of blood to the anterior part of the ambient cistern or to the basal part of the sylvian fissures; no complete filling of the anterior interhemispheric fissure and no extension to the lateral sylvian fissures, except for minute amounts of blood; and absence of frank intraventricular blood (Figure 1-3) KEY POINTS h All patients with a diagnostic CT scan or with either equivocal or diagnostic lumbar puncture must undergo further imaging with CT angiography or digital subtraction angiography h Any of the following clinical factors should prompt a workup for subarachnoid hemorrhage in patients older than 40: neck pain or stiffness, witnessed loss of consciousness, and symptom onset during exertion plus thunderclap headache and pain on neck flexion INITIAL EVALUATION Initial evaluation and management of patients with SAH should focus on www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1269 Subarachnoid Hemorrhage a TABLE 1-3 Reasons for Misdiagnosis of Subarachnoid Hemorrhage b Failure to Recognize Spectrum of Presentation of Subarachnoid Hemorrhage Not obtaining complete history from patients with unusual (for the patient) headaches (Was the onset abrupt? Is the quality different and severity greater than prior headaches?) Failure to appreciate that the headache can improve spontaneously or with non-narcotic analgesics Focusing on the secondary head injury resulting from syncope and fall or motor vehicle collision Focusing on ECG findings Focusing on elevated blood pressure Overreliance on the classic presentation Assuming symptoms may be related to other disorders (eg, viral syndrome, viral meningitis, migraine, tension-type headache, sinus-related headache, psychiatric disorder) b Failure to Understand the Limitations of Head CT Scanning Sensitivity decreases with increasing time from onset of headache False-negative results with small-volume bleeds Lack of experience of physician reader Motion artifacts or lack of thin cuts of posterior fossa False-negative results due to hematocrit of less than 30% b Failure to Perform Lumbar Puncture or Interpret the CSF Findings Correctly Failure to perform lumbar puncture in patients with negative or inconclusive CT scans Failure to distinguish a traumatic tap from true subarachnoid hemorrhage Failure to recognize that xanthochromia may be absent very early (less than 12 hours) and very late (more than weeks) CSF = cerebrospinal fluid; CT = computed tomography; ECG = electrocardiogram a Data from Edlow JA, et al, J Emerg Med.11 www.jem-journal.com/article/S0736-4679(07)00729-9/abstract KEY POINT h Mean arterial blood pressure should be maintained at less than 110 mm Hg or systolic blood pressure at less than 160 mm Hg until the ruptured aneurysm is secured, while avoiding hypotension 1270 stabilization of airway, breathing, and circulation.2,12,15,22,23 Once patients are deemed stable, a head CT scan must be performed Patients who are unable to protect their airway should be intubated immediately The most common indications for endotracheal intubation include coma, hydrocephalus, seizure, and need for sedation for significant agitation In addition, extreme blood pressure values should be avoided Hypertension control is predicated on the premise that it may precipitate rebleeding.33 No data from randomized controlled clinical trials exist, but usual practice and current recommendations are to maintain a mean arterial blood pressure of less than 110 mm Hg or a systolic blood pressure of less than 160 mm Hg until the ruptured aneurysm is secured, while using premorbid baseline blood pressures to refine targets and avoid hypotension Commonly, pain control may be sufficient to achieve blood pressure control; otherwise, administration of IV labetalol (5 mg to 20 mg), hydralazine (5 mg to 20 mg), or continuous infusion of nicardipine (5 mg/h to 15 mg/h) is preferred Pain control is best achieved with the administration of short-acting opiates (Case 1-1A) Disease Severity Scoring The severity of neurologic impairment and the amount of subarachnoid www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 Noncontrast head CT scan of a patient with nonaneurysmal perimesencephalic subarachnoid hemorrhage The center of the hemorrhage is located immediately anterior to the midbrain (A and C, arrows) and extends to the anterior part of the ambient cistern (B, arrow) FIGURE 1-3 bleeding on admission are the strongest predictors of neurologic complications and outcome.15,23 Therefore, it is essential that patients with SAH be scored promptly after arrival and stabilization There are several scoring systems available However, the World Federation of Neurological Surgeons Scale (WFNSS) and the modified Fisher Scale are the most reliable and simple to perform (Table 1-415,34,35).23 Higher WFNSS and modified Fisher Scale scores are associated with worse clinical outcome and a higher proportion of neurologic complications KEY POINT h The severity of neurologic Admission to High-Volume Centers The next immediate steps are to transfer the patient to a high-volume center (if not impairment and the amount of subarachnoid bleeding on admission are the strongest predictors of neurologic complications and outcome a TABLE 1-4 Clinical and Radiologic Grading Scales for Subarachnoid Hemorrhage World Federation of Neurological Surgeons Scale34 Modified Fisher Scale35 Grade Glasgow Coma Scale Neurologic Examination Grade Subarachnoid Hemorrhage Intraventricular Hemorrhage 15 No motor deficit Absent Absent 13Y14 No motor deficit Minimal Absent in both lateral ventricles 13Y14 Motor deficit Minimal Present in both lateral ventricles 7Y12 With or without motor deficit Thickb Absent in both lateral ventricles 3Y6 With or without motor deficit Thickb Present in both lateral ventricles a b Modified with permission from Suarez JI, et al, N Engl J Med.15 B 2006 Massachusetts Medical Society www.nejm.org/doi/full/10.1056/NEJMra052732 Thick is defined as a hemorrhage filling one or more cisterns or fissures out of a total of 10: interhemispheric fissure, the quadrigeminal cistern, both suprasellar cisterns, both ambient cisterns, both basal sylvian fissures, and both lateral sylvian fissures Continuum (Minneap Minn) 2015;21(5):1263–1287 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1271 Subarachnoid Hemorrhage already in one), admit the patient to a dedicated neurocritical care unit, and have the patient undergo a multidisciplinary evaluation for the management of an unsecured cerebral aneurysm (Table 1-5).2,12 It has been shown that admission of patients with SAH to low-volume centers is associated with higher 30-day mortality compared to admission to highvolume centers In addition, admission TABLE 1-5 Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Treatment Decision American Heart Association/American Stroke Association2,a Hospital/system characteristics Low-volume hospitals (eg, less than 10 subarachnoid hemorrhage [SAH] cases per year) should consider early transfer of patients with SAH to high-volume centers (eg, more than 35 SAH cases per year) with experienced cerebrovascular surgeons, endovascular specialists, and multidisciplinary neurointensive care services (Class I, Level B) After discharge, it is reasonable to refer patients with SAH for a comprehensive evaluation, including cognitive, behavioral, and psychosocial assessments (Class IIa, Level B) Aneurysm treatment 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 rebleeding after SAH (Class