Catastrophic Neurologic Disorders in the Emergency Department , 2nd Edition

Chapter 14. Intracerebral Hematomas

By and large, intracerebral hematomas are caused by a ruptured penetrating arterial branch damaged by the effects of long-standing hypertension.1 At one undefined moment in time, in some patients it may produce hemorrhages localized in either the caudate nucleus, putamen, thalamus, cerebellum, or pons. Hematomas involving the subcortical white matter and cortex may have different causes, including vascular malformations. This fundamental distinction is important because cerebral angiography may be urgently indicated in a lobar hematoma and of less importance in ganglionic hemorrhages in patients with known brittle hypertension.

Some types of intracerebral hematoma are surgically accessible, and early recognition of clinical and computed tomographic (CT) scan predictors of deterioration may lead to surgical evacuation. Thus, it is also important to separate cerebellar hematoma from brain stem hemorrhages. Another task is to determine at an early stage whether survival is remote or whether salvage with a reasonable opportunity for rehabilitation is possible.

In the first hours, intraparenchymal hemorrhage, in one form or another, poses significant management and triage problems.1 Interpretation of different aspects of neuroimaging, management, stabilization, and indications for neurosurgical treatment of spontaneous intracerebral hematomas are discussed. Traumatic intracerebral hematoma is discussed in Chapter 19.

Ganglionic Hemorrhages

Location of the hemorrhage typically is in the putamen or caudate nucleus. The cause is a ruptured lateral branch of the lenticulostriate artery. Equally common are hematomas in the thalamus from ruptured thalamoperforating arteries. Many of these hemorrhages are apoplectic, creating large, destructive volumes with extension into the ventricular system.

Clinical Presentation

Supratentorial intracerebral hemorrhage may be manifested in many ways. Coma or any impaired level of consciousness can be explained by the space-occupying effect of the hematoma, causing significant shift of the brain stem; extension of the hemorrhage of the putamen into the thalamus, compressing the opposite thalamic nuclei; and rupture into the ventricular system, resulting in profound hydrocephalus. A progression to loss of many brain stem functions is not unusual.

The clinical syndromes in patients with hemorrhages into the putamen have been further divided on the basis of whether the lesion affects only the anterior part of the putamen close to the anterior limb of the internal capsule, the middle part, or the posterior part. Hemorrhage localized to the anterior part of the putamen may produce purely motor hemiparesis, eye deviation to the site of the lesion, and abulia. Extension into the middle part of the putamen may additionally result in spatial neglect and decreased sensation evidenced by diminished awareness of pinprick, touch, and position. Extension of the clot into the posterior putamen leads to a more prominent left-sided neglect in right-sided lesions and fluent aphasia in left-sided lesions. Large hemorrhages, in the putamen may dissect along the white matter tracts into the temporal lobe, causing a Wernicke-type aphasia, but periclot edema may also impair the into of the temporal lobe.

Box 14.1. Growth of Parenchymal Hematoma

The volume of a hematoma may increase from continued bleeding, edema formation, and rebleeding. Continued bleeding occurs from a cascade effect. The mass exerts pressure and stretch on surrounding arteries, which subsequently rupture and build a mass in consecutive layers of fibrin. Edema in intracerebral hematoma is due to both cytotoxic and vasogenic mechanisms. It is maximal 1–3 days after the initial hemorrhage and resolves by day 5. The perilesional edematous regions contain significant clot-derived protein and expand the extracellular space, increasing the distance of white matter axons and cells from their Wood supply and creating hypoxia. This may be further enhanced by systemic hypoxemia.3 Thrombin is important in perilesional edema4,5 because it causes inflammation, reactive gliosis, and retraction of axons and dendrites. In one experimental study, the effects of thrombin could be blocked by hirudin, which is a specific thrombin inhibitor, and edema could not be produced by other blood products.4 Single-photon emission computed tomography suggested that edema is a form of reperfusion injury due to early ischemia after the hematoma, with flow improving significantly over time.6 A study of regional cerebral blood flow that used radiolabeled microspheres failed to detect an ischemic penumbra in nonhypertensive animals with large-volume clots.7

The neurologic deficit in a putaminal hemorrhage is commonly stable when the patient is admitted to the emergency department. However, neurologic deficits may become more pronounced, signaled by stupor instead of drowsiness or by development of a gaze preference. Progression of neurologic symptoms, indicating enlargement of the hematoma with more mass effect, is commonly noted clinically within the first 6 hours after presentation (Box 14.1).

Clinical features of a thalamic hematoma are excessive sleepiness and abulia. Stupor may ensue if the hematoma causes pressure effects on the opposite thalamus or acute hydrocephalus due to extension into the third ventricle. A thalamic hematoma with dissection into a mesencephalon causes a fluctuating level of consciousness, and episodes of stupor alternate with slow responses (see Chapter 8). Left-sided thalamic hemorrhages are associated with fluent aphasia, with nonexistent phrases and poor naming but conspicuously good comprehension of spoken language. When the hematoma affects the internal capsule, hemiplegia occurs. Right-sided thalamic hematomas produce left visual neglect and hemiplegia.

