Subarachnoid and Intracerebral Hemorrhage

A.L.O. Manoel, Cappy Lay, D. Turkel-Parrella, Joshua Stillman, and Alberto Goffi

BACKGROUND

Cerebrovascular disease is the fourth leading cause of death in North America and accounts for approximately 130,000 deaths per year. Eighty percent of strokes are ischemic; the remaining 20% are hemorrhagic. Hemorrhagic stroke is subdivided into spontaneous intracranial hemorrhage (ICH) (15%) and subarachnoid hemorrhage (5%). Although less common, hemorrhagic stroke has markedly worse outcomes than ischemic stroke, including higher mortality and poorer functional outcomes. This chapter reviews the management of both spontaneous ICH and aneurysmal subarachnoid hemorrhage.

SPONTANEOUS INTRACEREBRAL HEMORRHAGE

The estimated incidence of spontaneous ICH worldwide is 24.6/100,000 person-years; 67,000 cases are reported annually in the United States.¹ Among strokes, ICH carries the poorest prognosis for survival and functional recovery, with high rates of early mortality (median 30-day mortality 40.4%, with 50% of these deaths occurring within the first 2 days); poor long-term survival²; and moderate to severe persistent deficits among survivors (<40% ever achieve independent function).¹ Recent population-based studies, however, suggest that more than half of all patients present with small ICHs, where excellent and timely medical care can have a powerful, positive impact on morbidity and mortality.³ In fact, observational reports suggest that misguided prognostic pessimism has led to withdrawal of life support in patients who would have had acceptable clinical outcomes if properly managed.^4–6 ICH must therefore be considered an acute neurologic emergency with potential interventions that may significantly mitigate primary and subsequent secondary brain injury. The following discussion focuses exclusively on spontaneous (i.e., not traumatic) ICH.

Etiology and Risk Factors for ICH

An increased incidence of spontaneous ICH is associated with many underlying conditions, including hypertension, advanced age, and male gender. Other conditions associated with a poorer prognosis—after controlling for age and gender—include diabetes mellitus and a posterior fossa location (Table 21.1). The most common risk factor associated with spontaneous ICH is chronic arterial hypertension, which is present in approximately 75% of all patients with ICH and is associated with deep hemorrhage. The most common sites for hypertensive bleeds are deep perforator arteries in the pons, midbrain, thalamus, basal ganglia, and the deep cerebellar nuclei.⁷ The lobar region is the second most common location for ICH (45%). It is more common in the elderly and is associated with cerebral amyloid angiopathy. Posterior fossa hemorrhage accounts for the remaining 10% of ICH and carries the worst prognosis.

Important risk factors for secondary ICH are myriad: coagulopathies (resulting from the use of antithrombotic or thrombolytic agents or from congenital or acquired factor deficiencies); systemic diseases such as thrombocytopenia; lymphoproliferative disorders; and hepatic and renal failure. The increasing use of oral anticoagulants, especially vitamin K inhibitors (such as warfarin) and newer oral anticoagulants (such as dabigatran), has resulted in a surge of coagulopathy-associated ICH in recent years and now accounts for more than 15% of all cases of ICH.⁸ Other identified risk factors for ICH are advanced age, high alcohol intake, low cholesterol, and low triglyceride levels.^9,10 Socioeconomic and ethnic factors also appear to play a role in the prevalence of cerebral hemorrhage. ICH is twice as common in low-income and middle-income countries when compared with high-income countries; Asians, African Americans, and Hispanics are at higher risk than Caucasians.^11,12

Causes of ICH include intracranial aneurysms and arteriovenous malformations (AVMs). Aneurysms most commonly rupture into the subarachnoid space but may also cause intraparenchymal hematomas. AVMs typically remain asymptomatic; however, ICH is their most common presentation (60% of AVMs present with intraparenchymal hemorrhage).¹³ Hemorrhage due to an AVM may occur at any location within the cerebrum, brainstem, or cerebellum.

Brain tumors are a rare cause of intracerebral hemorrhage and account for <5% of all cases.¹⁴ These may be primary tumors, most commonly glioblastoma multiforme (GBM) or oligodendrogliomas, or they may be metastatic brain tumors. Lung cancer, because of its high prevalence, is the most common source for brain metastases causing ICH. Other sources of brain metastasis causing ICH include melanoma, renal cell carcinoma, thyroid carcinoma, and choriocarcinoma.¹⁵

Less frequent causes of secondary ICH include infections, vasculitis, sinus venous thrombosis, carotid endarterectomy, Moyamoya disease, and drug use (e.g., cocaine). Finally, it should be noted that hemorrhagic transformation of acute ischemic stroke is relatively common, but in the absence of anticoagulation or thrombolytic therapy, is most often asymptomatic.