I, Level B) For patients with ruptured aneurysms judged to be technically amenable to either endovascular coiling and neurosurgical clipping, endovascular coiling should be considered (Class I, Level B) Complete obliteration of the aneurysm is recommended whenever possible (Class I, Level B) Stenting of a ruptured aneurysm is associated with increased morbidity and mortality (Class III, Level C) For patients with an unavoidable delay in obliteration of aneurysm, a significant risk of rebleeding, and no compelling medical contraindications, short-term (less than 72 hours) therapy with tranexamic acid or aminocaproic acid is reasonable to reduce the risk of early aneurysm rebleeding (Class IIa, Level B) Neurocritical Care Society12,b Patients with SAH should be treated at high-volume centers (moderate quality of evidence, strong recommendation) High-volume centers should have appropriate specialty neurointensive care units, neurointensivists, vascular neurosurgeons, and interventional neuroradiologists to provide the essential elements of care (moderate quality of evidence, strong recommendation) Early aneurysm repair should be undertaken, when possible and reasonable to prevent rebleeding (high quality of evidence, strong recommendation) An early, short course of antifibrinolytic therapy prior to early aneurysm repair (begun at diagnosis and continued up to the point at which the aneurysm is secured or at 72 hours post ictus, whichever is shorter) should be considered (low quality of evidence, weak recommendation) Delayed (more than 48 hours after the ictus) or prolonged (more than days) antifibrinolytic therapy exposes patients to side effects of therapy when the risk of rebleeding is sharply reduced and should be avoided (high quality of evidence, strong recommendation) Continued on page 1273 1272 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 TABLE 1-5 Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Continued from page 1272 Treatment Decision American Heart Association/American Stroke Association2,a Blood pressure control Between the time of SAH symptom onset and aneurysm obliteration, blood pressure should be controlled with a titratable agent to balance the risk of stroke, hypertension-related rebleeding, and maintenance of cerebral perfusion pressure (Class I, Level B) The magnitude of blood pressure control to reduce the risk of rebleeding has not been established, but a decrease in systolic blood pressure to less than 160 mm Hg is reasonable (Class IIa, Level C) Neurocritical Care Society12,b Treat extreme hypertension in patients with an unsecured, recently ruptured aneurysm Modest elevations in blood pressure (mean blood pressure of less than 110 mm Hg) not require therapy Premorbid baseline blood pressures should be used to refine targets and hypotension should be avoided (low quality of evidence, strong recommendation) Intravascular volume status Maintenance of euvolemia and normal circulating blood volume is recommended to prevent delayed cerebral ischemia (Class I, Level B) Intravascular volume management should target euvolemia and avoid prophylactic hypervolemic therapy In contrast, there is evidence for harm from aggressive administration of fluid aimed at achieving hypervolemia (moderate quality of evidence, strong recommendation) Cardiopulmonary complications No recommendations given Baseline cardiac assessment with serial enzymes, ECG, and echocardiography is recommended, especially in patients with evidence of myocardial dysfunction (low quality of evidence, strong recommendation) Monitoring of cardiac output may be useful in patients with evidence of hemodynamic instability or myocardial dysfunction (low quality of evidence, strong recommendation) Seizures The use of prophylactic anticonvulsants may be considered in the immediate posthemorrhagic period (Class IIb, Level B) The routine long-term use of anticonvulsants is not recommended (Class III, Level B) Routine use of anticonvulsant prophylaxis with phenytoin is not recommended after SAH (low quality of evidence, strong recommendation) If anticonvulsant prophylaxis is used, a short course (3Y7 days) is recommended (low quality of evidence, weak recommendation) Continuous EEG monitoring should be considered in patients with poor-grade SAH who fail to improve or who have neurologic deterioration of undetermined etiology (low quality of evidence, strong recommendation) Continued on page 1274 Continuum (Minneap Minn) 2015;21(5):1263–1287 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1273 Subarachnoid Hemorrhage TABLE 1-5 Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Continued from page 1273 Treatment Decision American Heart Association/American Stroke Association2,a Neurocritical Care Society12,b Fever treatment Aggressive control of fever to a target of normothermia by use of standard or advanced temperature-modulating systems is reasonable in the acute phase of SAH (Class IIa, Level B) During the period of risk for delayed cerebral ischemia, control of fever is desirable; intensity should reflect the individual patient’s relative risk of ischemia (low quality of evidence, strong recommendation) Surface cooling or intravascular devices are more effective and should be employed when antipyretics fail in cases where fever control is highly desirable (high quality of evidence, strong recommendation) Glucose control Deep venous thrombosis prophylaxis Delayed cerebral ischemia Careful glucose management with strict avoidance of hypoglycemia may be considered as part of the general critical care management of patients with SAH (Class IIb, Level B) Hypoglycemia (serum glucose of less than 80 mg/dL) should be avoided (high quality of evidence, strong recommendation) Heparin-induced thrombocytopenia and deep venous thrombosis are relatively frequent complications after SAH Early identification and targeted treatment are recommended, but further research is needed to identify the ideal screening paradigms (Class I, Level B) Measures to prevent deep venous thrombosis should be employed in all patients with SAH (high quality of evidence, strong recommendation) Oral nimodipine should be administered to all patients with SAH (Class I, Level A) Oral nimodipine (60 mg every hours) should be administered after SAH for a period of 21 days (high quality of evidence, strong recommendation) Maintenance of euvolemia and normal circulating blood volume is recommended to prevent delayed cerebral ischemia (Class I, Level B) Prophylactic hypervolemia or balloon angioplasty before the development of angiographic spasm is not recommended (Class III, Level B) Transcranial Doppler is reasonable to monitor for the development of arterial vasospasm (Class IIa, Level B) Perfusion imaging with CT or MRI can be useful to identify regions of potential brain ischemia (Class IIa, Level B) Serum glucose should be maintained below 200 mg/dL (moderate quality of evidence, strong recommendation) The use of unfractionated heparin for prophylaxis could be started 24 hours after undergoing aneurysm obliteration (moderate quality of evidence, strong recommendation) The goal should be maintaining euvolemia, rather than attempting hypervolemia (moderate quality of evidence, strong recommendation) Transcranial Doppler may be used for monitoring and detection of large artery vasospasm with variable sensitivity (moderate quality of evidence, strong recommendation) Digital subtraction angiography is the gold standard for detection