Perspective

Intracranial hemorrhages have different clinical manifestations ranging from subtle to catastrophic. The efforts of the emergency physician (EP) are directed toward identifying the correct diagnosis, confirming the diagnosis by cranial computed tomography (CT) or other diagnostic tests, and providing supportive care. Liberal consultation plus collaboration with specialists is required. Strong evidence of the best course of action regarding basic treatment issues such as blood pressure management and the use of anticonvulsants is lacking. Definitive therapy is most often in the hands of consulting and admitting physicians.

It is tempting to place any intracranial hemorrhage in the diagnostic category head bleed. Different types of intracranial hemorrhage may have different causes, different natural histories, different diagnostic strategies, different treatments, and frequently different prognoses. It is important to delineate the various types of intracranial hemorrhage so that correct diagnostic steps and therapeutic interventions can be performed.

Epidemiology

Estimates of the incidence of intracranial hemorrhage in patients seen in the emergency department (ED) are difficult because the findings include isolated headache, stroke syndromes, and head trauma, but a few generalities may be made. It is estimated that approximately 800,000 strokes occur each year in the United States, with intracranial hemorrhages accounting for 20% of the strokes. About 1% to 2% of patients seek treatment in EDs with a primary complaint of headache, and it is thought that 1% of these patients may have subarachnoid hemorrhage (SAH). If a filter of “worst headache of my life” is used, that estimate increases to up to 12% of patients with SAH. Approximately 500,000 moderate and severe traumatic head injuries occur each year in the United States. One percent to 2% of these patients have epidural hematomas, with estimates of an additional 5% to 25% having acute subdural hematomas.

Pathophysiology

intracranial hemorrhage is the umbrella term used to encompass the many types of bleeding within the cranial vault (Figs. 103.1 to 103.5 and Table 103.1). Intraparenchymal hemorrhage implies blood within the substance of the brain. When the hemorrhage is not clearly secondary to a detectable cause, it is deemed a spontaneous hemorrhage. This term is often used synonymously with the terms hypertensive hemorrhage and, when anatomically appropriate, intracerebral hemorrhage. Intraparenchymal hemorrhages may also occur in the brainstem or cerebellum. SAH literally describes blood in the subarachnoid space, and if nontraumatic, a vascular lesion such as an aneurysm is the implied cause of the bleeding. SAH and intraparenchymal hemorrhage may coexist. Intraventricular hemorrhage means that blood is visualized within the ventricles by cranial CT, and it is most often present with other types of intracranial hemorrhage. intracranial hemorrhages outside the brain substance are referred to as extraaxial hemorrhages and include both subdural hemorrhages and epidural hemorrhages. Although uncommon exceptions exist, extraaxial hemorrhages almost always have a traumatic etiology. The term hemorrhagic stroke might literally describe abrupt symptoms with any of the previously mentioned hemorrhages, but it is sometimes used in a more restrictive sense to describe hemorrhagic changes in an area of ischemic stroke to the point of being visible on cranial CT; this is termed hemorrhagic transformation of ischemic stroke.

Fig. 103.1 Computed tomography scan: supratentorial intracerebral hematoma.

Note the bright white appearance consistent with an acute hemorrhage. The anatomic location is thalamic.

Fig. 103.2 Computed tomography scan: acute subarachnoid hemorrhage.

Blood density is not as dramatic as in Figure 103.13. Hydrocephalus with enlarged temporal horns of the lateral ventricle is present.

Fig. 103.3 Computed tomography scan: acute subdural hematoma.

Note the crescent-shaped hemorrhage extending the length of the left hemisphere. The mottled appearance is consistent with ongoing bleeding.

Fig. 103.4 Computed tomography (CT) scan: acute epidural hematoma with the “swirl” sign.

This is a slice from a repeated CT scan of the patient in Figure 103.10 taken approximately 1 hour later. The marbled density of the clot is consistent with ongoing hemorrhage. Note the lens shape of the hematoma.

Fig. 103.5 Computed tomography scan: hemorrhagic transformation of ischemic stroke.

