Subarachnoid hemorrhage

The author: Professor Yasser Metwally

http://yassermetwally.com

INTRODUCTION

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 represents 20% of all strokes.

Subarachnoid hemorrhage is a devastating condition with high morbidity and mortality, and in the US, 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 Procedure: Ancient 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 US, 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 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 are used as a first-line intervention in lieu of surgical treatment for patients without contraindications to endovascular therapy.

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.

Problem: Nontraumatic SAH usually is the result of a ruptured cerebral aneurysm or arteriovenous malformation. Blood extravasation into the subarachnoid space has a detrimental effect on both local and global brain function and leads to a high morbidity and mortality.

Frequency: Subarachnoid hemorrhage is a major clinical problem worldwide.

In the US: The annual incidence of aneurysmal SAH in the US is 6-16 per 100,000, 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.

Internationally: The incidence of SAH worldwide varies widely (2-49 per 100,000), with the highest rates occurring in Japan and Finland.

Age: Incidence increases with age and peaks at 50 years. Approximately 80% occur between ages 40-65 years, with 15% occurring between ages 20-40 years. Only 5% occur below the age of 20. The prevalence of SAH is rare in children under 10 years of age, accounting 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 arteriovenous malformation (AVM) rupture also has been reported during pregnancy.

Race: The risk is higher in blacks than in whites; however, 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.

Mortality/Morbidity: 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 males and 57% greater in blacks than whites. While advances in the management of SAH have led to an overall decrease in mortality, 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.

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 conflict regarding the relationship between hypertension and SAH. The following do not appear to be significant risk factors for SAH:

  • Use of oral contraceptives

  • Hormone replacement therapy

  • Hypercholesterolemia

  • Vigorous physical activity

The risk of AVM rupture is greater during pregnancy.

Etiology: Nontraumatic subarachnoid hemorrhages 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 comprise 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:

  • Clusters of familial occurrence, such as in Finland, where the incidence of familial cerebral aneurysm is 10%

  • Significant incidence of multiple aneurysms in patients with SAH (15%)

  • Aneurysms have been associated with specific congenital diseases (eg, coarctation of the aorta, Marfan syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia, polycystic kidney disease).

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 (>5 mm) and aneurysms in 5% of the population.

Acquired factors thought to be associated with aneurysmal formation include the following:

  • Atherosclerosis

  • Hypertension

  • Hemodynamic stress

AVMs are the second most identifiable cause of SAH, accounting for 10% of SAHs. Familial cases of AVM are rare, and it is thought that 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:

  • Fusiform and mycotic aneurysms

  • Fibromuscular dysplasia

  • Blood dyscrasias

  • Moyamoya disease

  • Infection

  • Neoplasm

  • Trauma (fracture at the base of the skull leading to internal carotid aneurysm)

  • Amyloid angiopathy (especially in the elderly)

  • Vasculitis

  • Idiopathic SAH

Pathophysiology: Aneurysms 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, it is clear that certain hypertensive states, such as those induced by use of cocaine and other stimulants, 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 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 given for the observation that small AVMs (<2.5 cm) rupture more frequently than large AVMs (>5 cm).

Figure 1. Massive subarachnoid hemorrhage due to ruptured berry aneurysm (Click to magnify figure)

Clinical: The signs and symptoms of SAH range from subtle prodromal events that often are misdiagnosed to the classic presentation of catastrophic headache. The history and physical, 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.

  • Sentinel or “warning” leaks that produce minor blood leakage are reported to occur in 30-50% of aneurysmal SAHs. Sentinel leaks produce sudden focal or generalized head pain that may be severe. Sentinel headaches precede aneurysm rupture by a few hours to a few months, with a reported mean of 2 weeks prior to discovery of the SAH. In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia, malaise, or, less commonly, neck pain. These symptoms may be ignored by the physician. Therefore, a high index of suspicion is necessary for accurate diagnosis. Sentinel leaks usually do not generate symptomatology suggestive of elevated intracranial pressure. Sentinel leaks usually do not occur in the setting of AVM.

  • Mass effect: Prodromal presentations occasionally are caused by the mass effect of an expanding aneurysm and have characteristic features based upon aneurysm location.

    • Posterior communicating artery/internal carotid artery – Focal, progressive retro-orbital headaches and oculomotor nerve palsy

    • Middle cerebral artery – Contralateral face or hand paresis; aphasia (left side); contralateral visual neglect (right side)

    • Anterior communicating artery – Bilateral leg paresis and bilateral Babinski sign

    • Basilar artery apex – Vertical gaze, paresis, and coma

    • Intracranial vertebral artery/posterior inferior cerebellar artery – Vertigo, components of lateral medullary syndrome

  • Emboli: Transient ischemic attacks can occur from emboli originating from intraaneurysmal thrombus formation. The classic symptoms and signs of aneurysmal rupture into the subarachnoid space comprise one of the most pathognomonic presentations in all of clinical medicine. Symptomatology is as follows:

    • A sudden onset of severe headache, often described as the “worst headache of my life.” Absence of headache in the setting of a ruptured intracranial aneurysm is rare, and probably represents amnesia for the event.

    • Nausea and/or vomiting

    • Symptoms of meningeal irritation, including nuchal rigidity and pain, back pain, and bilateral leg pain, occur in up to 80% of SAHs (but may take several hours to manifest).

    • Photophobia and visual changes are common.

    • A sudden loss of consciousness (LOC) occurs at the ictus in up to 45% of patients as intracranial pressure exceeds cerebral perfusion pressure.

    • LOC often is transient; however, approximately 10% of patients remain in a coma for several days, depending on the location of the aneurysm and the amount of bleeding.

    • Seizures during the acute phase of SAH occur in 10-25% of patients.

    • No correlation exists between seizure focus and the anatomical site of aneurysm rupture.

    • Less severe hemorrhages may present with headache of moderate intensity, neck pain, and nonspecific symptoms.

    Physical examination of the patient with SAH may be normal or consistent with one or more of the following:

    • Focal neurologic abnormalities, including hemiparesis, aphasia, hemineglect, cranial nerve palsies, and memory loss, are present in 25% of patients.