Mechanisms of Brain Injury

Acute neurologic injuries cause immediate damage (primary brain injury) and delayed damage (secondary brain injury). In ICH, primary injury is defined by local tissue destruction, which results from the rupture of a blood vessel into the brain parenchyma and ensuing ischemia and elevated intracranial pressure (ICP). In more than one-third of patients, substantial expansion of the hemorrhage is observed during the first few hours, resulting in further mechanical injury and early clinical deterioration.¹⁶ It is thought that much of this initial damage cannot be reversed.

Primary brain injury initiates a cascade of biochemical events at the cellular level, including ischemic and apoptotic cell injury cascades, edema, and excitotoxicity, resulting in delayed and often progressive secondary brain injury. Unlike primary injury, secondary brain injury is considered preventable or reversible in the first hours to days following the initial hemorrhagic event. If present, conditions that decrease cerebral oxygen and glucose delivery (e.g., hypotension, hypoxia, anemia, and hypoglycemia) or increase cerebral metabolic demand (e.g., fever, seizures, and hyperglycemia) exacerbate secondary brain injury.¹⁷ Minimization of secondary brain injury requires an early, aggressive, and well-structured approach to patient care and may result in improved long-term functional outcomes.

History and Physical Exam

Classically, ICH presents as a sudden onset of a focal neurologic deficit that evolves over minutes to hours. Clinical assessment, however, cannot reliably distinguish intracerebral hemorrhage from ischemic stroke.¹⁸ Neurologic signs and symptoms can help indicate the location of the hemorrhage: (1) hemiplegia/hemiparesis, hemisensory loss, or homonymous hemianopsia suggest putaminal and thalamic ICH; (2) ataxia, vomiting, headache, and coma indicate brainstem compression in cerebellar bleeding; (3) deep coma, total paralysis, and pinpoint pupils suggest pontine bleeding.

Common symptoms for all types of ICH include headache (~40%), nausea and vomiting (~40% to 50%), and alteration in level of consciousness (LOC) (~50%), particularly for large ICH. Seizures occur in up to one-third of patients and often reflect an expanding hemorrhage, an underlying vascular or neoplastic etiology, or a lobar hemorrhage affecting cortical tissue.¹⁹

Blood pressure (BP) is typically elevated in ICH. Nonspecific EKG abnormalities are common (e.g., prolonged QT interval, depressed ST segments, flat or inverted T waves) and are thought to result from a centrally mediated release of catecholamines. Ventricular arrhythmias have also been described with brainstem compression.

Progression of neurologic deficits with deterioration of LOC during the first 48 hours after hospital admission has been described in 22% to 50% of patients with ICH.^20,21

Diagnostic Evaluation

Recently published Emergency Neurological Life Support (ENLS) protocols²² emphasize the following aspects of emergent clinical assessment for patients presenting with suspicion of ICH: (1) a concise and targeted assessment of the patient’s clinical condition and (2) rapid and accurate diagnosis using neuroimaging to define ICH characteristics (i.e., location, volume, and possible etiology). Clinical assessment proceeds as follows:

The clinical presentation of ICH is indistinguishable from ischemic stroke, but its management can be very different; therefore, rapid neuroimaging is essential. Noncontrast computed tomography (CT) is the most commonly used imaging modality for emergency diagnosis and characterization of ICH (location and extent of the hematoma). Noncontrast CT is highly sensitive and specific for acute bleeding, which will appear hyperdense, then, over weeks, become isodense, and may have a ring-enhancing appearance. In addition to the location of the primary hematoma, the degree of bleeding (including volume, the presence of intraventricular hemorrhage [IVH], and signs of increased ICP or herniation) is among the strongest predictors of long-term outcome.