See Table 103.1, Types of Intracranial Hemorrhage, online at www.expertconsult.com

Table 103.1 Types of Intracranial Hemorrhage

Intracranial bleeding may be of either arterial or venous origin. Because of the closed nature of the cranial vault, any increase in intracranial volume from bleeding may result in increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). As a mass expands, some initial compensation occurs in the form of diminished intracranial vascular and cerebrospinal fluid volume. However, at some point the compensatory mechanisms fail and ICP will dramatically rise with a further increase in size of the mass. A key concept is CPP, the effective blood pressure exerted on the intracranial contents. CPP is equal to mean arterial pressure (MAP) minus ICP:

If ICP increases abruptly or if MAP falls, CPP decreases and central nervous system ischemia may follow and exacerbate the neuronal injury.

Hemorrhages also cause injury by direct tissue destruction or compression of adjacent structures. Edema formation around a hematoma may further increase the mass effect. For example, with cerebellar hemorrhages, tissue damage may cause the initial symptoms, but increased ICP and rapid progression to coma result from compression of the adjacent brainstem.

Spontaneous intraparenchymal hemorrhages (e.g., intracerebral hemorrhages, lobar hemorrhages, hypertensive hemorrhages) are most often associated with chronic hypertension. Cerebral amyloid angiopathy is increasingly being recognized as a contributing process in the elderly. Chronic excessive alcohol use is also a risk factor. Hemorrhage usually originates from rupture of small penetrating branch arteries of the vessels at the base of the brain¹ (Fig. 103.6).

Fig. 103.6 Common sites and sources of intracerebral hemorrhage.

Intracerebral hemorrhages most commonly involve the cerebral lobes, with origin from penetrating cortical branches of the anterior, middle, or posterior cerebral arteries (A); the basal ganglia, with origin from ascending lenticulostriate branches of the middle cerebral artery (B); the thalamus, with origin from ascending thalamogeniculate branches of the posterior cerebral artery (C); the pons, with origin from paramedian branches of the basilar artery (D); and the cerebellum, with origin from penetrating branches of the posterior inferior, anterior inferior, or superior cerebellar arteries (E).

Serial cranial CT demonstrates that many intracerebral hemorrhages expand over the course of several hours.² The initial hemorrhage may infiltrate the white matter with little direct destruction, but continued hematoma expansion, white matter edema, additional hemorrhage from surrounding vessels, and the development of hydrocephalus may all contribute to increased ICP and secondary neuronal injury. The frequency of anticoagulant-associated intracerebral hemorrhage is increasing.³ Warfarin therapy does not appear to increase hematoma volume initially, but it does increase the risk for later hematoma expansion.⁴

SAH literally means “blood in the subarachnoid space.” Trauma is the most common cause. Spontaneous, or nontraumatic, SAH has an entirely different differential diagnosis. About 80% of spontaneous SAHs are caused by rupture of saccular (berry) aneurysms of the intracranial vessels, which are commonly located near intracranial arterial bifurcations of the circle of Willis^5,6 (Fig. 103.7). Aneurysms are often named after the vascular site of origin, such as the anterior communicating artery or middle cerebral artery. Aneurysms that develop following vascular infection from endocarditis are termed mycotic aneurysms. Some aneurysms also cause symptoms without rupture from a mass effect or from emboli originating within the aneurysm. Rupture of an intracranial aneurysm abruptly raises ICP and leads to the onset of symptoms. The bleeding may be confined to the subarachnoid space, or a hematoma may extend into the brain substance and create an intraparenchymal hemorrhage, which in turn may rupture into the ventricles. Vasospasm of the vascular tree related to the aneurysm typically takes hours to develop and may worsen regional ischemia.

Fig. 103.7 The intracranial vasculature showing the most frequent locations of intracranial aneurysms.