Caudate hemorrhage is the least common of the classic hypertensive hemorrhages, and its clinical manifestations often can be inferred mainly from an extension to the ventricular system. More commonly, agitation, confusion, and thrashing around occur at the onset without localizing neurologic findings.2When the hematoma enlarges and extends from the caudate nucleus into the white matter, involving the internal capsule or putamen, level of consciousness decreases because of brain shift. Extension of the hemorrhage into the hypothalamus and diencephalon might produce complete Homer's syndrome on one side, a diagnostic clue to a large extending caudate hematoma. The clinical features are summarized in Table 14.1.

Interpretation of Diagnostic Tests

The volume in cubic centimeters can be measured on CT scan by the ellipsoid method: [(A × B × C)/2)] (Fig. 14.1). (A is the maximum diameter, B is the diameter perpendicular to A, and C is the number of slices on which the hematoma is seen, assuming 10-mm cuts.8 The projected grid on CT scan films is 1 cm per single step.) This approximation of hemorrhagic volume assumes that every hematoma is ellipsoidal. Nonetheless, the value obtained correlates well with a direct CT scan measurement; thus, the method is a simple, practical means of rapid volume measurement in the emergency department. In 25% of patients, enlargement of the ganglionic hematoma may appear on CT scans when reimaged within the first hours of presentation. In contrast, patients with CT scans obtained more than 6 hours after the ictus and a volume of less than 25 cm3 are unlikely to have deterioration from further growth of the hematoma. However, anticoagulation with warfarin, despite normal international normalized ratio (INR), is a major factor in enlargement of the hematoma.

Table 14.1. Ganglionic Hemorrhages

Primary Site


Telltale Signs

Caudate nucleus

Localized intraventricular hemorrhage

Headache, confusion, drowsiness-stupor, abulia

Capsule, putamen, diencephalons

Hemiparesis, eye deviation, Horner's syndrome



Hemiparesis, eye deviation, global aphasia

Posterior extension

Fluent aphasia



Paresthesia, hemineglect, nonfluent aphasia (often preserved repetition), disorientation to place


Slow syndrome.

Putaminal hemorrhages are most prevalent and not infrequently massive. The volume on CT scan commonly approaches 60 cm3, but smaller hematomas may occur without further enlargement on serial CT scans. Common types of putaminal hemorrhage are shown in Figure 14.2.

Thalamic hematomas are usually small; but because of close proximity to the ventricles, intraventricular hemorrhage may occur. Hydro-cephalus may develop from obstruction of the cerebrospinal fluid (CSF) at the level of the foramen of Monro, more commonly with medially located thalamic hemorrhages (Fig. 14.3). Enlargement of the hematoma has been observed in thalamic hemorrhages, typically in conjunction with progression to coma, and markedly reduces the outlook for independent recovery (Fig. 14.4).9 The CT scan and magnetic resonance imaging (MRI) features producing coma in patients with thalamic hematomas are shown in Figure 14.5. Caudate hemorrhage (Fig. 14.6) may be difficult to separate from intraventricular hemorrhage on CT scans, and often MRI is needed to locate the source in the caudate nucleus.

Finally, CT scan interpretation of spontaneous intracerebral hematoma may be deceiving. Some may represent hemorrhagic infarcts rather than primary intracerebral hematomas.10 This possibility should be particularly considered in patients who have had transient ischemic attacks; who have a potential cardioembolic source for emboli, such as atrial fibrillation or left ventricular hypokinesis; and who have silent infarcts revealed on CT scans (Fig. 14.7).9 Later, a localized putaminal hemorrhage may mimic an infarct by leaving a slit-like lesion (Fig. 14.8). This is in contrast to lobar hematomas, which may leave a hypodensity and deformity of the ventricle.11

Figure 14.1 Volume of a thalamic hemorrhage as measured by the ABC method (A × B × C / 2). In this example, A is 5 cm, B is 3 cm, and the number of slices (C) is four (hemorrhage is visible on four computed tomographic slices at 10 mm intervals). The total volume is calculated as 60 / 2, or 30 cm3.

Figure 14.2 Computed tomographic scan examples of putaminal hemorrhage (arrows): localized (A), extensions to capsule and frontal lobe and intraventricular extension (B), and extension into the thalamus (C).