A rapid estimate of ICH volume helps determine stroke severity and delineate treatment options. A simple and validated method that can be used in the emergency department (ED) is the ABC/2 formula,²³ where A is the greatest hemorrhage diameter on the CT slice with the largest area of ICH, B is the largest perpendicular diameter on the same CT slice, and C is the approximate number of CT slices with hemorrhage multiplied by the slice thickness in centimeters, which is often 0.5 cm. For calculation of C, a slice is counted as 1 if the hemorrhage area is >75% of the largest hematoma area on the reference slice; as 0.5 if the hemorrhage area is approximately 25% to 75%; and not counted if the area is <25%. ABC/2 gives the ICH volume in cm³. In children, the ABC/XYZ has been proposed, where X, Y, and Z are perpendicular measures of the supratentorial intracranial space (% of total brain volume).²⁴

Recently, it has been suggested that identification of active extravasation of intravenous contrast into the hematoma, called the “spot sign,” during contrast-enhanced CT and/or CT angiography (CTA) may predict hematoma expansion.^25,26

In patients with confirmed acute ICH, CT or MR angiography, or catheter angiography is recommended to exclude an underlying lesion such as an aneurysm, AVM, or tumor. However, in hypertensive patients with a well-circumscribed hematoma in a typical location for hypertensive bleeding (thalamus, basal ganglia, pons, and cerebellum), the yield of such studies is extremely low, and a decision not to proceed with these additional diagnostic tests is reasonable.²⁷ At the other extreme, young, nonhypertensive patients with isolated intraventricular hemorrhage (IVH) deserve aggressive workup.

Risk Stratification and Prognostication

Several clinical grading scales have been developed to assist with risk stratification and prognostication. An easy-to-use and well-validated model is the ICH score²⁸ (Table 21.2), which is based on patient demographics (age), clinical condition (GCS), and neuroimaging findings (ICH volume, presence of IVH, and supratentorial or infratentorial origin of ICH). The ICH score has been validated for stratification of 30-day mortality²⁸ and 12-month functional outcome²⁹; each point increase is associated with increased mortality risk and poorer functional outcome. However, it has been shown that withdrawal of life support in patients likely to have a poor outcome may significantly bias these predictive models. In the ED, clinical grading scales should be used only for communication about a patient’s condition, or for research purposes, and not to limit interventions in the initial management of patients with ICH.²²

Management Guidelines

Emergency Department management of patients with acute ICH entails (1) initial stabilization of airway and hemodynamics, (2) minimization of primary injury and (3) prevention of secondary brain injury. The most recent American Heart Association/American Stroke Association guidelines³⁰ and the recently published ENLS protocols²² are reviewed in the following sections.

Initial Stabilization

Management of ICH begins by ensuring adequate patient airway, breathing, and circulation. Early endotracheal intubation is essential for patients with a depressed LOC who are unable to protect their airway. Classically, a GCS ≤ 8, rapidly deteriorating LOC, and uncontrolled seizures are indications for intubation. Stable patients requiring transfer to another medical facility should be carefully assessed for the possibility of airway compromise in the the near term, and, if the risk is deemed high, be intubated prior to leaving the referring center. Whenever possible, a rapid and concise neurologic assessment should precede intubation in order to document the patient’s baseline functioning before the exam is confounded by use of sedative or paralytic drugs.

Maintenance of both brain perfusion and oxygenation is critical for prevention of secondary brain injury. To this end, steps should be taken to prevent elevations in ICP, including minimization of airway manipulation and use of ICP lowering medications. Oxygen saturation should be maintained >94% and carbon dioxide (PaCO₂) levels should be kept in the normal range (35–45 mm Hg). In mechanically ventilated patients, use of lung-protective ventilation strategies (pressure- and volume-limited mechanical ventilation) is appropriate. In a setting of increased ICP and/or signs of acute brain herniation, hyperventilation to a goal PaCO₂ of 28 to 32 mm Hg may be used. Hyperventilation is not a definitive treatment for elevated ICP because of the risk of increased brain ischemia and rebound elevations in ICP; a normal PaCO₂ should be reinstituted as soon as definitive treatments to control ICP are in place.³¹

Minimization of Primary Injury

Blood Pressure Management

Arterial blood pressure is elevated in the majority of patients who present with ICH. Mean arterial pressure (MAP) is >120 mm Hg in over two-thirds of ICH patients and >140 mm Hg in over one-third.³² Such acute elevations in BP have been implicated as a cause of bleeding and as a normal physiologic response to maintain cerebral perfusion pressure (CPP). Although there is general agreement that low BP levels are associated with poorer outcome and must be corrected, it is not clear at this time whether this observation simply reflects the fact that low BP levels occur more often in severe cases.³⁰