    • Motor neurologic deficits occur in 10-15% of patients, usually from middle cerebral artery aneurysms.

    • Ophthalmologic examination may reveal subhyaloid retinal hemorrhages (20-30%) and papilledema.

    • Blood pressure elevation is seen in about 50% of patients. Blood pressure often becomes labile as ICP increases.

    • Temperature elevation, secondary to a chemical meningitis from subarachnoid blood products, is common after the fourth day following bleeding.

    • Tachycardia often is present for several days after SAH.

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.

  • Hunt and Hess grading system

    Grade 1 – Asymptomatic or mild headache

    Grade 2 – Moderate to severe headache, nuchal rigidity, and no neurological deficit other than possible cranial nerve palsy

    Grade 3 – Mild alteration in mental status (confusion, lethargy), mild focal neurological deficit

    Grade 4 – Stupor and/or hemiparesis

    Grade 5 – Comatose and/or decerebrate rigidity

  • WFNS scale

    Grade 1 – Glasgow Coma Scale (GCS) of 15, motor deficit absent

    Grade 2 – GCS of 13-14, motor deficit absent

    Grade 3 – GCS of 13-14, motor deficit present

    Grade 4 – GCS of 7-12, motor deficit absent or present

    Grade 5 – GCS of 3-6, motor deficit absent or present

  • Fischer scale (CT scan appearance)

    Group 1 – No blood detected

    Group 2 – Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm

    Group 3 – Localized clots and/or vertical layers of blood 1 mm or greater in thickness

    Group 4 – Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present

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.

INDICATIONS FOR SURGERY FOLLOWING ANEURYSMAL RUPTURE

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 recently been described and include the following:

  • Large and giant aneurysm

  • Wide-necked aneurysms

  • Vessels emanating from the aneurysm dome

  • Mass effect or hematoma associated with the aneurysm

  • Recurrent aneurysm after coil embolization

Indications for endovascular treatment: Endovascular therapy (eg, coil embolization) has increasingly been utilized 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. In general, endovascular treatment of aneurysms is favored over surgery in the following situations:

  • Patients with poor clinical grades

  • Patients that are medically unstable

  • In situations where aneurysm location imparts an increased surgical risk, such as cavernous sinus and many basilar tip aneurysms

  • Small-neck aneurysms in the posterior fossa

  • Patients with early vasospasm

  • Cases where the aneurysm lacks a defined surgical neck (although these are also difficult to “coil”)

  • Patients with multiple aneurysms in different arterial territories if surgical risk is high

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; for instance, 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 of 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 age 65 years who have aneurysms larger than 1 cm in size. The impact of the size of the aneurysm is controversial.

RELEVANT ANATOMY AND CONTRAINDICATIONS

Relevant Anatomy:

Circle of Willis

Most 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.

  • The right internal carotid artery, along with the right external carotid artery, branches from the common carotid artery most often at C3 or C4, with a range of C1-T2.

  • The right common carotid artery originates from the brachiocephalic trunk, the first branch of the aorta.

  • The left common carotid artery, the second branch of the aorta, branches into the right internal and right external carotid arteries at about the same level as the right common carotid bifurcation.

  • The cerebral portions of the internal carotid arteries branch into the anterior and middle cerebral arteries at the medial end of the lateral sulcus.

  • The anterior communicating artery is a short segment that connects the 2 anterior cerebral arteries and forms the anterior border of the circle.

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.

  • The 2 posterior cerebral arteries arise from the terminal bifurcation of the basilar artery.

  • The basilar artery is formed by the union of the 2 vertebral arteries, each of which begins as a branch of the first part of the subclavian artery.

  • The posterior communicating arteries connect the internal carotid and the posterior cerebral arteries and form the posterior-lateral borders of the circle of Willis.

Location of aneurysm rupture: Approximately 85% of saccular aneurysms occur in the anterior circulation. The most common sites of rupture are as follows:

  • The internal carotid artery including the posterior communicating junction (41%)

  • Anterior communicating artery/anterior cerebral artery (34%)

  • Middle cerebral artery (20%)

  • Vertebral-basilar arteries (4%)

  • Other arteries (1%)

Contraindications: There are no strict contraindications to surgery for aneurysmal SAH other than unstable medical status or a lesion not amenable to surgical therapy. Patient stratification with respect to endovascular therapy versus surgery is discussed later in this chapter.

WORKUP

Lab Studies:

  • CBC – For evaluation of possible infection or hematologic abnormality

  • Prothrombin time (PT) and partial thromboplastin time (aPTT) – For evaluation of possible coagulopathy

  • Serum electrolytes – To establish a baseline for detection of future complications

  • Blood type and screen – In case intraoperative transfusion is required or in the setting of massive hemorrhage

  • Cardiac enzymes – For evaluation of possible myocardial ischemia

  • Arterial blood gas (ABG) – Assessment is necessary in cases with pulmonary compromise

Imaging Studies:

  • CT scan: The diagnosis of SAH usually depends on a high index of clinical suspicion combined with radiographic confirmation via CT scan without contrast. The sensitivity decreases with respect to increased time from ictus and decreased scanner resolution (older CT scanners). CT scan has a sensitivity of 98% within the first 12 hours of the ictus and 93% within 24 hours, decreasing to approximately 80% at 72 hours and 50% at 1 week. CT scans are positive in 92% of patients who have SAH. Sensitivity is less on older second- or first-generation scanners. Most North American hospitals have been using third-generation scanners since the mid 1980s.

    Thin (3 mm) cuts are necessary to properly identify the presence of smaller hemorrhages.

    CT scan results may be falsely negative in patients with small hemorrhages and in patients with severe anemia.

    The location of blood within the subarachnoid space correlates directly with the location of the aneurysm in 70% of cases. In general, blood localized to the basal cisterns, the sylvian fissure, or the intrahemispheric fissure indicates rupture of a saccular aneurysm. Blood found lying over the convexities or within the superficial parenchyma of the brain often is indicative of AVM or mycotic aneurysm rupture.

