Hypertensive intracerebral hemorrhage …

Alexis T Roy MD MSc

Stroke & Vascular Disorders

Updated 03.10.2026
Released 07.16.1996
Expires For CME 03.10.2029

Hypertensive intracerebral hemorrhage

Author: Alexis T Roy MD MSc

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Editor: Steven R Levine MD

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Hypertensive intracerebral hemorrhage

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Introduction

Overview

The author provides an update on the diagnosis and management of hypertensive intracerebral hemorrhage based on the latest guidelines. Highlights include updates on imaging modalities to predict hematoma expansion, acute blood pressure and intracranial pressure management, minimally invasive surgical hematoma evacuation, and the impact of early do-not-resuscitate orders.

Key points

	• Specific markers on head CT can predict an increase in hematoma size, which is associated with worse outcomes.
	• Smooth and sustained control of blood pressure may improve functional outcomes.
	• In patients presenting with mild to moderate severity intracerebral hemorrhage and systolic blood pressures between 150 and 220 mm Hg, blood pressure should be maintained between 130 and 150 mm Hg in the acute setting. Lowering blood pressure to less than 130 mm Hg may be harmful.
	• Coagulopathy associated with intracerebral hemorrhage increases the mortality rate and should be urgently corrected.
	• Routine use of continuous hyperosmolar therapy, platelet transfusion without a clear indication, or antiepileptic medications in the absence of seizures are not beneficial.
	• Minimally invasive surgery for supratentorial hemorrhage can reduce mortality and may improve functional outcomes in certain patients.
	• Surgical cerebellar hematoma evacuation is indicated to reduce mortality if the volume is greater than 15 ml, in neurologic deterioration, brainstem compression, or hydrocephalus.
	• Transfer of patients to a center with specialized neurosurgical services may improve outcomes, whether or not surgery is performed. Telemedicine may facilitate patient selection.
	• Caregiver education improves coping with the challenges posed by intracerebral hemorrhage.

Historical note and terminology

Intracerebral hemorrhage is bleeding into the brain parenchyma resulting from the rupture of a cerebral artery. Globally, it accounts for approximately 28% of incident strokes (100). Despite a lower incidence than ischemic stroke, intracerebral hemorrhage is associated with disproportionately higher mortality and disability-adjusted life-years lost. Hypertension is the leading risk factor for intracerebral hemorrhage.

Intracerebral hemorrhage was first demonstrated at autopsy by Wepfer in 1658, long before blood pressure could be measured (37). The term spontaneous, or primary, intracerebral hemorrhage implies the absence of a structural lesion, such as a vascular malformation or tumor. The most common causes of primary intracerebral hemorrhage are chronic hypertension and cerebral amyloid angiopathy.

The introduction of CT in 1973 markedly improved the diagnosis of intracerebral hemorrhage. CT reliably diagnoses bleeding and differentiates it from ischemic stroke. Brain MRI provides additional information regarding hemorrhage age, evolution, and underlying etiology. CT angiography improves the detection of secondary causes of intracerebral hemorrhage and has high sensitivity for identifying vascular lesions, although digital subtraction angiography remains the gold standard.

Surgical treatment of hypertensive intracerebral hemorrhage was first reported by Cushing (28) and continues to be an important part of management in select patients.

Clinical manifestations

Presentation and course

	• Focal neurologic deficits typically evolve over minutes to hours.
	• The type of neurologic deficit (eg, weakness, aphasia, vision loss) depends on the region of brain tissue affected.
	• Large hematomas may cause symptoms of increased intracranial pressure, including headache, vomiting, and decreased level of consciousness.
	• Intracerebral hemorrhage cannot be reliably differentiated from ischemic stroke based on symptoms alone and requires neuroimaging for diagnosis.

In hypertensive intracerebral hemorrhage, focal neurologic deficits depend on the location, size, and secondary effects of the hematoma, including mass effect and perihematomal edema. The classic signs of intracerebral hemorrhage are summarized in Table 1 (19). As the hematoma expands, neurologic deficits often progress to a maximum severity, usually within 10 to 30 minutes after onset, but it may take up to 3 hours to fully develop (19). Large hematomas characteristically cause progressive focal neurologic deficits accompanied by vomiting, headache, and decreased level of consciousness. Conversely, small hematomas can mimic ischemic lacunar syndromes.

Level of consciousness is impaired in approximately 40% to 60% of cases due to the involvement of the reticular activating system, mass effect, increased intracranial pressure, or hydrocephalus. Coma is more common in patients with large hemorrhages and hemorrhages involving the thalamus, pons, or intraventricular extension. Stupor and coma are associated with a worse prognosis.

Headache, thought to result from stretching of the pain-sensitive meninges or blood vessels, occurs in 40% to 60% of patients (86). Vomiting, related to intracranial pressure or brainstem involvement, is experienced in approximately half of patients (19).