Current guidelines³⁰ recommend the following BP targets in patients with spontaneous ICH:

• SBP > 200 mm Hg or MAP > 150 mm Hg: Aggressive reduction of BP with target MAP of 110 mm Hg or BP 160/90 mm Hg
  
• SBP > 180 mm Hg or MAP > 130 mm Hg and no clinical evidence of elevated ICP: Target MAP of 110 mm Hg or BP 160/90 mm Hg
  
• SBP > 180 mm Hg or MAP > 130 mm Hg with clinical evidence of ICP elevation on exam, CT, or ICP monitor; If ICP monitoring is available, target a CPP of ≥ 60 mm Hg (50 to 70 mm Hg); if ICP monitoring is not available, target a MAP of 80 to 90 mm Hg (assuming an ICP of 20 to 30 mm Hg)

The evidence underlying these guidelines is controversial. In the recent, large multicenter trial “Intracerebral Hemorrhage Acutely Decreasing Arterial Pressure Trial 2” (INTERACT 2), 2,839 patients with spontaneous ICH were randomized to rapid blood pressure lowering with a target SBP = 140 mm Hg within 1 hour; or to the standard guideline-recommended target SBP of 180 mm Hg. Analysis of a composite outcome of death and severe disability on the modified Rankin scale (mRS = 3 to 6) showed an 8% benefit in the more aggressive treatment group; however, the result was not statistically significant. Although the safety of this lower-BP target has been demonstrated, an evidence-based benefit in clinical outcome has yet to be confirmed. More answers are expected from the Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH) II trial.

If a decision is made to lower blood pressure, management should be started immediately. A short-acting, titratable, intravenous agent should be used to achieve the target quickly and with minimal risk for overshoot. Labetalol (initial bolus dose 5 to 20 mg titrated every 10 minutes to effect) is a reasonable agent if there are no contraindications. Nicardipine is another excellent option (initial dose 5 mg/hour, with titration by 2.5 mg/hour every 15 minutes as needed; maximum dose 15 mg/hour). Angiotensin-converting enzyme inhibitors (e.g., enalapril) and hydralazine may be used. Sodium nitroprusside and nitroglycerin increase ICP and lower cerebral blood flow and should be avoided.

Twenty-four to forty-eight hours following brain injury, oral/enteral antihypertensive medications should be initiated to help achieve individualized blood pressure targets for secondary stroke prevention.

Correction of Coagulopathy

Coagulopathy in patients with ICH is most commonly due to use of therapeutic anticoagulation; other risk factors include acquired or congenital coagulation factor deficiencies and qualitative or quantitative platelet abnormalities. Coagulopathies in ICH are associated with poor prognosis because of prolonged bleeding and hematoma expansion; whenever possible, these deficits should be immediately corrected.

Specific Anticoagulants

Antiplatelet Agents

Conflicting results have been published regarding the impact of antiplatelet agents on hematoma expansion and clinical outcomes. There is a small increased risk of ICH with the use of antiplatelet agents (0.2 events per 1,000 patient-years).^35,36 Some centers support empiric use of platelet transfusion, while others discourage this practice, or suggest assaying for platelet function to guide transfusion.²² Current guidelines highlight a lack of evidence and consider platelet transfusion in ICH patients with a history of antiplatelet use as experimental.³⁰ Additionally, some authors suggest the use of desmopressin (DDAVP, 0.3 mcg/kg), as has been used in the treatment of uremia-associated bleeding.²²

Fibrinolytic Agents

Symptomatic ICH is one of the most life-threatening complications of thrombolytic therapy. The incidence of symptomatic ICH following recombinant tissue plasminogen activator (rt-PA) therapy for ischemic stroke is approximately 6%; of interest, symptomatic ICH following thrombolysis for myocardial infarction (MI), for which a higher dose of rt-PA is used than in stroke (1.1 mg/kg in MI vs. 0.9 mg/kg in stroke), is quite rare (0.4% to 1.3%). The difference is thought to reflect the fact that healthy cerebral vessels do not readily bleed from thrombolysis. Management of suspected ICH during or after fibrinolytic infusion begins with immediate cessation of the infusion, clinical stabilization (ABCs), and emergent noncontrast CT head. The NINDS rt-PA study³⁷ protocol recommends empiric treatment in these cases with 6 to 8 units of cryoprecipitate or FFP and 6 to 8 units of platelets; however, evidence on the most effective treatment in this situation is lacking.