    Anterior communicating artery aneurysms often are associated with interhemispheric and intraventricular hemorrhages. Middle communicating artery and posterior communicating artery aneurysms are associated with intraparenchymal hemorrhages.

    CT scan allows for the detection of ventricular size and, thus, evaluation and surveillance of mass effect and hydrocephalus.

    A contrast-enhanced CT scan may reveal an AVM; however, this study should not be performed before a noncontrast CT scan, because the contrast may interfere with the visualization of subarachnoid blood.

    After the diagnosis of SAH, further imaging should be done to characterize the source of the hemorrhage. This effort can include standard angiography, CT-angiography, and MR-angiography. If the diagnosis of SAH is yet unclear, lumbar puncture should be done (see below).

  • Cerebral angiography: This test is particularly useful in the following scenarios:

    • In cases of diagnostic uncertainty (after CT scan and lumbar puncture)

    • In patients with septic endocarditis and SAH to search for the presence of mycotic aneurysms

    In cases where the diagnosis of SAH has been determined, the timing of cerebral angiography will depend on surgical considerations. Cerebral angiography can provide the following important surgical information in the setting of SAH:

    • Cerebrovascular anatomy

    • Aneurysm location and source of bleeding

    • Aneurysm size and shape, as well as orientation of the aneurysm dome and neck

    • Relation of the aneurysm to the parent artery and perforating arteries

    • Presence of multiple or mirror aneurysms (identically placed aneurysms in both the left and right circulations)

    A trial balloon occlusion of the parent artery can be performed and may help to guide preoperative surgical planning. If cerebral angiography is negative (10-20%) a repeat test should be performed 3-4 weeks later. Patients with SAH and a negative cerebral angiography may have an improved prognosis. A negative study can result from aneurysm obliteration secondary to clotting. Hemorrhage secondary to a ruptured AVM or spinal cord aneurysm may be present despite a negative cerebral angiogram. Perimesencephalic venous hemorrhage should also be considered.

    Follow-up angiogram also is useful in the postsurgical patient to detect the presence of aneurysmal obliteration and to evaluate for possible cerebral vasospasm.

    The management of moribund patients with CT scan evidence of a large SAH and focal hematoma is controversial.

    Performing angiography may result in a life-threatening delay in treatment.

  • Infusion CT scan and CT-angiography: Some centers have obtained good results with infusion CT scanning. This scan employs a contrast dye and can be performed immediately after a noncontrast CT scan. Reformatted image data can be viewed and rotated in 2-dimensional displays. Infusion CT scanning has been reported to detect aneurysms larger than 3 mm with a sensitivity of 97%, which may provide sufficient anatomic detail to allow for surgical management in the absence of angiography.

  • MRI: This is not sensitive for SAH within the first 48 hours. MRI is a useful tool to diagnose AVMs that are not detected by cerebral angiography, or spinal AVMs causing SAH. It can be useful for diagnosing and monitoring unruptured cerebral aneurysms.

    MRI can detect aneurysms 5 mm or larger with a high sensitivity and is useful for monitoring the status of small, unruptured aneurysms. MRI can be used to evaluate the degree of intramural thrombus in giant aneurysms.

  • Magnetic resonance angiography (MRA): The role of MRA in the detection of SAH currently is under investigation; however, many authors believe that MRA eventually will replace conventional transfemoral cerebral angiography. Given the current limitations of MRA (eg, failure to detect posterior inferior communicating artery and anterior communicating artery aneurysms in one series) most authors feel that the risk/benefit ratio still favors conventional angiography.

  • Transcranial Doppler studies are useful in the detection and monitoring of arterial vasospasm.

  • Chest radiograph: All patients with SAH should have a baseline chest radiograph to serve as a reference point for evaluation of possible pulmonary complications.

Other Tests:

  • All patients with SAH should have an admission ECG. Electrocardiogram abnormalities frequently detected in patients with SAH include the following:

    • Nonspecific ST and T wave changes

    • Decreased PR intervals

    • Increased QRS intervals

    • Increased QT intervals

    • Presence of U waves

    • Dysrhythmias, including premature ventricular contractions (PVCs), supraventricular tachycardia (SVT) and bradyarrhythmias

    These changes are attributed to myocardial ischemia and/or infarction caused by high levels of circulating catecholamines.

    Myocardial ischemia/infarction is present in 20% of SAH cases.

  • Anticoagulation and thrombolytic therapy are contraindicated in cases of suspected SAH.

  • Evaluation of ventricular wall motion via echocardiogram may be necessary in cases with suspected myocardial ischemia.

Diagnostic Procedures:

  • Lumbar puncture (LP): This should be performed when there is strong clinical suspicion of SAH with a negative CT scan or when a CT scan is not available.

    If possible, a CT scan should be performed before lumbar puncture to exclude significant intracranial mass effect, elevated ICP, obstructive hydrocephalus, or obvious intracranial bleed. LP often is negative within 2 hours of the ictus and is most sensitive 12 hours after the bleed.

    No consensus is found in the literature on the lower limit of RBCs in the CSF, which signifies a positive tap. However, most counts will range from a few hundred to a million or more cells per cubic millimeter.

    LP should not be performed if the CT scan demonstrates a SAH because of the (small) risk of further intracranial bleeding associated with a drop in ICP.

    • SAH often can be distinguished from traumatic lumbar puncture by comparing the red blood cell count of the first and last tubes of CSF. The RBC count usually will not decrease between the first and last tubes in the setting of SAH; however, case reports of this phenomenon do exist.

    • The most reliable method of differentiating SAH from a traumatic tap is to spin down the CSF and examine the supernatant fluid for the presence of xanthochromia,
      a pink or yellow coloration of the CSF supernatant caused by the breakdown of RBCs and subsequent release of heme pigments.

    • Spectrophotometry is much more sensitive than the naked eye in detecting xanthochromia. Xanthochromia typically will not appear until 2-4 hours after the ictus.
      In nearly 100% of patients with a SAH, xanthochromia is present 12 hours after the bleed and remains for approximately 2 weeks. Xanthochromia is present 3 weeks after the bleed in 70% of patients, and it is still detectable at 4 weeks in 40%.