of large artery vasospasm (high quality of evidence, strong recommendation) Continued on page 1275 1274 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 TABLE 1-5 Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Continued from page 1274 Treatment Decision American Heart Association/American Stroke Association2,a Neurocritical Care Society12,b Induction of hypertension is recommended for patients with delayed cerebral ischemia unless blood pressure is elevated at baseline or cardiac status precludes it (Class I, Level B) Patients clinically suspected of delayed cerebral ischemia should undergo a trial of induced hypertension (moderate quality of evidence, strong recommendation) Cerebral angioplasty and/or selective intra-arterial vasodilator therapy is reasonable in patients with symptomatic vasospasm, particularly those who are not responding to hypertensive therapy (Class IIa, Level B) Endovascular treatment using intra-arterial vasodilators and/or angioplasty may be considered for vasospasm-related delayed cerebral ischemia (moderate quality of evidence, strong recommendation) Anemia and transfusion The use of packed red blood cell transfusion to treat anemia might be reasonable in patients with SAH who are at risk of cerebral ischemia The optimal hemoglobin goal is still to be determined (Class IIb, Level B) Patients should receive packed red blood cell transfusions to maintain hemoglobin concentration above 8Y10 g/dL (moderate quality of evidence, strong recommendation) Hyponatremia The use of fludrocortisone acetate and hypertonic saline solution is reasonable for preventing and correcting hyponatremia (Class IIa, Level B) Fluid restriction should not be used to treat hyponatremia (weak quality of evidence, strong recommendation) Early treatment with hydrocortisone or fludrocortisone may be used to limit natriuresis and hyponatremia (moderate quality of evidence, weak recommendation) Mild hypertonic saline solutions can be used to correct hyponatremia (very low quality of evidence, strong recommendation) CT = computed tomography; ECG = electrocardiogram; EEG = electroencephalogram; MRI = magnetic resonance imaging a American Heart Association/American Stroke Association recommendations follow the American Heart Association Stroke Council’s methods of classifying the level of certainty of the treatment effect and the class of evidence b For the Neurocritical Care Society’s guidelines, the quality of the data was assessed and recommendations developed using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system to dedicated neurocritical care units staffed by dedicated neurointensivists is associated with decreased in-hospital mortality.36 Treatment of Unsecured Aneurysms Treatment of unsecured aneurysms has evolved, and two accepted efficacious management modalities currently exist: surgical clipping and endovascular coilContinuum (Minneap Minn) 2015;21(5):1263–1287 ing The choice of treatment depends on several factors, including the patient’s age and aneurysm location, morphology, and relationship to adjacent vessels Because of the complexity of determining the most appropriate treatment for individual patients, it is recommended that a multidisciplinary team made up of cerebrovascular neurosurgeons, endovascular practitioners, and neurointensivists confer KEY POINT h Admission of patients with subarachnoid hemorrhage to low-volume centers is associated with higher 30-day mortality compared to admission to high-volume centers www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1275 Subarachnoid Hemorrhage KEY POINTS h Overall, when considering treatment of unruptured aneurysms, endovascular coiling should be preferred over surgical clipping whenever possible h Patients with subarachnoid hemorrhage are at risk for several significant neurologic complications, including hydrocephalus, cerebral edema, delayed cerebral ischemia, rebleeding, seizures, and neuroendocrine abnormalities h The best measure to reduce the risk of rebleeding is the early treatment of unsecured aneurysms to reach a consensus.2,12,15,22,23,29 The International Subarachnoid Aneurysm Trial (ISAT) was a prospective randomized controlled clinical trial that evaluated patients with unsecured aneurysms who were considered suitable for either endovascular coiling or surgical clipping.13,14 Patients assigned to the endovascular coiling group had a significantly higher favorable outcome (defined as survival free of disability at year) and lower risk of epilepsy compared to those assigned to the surgical clipping group However, the risk of rebleeding and partial occlusion of aneurysms was lower with surgical clipping Overall, endovascular coiling should be preferred over surgical clipping whenever possible; however, many aneurysms are not equally suitable for either surgical clipping or endovascular coiling (Table 1-6) (Case 1-1A) Regardless of the treatment modality chosen, unsecured aneurysms must be treated as soon as possible to prevent rebleeding (Table 1-5) In the author’s institution, the median time for aneurysm treatment is hours from initial hospital arrival INTENSIVE CARE UNIT MANAGEMENT SAH is often accompanied by more severe initial systemic and intracranial responses than other cerebral insults.37Y40 More than 75% of patients with SAH experience systemic inflammatory response syndrome (SIRS), which is likely related to elevated levels of inflammatory cytokines SIRS has been associated with permanent neurocognitive dysfunction In addition, patients with SAH are at risk for several significant neurologic complications, including hydrocephalus, cerebral edema, delayed cerebral ischemia, rebleeding, seizures, and neuroendocrine abnormalities that lead to impaired body regulation of sodium, water, and 1276 glucose Furthermore, SAH unleashes hypothalamic-mediated changes, including increased sympathetic and parasympathetic drive, that result in cardiac and pulmonary complications For example, increased circulating catecholamines are thought to be the cause for several cardiac manifestations, including ECG changes, arrhythmias, impaired cardiac contractility (eg, Takotsubo cardiomyopathy), troponinemia, and myocardial necrosis Pulmonary complications, such as neurogenic pulmonary edema, most likely have a similar underlying pathophysiologic mechanism It is important to recognize and treat all these systemic complications as they are associated with increased risk for delayed cerebral ischemia and poor neurologic outcome after SAH Neurologic Complications Rebleeding Rebleeding is a major disabling complication of SAH, which carries high mortality and morbidity In the first 24 hours, 4% to 15% of patients will rebleed, with the highest risk occurring less than hours from symptom onset.33 Rebleeding risk decreases over the following weeks The main risk factors associated with rebleeding include high systolic blood pressure (ie, greater than 160 mm Hg), poor neurologic grade, intracerebral or intraventricular hematomas, ruptured posterior circulation aneurysms, and aneurysms of greater than 10 mm in size.33 The best measure to reduce the risk of rebleeding is the early treatment of unsecured aneurysms (Table 1-5).2,12 However, in some instances there may be a delay in surgical clipping or endovascular coiling of the aneurysm, and short-term (ie, less than 72 hours) treatment with tranexamic acid or aminocaproic acid has been recommended if no contraindications exist The use of these