Even patients without evidence of coagulopathy may experience hematoma expansion, especially in the first 24 hours. Because hematoma expansion is one of the major risk factors for poor outcome, it has been hypothesized that use of procoagulant agents could improve outcomes after ICH. Five randomized trials tested this hypothesis using recombinant factor VIIa (rFVIIa) (NovoSeven® RT) in non-coagulopathic patients with ICH (spontaneous and traumatic ICH). A meta-analysis³⁸ of these studies showed significant reduction in hematoma growth, but an increased rate of thromboembolic events and no overall net difference in mortality or long-term disability. Current guidelines do not recommend the use of rFVIIa in the treatment of ICH.³⁰ However, rFVIIa might benefit specific subsets of patients in whom the risk of hematoma expansion outweighs the risk of thromboembolic events. Two ongoing trials address this question in patients thought to be at high risk for hematoma expansion. The SPOTLIGHT trial (Spot Sign Selection of Intracerebral Hemorrhage to Guide Hemostatic Therapy) and the STOP-IT trial (Spot Sign for Predicting and Treating ICH Growth Study) are both addressing the role of rFVIIa in patients identified on CTA as having a positive “spot sign,” a finding indicative of extravasation of contrast into the hematoma and suggestive of significant risk for imminent hematoma expansion.³⁹

Surgical Interventions

Based on current evidence and guidelines, surgical intervention may be considered in the following conditions.

Infratentorial ICH

Although no randomized controlled trials (RCTs) of cerebellar hematoma evacuation have been undertaken, several case series suggest that surgical evacuation with cerebellar decompression is associated with improved outcomes in patients with ICH > 3 cm in diameter and clinical deterioration, or radiographic evidence of either brainstem compression or hydrocephalus. Treatment with external ventricular drainage (EVD) alone without posterior fossa decompression is not recommended because of the theoretical risk of upward herniation. Patients with cerebellar hemorrhage should be always referred for urgent neurosurgical consultation.

Supratentorial ICH

Current guidelines suggest that surgical evacuation of supratentorial ICH should be considered only in patients presenting with lobar clots >30 mL that are within 1 cm of the surface.^30,40,41 The recently published Surgical Trial in Intracerebral Hemorrhage (STICH) II⁴¹ did not show any difference in unfavorable outcomes at 6 months when comparing early surgery to conservative treatment in this specific subgroup of patients. The trial showed a slight survival advantage (OR = 0.86) for surgery within a few hours of the onset of hemorrhage in conscious patients with a modestly decreased GCS (9 to 12) and with lobar hematomas, but the survival advantage was far from achieving statistical significance.⁴² Expert consensus is that surgery should be considered as a life-saving procedure for treatment of refractory increased ICP, especially in patients with ongoing clinical deterioration, recent onset of hemorrhage, involvement of the nondominant hemisphere, and relatively accessible hematomas.

Intraventricular Hemorrhage and Hydrocephalus

IVH is quite common in spontaneous ICH (45% of patients), especially in patients with hypertensive hemorrhages involving the basal ganglia and the thalamus.⁴³ Acute hydrocephalus may develop after ICH, either in association with IVH or because of direct mass effect on ventricles. Patients with acute hydrocephalus require urgent neurosurgical consultation for possible EVD placement. Unfortunately, ventriculostomy in the setting of IVH is difficult to manage because of frequent obstruction secondary to blood clots. Flushing the catheter helps remove the thrombus but may cause ventriculitis. Recently, use of intraventricular thrombolytic agents has been suggested as adjunct to EVD for accelerating blood clearance and clot lysis. The safety phase 2 trial of the CLEAR-IVH trial (Clot Lysis: Evaluating Accelerated Resolution of IVH) prospectively evaluated the safety of intraventricular use of 3 mg rt-PA versus placebo in 48 patients. Results from this study suggest that intraventricular rt-PA is safe and can have a significant benefit on clot clearance. However, pending results of the ongoing phase III CLEAR-IVH trial, current guidelines consider this treatment experimental.³⁰

Prevention of Secondary Injury

Although this chapter focuses on the initial evaluation and management of patients with ICH, it is reasonable for the emergency physician to implement early intrventions that can help minimize secondary injury in the ensuing 24 to 72 hours.²²

Intracranial Pressure Monitoring

Few studies have addressed the incidence, management, and impact of elevated ICP on outcomes of ICH patients. Current guidelines are based on the principles and goals of traumatic brain injury (TBI) management.^22,30,44