  • D-Dimer assay: It has been suggested by some authors that the D-Dimer assay can be used to discriminate SAH from traumatic LP; however, results have been conflicting and further data are needed. Spinal fluid samples taken within 24 hours of the ictus usually show a WBC-to-RBC ratio that is consistent with the normal circulating WBC/RBC ratio of approximately 1:1000. After 24 hours, CSF samples may demonstrate a polymorphonuclear and mononuclear polycytosis secondary to a chemical meningitis caused by the degradation products of subarachnoid blood.

TREATMENT

Medical therapy: The 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 intracranial pressure. 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:

    • Cardiac monitoring

    • Pulse oximetry

    • Automated and/or arterial blood pressure monitoring (arterial BP monitoring is indicated in high-grade SAH or when blood pressure is labile)

    • End-tidal carbon dioxide, if applicable

    • Urine output via placement of a Foley catheter

  • Antihypertensive therapy: The traditional treatment of ruptured cerebral aneurysms included strict blood pressure control, with fluid restriction and antihypertensives. 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. Intravenous beta-blockers, which have a relatively short half-life, can easily be titrated and do not increase ICP and 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 intracranial pressure 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:

    • Osmotic agents (eg, mannitol), which can dramatically decrease ICP (50% after 30 minutes postadministration)

    • Loop diuretics (eg, furosemide) also can decrease ICP

    • The use of IV steroids (eg, Decadron) is controversial but is recommended by some authors.

  • 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 common complications of SAH.

Rebleeding
Vasospasm
Hydrocephalus
Hyponatremia
Seizures
Pulmonary complications
Cardiac complications

Ideally, management of the complications of SAH should take place in a Neurointensive 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:

    • Bedrest in a quiet room

    • Analgesia, preferably with a short-acting and reversible agent such as fentanyl. Pain is associated with a transient elevation in blood pressure and increased risk of rebleeding.

    • Sedation (used with caution to avoid distorting subsequent neurologic evaluation) with a short-acting benzodiazepine such as midazolam.

    • Stool softeners

    • Antifibrinolytics have been shown to reduce the occurrence of rebleeding. However, outcome likely does not improve because of a concurrent increase in the incidence of cerebral ischemia.

  • Vasospasm: 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 up to 70% of patients with SAH and is clinically symptomatic in up to 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:

    • Larger volumes of blood in the subarachnoid space

    • Clinically severe SAH

    • Female gender

    • Young age

    • Smoking

    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 is required to exclude the latter. Conventional angiography is the definitive imaging study for vasospasm. The diagnosis of vasospasm can be made at reliably 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% and severe morbidity in 7-10%.

    Measures used for prevention of vasospasm include the following:

    • Maintenance of normovolemia, normothermia, and normal oxygenation are paramount to vasospasm prophylaxis. Volume status should be monitored closely, with avoidance of volume contraction, which can predispose to vasospasm.

    • Prophylaxis with oral nimodipine: Calcium channel blockers have been shown to reduce the incidence of ischemic neurological deficits, and nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH. Although the mechanism is unproven, it appears that nimodipine may prevent the ischemic complications of vasospasm by the neuroprotective effect of blockading the influx of calcium into damaged neurons. Calcium channel blockers and other antihypertensives should be used cautiously to avoid the deleterious effects of hypotension.

    • Some evidence indicates that subarachnoid clot removal achieved via intracisternal injections of recombinant tissue plasminogen activator (rTPA) may dramatically reduce the risk of vasospasm. This is performed after the clipping of the aneurysm. Thrombolytic therapy is associated with the theoretical risk of intracranial bleeding, and although the results of preliminary studies are favorable, rigorous clinical trials are needed to establish the safety and efficacy of this approach. Intracisternal antioxidants and anti-inflammatory agents are of uncertain value.

    • Aspiration and irrigation of the subarachnoid clot at the time of aneurysmal clipping usually results in suboptimal removal of the clot and is associated with a significant risk of iatrogenic trauma to pial surfaces and small vessels.

    • Intraoperative saline lavage to clear blood products from the subarachnoid space may be of some benefit, but its effectiveness remains unproven.

    • Some authors suggest that early CSF drainage via a ventricular drain may decrease the incidence of vasospasm. This intervention is performed after the aneurysm has been secured. Caution must be taken in order to prevent rapid or overly aggressive drainage of CSF, which may precipitate aneurysmal rebleeding. One author suggests draining the CSF if the ICP exceeds 20 mm Hg. The drain should be set at a height to drain at 20 mm Hg to avoid an excessive reduction in ICP.

    Treatment of vasospasm: 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 between 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.

    Intraarterial 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.

  • Hydrocephalus: 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 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.

    Treatment of chronic hydrocephalus: Symptomatic cases may be managed by temporary lumbar CSF drainage, serial lumbar punctures, 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 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 saline (1.5% saline) at rates above maintenance requirements is usually efficacious for SAH-induced hyponatremia. Avoid fluid restriction in patients with SAH.

  • Seizures occur in up to 25% of patients following SAH and are most common after rupture of middle cerebral artery aneurysms. Seizures can give rise 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 seen after SAH.

    Agents used for seizure prophylaxis include the following:

    • Phenytoin, the agent of choice – Phenytoin can achieve rapid therapeutic concentrations when loaded intravenously and does not cause alterations in consciousness.

    • Phenobarbital – Phenobarbital produces a sedative effect, which may mask the neurological evaluation and is used less frequently than phenytoin.

    • Chronic anticonvulsants – Not recommended in patients without prior seizure activity or risk factors such as hematoma, infarct, or middle cerebral artery aneurysm.

  • Pulmonary complications: 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 as 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 complications: Cardiac dysfunction occurs in significant number of SAH patients. Neurogenic sympathetic hyperactivity, as well as increased levels of systemic catecholamines, has been implicated in SAH-associated cardiac dysfunction. Arrhythmias occur in up to 90% of patients and most commonly include the following:

    • Premature ventricular complexes (PVCs)

    • Bradyarrhythmias

    • Supraventricular tachycardia

    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.