First Priority in Management

Most academic institutions in the United States and Europe manage patients with ganglionic hemorrhage medically.12 This preference implies supportive care and monitoring of further deterioration from enlargement in volume caused by development of surrounding edema or continuous bleeding. Underlying coagulopathy should be corrected aggressively. Reversal of anticoagulation is essential, and fresh-frozen plasma (and vitamin K) or, if more appropriate, platelets should be infused in the emergency department.13 In patients with a metallic heart valve or otherwise high cardioembolic risk (e.g., marked ventricular hypokinesis or atrial fibrillation and echocardiographic evidence of atrial thrombus), there is an increased risk of thromboembolization or valve thrombosis. Current data suggest that discontinuation of anticoagulation and correction to an international normalized ratio <1.5 for less than a week in these patients rarely lead to systemic embolization.14,15

Figure 14.3 Computed tomographic scans of thalamic hemorrhage (arrows): lateral (A,B) and medial (C,D).

Hypertensive crisis is very common but seldom produces congestive heart failure or brief ventricular arrhythmias from a catecholamine surge. Only when blood pressure remains high (mean arterial pressure >140 mm Hg) and electrocardiographic changes or cardiac arrhythmias appear is reduction with β-blockers indicated.16 No evidence suggests that persistent acute hypertension provokes a recurrence of bleeding in patients with a spontaneous intracranial hematoma.17 However, vasogenic edema may develop, and persistent hypertension may contribute to an increase in intracranial pressure.18 Aggressive treatment of hypertension might theoretically reduce cerebral edema in these patients, but it may increase the risk of producing further perilesional ischemia in patients with prior hypertension. The presence of an ischemic perilesional penumbra is a matter of debate.19,20 It is generally accepted that when the mean arterial blood pressure reaches 145–150 mm Hg, the risk of enlargement of the hematoma from continuous leakage or cerebral edema is too high. Blood pressure should be reduced gradually to a mean arterial pressure of around 130 mm Hg.

Preliminary studies showed no significant change in the periclot blood flow when antihypertensives were administered 6 hours after onset.21 However, this major management dilemma remains unresolved in the first hours after the onset, particularly when blood pressures are high. The recommended antihypertensive medication is labetalol, ≈ 20 mg intravenously every 10 minutes up to 300 mg. In patients with bradycardia or other contraindications to β-blockers, one should consider intravenous enalaprilat 1.25 mg every 6 hours to a maximum of 5 mg.16,22

Figure 14.4 Computed tomographic images of enlargement of thalamic hemorrhage (arrow in A), intraventricular extension (left arrow in B), and hydrocephalus (right arrow in B).

There is no benefit from corticosteroids,23 and in susceptible patients, they may increase the risk of severe hyperglycemia or enhance pulmonary infection triggered by aspiration. The benefit of mannitol in deep ganglionic hemorrhage is not known. It is unlikely to result in improvement in outcome unless its effect on intracranial pressure and cerebral perfusion pressure is documented, nor is it known whether it may assist in the bridging period before surgical evacuation. More likely, the direct destructive effect of this type of hematoma rather than brain shift determines outcome in survivors.

Figure 14.5 Coma caused by thalamic hemorrhage. Left: Massive extension and enlargement of ventricles (arrows). Right: Magnetic resonance image of the thalamic hemorrhage with extension into the midbrain.

Figure 14.6 Computed tomographic images of caudate hemorrhage (left) and intraventricular extension (right, arrows).

Enlargement may have occurred during transport, and any further deterioration should be evaluated with a new CT scan. Enlargement 24 hours after onset is rare. Several systemic factors have been identified that increase the probability of enlargement, such as anticoagulation, liver disease, and poorly controlled diabetes with high systolic blood pressure (>200 mm Hg).9

Figure 14.7 Series of computed tomographic scans in a patient with rapidly progressing neurologic deficit. There is a hyperdense middle cerebral artery sign, but, except for a dubious difference in sylvian fissure width (arrow, left) and an old infarct in the posterior cerebral artery territory (arrow, right), there is no evidence of a recent ischemic stroke by computed tomography. Series of computed tomographic scans in a patient with rapidly progressing neurologic deficit. Several hours later, a large putaminal hemorrhage (arrows) represents a hemorrhagic infarct rather than a primary putaminal hemorrhage.

Hemostatic therapy (aminocaproic acid, apoprotein, or activated recombinant factor VII) used within 3 hours of the ictus of intracerebral hematoma could potentially reduce growth of the hematoma, but no data are available to justify its use.24 Its impact on outcome may be small because only 20%–30% of patients do demonstrate enlargement of the hematoma25 and clinical deterioration is not evident in all instances.

Craniotomy in large ganglionic hemorrhages is only lifesaving. Awakening from coma rarely occurs without devastating morbidity (Box 14.2), and thus it is a questionable procedure.

Figure 14.8 Putaminal hemorrhage (localized type) recognized 3 years later on subsequent computed tomographic scan as a slit-like lesion (arrows, right).