Arteriovenous malformations are another cause of intracranial hemorrhage of both the subarachnoid and intraparenchymal anatomic subtypes. These arteriovenous shunts vary in their anatomy, and many patients have saccular aneurysms as well. Lesions with deep venous drainage and high pressure in the feeding vessels are at increased risk for bleeding.⁷ Cavernous angiomas are low-pressure vascular lesions associated with small hemorrhages.

Closed head injury may cause diffuse or localized subarachnoid bleeding. Cerebral contusion is a loosely defined term that describes the CT appearance of low density consistent with edema and often with some hemorrhage within that region.

An epidural hematoma usually reflects arterial bleeding into the epidural space following injury to a meningeal artery. A common mechanism is a skull fracture in the temporal area with associated laceration of the middle meningeal artery. The arterial pressure hematoma may increase in size until tamponade occurs as a result of resistance of distorted intracranial structures and increased ICP (at the expense of CPP).

Subdural hematomas reflect bleeding from small vessel sources and from diffuse brain injury with hemorrhage accumulating over the surface of the brain. Again, distortion of the cranial contents may occur, as well as increased ICP. The cortical atrophy that occurs with aging is thought to make the bridging vessels from the cortex to the dura increasingly susceptible to rupture from even trivial trauma in the elderly.

Less common causes of intracranial hemorrhage include dural sinus thrombosis with venous infarction and hemorrhage, intracranial neoplasms, brain abscesses, coagulopathies, vasculitides, and toxins. Cocaine and other sympathomimetic agents are believed to cause transient severe hypertension with resultant hemorrhage.

The anatomic terminology regarding intracranial hemorrhage historically comes from postmortem neuropathology descriptions. In the ED, intracranial hemorrhages are most often diagnosed by cranial CT, which remains the initial diagnostic modality of choice. The appearance of acute hemorrhage usually contrasts vividly with that of the other intracranial contents. The types of intracranial hemorrhage are anatomically classified primarily by their relationship to the substance of the brain and the meninges.⁸ Simplistically, hemorrhages may be thought to be located in the brain substance (intraparenchymal, intracerebral), within the ventricles (intraventricular), in the subarachnoid space between the meninges and the brain, or outside the brain and meninges (subdural, epidural) (Figs. 103.8 and 103.9).

Fig. 103.8 Varieties of intracranial hemorrhage.

(From Snell RS, Smith MS. Clinical anatomy for emergency medicine. St. Louis: Mosby; 1993.)

Fig. 103.9 An axial section of a non–contrast-enhanced computed tomography scan of the head reveals four types of acute posttraumatic intracranial hemorrhage: an epidural hematoma (thin white arrow) on the left side, a laminated subdural hematoma (short black arrow) on the right side, right-sided periventricular and frontal lobe contusions containing an intraparenchymal hematoma (thick white arrow), and a subarachnoid hemorrhage (long black arrow) in the right frontal region.

Presenting Signs and Symptoms

intracranial hemorrhages of any type may be associated with a continuum of changes in mental status ranging from mild headache to agitation, confusion, and coma. Seizures and stroke symptoms are also common findings.

Patients with a large intracranial hemorrhage typically have a diminished level of consciousness with or without a focal neurologic deficit. Intracerebral hemorrhages are responsible for about 20% of acute strokes. It is not possible at the bedside to reliably distinguish between an ischemic stroke and an intracerebral hemorrhage.⁹ Patients with a diminished level of consciousness often have a larger hemorrhage and increased ICP or distortion of the thalamic and brainstem reticular activating system.¹

With increased ICP, the Cushing triad of hypertension, bradycardia, and irregular respirations may be present, but this is not specific for intracranial hemorrhage. If able to speak, many patients complain of headache and nausea. Depending on the region of brain injured, the examiner will often find corresponding neurologic deficits. With hemispheric lesions, the picture may be similar to ischemic stroke—that is, patients with a large left cerebral hemorrhage may have right-sided hemiparesis and aphasia. Other stroke syndromes of neglect, visual field defects, and cortical sensory abnormalities may be present. With frontal lesions, conjugate eye deviation toward the side of the lesion is common. Large hematomas with mass effects may present the clinical picture of uncal herniation with diminished consciousness and third nerve dysfunction, including a large, nonreactive pupil. Third nerve dysfunction usually occurs on the side of the mass lesion but in about 10% of cases is on the opposite side (falsely localizing third nerve palsy).