antifibrinolytic agents is based www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 KEY POINT h About 60% of patients TABLE 1-6 Preferences for Treatment of Unsecured Aneurysms Characteristics Preferred Treatment Modality Advanced age Endovascular coiling Poor clinical grade Endovascular coiling Multiple underlying systemic conditions Endovascular coiling Aneurysms with wide neck-to-body ratio Surgical clipping Normal arterial branches arising from dome or body of aneurysm Surgical clipping Middle cerebral artery aneurysm Surgical clipping Top-of-the-basilar aneurysm Endovascular coiling Aneurysm associated with large parenchymal hematoma Surgical clipping High surgical risk Endovascular coiling Patient preference Endovascular coiling a Endovascular coiling Clinical equipoise a with subarachnoid hemorrhage who undergo external ventricular drain insertion will have successful weaning and the others may require chronic ventriculoperitoneal shunt insertion Unsecured aneurysm is considered equally suitable for either endovascular coiling or surgical clipping on the premise that early risk for rebleeding is a consequence of activated fibrinolysis and reduced clot stability during the first hours In addition, blood pressure control is also very important to prevent rebleeding prior to aneurysm obliteration, as previously mentioned Patients suspected of rebleeding should be evaluated promptly, have a follow-up head CT scan and DSA (if not already done), and immediately undergo aneurysm obliteration Endovascular treatment of ruptured cerebral aneurysms should include coiling only Stenting of cerebral aneurysms in the setting of SAH should be avoided as it is associated with higher bleeding complications and poor outcome.2 Hydrocephalus Acute symptomatic hydrocephalus occurs in about 20% of patients with SAH, usually within the first few days after symptom onset.2,15,22 Patients manifest decreased levels of consciousness and other signs of increased ICP, such as impaired upward gaze and hypertension An immediate follow-up Continuum (Minneap Minn) 2015;21(5):1263–1287 head CT scan is warranted in any patient with suspected symptomatic hydrocephalus and must be followed by insertion of an external ventricular drain (EVD) Some centers perform lumbar drain insertion instead of EVD in patients with SAH who have communicating hydrocephalus Weaning the patient of an EVD should begin shortly after aneurysm obliteration or within 48 hours of insertion if the patient is neurologically stable A rapid weaning protocol is preferred About 60% of patients with SAH who undergo EVD insertion will have successful weaning, and the others may require chronic ventriculoperitoneal shunt insertion (Case 1-1B) Seizures Delineating the true frequency of seizures in patients with SAH has been difficult and controversial as many patients (20% to 26%) present with seizurelike episodes that are not easy to characterize as many of them occur at the time of symptom onset.2,12Y15 In general, patients with middle cerebral artery (MCA) aneurysms, concomitant www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1277 Subarachnoid Hemorrhage KEY POINTS h Anticonvulsant administration (particularly phenytoin) has been associated with worse clinical outcome h Delayed cerebral ischemia is defined as any neurologic deterioration (focal or global) presumed secondary to cerebral ischemia that persists for more than hour and cannot be explained by any other neurologic or systemic condition intraparenchymal hematomas, and poor clinical grade are at higher risk for seizures, whereas patients treated with endovascular coiling have lower rates of seizures Long-term risk for epilepsy is low The administration of prophylactic anticonvulsants in patients with SAH was common practice; however, anticonvulsant administration (particularly phenytoin) has been associated with worse clinical outcome and a high frequency of medication-related complications.2,12 Current recommendations are to avoid phenytoin, and, if desirable, short-term anticonvulsant administration for to days could be administered In addition, concern exists that the frequency of subclinical seizures may be high in patients with poor-grade SAH, and continuous EEG has been recommended in this setting.12 Delayed cerebral ischemia Delayed cerebral ischemia is one of the most dreaded complications after SAH and is the most important factor impacting functional outcome.39Y41 Delayed cerebral ischemia occurs in about 30% of patients with SAH, usually between and 14 days after the onset of symptoms Delayed cerebral ischemia is defined as any neurologic deterioration (focal or global) presumed secondary to cerebral ischemia that persists for more than hour and cannot be explained by any other neurologic or systemic condition The latter implies an absence of significant hydrocephalus, sedation, hypoxemia, seizures, and electrolyte or renal or hepatic impairment Thus, delayed cerebral ischemia is a diagnosis of exclusion Several factors have been implicated in the pathogenesis of delayed Case 1-1B The patient discussed in Case 1-1A continued to evolve satisfactorily with normal mean cerebral blood flow velocities by transcranial Doppler (TCD) On postbleed day 6, TCD revealed an increase in mean cerebral blood flow velocity in the right middle cerebral artery (MCA) to 160 cm/s from 80 cm/s on day The next morning, the patient developed a sudden onset of left hemiparesis and confusion A head CT scan revealed no rebleeding, cerebral edema, or hydrocephalus She was given an IV bolus of 500 mL of 0.9% saline and was started on a norepinephrine drip with some improvement of her left hemiparesis but without complete resolution The patient’s electrolytes, blood urea nitrogen, creatinine, and liver function tests were normal, and her white blood cell count was 14,000 cells/mm3 A follow-up TCD after neurologic deterioration showed a further increase in mean cerebral blood flow velocity of her right MCA to 220 cm/s and a Lindegaard ratio (MCA/extracranial internal carotid artery mean blood flow velocities) of Digital subtraction angiography (DSA) was performed 90 minutes after symptom onset, showing severe vasospasm of her right MCA and anterior cerebral artery (ACA) (Figure 1-4A) She underwent balloon angioplasty of the right MCA and subsequent intra-arterial infusion of nicardipine in both the right MCA and ACA with radiologic and clinical improvement (Figure 1-4B) The patient’s neurologic examination normalized, and her systolic blood pressure was maintained at greater than 180 mm Hg for more days Her TCD showed improvement in mean cerebral blood flow velocities to less than 100 cm/s by day 9, and the patient was slowly weaned off norepinephrine by day 10 On day 11 she developed a decreased level of consciousness without focal neurologic findings except for limited upward gaze A follow-up head CT scan showed communicating hydrocephalus, and an external ventricular drain (EVD) was inserted (Figure 1-4C) Several attempts at weaning the patient off the EVD failed and, therefore, she underwent programmable ventriculoperitoneal shunt placement (Figure 1-4D) on day 15, after which she was transferred to the regular floor The patient was discharged to home on day 17, after clearance by physical and occupational therapies, with instructions to continue nimodipine for more days and schedule follow-up in vascular neurology and neurosurgery outpatient clinics Continued on page 1279 1278 