You are in: eMedicine Specialties > Neurosurgery > Vascular Subarachnoid HemorrhageArticle Last Updated: Nov 16, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: Jennifer Krawczyk, MD, Clinical Assistant Professor, Department of Internal Medicine, Division of Emergency Medicine, University of California at Irvine Coauthor(s): Todd Newton, MD, Staff Physician, Department of Emergency Medicine, University of California at Irvine; Sean Lavine, MD, Department of Neurological Surgery, Columbia University Editors: Paul L Penar, MD, Program Co-Director, Associate Professor, Department of Surgery, Division of Neurosurgery, University of Vermont School of Medicine; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Allen R Wyler, MD, Medical Director, Northstar Neuroscience, Inc; Herbert H Engelhard III, MD, PhD, Director, UIC Neuro-Oncology Program, Chief, Division of Neuro-Oncology, Associate Professor, Department of Neurosurgery, University of Illinois at Chicago; Allen R Wyler, MD, Medical Director, Northstar Neuroscience, Inc Author and Editor Disclosure Synonyms and related keywords: SAH, nontraumatic subarachnoid hemorrhage, nontraumatic SAH, extravasation of blood into the subarachnoid space between the pial and arachnoid membranes, spontaneous atraumatic intracranial hemorrhage, ruptured cerebral aneurysm, ruptured arteriovenous malformation INTRODUCTIONSection 2 of 11
  The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH comprises half of spontaneous atraumatic intracranial hemorrhages, the other half consist of bleeding that occurs within the brain parenchyma. Intracranial hemorrhage as a whole comprises 20% of all strokes. SAH is a devastating condition with high morbidity and mortality, and, in the United States, it is associated with an annual cost of $1.75 billion. SAH occurs in various clinical contexts, the most common being head trauma. However, the familiar medical use of the term SAH refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM). The scope of this chapter is confined to nontraumatic SAH. History of the ProcedureAncient Greek, Egyptian, and Arabic literature all have references to intracranial aneurysms. The first successful treatment of an intracranial aneurysm was reported in the early 19th century; however, such outcomes did not become routine until the Dandy era and the advent of modern neurosurgical techniques. Dandy performed the first successful clipping of an aneurysm in 1937, using a vascular clip designed by Harvey Cushing. In the following years, advancements in microneurosurgical techniques, including the operating microscope, microsurgical instruments, better anesthesia, and improved management of SAH complications, have led to significant improvements in surgical outcomes. Endovascular therapy for the treatment of intracranial aneurysms was pioneered in the mid 1970s by Serbinenko at the Moscow Institute of Neurosurgery. This initial approach, which attempted to achieve parent vessel occlusion using latex balloons, was moderately successful in a limited subset of cases. However, it never gained widespread applicability. Other balloon devices, including detachable silicon and latex balloons, subsequently were developed in the United States, Europe, and Japan. The success of balloon embolization has been tempered by the associated complications of deflation and aneurysmal rupture. Arguably, the most significant recent development in endovascular therapy occurred in 1990, when Guglielmi and colleagues at the University of California Los Angeles (UCLA) Medical Center developed the Guglielmi detachable coil system (GDC). The GDC is a radiopaque platinum coil that is delivered through a microcatheter into an aneurysm, which then is detached by electrolysis. GDCs gained approval by the Food and Drug Administration (FDA) in 1995 for treatment of aneurysms that have the potential for high surgical morbidity and mortality. In Europe, GDCs have been used as a first-line intervention in lieu of surgical treatment for patients without contraindications to endovascular therapy. In the last 5 years, endovascular coiling has become first-line treatment for aneurysms at several centers in the United States and is continuing to gain popularity in those patients appropriate for the procedure. Other endovascular techniques under investigation include liquid embolic agents, intravascular laser treatments, and intravascular stents. As endovascular occlusive techniques evolve, it seems likely that they will play a larger role in the management of SAH. ProblemNontraumatic SAH usually is the result of a ruptured cerebral aneurysm or AVM. Blood extravasation into the subarachnoid space has a detrimental effect on both local and global brain function and leads to high morbidity and mortality rates. Although mortality rates of SAH have decreased since 1979, it remains a devastating neurological problem. An estimated 15% of patients die before reaching the hospital. Approximately 25% of patients die within 24 hours, with or without medical attention. The mortality rate at the end of 1 week approaches 40%. Half of all patients die in the first 6 months. Age-adjusted mortality rates are 62% greater in females than in males and 57% greater in blacks than in whites. While advances in the management of SAH have led to an overall decrease in mortality rates, approximately 40% of all survivors have major neurologic deficits. Morbidity and mortality increase with age and are related to the overall health status of the patient. FrequencySAH is a major clinical problem worldwide. The annual incidence of