Patients with brainstem and posterior fossa hematomas may show brainstem dysfunction, including alteration in consciousness, abnormalities in extraocular motion, other cranial nerve abnormalities, and the so-called crossed signs, with cranial nerve dysfunction on one side and long-tract findings of weakness on the opposite side. One pathognomonic finding on physical examination occurs in patients with pontine hemorrhage, in whom truly pinpoint pupils (not just small) may be present.

Patients with cerebellar hemorrhages may have profound vegetative signs of diaphoresis and vomiting. A common finding is acute headache and inability to ambulate. Smaller cerebellar hemorrhages may demonstrate nystagmus, ataxia, dysmetria, or abnormalities in extraocular motion. If brainstem compression develops, consciousness may deteriorate abruptly.

SAH is typically manifested as the “worst headache of my life.” Abrupt onset of a severe headache that quickly attains maximal intensity is the classic finding. This manifestation—abrupt severe headache reaching maximal intensity within seconds or moments of onset, perhaps occurring with exertion—often leads to the diagnosis. Syncope may be present at the onset of a hemorrhage. Meningismus may also be present. However, initial misdiagnosis of SAH occurs in up to 50% of cases.^10,11 The high-risk clinical characteristics of SAH have led to the derivation of preliminary decision rules, which remain under study.¹²

It is important to identify the diagnosis at the time of an initial or “sentinel” hemorrhage or warning leak. The sentinel hemorrhage may be manifested as a transient headache or confusional episode. If the patient complains of headache of abrupt onset or that the headache is different from the kind that the patient usually experiences, the possibility of SAH exists. Patients in whom the diagnosis is made at subsequent visits often have worse outcomes.

An expanding unruptured aneurysm may be accompanied by cranial nerve abnormalities. Typically, this is a third nerve paresis with asymmetric pupils and impairment of extraocular movement. The pupillary reflex may or may not be impaired.

With SAH and increased ICP, cardiac arrhythmias and changes on the electrocardiogram (ECG) consistent with myocardial ischemia may at times confound the diagnosis.¹⁰ Usually, these patients have severe neurologic symptoms, but cases in which the arrhythmia overshadows the clinical findings are reported as well.

intracerebral hemorrhage is the most common manifestation of arteriovenous malformations and accounts for roughly half the presentations. Other manifestations include seizures and focal neurologic deficits.⁷

A history of trauma suggests the possibility of an extraaxial hematoma. Progression of symptoms or deterioration in level of consciousness mandates investigation for an expanding mass lesion. With epidural hematoma, the classic description (present in only a minority of patients) is a transient loss of consciousness followed by an alert or lucid interval and later by progressively decreased level of consciousness. Headache out of proportion to the head blow or the presence of persistent vegetative symptoms such as nausea and vomiting is the more common manifestation. As the mass progresses, the neurologic findings may progress. Altered mental status following trauma is the typical clinical scenario.

Chronic large subdural hematomas may be found during evaluation of patients for altered mental status or headaches. Occult manifestations of intracranial injury are more common in the elderly.

Differential Diagnosis and Medical Decision Making

The major differential diagnosis of intracranial hemorrhage with focal neurologic signs or symptoms is ischemic stroke. Both processes may be associated with an abrupt onset of symptoms and focal neurologic deficits. Intracranial neoplasms are also in the differential diagnosis. However, the spectrum of findings in patients with intracranial hemorrhage is wide. Seizures are not a frequent initial complaint of patients with intracranial hemorrhage, although they do occur with enough frequency to include intracerebral hemorrhage and SAH in the differential diagnosis of seizures. Abnormal decerebrate posturing, which may occur with intracranial hemorrhage, is sometimes mistaken as seizure activity, particularly if it is brief and repetitive. Though counterintuitive, infectious processes such as encephalitis and meningitis may at times also have an abrupt onset of symptoms.