• Indications for ICP monitoring: GCS ≤ 8, large hematoma with mass effect suggestive of elevated ICP, or hydrocephalus
  
• Goals: ICP < 20 mm Hg, CPP 50 to 70 mm Hg (if possible, adjustments based on the patient’s cerebral autoregulatory status)
  
• Interventions: Initial measures: elevate the patient’s head (30 to 45 degrees), drain cerebral spinal fluid (CSF) using an EVD; provide analgesia and sedation to achieve a motionless state, and maintain normal body temperature
  
• Advanced measures: hypertonic solutions (e.g., mannitol and hypertonic saline); hyperventilation (as bridge to further management); neuromuscular blockade; hematoma evacuation/decompressive craniectomy; mild hypothermia; barbiturate coma

Seizure Prophylaxis

Seizures frequently complicate ICH; however, their incidence varies widely depending on diagnostic criteria, duration of follow-up, and the population studied. The estimated incidence of clinical seizures in patients with ICH is 4.2% to 20%, subclinical seizures 29% to 31%, and status epilepticus 0.3% to 21.4%. About 50% to 70% of seizures will occur within the first 24 hours, and 90% in the first 3 days.³⁹ Predisposing factors include ICH with a lobar location (typically nonoccipital and subcortical hemorrhages), large hematoma size, hydrocephalus, midline shift, and low GCS. Although seizures theoretically may exacerbate brain injury, conflicting results have been reported on seizure association with clinical outcome and mortality. No RCTs exist to guide decision making for seizure prophylaxis or treatment specifically in patients with ICH.

As in traumatic brain injury, prophylactic anticonvulsants in patients with lobar ICH may reduce the risk of early seizures but do not affect long-term risk of developing epilepsy. In addition, two recent studies found their use to be associated with worse functional outcomes.^45,46 Based on available data, current guidelines do not recommend routine use of prophylactic anticonvulsants.³⁰

However, if a patient with ICH develops clinical seizures, or there is a change in mental status associated with EEG evidence of seizures, experts recommend initiation of treatment with antiepileptic agents. The choice of initial drug should depend on individual patient characteristics (i.e., medical comorbidities, concurrent drugs, and contraindications). Initial treatment typically begins with an intravenous benzodiazepine (e.g., lorazepam 0.05 to 0.10 mg/kg), followed by a loading dose of an IV agent (e.g., phenytoin 15 to 20 mg/kg, valproic acid 15 to 45 mg/kg, levetiracetam 500 to 1,500 mg, or phenobarbital 10 to 20 mg/kg).

Glycemic Control

A high proportion of patients with ICH (~60%) will develop stress hyperglycemia in the first 72 hours, even in the absence of a previous history of diabetes mellitus.⁴⁰ Multiple studies have associated increased serum glucose in the acute phase of ICH with higher risk of poor outcome (hematoma expansion, increased edema, and death or severe disability).⁴¹ However, clear causality between hyperglycemia and poor outcome and, more interestingly, evidence of improved outcome with glycemic control have not been proven. Recent microdialysis studies have demonstrated increased cerebral hypoglycemic events in patients treated with tight glucose control strategy, and a large multicenter RCT in a general ICU population found increased mortality with intensive glucose control.⁴⁷ Current guidelines recommend close glucose monitoring and avoidance of both hypoglycemia (<70 mg/dL) and hyperglycemia (>180 mg/dL); most experts agree that an insulin infusion should aim for a serum glucose of 140 to 180 mg/dL.³⁹ By contrast, tight control (80 to 110 mg/dL) has been shown to increase mortality.⁴⁷

Temperature Control

Fever is relatively common in patients with ICH (up to 40%), and it has been independently associated with poor outcome. However, no RCT has yet demonstrated improved clinical outcome with induced normothermia.³⁹ Despite a lack of evidence, there is general agreement that the presence of fever should prompt an appropriately broad workup; infectious sources should be identified and treated, and hyperthermia should be corrected (target core temperature below 38°C–37.5°C).