aneurysmal SAH in the United States is 6-16 cases per 100,000 population, with approximately 30,000 episodes occurring each year. Unlike other subcategories of stroke, the incidence of SAH has not decreased over time. However, since 1970, population-based survival rates have improved. The incidence of SAH worldwide varies widely (2-49 cases per 100,000 population), with the highest rates occurring in Japan and Finland. Age: Incidence increases with age and peaks at age 50 years. Approximately 80% of cases of SAH occur in people aged 40-65 years, with 15% occurring in people aged 20-40 years. Only 5% of cases of SAH occur in people younger than 20 years. The prevalence of SAH is rare in children younger than 10 years; SAH in children younger than 10 years accounts for only 0.5% of all cases. Sex: Incidence of SAH in women is higher than in men (3:2). The risk of SAH is significantly higher in the third trimester of pregnancy, and SAH from aneurysmal rupture is a leading cause of maternal mortality, accounting for 6-25% of maternal deaths during pregnancy. A higher incidence of AVM rupture also has been reported during pregnancy. Race: The risk is higher in blacks than in whites; however, people of all ethnic groups develop intracranial aneurysms. The disparity in frequency of rupture has been attributed to population variance with respect to prevalence of risk factors and age distribution. EtiologyNontraumatic cases of SAH usually are caused by extravasation of blood from abnormal blood vessels onto the surface of the brain. Usually, this is the result of aneurysmal or AVM leakage or rupture. Rupture of "berry," or saccular, aneurysms of the basal vessels of the brain comprises 77% of nontraumatic SAH cases. The etiology of cerebral aneurysms is unknown, but both congenital and acquired factors are thought to play a role. Evidence supporting the role of congenital causes in aneurysm formation includes the following:
Congenital defects in the muscle and elastic tissue of the arterial media in the vessels of the circle of Willis are found in approximately 80% of normal vessels at autopsy. These defects lead to microaneurysmal dilatation in 20% of the population (<2 mm) and larger dilation (>5 mm) and aneurysms in 5% of the population. Acquired factors thought to be associated with aneurysmal formation include the following:
AVMs are the second most identifiable cause of SAH, accounting for 10% of cases of SAH. Familial cases of AVM are rare, and the problem may result from sporadic abnormalities in embryologic development. AVMs are thought to occur in approximately 4-5% of the general population, of which 10-15% are symptomatic. Less common causes of SAH include the following:
Risk factors Although risk factors for SAH have been evaluated extensively, little conclusive evidence has been derived. Smoking appears to be a significant risk factor, as does heavy alcohol consumption. Data regarding the relationship between hypertension and SAH are conflicting. The following do not appear to be significant risk factors for SAH:
The risk of AVM rupture is greater during pregnancy. PathophysiologyAneurysms usually occur at the branching sites on the large cerebral arteries of the circle of Willis. The early precursors of aneurysms are small outpouchings through defects in the media of the arteries. These defects are thought to expand as a result of hydrostatic pressure from pulsatile blood flow and blood turbulence, which is greatest at the arterial bifurcations. A mature aneurysm has a paucity of media, replaced by connective tissue, and has diminished or absent elastic lamina. The probability of rupture is related to the tension on the aneurysm wall. The law of La Place states that tension is determined by the radius of the aneurysm and the pressure gradient across the wall of the aneurysm. Thus, the rate of rupture is directly related to the size of the aneurysm. Aneurysms with a diameter of 5 mm or less have a 2% risk of rupture, whereas 40% of those 6-10 mm have already ruptured upon diagnosis. Although hypertension has been identified as a risk factor for aneurysm formation, the data with respect to rupture are conflicting. However, certain hypertensive states, such as those induced by use of cocaine and other stimulants, clearly promote aneurysm growth and rupture earlier than would be predicted by the available data. Brain injury from cerebral aneurysm formation can occur in the absence of rupture via compressive forces that cause injury to local tissues and/or compromise of distal blood supply (mass effect). When an aneurysm ruptures, blood extravasates under arterial pressure into the subarachnoid space and quickly spreads through the cerebrospinal fluid (CSF) around the brain and spinal cord. Blood released under high pressure may directly cause damage to local tissues. Blood extravasation causes a global increase in intracranial pressure (ICP). Meningeal irritation occurs. Rupture of AVMs can result in both intracerebral hemorrhage and SAH. Currently, no explanation can be provided for the observation that small AVMs (<2.5 cm) rupture more frequently than large AVMs (>5 cm). ClinicalThe signs and symptoms of SAH range from subtle prodromal events, which often are misdiagnosed, to the classic presentation of catastrophic headache. The history and physical examination, especially the neurologic examination, are essential components in the diagnosis and clinical staging of SAH. Prodromal signs and symptoms usually are the result of one or more of the following: sentinel leaks, mass effect of aneurysm expansion, or emboli.