    Since the majority of ECG abnormalities that occur with SAH are benign and reversible, it is important to differentiate true myocardial ischemia from these benign changes. 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 is useful in the setting of SAH.

Surgical therapy: Surgical methods for treatment of SAH have improved dramatically with the advent of modern microsurgical techniques and, more recently, with the success of endovascular therapy. The indications for treating an aneurysm surgically, endovascularly, or both have been discussed earlier in this chapter.

Current surgical options include the following:

  • Direct aneurysmal clipping – Still considered first line treatment in the US. 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).

  • Endovascular treatment – 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 3D 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 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 details: The 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 arterial blood gas monitoring. Hemodynamic status should be monitored with a pulmonary artery catheter in patients that show evidence of compromise. A funduscopic examination should be performed. Up to 10% of patients with SAH have subretinal hemorrhage, which can lead to loss of vision.

  • Neurologic assessment: Serial neurologic examinations should be performed up 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 intervention: The timing of surgery for SAH has been a controversial topic for over 3 decades. Early surgery (0-3 days) has the following advantages:

  • Prevention of rebleeding, which is associated with a high mortality

  • Possible prophylaxis against vasospasm by removal of subarachnoid clot

  • Prevention and treatment of ischemic complications

  • Prevention of medical complications

  • Decreased duration of hospitalization

Disadvantages of early surgery for SAH include the following:

  • Technical problems associated with edematous brain tissue

  • High risk of intraoperative rupture of fragile aneurysm

  • A higher surgical morbidity and mortality

Delayed surgery for SAH (>10 days posthemorrhage) has the following advantages:

  • Brain tissue is less edematous.

  • Lower risk of intraoperative aneurysm rupture

  • A lower surgical morbidity and mortality

  • Flexibility of scheduling

The disadvantages of delayed surgery are as follows:

  • Increased rate of morbidity and mortality due to rebleeding

  • Technical difficulties due to adhesions around the aneurysm

The International Cooperative Study on Timing of Aneurysm Surgery findings are as follows:

  • Surgical outcomes usually are superior with delayed surgery; however, the increased morbidity and mortality associated with delay (up to 30% in some studies for patients with low-grade SAH) negated these results.

  • Overall results were comparable for early and delayed surgery with the exception that patients with low-grade SAH (Hunt and Hess/WFNS grades 1-2) had a better outcome with early surgery.

  • Subsequently, many centers have published favorable results with early surgery for low-grade SAH and it now is a common treatment decision.

For patients with an intermediate grade of SAH (Hunt and Hess/WFNS grade 3), the published results are less conclusive.

  • Several studies show no difference in morbidity and mortality between early and delayed surgery.

  • A 1995 study in Japan suggests that early surgery was beneficial in this group of patients.

  • Greater microsurgical experience and advances in neuroanesthesia and neurointensive management are likely to improve the outcomes for early surgery in this group of patients.

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:

  • Admission clinical examination and GCS

  • CT scan evidence of brain destruction

  • Intracranial pressure

  • Concurrent medical problems

  • Presence of absence of cerebral vasospasm

Data suggest that some patients with an initial GCS less than 5 can have good outcomes if the following occur:

  • A ventricular drain is placed emergently.

  • ICP does not exceed 30

  • Angiography shows normal intracranial filling

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; since surgical treatment seems to benefit some patients, many authors suggest an aggressive approach to management.

Intraoperative details: Surgical clipping: Most anterior circulation aneurysms can be approached pterionally. 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.

  • The modified pterional approach can be employed for aneurysms arising from the head of the basilar artery where the head is above the dorsum sellae.

  • The subtemporal approach is used for aneurysms that initiate at the head of the basilar artery in which the bifurcation of the basilar artery is below the dorsum sellae.

  • A posterior subtemporal approach can be used for most aneurysms arising from the trunk of the basilar artery.

  • A far lateral inferior approach can be used for certain lower basilar trunk and midline vertebral artery aneurysms. A midline suboccipital approach can be utilized for aneurysms extending from the vertebral artery where it pierces the dura. The midline suboccipital approach also may be used for a group of aneurysms that arise from the distal posterior inferior communicating artery.

Skillful brain retraction is paramount in aneurysm surgery, with care taken to minimize tissue and vessel damage. Use of 1 blade only of a self-retaining retractor (eg, Yasargil, Greenburg, Sugita) usually is often 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:

  • Dissection is done to identify the parent artery for possible temporary clipping in the event of aneurysmal rupture.

  • Incision of the arachnoid overlying the aneurysm is accomplished with the tip of a No. 11 blade scalpel.

  • The walls of the aneurysm are dissected away from the perforating vessels with a small aneurysm dissector or spatula. Aneurysmal sac volume can be decreased, under hypotension, by compression with a suction device placed over a cotton pad.

  • Mobilization of the aneurysm in all directions is necessary for visualization of any perforating vessels that might inadvertently be incorporated by clip misplacement.

  • Occlusion of the aneurysm is accomplished with an appropriately sized clip placed across the base. Use of as small a clip as possible will help facilitate the visualization of perforating vessels after aneurysm repair.

    • Avoid placing the clip too close to the parent artery, which may cause a tear in the aneurysmal sac.

    • If a tear does occur, a clip graft is used for repair. Use of a clip graft is associated with the risk of damage to perforating vessels, so it should be employed only when necessary.

    • Suturing in close proximity to an aneurysm can result in damage to the parent artery and should be avoided.

  • An attempt should be made to gently open the basal cisterns and to carefully remove as much of the subarachnoid blood as possible with suction, lavage, and, possibly, intracisternal infusion of antifibrinolytics, when appropriate.

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.

  • After the femoral artery puncture and initial angiogram, anticoagulation is initiated with heparin. The risk of thromboembolic events during the procedure in patients with acute SAH eclipses the risk of hemorrhage.