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 Continued from page 1278 Subsequent imaging studies for the patient in Case 1-1 A, A two-dimensional digital subtraction angiogram reveals severe vasospasm of the right middle cerebral artery and anterior cerebral artery (arrows) B, A two-dimensional digital subtraction angiogram after balloon angioplasty of the right middle cerebral artery and intra-arterial infusion of nicardipine of the right middle cerebral artery and anterior cerebral artery reveals improved vessel diameter of both arteries (arrows) C, Nonenhanced head CT scan shows communicating hydrocephalus and placement of an external ventricular drain (arrow) after patient developed decreased level of consciousness D, Noncontrasted head CT scan shows placement of a ventriculoperitoneal shunt FIGURE 1-4 Comment This case exemplifies the clinical presentation and management of two of the most common neurologic complications of SAH: delayed cerebral ischemia and hydrocephalus This patient was treated with recommended therapies, including maintenance of euvolemia, oral nimodipine, and liberal blood pressure parameters In addition, she was monitored in the neurocritical care unit and had frequent TCDs This patient had important risk factors for the development of delayed cerebral ischemia secondary to vasospasm, including cigarette smoking, cocaine use, and a high burden of subarachnoid blood Her TCD recordings revealed an increase in mean cerebral blood flow velocities of greater than 50 cm/s within 24 hours followed by focal neurologic signs Once the diagnosis of cerebral vasospasm was confirmed (after ruling out other neurologic and systemic disorders), she was treated with induced hypertension and endovascular therapy with complete resolution of her symptoms As this case demonstrates, the management of delayed cerebral ischemia is carried out in a stepwise fashion, and final confirmation and treatment of vasospasm must be done within hours of symptom onset Furthermore, this case highlights that, frequently, more than one neurologic complication is present in the same patient Treatment of hydrocephalus entails the immediate insertion of an EVD Continuum (Minneap Minn) 2015;21(5):1263–1287 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1279 Subarachnoid Hemorrhage KEY POINTS h Possible underlying conditions implicated in the pathogenesis of delayed cerebral ischemia include cerebral vasospasm, microcirculatory constriction, microthrombosis, cortical spreading depression, and delayed cellular apoptosis h Nimodipine should be administered to all patients with subarachnoid hemorrhage to decrease the risk of delayed cerebral ischemia and poor functional outcome h Euvolemia should be maintained at all times, while prophylactic hypervolemia should be avoided 1280 cerebral ischemia, including cerebral vasospasm, microcirculatory constriction, microthrombosis, cortical spreading depression, and delayed cellular apoptosis.39 Most likely, the main driver of all these processes is the release of oxyhemoglobin and erythrocyte contents through hemolysis, which unleashes a host of inflammatory and proapoptotic factors The risk for cerebral vasospasm increases with the thickness, density, location, and persistence of the subarachnoid blood In addition, poor clinical grade, loss of consciousness at ictus, cigarette smoking, cocaine use, SIRS, hyperglycemia, and hydrocephalus also increase the risk of delayed cerebral ischemia and poor neurologic outcome.39,40 However, predicting who will develop delayed cerebral ischemia has proven very difficult The latter has important implications for the reduction of level of monitoring in patients with SAH who are at low risk for delayed cerebral ischemia, thus avoiding potential adverse effects of aggressive management and potentially decreasing resource utilization The best predictors for patients requiring less frequent monitoring include older age (more than 65 years), a WFNSS score of to 3, and a modified Fisher Scale score less than (Table 1-5).39 Prophylaxis The best studied of the available interventions aimed at preventing delayed cerebral ischemia are calcium channel blockers and intravascular volume status The use of nimodipine to decrease the risk of delayed cerebral ischemia and poor functional outcome is well supported and recommended (Table 1-5).2,12,23,39 Nimodipine is administered by enteral route at 60 mg every hours for 21 days Nimodipine affords neuroprotection without decreasing the frequency of angiographic vasospasm The most common adverse effects of nimodipine include constipation and hypotension The latter could be problematic as it could lead to hypoperfusion due to decreased cerebral perfusion pressure (CPP) Therefore, it is important that systolic blood pressure not be compromised when administering nimodipine One solution employed by the author is to half the nimodipine dose to 30 mg every hours while maintaining adequate intravascular volume Patients with SAH frequently experience decreased intravascular volume and negative fluid balance, which have been associated with higher incidence of cerebral infarction and poor neurologic outcome These findings led to the institution of prophylactic hypervolemic therapy However, this strategy has not been shown to improve cerebral blood flow (CBF) or decrease the frequency of cerebral vasospasm or delayed cerebral ischemia, and it increases the frequency of cardiopulmonary complications Therefore, prophylactic hypervolemia should not be pursued Current recommendations are to maintain euvolemia at all times after SAH.2,12 It is important to emphasize that controversy still exists about the methodology to follow to determine euvolemia Many neurointensivists use a combination of methods, including strict monitoring of fluid balance, central venous pressure, echocardiogram, and stroke volume variation, among others In practice, maintenance of euvolemia can generally be ensured by replacing urine output and even administering fludrocortisone or hydrocortisone in patients with significant diuresis (Table 1-5) Diagnosis and monitoring Diagnosing delayed cerebral ischemia is not easy However, the combination of neurologic examination and imaging studies can enhance the chances of early detection and management Patients with SAH must be in the neurocritical care unit where they can be examined very frequently, preferably at least every hours Delayed cerebral ischemia must be suspected www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 when patients with SAH develop focal neurologic impairment or a decrease of at least points on the Glasgow Coma Scale that lasts for more than hour and cannot be explained by any other cause In addition, all patients with SAH should undergo head CT or MRI 24 to 48 hours after aneurysm occlusion Therefore, any new hypodensities on CT imaging after this period not attributable to EVD insertion or intraparenchymal hematoma should be regarded as cerebral infarctions from delayed cerebral ischemia regardless of clinical signs.41 The general consensus among practitioners indicates that patients with SAH should undergo additional imaging and/or physiologic monitoring routinely during the risk period for delayed cerebral ischemia (Table 1-5).2,12 Such monitoring is usually multimodal and includes ICP, CPP, CBF, EEG, transcranial Doppler (TCD), DSA, CTA, CT perfusion (CTP), and brain tissue oxygenation TCD has been the longest and best studied