If altered mental status is the initial finding, all the causes of altered mental status should be included in the differential diagnosis (see Chapter 104). The expanded differential diagnosis for hemorrhages without focal lesions or altered mental status includes the universe of headache types. Functional headaches or thunderclap headaches are at times related to different types of exertion; however, they must be part of a diagnosis of exclusion for the EP.

Cranial CT is the current initial imaging test of choice for evaluation of intracranial hemorrhage because of the ability of non–contrast-enhanced cranial CT to demonstrate the presence of acute hemorrhage. Cranial CT is readily available in most U.S. EDs. Expert interpretation of cranial CT scans is sometimes not as readily obtainable, however, and EPs should be familiar with the basics of CT interpretation as it applies to immediate patient care.

In patients with suspected SAH, CT is very sensitive in detecting acute hemorrhage, with estimates of 95% or better.^11,13 Sensitivity starts to diminish as time from the hemorrhage increases, and CT sensitivity is estimated to be less than 50% 7 days after the event.

A suggested approach to analyzing CT scans (see Chapter 74) and a useful structure for communicating with consultants can be determined by asking the following series of simple questions:

Question 1—Is Blood Present?

Acute blood appears white or hyperdense on non–contrast-enhanced CT scans (Fig. 103.10). Some intracranial structures such as the dura or choroid plexus may calcify and at times simulate hemorrhage. As blood ages, it becomes increasingly low density or dark (Fig. 103.11). There is a time during this evolution when blood is nearly the same CT density as brain parenchyma and is therefore termed isodense. Rarely, the existence of an isodense hematoma must be inferred from cortical sulcus markings that do not reach the cranium. Clinically, the terms acute, subacute, and chronic are used to reflect the change in appearance on the CT scan, from hyperdense to isodense and finally hypodense. Nonhomogeneous density may be observed in some cases and is an indication of acute or acute on chronic bleeding. The possibility of hyperacute bleeding should always be kept in mind, with the areas of rapid bleeding appearing relatively hypodense within a larger, more dense area on CT (see Fig. 103.4).

Fig. 103.10 Computed tomography scan: acute epidural hematoma.

Note the high density of the hemorrhage and the lens-shaped clot.

Fig. 103.11 Computed tomography scan: chronic subdural hematoma (left hemispheric and bifrontal section).

Low density is consistent with the presence of hemorrhage for some days to weeks.

Question 2—Where is the Hemorrhage?

If hemorrhage is present, it is then described as external to the brain substance (extraaxial), within the substance of the brain (intraaxial or intraparenchymal), or visible in the intraventricular and subarachnoid or cisternal spaces. Extraaxial hematomas have two basic types of appearance. Subdural hematomas are most often crescentic (see Fig. 103.3), whereas epidural hematomas have a typical lens-shaped pattern (see Fig. 103.4). An intraparenchymal hemorrhage may be located in the cerebrum (intracerebral hemorrhage) or in subcortical or brainstem structures. Intracerebral hemorrhages of hypertensive origin tend to be situated in deep white matter or the basal ganglia or are confined to one lobe of the brain (lobar) (see Fig. 103.1). These hemorrhages tend to have a stereotypic pattern, and deviation from these patterns may suggest an uncommon cause of the hemorrhage.

Cerebellar hemorrhages may be midline or hemispheric (Fig. 103.12) and may cause brainstem compression. SAH may be detected by high density in the suprasellar or perimesencephalic cistern or by blood in the cortical sulci, where ordinarily there should be low-density images from the cerebrospinal fluid signal. Depending on the degree of hemorrhage, SAH may be obvious (Fig. 103.13) or relatively subtle (see Fig. 103.2). Intraventricular hemorrhage (literally “blood within the ventricles”) may result from rupture of an intracerebral hemorrhage into the ventricular system, from trauma, or from SAH (Fig. 103.14).

Fig. 103.12 Computed tomography scan: acute hemispheric cerebellar hemorrhage.