  • A guide catheter (6F) is placed in the internal carotid or vertebral artery. This allows for the passage of the microcatheter and facilitates contrast injection for angiograms and road mapping. Road mapping is a computer-generated technique that allows for real-time visualization of endovascular equipment superimposed over a map of the intracranial arteries.

  • The size of the aneurysm must be approximated before embolization either by estimation based on the size of the adjacent intracranial arteries, by using objects such as coins for reference, or by use of a guiding catheter with a known size.

  • The clinician should find the projection that allows for optimal visualization of the parent artery in relation to the aneurysm; this usually requires views in multiple planes.

  • The plastic microcatheter tip and the Micro-Guide wire are shaped according to the configuration of the aneurysm.

  • The aneurysm is catheterized with the microcatheter and guide wire using road mapping. The microcatheter should not touch the walls of the aneurysm.

  • When the microcatheter is in the desired position within the aneurysm, the first GDC can be delivered.

    • The first coil should be slightly smaller than the diameter of the aneurysm, and it should cross the neck of the aneurysm several times to form a receptacle.

    • Delivery of the GDC typically takes 1-4 minutes; however, newer GDC systems can detach in 20-30 seconds.

  • After placement of the first coil has been achieved, the aneurysm is filled with coils of decreasing size until densely packed.

    • Complete packing of the aneurysmal sac and neck usually is possible with small aneurysms.

    • In some larger aneurysms, the neck cannot be completely occluded. These aneurysms have a higher risk of recurrence.

    • Often, aneurysms with larger necks can be treated successfully with a balloon-assisted GDC technique.

  • The microcatheter is cautiously withdrawn from the aneurysm, and a final angiogram is obtained.

  • Heparinization is reversed with protamine, the femoral sheath is removed, and the patient is transferred to the neurointensive care unit.

Postoperative details: The postoperative management of SAH is directed at prophylaxis and treatment of the complications of SAH, as discussed previously.

Follow-up care: Patients 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:

  • Headache

  • Dizziness

  • Blurred vision

  • Poor concentration

  • Poor short term memory

  • Emotional lability

  • Insomnia

  • Fatigue

Specific postsurgical problems include the following:

  • Jaw pain and stiffness due to temporalis muscle scarring

  • Paralysis of the frontalis muscle

  • Deranged or absent sense of smell due to intraoperative traction on the olfactory tract

  • Local neuralgias

  • Wound infection

Some patients may require steroid and/or anticonvulsant therapy as outpatients. Oral nimodipine therapy often is continued for 3-4 weeks after SAH.

COMPLICATIONS

Complications of surgical clipping include the following:

  • Hemorrhagic complications

  • Ischemic complications

  • Damage to parent artery or perforating arteries

  • Acute or delayed neurological deficits from iatrogenic trauma

  • Meningitis

  • Cellulitis and wound infection

  • Nonspecific postsurgical syndrome similar to postconcussive syndrome

Common complications of endovascular therapy include the following:

  • Aneurysm rupture (GDCs, balloons)

  • Thromboembolism (GDCs) with acute or delayed neurologic deficit

  • Balloon rupture or deflation

OUTCOME AND PROGNOSIS

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 shows an approximate 70% survival 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, age of the patient, presence or absence of comorbid conditions, and occurrence of medical complications.

FUTURE AND CONTROVERSIES

The future of SAH management most likely will revolve around the continuing development and refinement of minimally invasive endovascular techniques.

Currently, controversy remains over 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.

References

  1. Allen GS, Ahn HS, Preziosi TJ, et al: Cerebral arterial spasm–a controlled trial of nimodipine in patients with subarachnoid hemorrhage. N Engl J Med 1983 Mar 17; 308(11): 619-24.