Box 14.2. Surgical Management of Ganglionic Supratentorial Hemorrhage

Most neurosurgeons prefer surgical evacuation in a deteriorating patient. Randomized surgical trials of supratentorial hemorrhage have been hampered by marginal statistical power26,27,28,29 imbalances in baseline characteristics between groups. Surgical evacuation of a ganglionic hematoma through open craniectomy did not improve outcome. Endoscopic aspiration reduced mortality, with no improvement in morbidity in large hematomas (>50 mL) but a trend in improved outcome in smaller hematomas. Stereotactic aspiration may result in lower incidence of complications.30 Ventriculostomy may be performed in patients with intraventricular rupture, but its effect on outcome is marginal, if any. Stereotactic treatment using thrombolytics and aspiration reduced volume but not disability or mortality.29

A recent small randomized pilot trial, the Surgical Treatment for Intracerebral Hemorrhage (STICH) study,31 documented reduced mortality at 1 month but not at 6 months in. patients treated with surgery (median Glasgow coma score = 11, median volume = 49 mL) compared with those given medical management (median Glasgow coma score = 11, median volume = 44 mL). Future trials should analyze lobar hematomas separately from ganglionic hemorrhage and study patients at high risk of deterioration to demonstrate a possible surgical benefit.

Predictors of Outcome

A large clot (>60 cm3 by ellipsoid volume measurement) associated with Glasgow coma score < 4 intraventricular hematoma and acute hydrocephalus is likely to result in death.32,33,34 A study from Sweden extrapolated that supposedly unrelated comorbidity such as preictal coronary artery disease or atrial fibrillation was an independent predictor for 30 days' mortality.35 Extension of the hematoma into the middle putamen most likely results in persistent hemiplegia. The prognosis in thalamic hemorrhage is determined by diameter and extension to the mesencephalon. If a thalamic hematoma exceeds 2.5 cm in greatest diameter, outcome is worse. Unilateral hydrocephalus in ganglionic hemorrhage caused by trapping of the ventricular system is a CT scan sign that indicates poor outcome despite surgical evacuation or ventriculostomy.


·     Observation for at least 24 hours in a neurologic-neurosurgical intensive care unit.

·     Evacuation of hematoma if enlargement causes brain herniation syndromes.

Lobar Hemorrhages

In this type of intracranial hematoma, the blood dissects throughout the subcortical white matter and often involves the cortex. The clinical features are related to topography. The source of lobar hematomas is unclear in many instances. Mechanisms include a ruptured vascular malformation, cerebral amyloid angiopathy,36 hemorrhage inside an existing brain tumor or metastatic lesion, infectious lesions (e.g., aspergillosis, toxoplasmosis), coagulation disorders, and use of sympathomimetic drugs or fibrinolytic agents.

A temporal lobe hematoma may be caused by a ruptured middle cerebral artery aneurysm.37 Any patient with a temporal lobe hematoma, transient loss of consciousness, and a much lower level of consciousness than expected on the basis of size or brain shift should be considered to have a ruptured aneurysm of the middle cerebral artery. A CT scan should be scrutinized for basal cistern clots. A temporal lobe hematoma may indicate a hemorrhagic necrotic mass due to herpes simplex encephalitis, and febrile agitation may be the only manifestation (see Chapters 7 and 17). Multiple hematomas should point to a possible devastating sagittal sinus thrombosis with multiple hemorrhagic infarcts (see Chapter 15).

Use of thrombolytic agents has increased the frequency of intracerebral hematomas associated with thrombolysis.38 The frequency of symptomatic intracerebral hematomas associated administration of tissue-type plasminogen activator (tPA) for ischemic stroke has increased to 6%. These hemorrhages occur within 36 hours after infusion. Decrease in level of consciousness is most prevalent, but increased hemiparesis, headaches, and a surge in blood pressure have also been noted.38 A major neurologic deficit (defined as a score of more than 20 on the National Institutes of Health Stroke Scale; see Chapter 15, Table 15.1) and early hypodensity or edema on CT scans increase the odds of later development of symptomatic intracerebral hematoma after tPA use. The risk of intracerebral hematoma after tPA for myocardial infarction is very low, but old age, dose, and history of stroke are major predisposing factors.39

Clinical Presentation

Frontal lobe hematomas cause abulia, contralateral arm weakness, and gaze preference toward the side of the hematoma; but when the hemorrhages are located superiorly above the frontal horn, leg weakness may be more apparent.40 Headache is frequently present and associated with vomiting. Approximately one-third of patients have seizures within the first hours of presentation. Temporal lobe hematomas may cause Wernicke's aphasia and right-sided homonymous hemianopia. Temporal lobe hematomas in the nondominant hemisphere may produce only confusional episodes without any localizing neurologic symptoms. Parietal lobe hematoma produces prominent hemisensory symptoms, but if it extends into the posterior parietal lobe, constructional apraxia or dressing apraxia may be found if specific testing is done. Patients with an occipital lobe hematoma have a sudden visual field defect, most commonly an easily identifiable homonymous hemianopia. Multiple hematomas commonly immediately involve the level of consciousness unless they are localized within one hemisphere or are small. Clinical features are determined by the largest hematoma.