The expanding mass in the posterior fossa places the brainstem at risk for compression.

Fig. 103.13 Computed tomography scan: acute subarachnoid hemorrhage.

Blood is present in the suprasellar cistern and over the hemispheres.

Fig. 103.14 Computed tomography scan: intraventricular blood from extension of deep intracerebral hemorrhage.

The right lateral and third ventricles are filled with blood casts.

Treatment

Supportive care including appropriate management of the ABCs—airway, breathing, and circulation—is of course important. The decision to perform endotracheal intubation is based on the judgment of the physician who assesses the patient’s ability to protect the airway. It is recommended that certain steps be taken for rapid-sequence induction in patients with intracranial hemorrhage or other conditions with suspected increased ICP, including the use of lidocaine and a defasciculating dose of a paralytic agent, although rigorous proof of efficacy is lacking. In the past, hyperventilation was recommended with the goal of reducing abnormally increased ICP. Again, evidence is lacking, but the consensus is that hyperventilation beyond that needed to reduce PaCO₂ to only a small degree (PaCO₂ of 30 to 35 mm Hg) is not indicated.¹⁵

Blood pressure management in the setting of intracranial hemorrhage is controversial. In multiple-trauma patients with central nervous system injury, hypotension is associated with a poor outcome. In patients with intracerebral hemorrhage, the risk of expanding a hematoma associated with sustained hypertension must be weighed against the risk of impairing cerebral perfusion if blood pressure is reduced. A 2010 study suggested a trend toward more favorable outcomes in patients with aggressive blood pressure reduction but admitted that the study was underpowered and called for further investigation.¹⁶ In patients with established intracerebral hematoma and hypertension, consensus at this time is to use intravenous agents that can be titrated, such as nitroprusside, labetalol, esmolol, or carvedilol, if needed, to maintain blood pressure with an MAP of less than 130 mm Hg. Systolic blood pressure greater than 180 mm Hg or diastolic blood pressure higher than 105 mm Hg on two readings taken 5 minutes apart are the criteria recommended for intervention.¹⁵

In patients with SAH, there is also no clear evidence-supported management strategy. Hypertension should be avoided in patients with a ruptured aneurysm by administering intravenous titratable agents, as described previously. Some experts argue that relative hypotension should be induced based on the theory that a ruptured aneurysm is at risk for rebleeding in the presence of hypertension. Once the aneurysm is secured by interventional techniques, blood pressure is allowed to return to normal levels. The calcium channel antagonist nimodipine is recommended to reduce the chance of ischemia from vasospasm.^5,6

Management of increased ICP is conjectural if its existence is unknown. However, basic steps such as elevating the head of the bed, keeping the head midline, and avoiding painful stimulation are clearly indicated. Hyperventilation with the goal of reducing ICP is currently out of favor. Steroids have no proven benefit in patients with intracranial hemorrhage. Use of osmotic agents such as mannitol in cases in which a herniation syndrome is present may be useful as a temporizing measure when decompressive neurosurgical therapy is planned.

ICP monitoring may be useful in the ED but should be performed under the direction of a neurosurgeon or neurointensivist. Ventriculostomy may be performed in the ED by a neurosurgeon.

If a patient with intracranial hemorrhage has a seizure, the use of anticonvulsants is clearly indicated. Phenytoin and fosphenytoin are the current drugs of choice. Increasingly, levetiracetam seems to be used in these settings, though rigorous evidence for superiority is lacking. Use of anticonvulsants is common in patients with intracerebral hematomas who have not had seizures, although their efficacy is not based on evidence. Likewise, use of anticonvulsants in patients with SAH who have not had seizures is controversial.

Hyperglycemia and hyperthermia are associated with neuronal injury and should be avoided if possible and treated if present. No specific guidelines exist for the clinician at this time. If a coagulopathy is detected, appropriate treatment should be initiated (see the following discussion on warfarin coagulopathy).

