Intracerebral Hemorrhage

Key Points

Spontaneous intracerebral hemorrhage (ICH) is the most serious form of acute stroke, which causes enormous loss of life and suffering on a global scale but particularly so in older and socioeconomically disadvantaged populations where the prevalence of hypertension, unhealthy lifestyles, and antithrombotic use are high.
Although there are few clearly proven treatments for ICH, an urgent approach is required for diagnosis and management with careful consideration of the location, size, and morphology of the hematoma, and any associated background cerebrovascular features on brain imaging.
There is reasonable evidence to support that chances of recovery may be improved from the early smooth control of elevated blood pressure, and for better chances of survival after surgical decompression of serious hematoma and/or intraventricular extension.
ICH management broadly involves active and well-coordinated systems of interdisciplinary care, with efforts to avoid and carefully manage potential complications, and to seriously consider effective long-term blood pressure control and use of antithrombotic therapy and other cardiovascular risk management.
An improved understanding of pathophysiology, its similarly short therapeutic time window to that of acute ischemic stroke, and broad range of health consequences including cognitive loss has fostered greater collaborative efforts to improve the prevention and management of ICH.

Introduction

Acute spontaneous (nontraumatic) intracerebral hemorrhage (ICH) is the most serious and least treatable type of stroke, accounting for approximately one-quarter of the 12 million incident strokes that occur in the world each year. It is a dynamic condition, usually manifesting radiologically as an isolated hematoma within the deep structures of brain parenchyma, and with high potential to rapidly expand or “grow” to cause pressure on vital structures and/or extend into the ventricular system or subarachnoid and dural spaces, with varying degrees of perihematomal edema. On average, one in three patients with ICH will die within the first month of onset, most within the first few days, and survivors are left with varying degrees of disability and high risk of recurrent ICH, ischemic cerebral and cardiac events, ^, and cognitive decline and dementia. In comparison to progress that has been made in the management of acute ischemic stroke, there is still no clearly proven treatment for ICH and few established protocols of care. This contributes to wide variation in the manner in which these patients are managed across the world, with differing regional patterns of neurosurgical practice and clinical opinions as to the amount of active care needed for a condition with a poor prognosis. Because most cases of ICH occur in adults of working age in low- and middle-income countries (LMICs), where the prevalence of hypertension and other adverse lifestyle and environmental factors are high, the socioeconomic impact of this condition is enormous, such that the overall global loss of productive life years from ICH is at least as great as the more common, acute ischemic stroke. Although temporal epidemiologic data are limited, these suggest divergent trends of the incidence of ICH across the world, with modest declines in LMIC ^, presumably due to improved blood pressure (BP) control and the benefits of urbanization, whereas rates are stable or increasing in high-income countries in relation to greater use of anticoagulation and antithrombotic treatment for atrial fibrillation and cardiovascular risk management in aging populations. ^, Conversely, there are some encouraging outcome data suggesting improved survival after ICH, possibly due to improved systems of care.

Etiology and Risk Factors

A longstanding convention is to use the terms “primary” or “hypertensive” when referring to the typical case of ICH originating in the basal ganglia or thalamus, which is understandable given the historical recognition of associations with severe hypertension in middle-aged adults and neuropathologic changes in the perforating vessels of proximal intracranial arteries. However, this approach is less appropriate for contemporary clinical practice because it can block enquiry over pathophysiology and investigations that can allow potentially treatable secondary causes to be readily identified.

ICH is the most common type of intracranial hemorrhage, which can occur in different locations with varying but overlapping etiologies ( Figs. 28.1 and 28.2 ). Deep perforating vasculopathy is the main cause of ICH, most often located in the vessels of the basal ganglia and brainstem, but this pathology can be accompanied by a broader process of chronic cerebral damage due to cerebral small vessel disease (CSVD), which can manifest as varying degrees of white matter lesions (“leukoaraiosis”), infarcts in relation to small perforating vessels (“lacunes”), small ICH (“microbleeds”), superficial siderosis, and lesions of old ICH and cerebral atrophy. Because there is overlap in mechanisms and risk factors, even in the presence of arteriolosclerosis elsewhere in body of a middle-aged or elderly “hypertensive” patient, clinicians should consider searching for secondary causes, especially for small deep arteriovenous malformations (AVMs) for which surgical intervention may reduce the risk of recurrent ICH. Simple clinical parameters, such as younger age (<60 years), superficial cortical or posterior fossa ICH, absence of any features of CSVD, and a suspicious or inconclusive abnormality on computed tomographic angiography (CTA), should prompt consideration of formal digital subtraction angiography from suspicion of an underlying structural cause of ICH.