Table 14.2. Computed Tomographic Scan Characteristics of Lobar Hematoma that Suggest the Cause


Multiple locations and compartments

Fluid level from poor clot formation

Amyloid angiopathy

Superficially located

Irregular border

Recurrent hematomas

White matter hypodensities

Tumoral hemorrhage

Central or eccentric location of hemorrhage

Tumor mass visible

Proportionally more white matter edema

Arteriovenous malformation

Calcification in hemorrhage mass

Enhancement with contrast medium

Interpretation of Diagnostic Tests

Several CT scan characteristics of hematoma suggesting its origin should be recognized,41 and they are summarized in Table 14.2. Shift of midline structures on the initial CT scan in patients with lobar hematoma admitted to the emergency department is highly predictive of further clinical deterioration.

The specific features are shift of the septum pellucidum, obliteration of the opposite ambient cistern, and early trapping of the temporal horn (Fig. 14.9).35Some of the CT scan changes may be subtle and involve effacement of the supracerebellar cistern from edema (Fig. 14.10).

Figure 14.9 Computed tomographic scan signs predictive of deterioration in lobar hematoma (arrow). Note shift of septum pellucidum and pineal gland (arrows) and early temporal horn entrapment (arrow, left).46

Figure 14.10 Computed tomographic scans showing lobar hematoma (left) with some mass effect and bowing of the midline structures. Right: Two days later, the hematoma is resolving but edema is more pronounced, with progressive obliteration of the supracerebellar cistern without appreciable shift of the pineal gland from edema.

Lobar hematoma may indicate an underlying metastatic lesion or primary brain tumor, and it is evident by marked fingerlike white matter edema notably out of proportion to the size of the hematoma and seldom causing brain shift (Fig. 14.11).

Figure 14.11 Hemorrhage in metastasis. Note the comparatively large, fingerlike edema in the white matter out of proportion to the size of the hematoma. Computed tomographic scans mask underlying metastasis, which may be more evident by magnetic resonance imaging.

Figure 14.12 Amyloid angiopathy-associated hematoma. Magnetic resonance images show a thalamic hemorrhage (black arrow) and multiple areas of hemosiderin (white arrows), which are clues to earlier hemorrhages.

Superficially located hematomas commonly are a result of amyloid angiopathy, and MRI (preferably gradient-echo) may show earlier hemorrhages (Fig. 14.12). Coagulation-associated hematomas are commonly multiple, involving multiple compartments (Fig. 14.12).

Intracerebral hematomas after intravenous tPA for myocardial infarction characteristically are hemorrhages in multiple compartments, and fluid levels from continuing anticoagulation are evident (Fig. 14.14).

MRI is a crucial study in lobar hematoma because it may identify an underlying structural lesion. In young adults, an arteriovenous malformation is common; in older adults, earlier amyloid hemorrhages may be found, and, as alluded to, routine T1 and T2 MRI may initially be unrewarding and a gradient echo image may be needed.42

Figure 14.13 Computed tomographic scan shows multiple hemorrhages in coagulopathy.

Cerebral angiography is warranted in patients with a lobar hematoma and MRI evidence of arteriovenous malformation (Fig. 14.15). Its yield in a patient with normal findings on MRI is very low.

First Priority in Management

The approach to lobar hematoma is similar to that in ganglionic hemorrhages.

Multiple intracranial lobar hematomas are often found in patients who have recently received tPA for acute myocardial infarction.43 Fresh-frozen plasma (2 units) should be used initially. It is important to repeat a CT scan, preferably 1–3 hours after the onset, to assess the true extension and dimension of the hematomas.38

The decision to proceed with surgery is determined by clinical presentation. Craniotomy with evacuation of a lobar hematoma should be strongly considered in patients with evidence of brain shift on CT scan and a decrease in the Glasgow coma score because there is a high probability of further deterioration in the next hours. With expanding hematomas, emergency surgery is effective in 25% of patients if young and the hematoma is located in the parietal lobe.44 Early surgical management is also indicated if an intracerebral hematoma is associated with a ruptured middle cerebral artery aneurysm or arteriovenous malformation, but mostly after further definition by cerebral angiography.45

Figure 14.14 Examples of hemorrhage associated with tissue-type plasminogen activator. A: Arrows point to different compartments, convexity subarachnoid hemorrhage, and lobar (arrowheads) and intraventricular hemorrhages with fluid level. B: Massive sub-arachnoid hemorrhage and lobar hematomas.