of all the monitoring modalities TCD has adequate sensitivity and specificity to detect delayed cerebral ischemia secondary to cerebral vasospasm in large arteries compared to DSA, but is limited by the operator’s experience and the patient’s cranial windows.42 TCD thresholds for vasospasm are the following: mean cerebral blood flow velocities of less than 120 cm/s for absence and more than 200 cm/s or a Lindegaard ratio (MCA mean cerebral blood flow velocity/extracranial internal carotid artery mean cerebral blood flow velocity) of greater than for presence In addition, mean cerebral blood flow velocity increases by more than 50 cm/s within 24 to 48 hours also have been associated with delayed cerebral ischemia DSA is the gold standard for detection of large artery vasospasm.2,12 CTA has become more widely available and may replace DSA for screening of vasospasm Continuum (Minneap Minn) 2015;21(5):1263–1287 with a high degree of specificity CTP findings of an elevated mean transit time (MTT) of greater than 6.4 seconds may be additive to CTA in predicting delayed cerebral ischemia and has been recommended as a threshold for decreased cerebral perfusion Qualitative visual interpretation of CTP can also be useful Brain tissue oxygenation and CBF monitoring can provide additional information when used in the context of a multimodality approach, bearing in mind their limitations, such as limited tissue sampling and location in relation to pathology Continuous EEG offers the advantage of being able to monitor broad regions of the brain to detect epileptiform discharges noninvasively Continuous EEG is particularly useful in patients with poorgrade SAH where neurologic examination is limited Some variability exists regarding the timing and frequency of use of the various neuromonitoring techniques mentioned above The author’s institution follows an algorithm for identifying and treating subarachnoid hemorrhage similar to the one proposed by Macdonald as shown in Figure 1-5.39 Patients with SAH are stratified into low risk (ie, older age, a WFNSS score of to 2, and a modified Fisher Scale score of less than 3), high risk (ie, a WFNSS score of to and a modified Fisher Scale score of 3), and high risk with poor neurologic status (ie, clouded examination due to sedation, a WFNSS score of to 5, and a modified Fisher Scale score of 4) All patients with aneurysmal SAH undergo TCD (daily or every other day) and head CT/CTA/CTP on admission and on days to and days to 10 for screening of decreased cerebral perfusion or vasospasm DSA also can be performed in lieu of CTA/CTP High-risk patients with poor neurologic status undergo additional neuromonitoring, including EEG, brain tissue oxygenation, and CBF determination KEY POINTS h Delayed cerebral ischemia must be suspected when patients with subarachnoid hemorrhage develop focal neurologic impairment or a decrease of at least points on the Glasgow Coma Scale that lasts for more than hour and cannot be explained by any other cause h Any new hypodensities on CT imaging 24 to 48 hours after aneurysm treatment should be regarded as cerebral infarctions from delayed cerebral ischemia h Transcranial Doppler thresholds for vasospasm include mean cerebral blood flow velocities of less than 120 cm/s for absence and more than 200 cm/s or a Lindegaard ratio of greater than for presence h Digital subtraction angiography is the gold standard for detection of large artery vasospasm h CT perfusion findings of elevated mean transit time of greater than 6.4 seconds may be additive to CT angiography in predicting delayed cerebral ischemia and has been recommended as a threshold for decreased cerebral perfusion www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1281 Subarachnoid Hemorrhage FIGURE 1-5 Management approach to delayed cerebral ischemia BP = blood pressure; CPP = cerebral perfusion pressure; CT = computed tomography; CTA = computed tomography angiography; CTP = computed tomography perfusion; DCI = delayed cerebral ischemia; ICP = intracranial pressure; IVH = intraventricular hemorrhage; MTT = mean transit time; SAH = subarachnoid hemorrhage; TCD = transcranial Doppler; WFNSS = World Federation of Neurological Surgeons Scale Reprinted with permission from Macdonald RL, Nat Rev Neurol B 2014 Macmillan Publishers Limited www.nature.com/nrneurol/journal/v10/n1/full/ nrneurol.2013.246.html 39 Management All of the patients with SAH in the author’s institution are treated with nimodipine and euvolemia as mentioned above (Table 1-5) (Figure 1-5) Low-risk patients whose neurologic examination remains unchanged along with absence of vasospasm and hypoperfusion on TCD and CTA/CTP are considered for transfer to a lower level 1282 of care as early as days post ictus High-risk patients who have good neurologic status and whose neurologic examination remains unchanged along with normal TCD and CTA/CTP are transferred out of the neurocritical care unit as early as days after symptom onset High-risk patients with poor neurologic status, whose examination www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 remains unchanged, and all neuromonitoring values remain within normal limits, are considered for transfer to a lower level of care 14 days after SAH If at any given time low-risk or high-risk patients develop elevated TCD mean cerebral blood flow velocities or abnormal CTA/CTP, the intensity and frequency of neurologic monitoring is escalated Once patients experience neurologic deterioration suggestive of delayed cerebral ischemia, rescue therapies are initiated Current guidelines indicate that induced hypertension is indicated (Table 1-5) (Figure 1-5).2,12 At the author’s institution, typically, an IV fluid bolus (1 to liters of 0.9% saline) is administered and hypertension is induced with norepinephrine as our drug of choice Blood pressure augmentation progresses in stepwise fashion with frequent assessment of neurologic function at each 10 mm Hg change in systolic (up to 200 mm Hg) or mean arterial blood pressures to determine whether a higher blood pressure target is needed The author’s institution reserves the use of inotropes (dobutamine or milrinone) for those patients with known poor cardiac function If neurologic deficits persist, then the patient undergoes CT/CTA/ CTP or DSA with subsequent endovascular therapy once cerebral vasospasm is confirmed Endovascular treatment using intra-arterial vasodilators and/or angioplasty is supported by prospective and retrospective observational data and is currently recommended (Table 1-5).2,12 Induced hypertension is maintained for at least 72 hours or until stability is achieved and is slowly weaned off after that We not perform prophylactic angioplasty when cerebral vasospasm is discovered during the screening CT/CTA/CTP or DSA without neurologic deterioration because this practice is associated with higher complication rates.2,12 In high-risk patients with poor neurologic status, diagnosis and treatContinuum (Minneap Minn) 2015;21(5):1263–1287 ment of delayed cerebral ischemia may be somewhat subjective and mostly based on neuromonitoring findings The protocol at the author’s institution dictates induced hypertension and CT/CTA/CTP or DSA when these patients experience elevated TCD mean cerebral blood flow velocities indicative of vasospasm, abnormal brain tissue oxygenation, or CBF (Figure 1-5) Medical Complications Cardiopulmonary Cardiopulmonary alterations are among the most common systemic