  2. Bejjani GK, Bank WO, Olan WJ, Sekhar LN: The efficacy and safety of angioplasty for cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery 1998 May; 42(5): 979-86; discussion 986-7.
  3. Bonita R, Thomson S: Subarachnoid hemorrhage: epidemiology, diagnosis, management, and outcome. Stroke 1985 Jul-Aug; 16(4): 591-4.
  4. Brilstra EH, Rinkel GJ, van der Graaf Y, et al: Treatment of intracranial aneurysms by embolization with coils: a systematic review. Stroke 1999 Feb; 30(2): 470-6.
  5. Brouwers PJ, Wijdicks EF, Van Gijn J: Infarction after aneurysm rupture does not depend on distribution or clearance rate of blood. Stroke 1992 Mar; 23(3): 374-9.
  6. Bryan RN, Rigamonti D, Mathis JM: The treatment of acutely ruptured cerebral aneurysms: endovascular therapy versus surgery. AJNR Am J Neuroradiol 1997 Nov-Dec; 18(10): 1826-30.
  7. Dandapani BK, Suzuki S, Kelley RE, et al: Relation between blood pressure and outcome in intracerebral hemorrhage. Stroke 1995 Jan; 26(1): 21-4.
  8. Dandy WE: Intracranial aneurysm of the internal carotid artery: cured by operation. Ann Surg 1938; 107: 654-659.
  9. Dias MS, Sekhar LN: Intracranial hemorrhage from aneurysms and arteriovenous malformations during pregnancy and the puerperium. Neurosurgery 1991; 27: 855.
  10. Edlow JA, Caplan LR: Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage. N Engl J Med 2000 Jan 6; 342(1): 29-36.
  11. Edlow JA, Wyer PC: Evidence-based emergency medicine/clinical question. How good is a negative cranial computed tomographic scan result in excluding subarachnoid hemorrhage? Ann Emerg Med 2000 Nov; 36(5): 507-16.
  12. Elliott JP, Newell DW, Lam DJ, et al: Comparison of balloon angioplasty and papaverine infusion for the treatment of vasospasm following aneurysmal subarachnoid hemorrhage. J Neurosurg 1998 Feb; 88(2): 277-84.
  13. Eskridge JM, Song JK: Endovascular embolization of 150 basilar tip aneurysms with Guglielmi detachable coils: results of the Food and Drug Administration multicenter clinical trial. J Neurosurg 1998 Jul; 89(1): 81-6.
  14. Feigin VL, Rinkel GJ, Algra A, et al: Calcium antagonists in patients with aneurysmal subarachnoid hemorrhage: a systematic review. Neurology 1998 Apr; 50(4): 876-83.
  15. Firlik KS, Kaufmann AM, Firlik AD, et al: Intra-arterial papaverine for the treatment of cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Surg Neurol 1999 Jan; 51(1): 66-74.
  16. Fisher CM, Kistler JP, Davis JM: Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery 1980 Jan; 6(1): 1-9.
  17. Guglielmi G, Vinuela F, Sepetka I, Macellari V: Electrothrombosis of saccular aneurysms via endovascular approach. Part 1: Electrochemical basis, technique, and experimental results. J Neurosurg 1991 Jul; 75(1): 1-7.
  18. Guglielmi G, Vinuela F, Dion J, Duckwiler G: Electrothrombosis of saccular aneurysms via endovascular approach. Part 2: Preliminary clinical experience. J Neurosurg 1991 Jul; 75(1): 8-14.
  19. Hacein-Bey L, Connolly ES, Mayer SA, et al: Complex intracranial aneurysms: combined operative and endovascular approaches. Neurosurgery 1998 Dec; 43(6): 1304-12; discussion 1312-3.
  20. Hackett ML, Anderson CS: Health outcomes 1 year after subarachnoid hemorrhage: An international population-based study. The Australian Cooperative Research on Subarachnoid Hemorrhage Study Group. Neurology 2000 Sep 12; 55(5): 658-62.
  21. Haley EC, Kassell NF, Apperson-Hansen C, et al: A randomized, double-blind, vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in North America. J Neurosurg 1997 Mar; 86(3): 467-74.
  22. Hop JW, Rinkel GJ, Algra A, et al: Randomized pilot trial of postoperative aspirin in subarachnoid hemorrhage. Neurology 2000 Feb 22; 54(4): 872-8.
  23. Hunt WE, Hess RM: Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg 1968 Jan; 28(1): 14-20.
  24. Johnston SC, Selvin S, Gress DR: The burden, trends, and demographics of mortality from subarachnoid hemorrhage. Neurology 1998 May; 50(5): 1413-8.
  25. Johnston SC, Dudley RA, Gress DR, Ono L: Surgical and endovascular treatment of unruptured cerebral aneurysms at university hospitals. Neurology 1999 Jun 10; 52(9): 1799-805.
  26. Juvela S, Heiskanen O, Poranen A, et al: The treatment of spontaneous intracerebral hemorrhage. A prospective randomized trial of surgical and conservative treatment. J Neurosurg 1989 May; 70(5): 755-8.
  27. Kasner SE: Stroke treatment-specific considerations. Neurol Clin 2000 May; 18(2): 399-417.
  28. Kassell NF, Boarini DJ, Adams HP, et al: Overall management of ruptured aneurysm: comparison of early and late operation. Neurosurgery 1981 Aug; 9(2): 120-8.
  29. Kassell NF, Torner JC: Aneurysmal rebleeding: a preliminary report from the Cooperative Aneurysm Study. Neurosurgery 1983 Nov; 13(5): 479-81.
  30. Kassell NF, Torner JC, Jane JA, et al: The International Cooperative Study on the Timing of Aneurysm Surgery. Part 2: Surgical results. J Neurosurg 1990 Jul; 73(1): 37-47.
  31. Kassell NF, Torner JC, Haley EC, et al: The International Cooperative Study on the Timing of Aneurysm Surgery. Part 1: Overall management results. J Neurosurg 1990 Jul; 73(1): 18-36.
  32. Kassell NF, Peerless SJ, Durward QJ, et al: Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery 1982 Sep; 11(3): 337-43.
  33. Kazzi AA, Ellis K: Subarachnoid Hemorrhage. In: Adler JN, Krause RS, Huff JS, Halamka J, Pollack CV, eds. eMedicine:Emergency Medicine[textbook online] . St. Petersburg, Fla: eMedicine Corporation, 1998-2001; Available at: http://www.emedicine.com/emerg/topic559.htm.
  34. Lang DT, Berberian LB, Lee S, Ault M: Rapid differentiation of subarachnoid hemorrhage from traumatic lumbar puncture using the D-dimer assay. Am J Clin Pathol 1990 Mar; 93(3): 403-5.
  35. Le Roux PD, Newell DW, Eskridge J, et al: Severe symptomatic vasospasm: the role of immediate postoperative angioplasty. J Neurosurg 1994 Feb; 80(2): 224-9.
  36. Le Roux PD, Winn HR: Intracranial aneurysms and subarachnoid hemorrhage management of the poor grade patient. Acta Neurochir Suppl (Wien) 1999; 72: 7-26.