Figure 14.15 Magnetic resonance features of large arteriovenous malformation in left frontal lobe with large vein draining to the sagittal sinus.

Predictors of Outcome

Poor outcome can be expected in patients with deterioration from hematoma enlargement who need emergency surgical evacuation. Poor outcome is more common in patients with a decreased Glasgow coma score and a septum pellucidum shift of more than 6 mm.46 Lobar hematomas associated with tPA administration are commonly fatal. Outcome is good after rehabilitation if the lobar hematoma is less than 40 cm3 on CT scan and there is no shift on CT scan in a patient seen several hours after ictus.47 Recurrent hemorrhage has been estimated at a 2.1% annual rate, but it is tripled when anticoagulation is administered.48 Resumption of anticoagulation in a patient with a definitive need and prior intracranial hematoma is safe for 30 days, but long-term risk is not known.


·     Neurologic intensive care unit if level of consciousness is decreased and mass effect appears on CT scan.

·     Smaller hematomas (<30 cm3) in alert patients can be observed in the ward if the time of ictus and presentation is beyond 6 hours.

·     Surgical evacuation in patients with CT scan evidence of mass effect and documented deterioration.

Intraventricular Hemorrhage

It may be difficult clinically and by CT scan criteria to differentiate spontaneous intraventricular hemorrhage from a small thalamic or caudate nucleus hemorrhage with overwhelming filling of the lateral portion of the ventricles. In many situations, intraventricular hemorrhage is caused by a rupture of the anterior communicating aneurysm, which can dissect through the lamina terminalis to enter the third ventricle and connecting ventricles (see Chapter 13). Primary intraventricular hemorrhage may be caused by arteriovenous malformations in the proximity of the ventricular system, intraventricular tumors, and, more recently, use of thrombolytic agents. Uncommon causes are coagulopathy in patients with severe thrombocytopenia associated with a hematologic malignancy and moyamoya disease from rupture of the dilated periventricular arteries.

Clinical Presentation

Primary intraventricular hemorrhage has a clinical presentation similar to that of poor-grade aneurysmal subarachnoid hemorrhage.49,50,51 Onset is acute, with immediate loss of consciousness but with extensor posturing that occurs spontaneously or with any manipulation of the patient. Nonspecific shivering, myoclonic jerks, and well-characterized generalized tonic-clonic seizures are common. Many patients have rapid breathing with periods of apnea or barely audible air displacement and need to be immediately placed on a mechanical ventilator. Increased blood pressure most likely is a consequence of transmitted intracranial pressure affecting the brain stem, particularly at the flush of arterial blood through the ventricular system. Pupil reflexes may become sluggish and pupil size smaller if acute hydrocephalus develops rapidly. Any change in this direction should prompt a repeat CT scan to evaluate progression of ventricular enlargement and need for ventriculostomy.

Interpretation of Diagnostic Tests

Entire filling of all parts of the ventricular system is characteristic, with acute ballooning out of the ventricular system (Fig. 14.16). The CT scan is notoriously unreliable in demonstrating a potential cause of intraventricular hemorrhage. Thus, some patients with a thalamic or caudate hemorrhage have only a hint of parenchymal bleeding on CT scanning, and this is markedly overshadowed by the massive intraventricular hemorrhage, often filling only one ventricle. The anatomic location may indicate the origin of the hemorrhage (Table 14.3).52,53

Figure 14.16 Left: Primary intraventricular hemorrhage. Right: Cerebral angiography disclosed an arteriovenous malformation.

Table 14.3. Intraventricular Hemorrhage


Unilateral ventricular

Caudate hemorrhage
Thalamic hemorrhage


Arteriovenous malformation of ependymal lining or choroid plexus


Cocaine or amphetamine

Head injury

Cavum septum pellucidum

Anterior artery cerebral aneurysm

Fourth ventricle only

Posterior inferior cerebral artery aneurysm

Source: Terayama et al.17

MRI can demonstrate hemorrhage into the thalamus or caudate nucleus and is also more sensitive to visualization of arteriovenous malformations and cavernous angiomas. Cavernous angiomas may be found at other locations inside the parenchyma, providing further clues to cavernous angioma as the main culprit in the ventricular hemorrhage. Magnetic resonance angiography should also be performed to exclude the possibility of an anterior communicating aneurysm or to document a much less common moyamoya vascular pattern. This pattern is the consequence of bilateral internal carotid artery occlusion causing dilatation to develop in the lenticulostriate, thalamoperforating, and thalamogeniculate arteries. Microaneurysms are often formed in these arteries, and they may rupture into the ventricular system.