Fig. 28.1, Right thalamic intracerebral hemorrhage with intraventricular extension.

Fig. 28.2, Locations of intracranial hemorrhage.

Another cause of ICH is cerebral amyloid angiopathy (CAA), which has received much attention as an explanation for cortical ICH in older people despite uncertainty over how much of CAA causes ICH, alone versus in combination with elevated BP and antithrombotic use. Characterized by the presence of amyloid-ß protein in the walls of cortical and leptomeningeal blood vessels, CAA has a different natural history to deep ICH: there is a higher risk of recurrent ICH (approximately 9% per annum) and cognitive decline and dementia. Various diagnostic clinical criteria exist, of which the magnetic resonance imaging (MRI)-based “modified Boston criteria” are the most popular and has good sensitivity and specificity for CAA: age older than 55 years, previous lobar ICH, cerebral microbleeds, and/or cortical superficial siderosis. However, the Edinburgh criteria of subarachnoid hemorrhage (SAH) and finger-like hematoma projections from a cortical ICH in apolipoprotein E (APOE)-positive patients is also moderately predictive for CAA, when MRI is contraindicated, intolerable, or unavailable. Although a presumed diagnosis of CAA can be made, the challenge to management is whether these patients should be managed differently to those with other types of spontaneous ICH (e.g., in balancing the benefits over risks of [re]starting antithrombotic agents for another clear indication). Even in high-risk patients with established cerebrovascular disease and multiple cerebral microbleeds, observational data suggest that the risk of future ischemic events far exceeds the risks of recurrent ICH.

The major risk factors for ICH are increasing age, elevations in BP or “hypertension” (currently defined as a systolic level >130 mm Hg), male sex, various dietary and lifestyle factors including smoking, high salt intake, excessive alcohol, and low consumption of fruit and fresh vegetables, use of antithrombotics (i.e., antiplatelet agents and anticoagulation) and antifibrinolytics, illicit drugs (i.e., amphetamines, cocaine), and the environment (e.g., cold ambient temperature). Although many of these factors indirectly elevate BP and overlap with those for acute ischemic stroke, they appear to preferentially damage the endothelium, leading to vessel “leakage” or rupture, rather than atheroma. Moreover, frequent systolic BP peaks in relation to chronic BP variability, and acute transient surges in BP in the context of a strong emotional reaction, sudden exertion, or alcohol/drugs, are also important triggers in predisposed individuals.

Diagnostics and Prognosis

Brain Imaging

Although certain clinical features are more suggestive of ICH than acute ischemic stroke, such as severe headache, vomiting, seizures, meningism, and rapid loss of consciousness ( Box 28.1 ), an early noncontrast computed tomography (NCCT) scan is the most reliable way of establishing the diagnosis, as in the management of anyone presenting with features suggestive of acute stroke. MRI is a more informative imaging modality in acute stroke, but its low accessibility means that it is more often performed 24–48 hours later for evaluation of the underlying etiology and background cerebrovascular disease and to exclude an underlying structural lesion. NCCT allows identification of the volume and location of ICH, any intraventricular hemorrhage (IVH), which have prognostic relevance, and of any SAH that may suggest CAA or an alternative underlying diagnosis (e.g., cerebral aneurysm or cerebral venous thrombosis). There are several CT features to suggest a secondary cause of ICH ( Box 28.2 ) as well as markers of heterogeneous shape and density that help to predict prognosis ( Box 28.3 ).

BOX 28.1

Clinical Features Suggestive of Acute Intracerebral Hemorrhage

1.
Severe headache
2.
Nausea and vomiting
3.
Neck stiffness (meningism) from subarachnoid hemorrhage
4.
Rapid loss of consciousness (rapid evolution)
5.
Loss of vertical gaze (midbrain compression)
6.
Behavior change disproportionate to any motor deficit (possible frontal lobe location)
7.
Extreme elevation of systolic blood pressure (>200 mm Hg)
8.
Seizures

BOX 28.2

Cranial Computed Tomography Features Suggestive of Secondary Causes of Intracerebral Hemorrhage

For example, arteriovenous malformation or primary metastatic tumor.