Venous Thromboembolism Prophylaxis

Patients with ICH are at high risk of venous thromboembolism (VTE). Independent risk factors for thromboembolic disease in patients with ICH include greater severity of stroke, prolonged immobilization, advanced age, female gender, African–American ethnicity, and thrombophilia. Discontinuation of antithrombotic agents is itself, of course, associated with an increased risk of deep vein thrombosis (DVT).³⁹ Guidelines suggest the use of intermittent pneumatic compression (IPC) devices in addition to elastic stockings in patients admitted for ICH, based on an RCT showing a reduced occurrence of asymptomatic DVT (4.7% vs. 15.9%).⁴⁸ Evidence regarding use of prophylactic UFH or LMWH is less definitive. Based on small studies showing safety of pharmacologic prophylaxis (no increased risk of hematoma expansion or further bleeding), current guidelines suggest consideration of LMWH starting 1 to 4 days after ICH, provided follow-up imaging has documented cessation of bleeding.³⁰

Disposition

Patients with ICH are frequently medically and neurologically unstable and are at significant risk for sudden clinical deterioration, particularly in the immediate poststroke period. Care of ICH patients in highly specialized stroke or neurointensive intensive care units has been associated with lower mortality and better functional outcome,⁴⁹ and admission to such a unit is considered standard of care.³⁰ An institutional algorithm for referral protocol and/or transfer to centers with higher levels of care is recommended.

ANEURYSMAL SUBARACHNOID HEMORRHAGE

The challenge of emergency medicine lies in identifying those patients who can be treated and released and those patients whose complaints represent a life-threatening process requiring urgent intervention. Among the diseases with the greatest potential for catastrophic consequence when undiagnosed is subarachnoid hemorrhage from a ruptured cerebral aneurysm. When an emergency department patient presents with headache due to aneurysmal rupture, timely diagnosis by the emergency physician is the best chance for avoiding the devastating effects of rebleeding that so often result in severe disability or death.

Aneurysmal subarachnoid hemorrhage (aSAH) accounts for only a small proportion of patients who present to the ED with a complaint of headache. Unfortunately, despite our awareness of the severity of this disease, 12% of aSAH patients are misdiagnosed on initial presentation. Misdiagnosed patients are more likely to have normal mental status, to present more than a day after the onset of symptoms, be unmarried, less educated, and speak English as a second language.⁵⁰

Epidemiology

Subarachnoid hemorrhage (SAH) is classified as either traumatic or spontaneous. Ruptured intracranial aneurysms are the leading cause of spontaneous SAH, followed by AVMs and nonaneurysmal “perimesencephalic” bleeding (characterized by a typical CT pattern and a benign clinical course). Cerebral aneurysms are vascular outpouchings that occur most frequently in the circle of Willis, where they typically form at branch points of the major cerebral arteries. Although cerebral aneurysms may be found at any arterial location in the cerebral circulation, the most common sites are the anterior communicating artery (30%), the posterior communicating artery (25%), the middle cerebral artery (20%), internal carotid bifurcation (7.5%), basilar tip (7%), and the posterior–inferior cerebellar artery (3%).⁵¹

Autopsy studies have shown that 6% to 8% of the general population harbors a cerebral aneurysm. The risk of rupture depends on many factors, including aneurysm location, size, and previous history of rupture.⁵² In the United States, aSAH affects 30,000 persons per year and is twice as common in women (average age of 55 years old).^53–57 Although aSAH accounts for only 5% of all types of stroke, it is responsible for 27% of productive years of life lost from cerebrovascular diseases.⁵⁸

Hypertension and smoking have a causative role in both aneurysm formation and rupture.⁵⁹ A recent study reported that smoking increased the odds of aneurysm rupture threefold.⁶⁰ Several heritable conditions are associated with the development of cerebral artery aneurysms, including a first-degree relative with aSAH, autosomal dominant polycystic kidney disease (PKD), neurofibromatosis type I, Marfan syndrome, multiple endocrine neoplasia (MEN) type I, pseudoxanthoma elasticum, hereditary hemorrhagic telangiectasia, and Ehlers-Danlos syndrome type II and IV.⁶¹ Family history and PKD account for 10% and 1% of all cases of aSAH, respectively.

History and Physical Exam

Aneurysmal SAH patients typically present with a sudden onset of severe headache. It is commonly described as the “worst headache of life,” but unfortunately, this description is given by more than 78% of all patients with headache of any etiology who present to the ED.⁶² The development of pain from aSAH is almost always rapid, though not instantaneous, and will usually reach peak intensity within 30 minutes of onset. Pain can be accompanied by loss of consciousness, vomiting, and neck pain or stiffness. Clinical grading scales have been developed to classify the severity and to predict the long-term outcome of aSAH (Table 21.3).^63,64

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