Not only is cerebral angiography imperative to exclude an anterior communicating artery aneurysm, but the posterior circulation should also be visualized bilaterally with multiple projections because blood in the fourth ventricle might be due to a ruptured aneurysm of the distal posteroinferior cerebellar artery. One study claimed an arteriovenous malformation or an aneurysm in 50%–70% of patients, with a higher yield in patients younger than 45 years.54

First Priority in Management

The management of primary ventricular hemorrhage is immediate ventriculostomy in patients with a Glasgow coma score of less than 8 and marked ventricular dilatation on CT scan (see Chapter 11). A trial is under way using 3 mg of intraventricular recombinant tPA every 12 hours when no cause is found by cerebral angiography (which should then be performed immediately).55,56 Dramatic resolution of the obstructing clot has been described, but experience with this potentially dangerous therapy is very limited and clinicoradiologic correlation has not been studied well. Recent experimental work also suggests an unwanted inflammatory response, edema of periventricular tissue and choroid plexus using tPA.55 It should not be used in intraparenchymal hemorrhages with intraventricular extension, even if the intraventricular compartment produces most of the clot volume.57,58

Predictors of Outcome

Outcome remains poor (severe disability or vegetative state) in patients with primary intraventricular hemorrhage associated with acute hydrocephalus. In others, survival is common but with a severe amnesic state.50


·     Neurologic-neurosurgical intensive care unit for monitoring of development of acute hydro-cephalus or drainage with a ventriculostomy.

·     Consider immediate cerebral angiography.

Cerebellar Hemorrhages

Cerebellar hemorrhages are commonly caused by rupture of a branch of the superior cerebellar artery afflicted by fibroid necrosis from long-standing hypertension. Much less frequent causes are hemorrhages associated with anticoagulation, arteriovenous malformation, or a metastatic lesion. Patients arriving in the emergency department often are initially alert but may have rapid deterioration to a lower level of consciousness and development of new brain stem signs. Features that predict clinical deterioration have been identified, as have clinical and CT scan features associated with such a poor prospect that even suboccipital craniotomy for clot evacuation may be discouraged.59,60

Clinical Presentation

Acute severe headache associated with vertigo and vomiting and acute gait imbalance are presenting findings. At onset, patients are unable to take a single step if standing and cry out for immediate assistance; some fall, are unable to stand up, and have to roll themselves to a telephone. Speech is slurred, and clumsiness may become apparent in one limb. A cerebellar hematoma can be further suspected if the clinical triad of ipsilateral limb ataxia, horizontal gaze palsy, and peripheral facial palsy is demonstrated, although two or fewer of these signs may be present. Other common neurologic findings are skew deviation, horizontal nystagmus, and decreased corneal reflex. In this condition, pinpointsized pupils indicate significant pontine compression and imply a high risk of further deterioration. Unilateral ataxia and dysarthria point to a cerebellar hemispheric hematoma. Dysautonomic features are frequent in large cerebellar hematomas, and they include episodic bradycardia and hypertension, not necessarily coupled together.

Interpretation of Diagnostic Tests

Two major types of cerebellar hemorrhage have been described. Cerebellar hemispheric hemorrhages are most common (Fig. 14.17A-C). For unclear reasons, vermis hematomas are more frequently seen in hemorrhages associated with acquired coagulopathy (Fig. 14.17D). Both may involve extension into the ventricle and compression of the brain stem. The typical features of brain stem compression often involve effacement of the quadrigeminal cistern, and when cerebellar tissue is herniated upward, it causes additional effacement of the supracerebellar cisterns (so-called tight posterior fossa). These CT findings should be regarded as an urgent indication for evacuation of the hematoma. CT scan features highly predictive of further deterioration are extension to the vermis and acute hydrocephalus.57

A cerebral angiogram can be deferred in most cases, but a ruptured posterior circulation aneurysm or arteriovenous malformation should be considered. An arteriovenous malformation should be considered in a young patient with no history of hypertension. Cerebellar hemispheric arteriovenous malformations have a characteristic bleeding pattern on CT scans and blood tracts in the direction of the cerebellar folia, particularly in the primary cerebellar fissure. The malformation may extend, rather symmetrically, into the midline as well. Blood in the quadrigeminal cisterns and tracts on the tentorium is characteristic (Fig. 14.17E). These cerebellar hemispheric arteriovenous malformations are unmasked by MRI and should be further defined by cerebral angiography.

Figure 14.17 Types of cerebellar hematoma on computed tomography. A-C: Cerebellar hemisphere. Note effacement of the quadrigeminal cisterns, intraventricular extension, and hydrocephalus. D: Vermis hemi-sphere. E: Cerebellar hemorrhage from arteriovenous malformation. F: Cerebellar hematoma with marked fluid levels (arrows) due to use of warfarin.

First Priority in Management

Attending physicians should be primed for surgical evacuation in many patients. At our institution, clinicians usually wait for clinical deterioration before operating. Another commonly accepted precept is to remove a clot when it is 3 cm or larger in axial diameter on CT scans.61 In patients with significant swelling, a bolus of mannitol, 1 g/kg, should be administered to bridge the time to the operating room. Administration of a corticosteroid can be considered, but valid data about its efficacy are not available.