  37. Leblanc R: The minor leak preceding subarachnoid hemorrhage. J Neurosurg 1987 Jan; 66(1): 35-9.
  38. Linn FH, Rinkel GJ, Algra A, van Gijn J: Incidence of subarachnoid hemorrhage: role of region, year, and rate of computed tomography: a meta-analysis. Stroke 1996 Apr; 27(4): 625-9.
  39. Mancuso PA, Weinstein PR: Pathophysiology and management of hydrocephalus after subarachnoid hemorrhage. In: Ratchenson RA, Wirth FP, eds. Ruptured cerebral aneurysms: Perioperative management. Concepts in Neurosurgery. Vol 6. 1994:124-133.
  40. Martin NA: The combination of endovascular and surgical techniques for the treatment of intracranial aneurysms. Neurosurg Clin N Am 1998 Oct; 9(4): 897.
  41. Mayberg MR, Batjer HH, Dacey R, et al: Guidelines for the management of aneurysmal subarachnoid hemorrhage. A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1994 Nov; 25(11): 2315-28.
  42. Miller J, Diringer M: Management of aneurysmal subarachnoid hemorrhage. Neurol Clin 1995 Aug; 13(3): 451-78.
  43. Mizoi K, Yoshimoto T, Takahashi A, et al: Prospective study on the prevention of cerebral vasospasm by intrathecal fibrinolytic therapy with tissue-type plasminogen activator. J Neurosurg 1993 Mar; 78(3): 430-7.
  44. Morgenstern LB, Luna-Gonzales H, Huber JC Jr, et al: Worst headache and subarachnoid hemorrhage: prospective, modern computed tomography and spinal fluid analysis. Ann Emerg Med 1998 Sep; 32(3 Pt 1): 297-304.
  45. Muizelaar JP, Becker DP: Induced hypertension for the treatment of cerebral ischemia after subarachnoid hemorrhage. Direct effect on cerebral blood flow. Surg Neurol 1986 Apr; 25(4): 317-25.
  46. Newell DW, Winn HR: Transcranial Doppler in cerebral vasospasm. Neurosurg Clin N Am 1990 Apr; 1(2): 319-28.
  47. Newell DW, Elliott JP, Eskridge JM, Winn HR: Endovascular therapy for aneurysmal vasospasm. Crit Care Clin 1999 Oct; 15(4): 685-99, v.
  48. Nichols DA, Meyer FB, Piepgras DG: Endovascular treatment of intracranial aneurysms. Mayo Clin Proc 1994 Mar; 69(3): 272-85.
  49. Ohman J, Servo A, Heiskanen O: Effect of intrathecal fibrinolytic therapy on clot lysis and vasospasm in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 1991 Aug; 75(2): 197-201.
  50. Olafsson E, Hauser WA, Gudmundsson G: A population-based study of prognosis of ruptured cerebral aneurysm: mortality and recurrence of subarachnoid hemorrhage. Neurology 1997 May; 48(5): 1191-5.
  51. Oropello JM, Weiner L, Benjamin E: Hypertensive, hypervolemic, hemodilutional therapy for aneurysmal subarachnoid hemorrhage. Is it efficacious? No. Crit Care Clin 1996 Jul; 12(3): 709-30.
  52. Pickard JD, Murray GD, Illingworth R: Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ 1989 Mar 11; 298(6674): 636-42.
  53. Pinto AN, Canhao P, Ferro JM: Seizures at the onset of subarachnoid haemorrhage. J Neurol 1996 Feb; 243(2): 161-4.
  54. Rhoney DH, Tipps LB, Murry KR, et al: Anticonvulsant prophylaxis and timing of seizures after aneurysmal subarachnoid hemorrhage. Neurology 2000 Jul 25; 55(2): 258-65.
  55. Rinkel GJ, van Gijn J, Wijdicks EF: Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke 1993 Sep; 24(9): 1403-9.
  56. Roginski RS, Abramowicz AS: Intracranial hypertension and neurosurgery. Anesthesiol Clin North America 1999; 17(3): 633-643.
  57. Roos EJ, Rinkel GJ, Velthuis BK, Algra A: The relation between aneurysm size and outcome in patients with subarachnoid hemorrhage. Neurology 2000 Jun 27; 54(12): 2334-6.
  58. Roos Y: Antifibrinolytic treatment in subarachnoid hemorrhage: a randomized placebo-controlled trial. STAR Study Group. Neurology 2000 Jan 11; 54(1): 77-82.
  59. Roos YB, Vermeulen M, Rinkel GJ, et al: Systematic review of antifibrinolytic treatment in aneurysmal subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 1998 Dec; 65(6): 942-3.
  60. Schievink WI: Intracranial aneurysms. N Engl J Med 1997 Jan 2; 336(1): 28-40.
  61. Schwartz RB, Tice HM, Hooten SM, et al: Evaluation of cerebral aneurysms with helical CT: correlation with conventional angiography and MR angiography. Radiology 1994 Sep; 192(3): 717-22.
  62. Shah MV, Heros RC: Intracerebral hemorrhage due to cerebral arteriovenous malformations. Neurosurg Clin N Am 1992 Jul; 3(3): 567-76.
  63. Solenski NJ, Haley EC Jr, Kassell NF, et al: Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter Cooperative Aneurysm Study. Crit Care Med 1995 Jun; 23(6): 1007-17.
  64. Solomon RA, Fink ME, Pile-Spellman J: Surgical management of unruptured intracranial aneurysms. J Neurosurg 1994 Mar; 80(3): 440-6.
  65. Stieg PE, Kase CS: Intracranial hemorrhage: diagnosis and emergency management. Neurol Clin 1998 May; 16(2): 373-90.
  66. Sztajnkrycer M, Jauch EC: Unusual headaches. Emerg Med Clin North Am 1998 Nov; 16(4): 741-60, vi.
  67. Thrift AG, McNeil JJ, Forbes A, Donnan GA: Risk factors for cerebral hemorrhage in the era of well-controlled hypertension. Melbourne Risk Factor Study (MERFS) Group. Stroke 1996 Nov; 27(11): 2020-5.
  68. Ullman JS, Bederson JB: Hypertensive, hypervolemic, hemodilutional therapy for aneurysmal subarachnoid hemorrhage. Is it efficacious? Yes. Crit Care Clin 1996 Jul; 12(3): 697-707.
  69. van der Wee N, Rinkel GJ, Hasan D, van Gijn J: Detection of subarachnoid haemorrhage on early CT: is lumbar puncture still needed after a negative scan? J Neurol Neurosurg Psychiatry 1995 Mar; 58(3): 357-9.
  70. van Gijn J, Bromberg JE, Lindsay KW, et al: Definition of initial grading, specific events, and overall outcome in patients with aneurysmal subarachnoid hemorrhage. A survey. Stroke 1994 Aug; 25(8): 1623-7.
  71. Vermeulen M: Subarachnoid haemorrhage: diagnosis and treatment. J Neurol 1996 Jul; 243(7): 496-501.
  72. Vespa PM, Gobin YP: Endovascular treatment and neurointensive care of ruptured aneurysms. Crit Care Clin 1999 Oct; 15(4): 667-84.
  73. Weaver JP, Fisher M: Subarachnoid hemorrhage: an update of pathogenesis, diagnosis and management. J Neurol Sci 1994 Sep; 125(2): 119-31.

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