Clinical grading scales Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical scales most often employed are the Hunt and Hess and the World Federation of Neurological Surgeons (WFNS) grading systems. A third, the Fischer scale, classifies SAH based on CT scan appearance and quantification of subarachnoid blood.
The Hunt and Hess and the WFNS grading systems have been shown to correlate well with patient outcome. The Fischer classification has been used successfully to predict the likelihood of symptomatic cerebral vasospasm, one of the most feared complications of SAH. All 3 grading systems are useful in determining the indications for and timing of surgical management. For an accurate assessment of SAH severity, these grading systems must be used in concert with the patient's overall general medical condition and the location and size of the ruptured aneurysm. INDICATIONSSection 3 of 11
The indications for surgery in patients with SAH can be stratified based on clinical grade. Other factors, such as overall medical condition of the patient, aneurysm size and location, accessibility of the aneurysm for surgical repair, and presence or absence of thrombus, also are important. For patients with a mild- or intermediate-grade SAH (Hunt and Hess/WFNS grades 1-3), surgical treatment is strongly recommended because the risks of SAH complications greatly exceed the risk of surgical complications. For patients with a poor grade of SAH (Hunt and Hess/WFNS grades 4-5), the decision whether to operate is controversial and largely institution-dependent. The overall outcome is poor, with or without surgical intervention. Patients with a higher grade of SAH or poor medical status that do not qualify for early surgery may be candidates for delayed surgery or endovascular obliteration of the aneurysm. Other indications for surgical management have been described recently and include the following:
Indications for endovascular treatment Endovascular therapy (eg, coil embolization) has been used increasingly in recent years in lieu of surgical clipping, with promising results. More definitive data are required comparing the traditional treatment modality (aneurysmal clipping) with newer endovascular techniques before conclusive recommendations can be made.
Surgery remains the standard reference for therapy and is favored over endovascular treatment when surgical risk is low or equal to that of endovascular therapy. However, many patients may be treated adequately with either method, and the ultimate choice of intervention often is guided by physician and institution preference. A combined approach may benefit a particular subset of patients, eg, those with a poor clinical grade and an aneurysm that cannot be occluded completely by endovascular therapy. Surgical indications for unruptured symptomatic aneurysms Surgery usually is indicated in patients with unruptured symptomatic aneurysms because the rate of subsequent rupture is high. Most symptomatic aneurysms are giant (large) aneurysms rather than saccular aneurysms. Patients with giant aneurysms face an increased surgical risk; however, this risk usually is much less than the morbidity and mortality associated with aneurysm rupture. Surgical indications for asymptomatic aneurysms The risk of aneurysmal rupture increases relative to the size of the aneurysm; however, the critical size with respect to increased risk of rupture is unknown. Unruptured aneurysms are reported to rupture at a rate of 1-1.4% per year. Most authors propose that surgical risks are eclipsed by the risks of mass effect and aneurysm rupture in patients younger than 65 years who have aneurysms larger than 1 cm in size. The impact of the size of the aneurysm is controversial. RELEVANT ANATOMYSection 4 of 11
Circle of WillisMost saccular aneurysms occur at bifurcations of the vessels that comprise the circle of Willis. The circle of Willis is in close proximity to the ventral surface of the diencephalon and is adjacent to the optic nerves and tracts. It extends from the superior border of the pons to the longitudinal fissure between the cerebral hemispheres. The circle of Willis is an important anastomosis for the 4 arteries that supply the brain—the 2 vertebral and the 2 internal carotid arteries. It can be divided into anterior and posterior sections. Anterior portion of the circle of Willis The anterior section of the circle of Willis consists of the internal carotid arteries, the anterior cerebral artery, and the anterior communicating artery.