Bradycardia may be frequently observed but should be left alone. Runs of bradycardia, however, should be treated with atropine administered intravenously (0.5 mg) if hypotension occurs.

Predictors of Outcome

Alert or minimally drowsy patients are at high risk of further deterioration when they have a midline extension of the hematoma or acute hydrocephalus. Poor outcome after surgery is very likely when acute hydrocephalus is present and corneal and doll's eye reflexes are absent. Good outcome after surgery can be expected in younger patients with intact brain stem reflexes.59,62


·     Surgical evacuation if CT scan shows signs of tight posterior fossa.

·     Observation on the ward if the hematoma is small (<3 cm) and not localized in the vermis, no deterioration has occurred, and the patient does not have an abnormal coagulation parameter.

Pontine Hemorrhage

A pontine hemorrhage is associated with high rates of death and neurologic morbidity. Hypertension is the usual cause, and arteriovenous malformation or rupture of a cavernous angioma is less common. At presentation, most patients are in a cataclysmic state and comatose with small, reactive pupils (diameter 2–3 mm), loss of horizontal gaze, and apneic spells requiring mechanical ventilation. Extension to the mesencephalon may cause significant anisocoria, which can be clinically misinterpreted as an uncal herniation syndrome (see Chapter 8). Abnormalities of eye movement have been described, such as ocular bobbing (sudden downward jerking with slow return to midcentral position), skew deviation, and abnormal horizontal conjugate gaze that is more apparent after caloric stimulation with ice water. Quadriplegia with extreme rigidity is frequent, but if the hematoma is unilaterally localized in the pons, hemiplegia may occur. Complete destruction of the mid-pons is common, and the tegmentum is seldom spared; thus, locked-in syndrome is rarely found in this condition. Dysautonomic features with marked hypertension, tachycardia, and hyperthermia (>39.5°C) may be profound.63 In contrast, pontine hemorrhages in cavernous hemangioma are not catastrophic and are manifested by acute oculomotor abnormalities or ataxia only.64

Interpretation of Diagnostic Tests

The CT scan patterns are shown in Figure 14.18. Pontine hemorrhages can be divided into massive pontine hemorrhage with extension to the mid-brain and thalamus, pontine hemorrhage with unilateral extension to the midbrain, and basal tegmental pontine hemorrhage. The lesion should be differentiated from a large fusiform aneurysm, which may produce identical clinical features due to basilar artery thrombosis (Fig. 14.19). Rarely, a unilateral tegmental hemorrhage is found; it is usually very circumscribed and barely involves major pontine structures. It may be caused by a cavernous hemangioma (Fig. 14.20).

Figure 14.18 Types of pontine hemorrhage on computed tomographic images. A-C: Extension to midbrain and thalamus. D: Massive destructive hemorrhage limited to pons. E,F: Basal tegmental hemorrhage.

First Priority in Management

Endotracheal intubation is needed in virtually all patients. Blood pressure is markedly increased, but aggressive management does not appear to have much effect on size. Blood pressure may become very high, with diastolic pressure in the range of 140–150 mm Hg. Labetalol may be needed to reduce the blood pressure to a more acceptable level. Ventriculostomy is not helpful because deterioration is related to extension or evolving swelling surrounding the hematoma. Stereotactic surgical evacuation has not been shown to improve outcome, and morbidity remains substantial. The effect of corticosteroids is unknown.

Predictors of Outcome

Good recovery occurs only in patients who are alert on admission and have small unilateral pontine hemorrhages.64 Cavernous malformations of the brain stem may continue to cause repeated hemorrhages. In one selected population of treated patients, the rate was up to 30% per person per year. Whether Stereotactic radiosurgery improves outcome is uncertain, but resection should be strongly considered to prevent devastating future morbidity.65 Clinical or CT scan features observed only in patients with a fatal outcome are a core temperature in excess of 39.8°C, tachycardia defined as more than 110 beats/ minute, CT evidence of extension to the midbrain and thalamus, and acute hydrocephalus on the initial CT scans.63

Figure 14.19 Pseudopontine hemorrhage. Left: Fusiform basilar aneurysm associated with acute basilar artery occlusion mimics pontine bleeding. Right: Note development of hypodensities on follow-up computed tomographic scan and better delineation of the aneurysm.

Figure 14.20 Magnetic resonance images showing limited pontine hemorrhage from cavernous hemangioma.


·     Neurologic intensive care unit for support, observation, and, if appropriate, discussion of level of care.

·     Patients with small pontine hemorrhages may be transferred to a ward for elective MRI, cerebral angiography, and surgical evacuation.


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