Hematoma location	Superficial subcortical or temporal region
Hematoma pattern	Heterogeneous pattern Multiple hemorrhages in different regions
Perihematomal edema	Disproportionately large to the size of the hematoma Finger- or root-like pattern
Associated features	Enlarged feeding vessel into the hematoma Dense vein sign on noncontrast computed tomography (CT) Empty delta sign on noncontrast CT Calcification pattern within or around the hematoma

BOX 28.3

Key Management Steps in Intracerebral Hemorrhage

ICH , Intracerebral hemorrhage; MRA , magnetic resonance angiography; MRI , magnetic resonance imaging.

1.
Intracerebral hemorrhage is a medical emergency—work quickly with assessments
2.
Brain and vascular imaging
- Poor prognostic features—large (>20 mL), irregular and heterogeneous density of hemispheric hematoma early (<3 h) after symptom onset; brainstem hematoma; intraventricular hemorrhage
- Any underlying cause—vascular malformation? cerebral venous thrombosis? vasculitis? reversible cerebral vasoconstrictor syndrome (“young” age), hematoma location (“peripheral/cortical”), history of hypertension (“absent”), and cerebral small vessel disease (“absent”)
3.
Stroke unit multidisciplinary care
4.
Control blood pressure—lower to systolic target <140 mm Hg over 1 h, and maintain smooth control for 72 h
5.
Correct hemostatic abnormalities
- Consider if there is a specific disease (e.g., hematologic disorder)
- Is this due to a specific anticoagulant drug, and is a reversal agent or antidote required?
6.
Correct other physiologic abnormalities
- Control elevated blood glucose
- Maintain hydration
- Is airway support required?
7.
Prevent complications
- Careful identification of deteriorating patients requiring neurosurgical intervention
- Use intermittent pneumatic compression therapy for venous thromboembolism prophylaxis, or subcutaneous heparin after several days
- Manage clinical seizures
8.
Search for the cause of the ICH
- MRA and digital subtraction angiography for high-risk clinical and imaging signs
- MRI to detect chronic microhemorrhages and cerebral superficial siderosis suggesting cerebral amyloid angiopathy
9.
Prevention
- Lower blood pressure (systolic target <130 mm Hg) to prevent recurrent ICH and other serious vascular events
- Consider restarting antiplatelet or anticoagulation to prevent ischemic events unless the patient is at very high risk of recurrent ICH
- Screen for cognitive impairment during follow-up

As an underlying vascular lesion, such as an AVM, cerebral aneurysm, or dural fistula, occurs in approximately 15% of adults with ICH, deciding whether to proceed to more extensive vascular imaging (CTA or magnetic resonance angiography [MRA] and intra-arterial digital subtraction angiography) can be made on the probability of finding a structural lesion using simple criteria: patient age, ICH location, history of hypertension, and presence of CSVD (see Box 28.2 ).

Computed Tomography Angiography Spot Sign

The CTA spot or leakage sign, which is the extravasation of contrast within or around the hematoma, has received considerable attention over the last decade as a reliable marker of hematoma growth and thus for identifying a “high-risk” patient group who could benefit from early hemostatic treatment. With some training, the accuracy of clinicians in detecting the spot sign is quite good, and studies have been consistent in showing that has moderate to high probability for further ongoing hemorrhage and adverse clinical outcome compared with spot sign–negative patients. However, hematoma growth occurs in all ICH, especially within the first few hours, and the spot sign can be easily missed if insufficient time has been allowed for the contrast to reach the leak point; although meta-analysis indicates the predictive ability of the spot sign is best in the first few hours of ICH, detection can be increased in later arterial, early venous, or delayed phases or multiphase CTA. ^, In the absence of a proven early treatment in ICH, the clinical utility of the CTA spot sign for clinical practice and research has not been defined.

Prognostic Scales

In addition to the anatomic location (i.e., lobar, deep, brainstem, cerebellum), the chances patients will survive free of major disability from ICH declines with increasing age, premorbid frailty, greater vascular comorbidity, and increasing severity of neurologic impairment and volume and extent of the hematoma in relation to the time from the onset of symptoms. The ICH score is the most commonly used prognostic scale that combines demographic and clinical information, with the location and volume of ICH, and presence of IVH. Although several other scores have been developed, none have shown substantial improvements in outcome prediction, particularly for early death. One problem is that loss of consciousness, a prominent feature of ICH, complicates the use of neurologic assessment scales (e.g., the National Institutes of Health stroke scale [NIHSS]) and can be related to the complications of ICH such as seizures, dehydration, head injury from falling, cerebral anoxia from airway obstruction, or even cardiac arrest.

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