Posterior portion of the circle of Willis The posterior segment of the circle of Willis consists of the proximal portions of the posterior cerebral arteries and the paired posterior communicating arteries.
Location of aneurysm ruptureApproximately 85% of saccular aneurysms occur in the anterior circulation. The most common sites of rupture are as follows:
CONTRAINDICATIONSSection 5 of 11
No strict contraindications to surgery for aneurysmal SAH exist other than unstable medical status or a lesion not amenable to surgical therapy. Patient stratification with respect to endovascular therapy versus surgery is discussed in Treatment. WORKUPSection 6 of 11
Lab Studies
Imaging Studies
Other Tests
Diagnostic Procedures
TREATMENTSection 7 of 11
Medical therapyThe initial management of patients with SAH is directed at patient stabilization. Assess the level of consciousness and airway, as well as breathing and circulation (ABCs). Endotracheal intubation should be performed for patients presenting with coma, depressed level of consciousness, inability to protect their airway, or increased ICP. Rapid sequence intubation should be employed, if possible, including the use of sedation, defasciculation, short-acting neuromuscular blockade, and agents to blunt an increase in ICP. Intravenous (IV) access should be obtained, including central and arterial lines. A short-acting benzodiazepine, such as midazolam, should be administered prior to all procedures. Monitoring should include the following:
The traditional treatment of ruptured cerebral aneurysms included strict blood pressure control, with fluid restriction and antihypertensive therapy. This approach was associated with a high rate of morbidity and mortality from the ischemic complications of hypovolemia and hypotension. The current recommendations advocate the use of antihypertensive agents when the mean arterial pressure (MAP) exceeds 130 mm Hg. Intravenous beta-blockers, which have a relatively short half-life, can be titrated easily and do not increase ICP. Beta-blockers are the agents of choice in patients without contraindications. Most clinicians avoid the use of nitrates, such as nitroprusside or nitroglycerin, which elevate ICP. Hydralazine and calcium channel blockers have a fast onset and lead to relatively less increase in ICP than do nitrates. Angiotensin-converting enzyme inhibitors have a relatively slow onset and are not first-line agents in the setting of acute SAH. Patients with signs of increased ICP or herniation should be intubated and hyperventilated. Minute ventilation should be titrated to achieve a PCO2 of 30-35 mm Hg. Avoid excessive hyperventilation, which may potentiate vasospasm and ischemia. Other interventions for increased ICP include the following:
All patients should receive frequent neurological evaluation. Use sedatives and analgesics cautiously to avoid masking the neurological examination. Emergent neurosurgical consultation should be obtained in all cases of suspected SAH. Prophylaxis and treatment of complications Additional medical management is directed to prevent and treat the following common complications of SAH:
Ideally, management of the complications of SAH should take place in a neurologic intensive care unit or in an intensive care unit similarly equipped. Rebleeding is the most dreaded early complication of SAH. The greatest risk of rebleeding occurs within the first 24 hours of rupture (4.1%). The cumulative risk of rebleeding is 19% at 14 days. The overall mortality rate from rebleeding is reported to be as high as 78%. Measures to prevent rebleeding include the following:
Cerebral vasospasm, the delayed narrowing of the large capacitance vessels at the base of the brain, is a leading cause of morbidity and mortality in survivors of nontraumatic SAH. Vasospasm is reported to occur in as many as 70% of patients with SAH and is clinically symptomatic in as many as 30% of patients. Most commonly, this occurs 4-14 days after the hemorrhage. Vasospasm can lead to impaired cerebral autoregulation and may progress to cerebral ischemia and infarction. Most often, the terminal internal carotid artery or the proximal portions of the anterior and middle cerebral arteries are involved. The arterial territory involved is not related to the location of the ruptured aneurysm. Risk factors for vasospasm include the following:
Symptoms vary with the arterial territory involved, but patients typically present with a new-onset general decrease in consciousness or focal neurological deficit. Vasospasm may be clinically indistinguishable from rebleeding; imaging studies are required to exclude the latter. Conventional angiography is the definitive imaging study for vasospasm. The diagnosis of vasospasm can be made reliably at the bedside in a noninvasive fashion with transcranial Doppler. Other tests, such as single photon emission computed tomography (SPECT), positron emission tomography (PET), xenon CT scan, and radioactive xenon clearance, can be useful for evaluation of regional cerebral blood flow in patients with vasospasm but often are difficult to perform on critically ill patients. Approximately 15-20% of patients with symptomatic vasospasm will have a poor outcome despite maximal medical therapy, including mortality in 7-10% of patients and severe morbidity in 7-10% of patients. Measures used for prevention of vasospasm include the following:
If vasospasm becomes symptomatic, most authors advocate the use of hypertensive, hypervolemic, and hemodilutional (HHH) therapy. While the efficacy of HHH therapy still is subject to debate, a number of studies have demonstrated improved cerebral blood flow and resolution of the ischemic effects of vasospasm. Initiation of HHH therapy requires placement of a pulmonary artery catheter in order to guide volume expansion and inotropic or vasopressor therapy. This therapy should be reserved for patients with aneurysms secured by surgical clipping or endovascular techniques in order to reduce the risk of rebleeding. Hypervolemia may be achieved by using packed erythrocytes, isotonic crystalloid, and colloid and albumin infusions in conjunction with vasopressin injection. Corticosteroids may be of some benefit; however, such treatment remains controversial. The hematocrit should be maintained at 30-35% via hemodilution or transfusion in order to optimize blood viscosity and oxygen delivery. Central venous pressure (CVP) should be maintained at 10-12 mm Hg. Pulmonary artery wedge pressure (PAWP) should be maintained at 19-20 mm Hg. Aggressive hypertensive therapy with inotropes and vasopressors (eg, dobutamine) can be initiated, if warranted. Transluminal balloon angioplasty is recommended for treatment of vasospasm after failure of conventional therapy. One study reported improved neurologic outcome in 70% of patients with symptomatic vasospasm after transluminal angioplasty. Case series reports have indicated that angioplasty appears to be effective in treating vasospasm of large proximal vessels. It is not effective in direct treatment of vasospasm of more distal vessels; however, distal blood flow may be increased as a result of increased proximal vessel diameter. The potential complications of angioplasty include vessel rupture, dissection, or occlusion, as well as intracerebral hemorrhage. Intra-arterial injection of papaverine has been reported to improve outcome, but more data are needed before routine use can be recommended. The beneficial effects of papaverine infusion appear to be short-lived compared to those of angioplasty. Acute obstructive hydrocephalus complicates 20% of SAH cases and usually occurs within the first 24 hours after hemorrhage. This condition can precipitate life-threatening brainstem compression and occlusion of blood vessels. Hydrocephalus presents as a relatively abrupt mental status change, including lethargy, stupor, or coma. CT scan differentiates hydrocephalus from rebleeding. Treatment for acute hydrocephalus includes external ventricular drainage, depending on the severity of clinical neurologic dysfunction or CT scan findings. Rapid lowering of ICP during intraventricular catheter placement is associated with a higher risk of rebleeding and should be avoided. Resolution of hydrocephalus may be assessed periodically by blocking CSF drainage while monitoring ICP. Late or chronic hydrocephalus, caused by scarring of the arachnoid granulations and alterations in CSF absorption, occurs in 10-15% of patients with SAH. Typically, late hydrocephalus is of the communicating type and develops 10 or more days after SAH. Patients may present with incontinence, gait instability, and cognitive deterioration. It may be impossible to distinguish late hydrocephalus from vasospasm clinically. Symptomatic cases of hydrocephalus may be managed by temporary lumbar CSF drainage, serial LPs, or placement of a permanent ventricular shunt. Shunt placement may not be necessary in mild cases. Hyponatremia following SAH occurs in 10-34% of cases. Elevated levels of atrial natriuretic factor (ANF) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been implicated in recent studies of post-SAH hyponatremia. Administration of isotonic fluid can prevent volume contraction but not hyponatremia. Use of slightly hypertonic sodium chloride (1.5% sodium chloride) at rates above maintenance requirements usually is efficacious for SAH-induced hyponatremia. Avoid fluid restriction in patients with SAH. Seizures occur in as many as 25% of patients following SAH and are most common after rupture of middle cerebral artery aneurysms. Seizures can lead to increased cerebral blood flow, hypertension, and elevated ICP, thereby escalating the risk of rebleeding and neurologic deterioration. Generalized, partial, and complex-partial seizures are observed after SAH. Agents used for seizure prophylaxis include the following:
Acute pulmonary edema and hypoxia are almost universal in severe SAH. The pulmonary edema in SAH is believed to be neurogenic in origin and unrelated to HHH therapy; however, the latter is associated with an increased risk of fluid overload. SAH-induced hypoxemia likewise is believed to be partially neurogenic in origin because it is out of proportion to what would be expected from cardiac insufficiency or fluid overload. Treatment of acute pulmonary edema may include the use of gentle diuresis, dobutamine, and positive end-expiratory pressure (PEEP). Cardiac dysfunction occurs in a significant number of people with SAH. Neurogenic sympathetic hyperactivity, as well as increased levels of systemic catecholamines, has been implicated in SAH-associated cardiac dysfunction. Arrhythmias occur in as many as 90% of patients and most commonly include the following:
Arrhythmias are most prevalent in the first 48 hours following SAH. Only a small percentage of arrhythmias (usually those associated with hypokalemia) are life threatening. Because most ECG abnormalities that occur with SAH are benign and reversible, differentiating true myocardial ischemia from these benign changes is important. The perioperative therapy to prevent secondary cerebral ischemia (hypervolemia, hypertension) may exacerbate myocardial ischemia. Conversely, therapy for myocardial ischemia, such as nitrates, may increase ICP, lower cerebral perfusion pressure, and exacerbate cerebral ischemia. Two-dimensional echocardiography often is more sensitive in detecting myocardial ischemia than is ECG, and 2-dimensional echocardiography is useful in the setting of SAH. Surgical therapySurgical methods for treatment of SAH have improved dramatically with the advent of modern microsurgical techniques and, more recently, with the success of endovascular therapy. See Indications for discussion of the specific indications for treating an aneurysm surgically, endovascularly, or both. Current surgical options include the following: Direct aneurysmal clipping is still considered first-line treatment in the United States. The aneurysmal neck is obliterated via application of a clip that occludes blood flow to the aneurysmal dome without compromising flow to the parent artery. Clips are available in various sizes and shapes. Giant aneurysms or aneurysms with a calcified neck require specialized clips with added strength (tandem or booster clips). Of the various endovascular options currently available, most authors believe that GDCs will have the largest influence with respect to treatment of SAH. GDCs are first-line therapy in Europe. They are soft, flexible, and can be contoured to the configuration of the aneurysm. Sizes range from 2-20 mm in diameter and 2-30 cm in length. In limited clinical trials, GDCs have been reported to achieve excellent rates of aneurysmal occlusion combined with a low complication rate in appropriate patients. Two experimental coils, the bidimensional GDC and the 3-dimensional GDC may have even better potential for aneurysm occlusion than the current generation of GDCs, but further study is needed. Balloon embolization is efficacious in selected patients, but it has a higher incidence of complications than coil embolization. Other surgical options include the following: Proximal ligation of the parent artery or trapping of aneurysms with or without bypass: Proximal ligation is effective for giant aneurysms. Trial balloon occlusion can be used to assess which cases necessitate a bypass graft during the trapping procedure. Wrapping or coating of aneurysms may be the only option in rare cases of dissecting or fusiform aneurysms Preoperative detailsThe presurgical examination should consist of a general assessment, a neurologic assessment, and a radiologic assessment. General assessment Cardiac and pulmonary function can decline with SAH; therefore, all patients should undergo ECG and ABG monitoring. Hemodynamic status should be monitored with a pulmonary artery catheter in patients that show evidence of compromise. A funduscopic examination should be performed. As many as 10% of patients with SAH have subretinal hemorrhage, which can lead to loss of vision. Neurologic assessment Serial neurologic examinations should be performed until the time of surgery for early detection of complications. Minor changes in mood, mentation, or focal neurologic function can be an early indicator of an impending complication, such as arterial vasospasm. Radiologic assessment Transfemoral cerebral angiography can provide important information about the size, shape, and configuration of the aneurysmal dome and neck, as well as the relationship of the parent vessel and perforators. Multiple views should be obtained to best delineate the anatomy of the aneurysmal neck. During diagnostic angiography, a trial balloon occlusion of the parent artery can be performed. This can be important in giant and fusiform aneurysms that may need to be "trapped" because they lack a defined neck for surgical clipping. A trial balloon occlusion also may provide important information about collateral blood flow. Transcranial Doppler studies are useful in detecting and following the course of arterial vasospasm. CT scan may detect calcification of the aneurysmal dome and neck, as well as the presence of thrombus. This information can have important surgical implications. CT angiography may be helpful in demonstrating the anatomy and relationships to other vessels. An MRI can help delineate the degree of intramural thrombus in giant aneurysms. Timing of surgical interventionThe timing of surgery for SAH has been a controversial topic for over 3 decades. Early surgery (0-3 d) has the following advantages:
Disadvantages of early surgery for SAH include the following:
Delayed surgery for SAH (>10 d posthemorrhage) has the following advantages:
The disadvantages of delayed surgery are as follows:
The International Cooperative Study on Timing of Aneurysm Surgery findings are as follows:
For patients with an intermediate grade of SAH (Hunt and Hess/WFNS grade 3), the published results are less conclusive.