complications of SAH and can range from minor ECG changes to severe dilated cardiomyopathy and acute respiratory distress syndrome (ARDS).38 ECG alterations and cardiac enzyme (troponin T) elevations are quite frequent after SAH and, depending on their severity, are also significant surrogates for clinical outcome ECG changes include sinus tachycardia, peaked T waves, T-wave inversions, ST segment depression or elevation, and QT prolongation Troponin elevation can be seen in up to 30% of patients The exact pathogenesis behind cardiac abnormalities is not completely understood but may reflect a catecholamine-related myocardial injury Echocardiogram can help differentiate patients with diffuse cardiac dysfunction related to SAH from those with underlying cardiac ischemia showing regional wall motion abnormalities restricted to the territory of a coronary vessel Clinically, patients with SAH can develop significant cardiac dysfunction manifesting as left ventricular failure, with impaired cardiac output, hypotension, and pulmonary edema These cardiovascular dysfunctions can lead to severe hypoperfusion, reduced CPP or brain tissue oxygenation, with added catastrophic consequences for an already-injured brain prone to delayed cerebral ischemia and poor neurologic outcome KEY POINTS h Once patients experience neurologic deterioration suggestive of delayed cerebral ischemia, rescue therapies are initiated with induced hypertension as first-line modality h In high-risk patients with poor neurologic status, diagnosis and treatment of delayed cerebral ischemia may be somewhat subjective and mostly based on neuromonitoring findings h Cardiopulmonary alterations are among the most common systemic complications of subarachnoid hemorrhage www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1283 Subarachnoid Hemorrhage KEY POINTS h Pulmonary edema or acute respiratory distress syndrome in patients with subarachnoid hemorrhage should be treated with judicious use of diuretics and other standard heart failure therapies targeting euvolemia and normal cerebral perfusion pressure h Fever is the most common non-neurologic complication in patients with subarachnoid hemorrhage h Fever in patients with subarachnoid hemorrhage has been associated with poor clinical outcome h Deep venous thrombosis prophylaxis should be administered to all patients with subarachnoid hemorrhage 1284 The term stunned myocardium has been applied to patients with SAH who present with hypoxemia and cardiogenic shock with pulmonary edema within hours of disease onset Takotsubo cardiomyopathy (typically characterized by apical ballooning on echocardiogram) can be seen in those patients with poor neurologic status and increases the risk of delayed cerebral ischemia.12 Current recommendations for the treatment of pulmonary edema or ARDS in patients with SAH are to avoid excessive fluid intake and to use diuretics judiciously to target euvolemia In addition, standard management of heart failure is indicated, keeping in mind that CPP should be maintained within normal limits.12 Although lung-protective mechanical ventilation should be tried whenever possible, hypercarbia should be closely monitored and managed to avoid ICP elevations Cardiopulmonary function should be supported, even with the insertion of an intra-aortic balloon pump if necessary, as these abnormalities usually improve a few days after onset Fever Fever is the most common nonneurologic complication of SAH, occurring in up to 70% of patients during their hospitalization.2,12 Fever is more likely to occur in patients with poor neurologic status and higher modified Fisher Scale scores Fever in SAH has been associated with poor clinical outcome and is more likely related to SIRS rather than infectious in origin There is currently no clear evidence indicating that fever control is beneficial for patients with SAH However, current recommendations are to monitor body temperature frequently and to seek and treat infectious processes In addition, during the period of risk for delayed cerebral ischemia, fever control should be achieved in a stepwise fashion starting with standard antipyretic medications and escalating to surface cooling or intravascular devices while avoiding shivering Thromboembolism The incidence of deep venous thrombosis (DVT) after SAH ranges from 2% to 20% depending on the screening methodology used.12 The risk of DVT is higher in patients with poor neurologic status Because of the high incidence of DVT and its potential life-threatening consequences, prophylaxis should be administered to all patients with SAH Sequential compression devices are recommended for all patients with SAH (Table 1-5) The use of unfractionated heparin for prophylaxis is indicated after aneurysm obliteration and can be started 24 hours after the procedure Glucose abnormalities Hyperglycemia is a common phenomenon following SAH Its real impact is still unclear, but hyperglycemia has been associated with the development of delayed cerebral ischemia and poor clinical outcome Hypoglycemia also is associated with worse clinical outcome The methods, timing, and aggressiveness of glucose control are not well studied in patients with SAH Current recommendations are to maintain a blood glucose between 80 mg/dL and 200 mg/dL pending further investigations (Table 1-5).12 Hyponatremia Hyponatremia is the most common electrolyte disorder in SAH and can occur in about 30% of patients.2,12,15 Hyponatremia has been associated with development of delayed cerebral ischemia and poor clinical outcome Hyponatremia can be secondary to cerebral salt wasting or inappropriate secretion of antidiuretic hormone Traditionally, in patients without SAH, the former is treated with volume infusion and the latter with fluid restriction However, because determination of fluid status can be difficult in the neurocritical care unit and because hypovolemia is associated with poor clinical outcome, fluid restriction should be avoided in patients with SAH Treatment goals for hyponatremia in SAH should be oral free water www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 restriction while maintaining euvolemia Patients can be treated with continuous infusion of hypertonic saline (1.5% to 3%) and fludrocortisone if diuresis is active and impedes maintenance of adequate fluid balance It is important to test for thyroid and adrenal dysfunction, particularly in those patients with SAH who require vasopressors to maintain blood pressure goals Hemoglobin The majority of patients with SAH experience a drop in hemoglobin during hospitalization, which could be due to several factors, including excessive blood draws, blood loss for other reasons, or systemic inflammation.12 Anemia has been associated with delayed cerebral ischemia and poor clinical outcome in patients with SAH However, the optimal hemoglobin concentration in patients with SAH has not been determined, and whether blood transfusion improves clinical outcome remains to be proven Current recommendations are to minimize blood loss from blood drawing and to maintain a hemoglobin concentration of above g/dL to 10 g/dL (Table 1-5) CONCLUSION SAH is a neurologic emergency associated with high morbidity and mortality SAH is more frequent in women than men and more frequent in minority populations compared to white Americans The main areas of emphasis when caring for patients with SAH should be the following: prompt evaluation and diagnosis, immediate transfer