In patients with intracranial hemorrhage, most activity in the ED is directed at diagnosis. Treatment is governed by the type of hemorrhage, its cause, and any associated medical and surgical conditions. Definitive treatment is under the direction of the consulting and admitting physicians, and the EP should work in concert with them. In most institutions, SAH and traumatic hemorrhage will be managed by neurosurgeons. Intracerebral hemorrhage is also often managed by neurosurgeons, but institutional management patterns vary. Intensive care and monitoring are necessary in many cases.

For deeply comatose patients, intensive supportive care is indicated in the short term. Evidence of the development of hydrocephalus on CT should lead to consideration of ventriculostomy. Drainage of cerebrospinal fluid and other supportive measures may be guided by continuous measurement of ICP by a variety of invasive techniques.

Cerebellar hemorrhage is an emergency requiring removal of the hematoma and relief of brainstem compression, which offers the possibility of good recovery in selected cases.¹ Surgery for removal of supratentorial intracerebral hematomas is controversial and not generally recommended.¹⁷ Other inpatient supportive measures for intracerebral hemorrhage might include prophylaxis for thromboembolic events.

Patients with an acute intracerebral hematoma who are taking warfarin should receive fresh frozen plasma (FFP) and vitamin K as soon as possible to correct the coagulopathy. The best dosing regimens are not known, but for patients with a prolonged international normalized ratio, a reasonable recommendation is 5-10 mg of vitamin K (administered intravenously over a 10-minute period) plus 10 mL/kg of FFP administered as soon as possible. Type AB FFP is available in some blood banks and can speed administration time by eliminating the time needed for cross-matching. Institutional recommendation many vary. Time to treatment of warfarin-associated coagulopathy in patients with intracerebral hemorrhage has been found to be the most important determinant of 14-hour reversal of anticoagulation.¹⁸ Antiplatelet therapy has been noted to be associated with clinical deterioration.

Acute administration of recombinant activated factor VII limits expansion of hematomas, but it has limited use for thromboembolic complications.^19,20 Other procoagulant pharmaceutical preparations are under study.

In recent years the trend has continued for early surgical intervention for SAH—that is, intervention to isolate the aneurysm or occlude it within 1 to 2 days of bleeding.^5,6 Until the aneurysm is secured, the consensus is that blood pressure should be lowered with parenteral medications if necessary. A recent study reported that interventional endovascular coiling may lead to better outcomes in selected patients with ruptured aneurysms.²¹

Treatment of arteriovenous malformations is complex, controversial, and outside the practice of EPs other than providing supportive care as outlined previously. The risk for rebleeding is less than that with saccular aneurysms. Should seizures occur, anticonvulsant medication should be administered. Additional diagnostic vascular studies besides cranial CT are required and may include angiography, CT angiography, and MRI. Treatment may include radiotherapy, embolization of the arteriovenous malformation, resection, or any combination of these modalities.

All but the smallest epidural hematomas must be treated by craniotomy and surgical evacuation plus investigation of the bleeding site to secure hemostasis. Treatment of subdural hematomas depends on the size and chronicity of the hematoma, the general medical condition of the patient, and signs and symptoms referable to the hematoma. In some patients, chronic subdural hematomas may be of large size with seemingly minimal or no effect on the patient; the problem is underlying atrophy, with the subdural hematoma filling the void. Acute subdural hematomas are generally evacuated if they are causing any mass effect, but at times this may be difficult to assess because the underlying brain is usually injured and edematous.

In hemorrhages complicating abscesses, tumors, or other conditions, treatment is generally directed at the underlying lesion.

Follow-Up, Next Steps in Care, and Patient Education

If the facility does not have the necessary specialty care, the patient should be transferred after stabilization to an appropriate facility. The urgency of transport corresponds roughly with the clinical condition of the patient; for example, patients with a headache, a chronic subdural hematoma, and no other findings may probably be transferred electively. The necessity for transfer of stable alert patients with minimal symptoms and minute traumatic hemorrhages detected on CT has not been studied. The notable exceptions in which emergency transport is indicated include acute SAH, cerebellar hemorrhage, and epidural hematoma when the natural history includes early clinical deterioration.