The timing of surgical management for patients with high-grade SAH (Hunt and Hess/WFNS grades 4-5) must be individualized depending on the following criteria:
Data suggest that some patients with an initial GCS less than 5 can have good outcomes if the following occur:
Patients with significant evidence of brain destruction, increased ICP, and angiogram revealing poor intracranial filling have a universally poor outcome regardless of treatment. The overall outcome in patients with high-grade SAH is poor with or without surgical intervention; however; because surgical treatment seems to benefit some patients, many authors suggest an aggressive approach to management. Intraoperative detailsSurgical clipping Most anterior circulation aneurysms can be approached from the pterion. Exceptions include (1) aneurysms arising from the division of the anterior cerebral artery into the pericallosal and callosal marginal branches and (2) small mycotic aneurysms on distal branches of the middle cerebral artery. Posterior circulation aneurysms are less accessible, and a number of modified approaches have been developed.
Skillful brain retraction is paramount in aneurysm surgery, with care taken to minimize tissue and vessel damage. Use of one blade only of a self-retaining retractor (eg, Yasargil, Greenburg, Sugita) usually is sufficient for adequate exposure of most saccular aneurysms and allows for the compensatory expansion and displacement of nonretracted areas of the brain, thus minimizing tissue trauma. The general approach to surgical clipping of saccular aneurysms is as follows:
Endovascular treatment with the Guglielmi detachable coil system Adequate airway protection, oxygenation, sedation, blood pressure management, and ICP management are paramount during the procedure. Ideally, endovascular treatment for patients with SAH should be performed under general anesthesia. Complete immobilization of the patient during catheterization and embolization is mandatory.
Postoperative detailsThe postoperative management of SAH is directed at prophylaxis and treatment of the complications of SAH (see Prophylaxis and treatment of complications). Follow-upPatients with neurologic deficits may require outpatient rehabilitation. Cognitive and psychological rehabilitation often is needed. SAH often causes nonspecific symptoms similar to postconcussion syndrome and include the following:
Specific postsurgical problems include the following:
Some patients may require steroid and/or anticonvulsant therapy as outpatients. Oral nimodipine therapy often is continued for 3-4 weeks after SAH. COMPLICATIONSSection 8 of 11
Complications of surgical clipping include the following:
Common complications of endovascular therapy include the following:
OUTCOME AND PROGNOSISSection 9 of 11
Despite advances in medical and surgical therapy, the mortality rate for aneurysmal SAH remains 50% at 1 year. Survival is inversely proportional to SAH grade upon presentation. Reported data demonstrate an approximate 70% survival rate for Hunt and Hess grade 1, 60% for grade 2, 50% for grade 3, 20% for grade 4, and 10% for grade 5. Approximately 25% of survivors have persistent neurologic deficits. Most survivors have either a transient or a permanent cognitive deficit. Mortality and morbidity are influenced by the magnitude of the bleed, the age of the patient, the presence or absence of comorbid conditions, and the occurrence of medical complications. For excellent patient education resources, visit eMedicine's Headache Center and Procedures Center. Also, see eMedicine's patient education article Aneurysm, Brain and Spinal Tap. FUTURE AND CONTROVERSIESSection 10 of 11
The future of SAH management most likely will revolve around the continuing development and refinement of minimally invasive endovascular techniques. Currently, controversy remains regarding the question of which aneurysms are appropriate for surgical or endovascular treatment; rigorous studies coupled with additional clinical experience will help with the formation of guidelines. Some aneurysms may require a combined approach. While GDC therapy is, to date, the most promising development in the realm of endovascular methodologies for SAH, the future almost certainly will provide materials that are even safer and more efficacious in occluding aneurysms. REFERENCESSection 11 of 11
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