to appropriate centers, expeditious diagnosis and treatment of the bleeding source, and overall good neurocritical care adhering to available treatment guidelines The main neurologic complications of SAH include hydrocephalus, seizures, cerebral edema, delayed cerebral ischemia, and neuroendocrine disorders Patients with SAH frequently experience cardiopulmonary complications, which can be life threatening Continuum (Minneap Minn) 2015;21(5):1263–1287 KEY POINTS REFERENCES Go AS, Mozaffarian D, Roger VL, et al Heart disease and stroke statisticsV2014 update: a report from the American Heart Association Circulation 2014;129(3):e28Ye292 doi:10.1161/01.cir.0000441139.02102.80 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(6):1711Y1737 doi:10.1161/STR.0b013e3182587839 Lovelock CE, Rinkel GJ, Rothwell PM Time trends in outcome of subarachnoid hemorrhage: population-based study and systematic review 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J Emerg Med 2005;29(1):23Y27 doi:10.1016/j.jemermed.2005.02.002 32 Rinkel GJ, Wijdicks EF, Vermeulen M, et al Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture AJNR Am J Neuroradiol 1991;12(5):829Y834 22 Raya AK, Diringer MN Treatment of subarachnoid hemorrhage Crit Care Clin 2014; 30(4):719Y733 doi:10.1016/j.ccc.2014.06.004 1286 23 Rabinstein AA, Lanzino G, Wijdicks EF Multidisciplinary management and emerging therapeutic strategies in aneurysmal subarachnoid haemorrhage Lancet Neurol 2010;9(5):504Y519 doi:10.1016/ S1474-4422(10)70087-9 33 Tang C, Zhang TS, Zhou LF Risk factors for rebleeding of aneurysmal subarachnoid hemorrhage: a meta-analysis PLos One 2014; 9(6):e99536 doi:10.1371/journal.pone.0099536 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 34 Report of World Federation of Neurological Surgeons committee on a universal subarachnoid hemorrhage grading scale J Neurosurg 1988;68(6):985Y986 35 Claassen J, Bernardini GL, Kreiter K, et al Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited Stroke 2001;32(9):2012Y2020 36 Suarez JI, Zaidat OO, Suri MF, et al Length of stay and mortality in neurocritically ill patients: impact of a specialized neurocritical care team Crit Care Med 2004;32(11):2311Y2317 doi:10.1097/01.CCM.0000146132.29042.4C 37 Macdonald RL, Diringer MN, Citerio G Understanding the disease: aneurysmal subarachnoid hemorrhage Intensive Care Med 2014;40(12):1940Y1943 doi:10.1007/ s00134-014-3483-5 38 Etminan N, Macdonald RL Medical complications after aneurysmal subarachnoid hemorrhage: an emerging contributor to poor outcome World Neurosurg 2014;pii: S1878-8750(14)00577-4 doi:10.1016/ j.wneu.2014.06.031 Continuum (Minneap Minn) 2015;21(5):1263–1287 39 Macdonald RL Delayed neurological deterioration after subarachnoid hemorrhage Nat Rev Neurol 2014;10(1):44Y58 doi:10.1038/ nrneurol.2013.246 40 Vergouwen MD, Ilodigwe D, Macdonald RL Cerebral infarction after subarachnoid hemorrhage contributes to poor outcome by vasospasm-dependent and -independent effects Stroke 2011;42(4):924Y929 doi:10.1161/STROKEAHA.110.597914 41 Vergouwen MD, Vermeulen M, van Gijn J, et al Definition of delayed cerebral infarction after aneurysmal subarachnoid hemorrhage as an outcome event in clinical trials and observational studies: proposal of a multidisciplinary research group Stroke 2010;41(10):2391Y2395 doi:10.1161/ STROKEAHA.110.589275 42 Suarez JI, Qureshi AI, Yahia AB, et al Symptomatic vasospasm diagnosis after subarachnoid hemorrhage: evaluation of transcranial Doppler ultrasound and cerebral angiography as related to compromised vascular distribution Crit Care Med 2002;30(6):1348Y1355 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1287 [...]... common systemic complications of subarachnoid hemorrhage www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1283 Subarachnoid Hemorrhage KEY POINTS h Pulmonary edema or acute respiratory distress syndrome in patients with subarachnoid hemorrhage should be treated with judicious use of diuretics and other standard heart failure therapies... American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 34 Report of World Federation of Neurological Surgeons committee on a universal subarachnoid hemorrhage grading scale J Neurosurg 1988;68(6):985Y986 35 Claassen J, Bernardini GL, Kreiter K, et al Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the... institution follows an algorithm for identifying and treating subarachnoid hemorrhage similar to the one proposed by Macdonald as shown in Figure 1-5.39 Patients with SAH are stratified into low risk (ie, older age, a WFNSS score of 1 to 2, and a modified Fisher Scale score of less than 3), high risk (ie, a WFNSS score of 1 to 3 and a modified Fisher Scale score of 3), and high risk with poor neurologic status... undetermined etiology (low quality of evidence, strong recommendation) Continued on page 1274 Continuum (Minneap Minn) 2015;21(5):1263–1287 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited 1273 Subarachnoid Hemorrhage TABLE 1-5 Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Continued from page... communicating hydrocephalus and placement of an external ventricular drain (arrow) after patient developed decreased level of consciousness D, Noncontrasted head CT scan shows placement of a ventriculoperitoneal shunt FIGURE 1-4 Comment This case exemplifies the clinical presentation and management of two of the most common neurologic complications of SAH: delayed cerebral ischemia and hydrocephalus This... Treatment of Unsecured Aneurysms Treatment of unsecured aneurysms has evolved, and two accepted efficacious management modalities currently exist: surgical clipping and endovascular coilContinuum (Minneap Minn) 2015;21(5):1263–1287 ing The choice of treatment depends on several factors, including the patient’s age and aneurysm location, morphology, and relationship to adjacent vessels Because of the complexity... Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Continued from page 1272 Treatment Decision American Heart Association/American Stroke Association2,a Blood pressure control Between the time of SAH symptom onset and aneurysm obliteration, blood pressure should be controlled with a titratable agent to balance the risk of stroke, hypertension-related rebleeding, and. .. oxyhemoglobin and erythrocyte contents through hemolysis, which unleashes a host of inflammatory and proapoptotic factors The risk for cerebral vasospasm increases with the thickness, density, location, and persistence of the subarachnoid blood In addition, poor clinical grade, loss of consciousness at ictus, cigarette smoking, cocaine use, SIRS, hyperglycemia, and hydrocephalus also increase the risk of delayed... Fever treatment Aggressive control of fever to a target of normothermia by use of standard or advanced temperature-modulating systems is reasonable in the acute phase of SAH (Class IIa, Level B) During the period of risk for delayed cerebral ischemia, control of fever is desirable; intensity should reflect the individual patient’s relative risk of ischemia (low quality of evidence, strong recommendation)... is the gold standard for detection of large artery vasospasm (high quality of evidence, strong recommendation) Continued on page 1275 1274 www.ContinuumJournal.com Copyright © American Academy of Neurology Unauthorized reproduction of this article is prohibited October 2015 TABLE 1-5 Summary of Key Recommendations for the Management of Patients With Subarachnoid Hemorrhage Continued from page 1274