Table 1. Signs of Intracerebral Hemorrhage at Various Sites

Motor and sensory signs
	Putaminal	• Contralateral hemiparesis if hemorrhage extends into the internal capsule, hemisensory loss if hemorrhage extends into thalamocortical fibers, homonymous hemianopsia if hemorrhage extends into optic radiations
	Thalamic	• Contralateral sensory loss; variable contralateral hemiparesis if the internal capsule is involved
	Pontine	• Contralateral hemiparesis or quadriparesis (larger lesions affecting bilateral pons)
	Cerebellar	• Ipsilateral limb or truncal ataxia
Oculomotor signs
	Putaminal	• Rare; can see conjugate deviation to the same site with large hemorrhages that extend into frontal eye field projections
	Thalamic	• Conjugate deviation to the same site or opposite site, eyes down or down and in, hyperconvergence, skew, vertical gaze palsy
	Pontine	• Bilateral horizontal gaze paresis, preserved vertical reflex movements, ocular bobbing (classic sign)
	Cerebellar	• Nystagmus, skew deviation, hyper- or hypometric saccades
Pupils *
	Putaminal	• Usually normal
	Thalamic	• Small but reactive or normal
	Pontine	• Small, reactive pupils
	Cerebellar	• Usually normal
	* Large hemorrhages of any location can cause uncal herniation with cranial nerve III palsy, leading to the classic “down and out” eye position with dilated and fixed (“blown”) pupil
Alertness
	Putaminal	• Normal if small lesion; decreased levels of arousal with large hemorrhages that result in midline shifts or downward herniation
	Thalamic	• Frequently associated with decreased alertness
	Pontine	• Can be associated with early coma
	Cerebellar	• Normal to decreased levels of arousal due to brainstem compression or the development of hydrocephalus
Behavioral signs
	Thalamic	• Confusion, poor memory, aphasia (dominant/left thalamus), left-side neglect (nondominant/right thalamus)

Ocular bobbing

A 68-year-old woman presented with deep coma (E1, V1, and M2) of 2 days duration. On examination the patient had pinpoint sluggishly reacting pupils, absence of extraocular movements on oculocephalic maneuvers, ocular bobbing, ...

Prognosis and complications

Perihematoma edema. Swelling around the hematoma site contributes to secondary brain injury through mass effect, disruption of adjacent neuronal tissue, and increased intracranial pressure. Large hematomas and associated edema can cause midline shift and compression of the brainstem’s vital centers, potentially leading to coma and death. Elevated blood pressure in the first 24 hours after symptom onset is associated with a greater risk of perihematomal edema (134) and higher morbidity and mortality (29). Edema formation begins within the first few hours (127), increases over several days, and peaks at 1 to 2 weeks (60). Perihematomal edema has also been associated with hyperthermia, likely reflecting activation of inflammatory cascades and cytokine-mediated injury (59).

Hematoma expansion. Hematoma expansion is associated with increased mortality and worse functional outcomes (30). Serial CT scans have demonstrated hematoma expansion in approximately 26% of patients within the first hour after the initial CT scan and in another 12% after 20 hours of the initial scan (13). The strongest imaging predictor of hematoma expansion is the CT angiography “spot sign,” defined as one or more small foci of contrast enhancement within the hematoma, suggesting active contrast extravasation and ongoing bleeding (145). Other predictors of hematoma expansion include larger baseline hematoma, irregular hematoma shape, presence of intraventricular hemorrhage, anticoagulant use, and elevated inflammatory biomarkers, such as matrix metalloproteinase-9 (146; 73).

Hydrocephalus. Hydrocephalus may develop after intracerebral hemorrhage due to intraventricular extension of blood or from mass effect from the hematoma. Communicating hydrocephalus occurs when blood products impair cerebrospinal fluid reabsorption at the arachnoid granulations, whereas obstructive (noncommunicating) hydrocephalus results from blockage of cerebrospinal fluid flow within the ventricular system due to intraventricular clot, compression of ventricular pathways, or brain tissue displacement. Hydrocephalus can lead to elevated intracranial pressure, decreased level of consciousness, and neurologic deterioration, and its presence is a predictor of increased mortality and poorer functional outcome (139).

Seizures. Seizures, either clinical or electrographic-only, are relatively common after intracerebral hemorrhage and may occur in the acute phase or months to years later. The reported incidence varies depending on seizure definition, monitoring methods, and duration of follow-up. One continuous EEG study found that seizures occurred in 31% of patients, with more than half being electrographic seizures only (26). In contrast, one meta-analysis found the seizure incidence to be approximately 10% after intracerebral hemorrhage (43). Many seizures will occur within the first 24 to 48 hours after hemorrhage onset. Several factors may increase the risk for seizures, including cortical location, larger hematoma volume, and alcohol use (43). The relationship between seizure and clinical outcomes is harder to quantify, with some studies suggesting that seizures do not worsen outcomes when correcting for hemorrhage severity (83).

Hyperthermia. Hyperthermia occurs in more than 30% of patients during their index hospitalization and is associated with increased mortality (59). However, it remains uncertain whether treatment of fever independently improves outcomes (32). Larger hemorrhage volume, intraventricular extension, external ventricular drainage or surgical evacuation, and positive blood cultures are associated with increased risk of hyperthermia (44; 40). Fever can be caused by thermoregulatory dysfunction, particularly in those with pontine or hypothalamic involvement, and can be difficult to treat (120) or secondary to other medical illnesses, such as infection.

Coma. Coma at presentation is strongly associated with poorer outcomes and has been associated with a 64% mortality rate in early observational studies (124). One study found that mortality within the first week is 32 times higher in patients with a Glasgow Coma Scale score less than 8 and 14.5 times higher in those with signs of brainstem compression (143).

Mortality. One large retrospective cohort study of over 20,000 patients reported an in-hospital mortality of approximately 32%, with mortality increasing to approximately 45% at 1 year and 50% at 2 years. Mortality correlates with hematoma size and Glasgow Coma Scale score (68). Additional predictors of mortality include older age, elevated systolic blood pressure on admission, fever, hyperglycemia, elevated neutrophil count, elevated serum fibrinogen levels, and hypodensities on CT head (70; 58; 130; 10).

Thirty-day mortality increases when the hematoma volume exceeds approximately 30 ml in the supratentorial compartment and 20 ml in the infratentorial compartment (119). Mortality is particularly high in brainstem hemorrhages, especially greater than 1 cm in diameter in the pons and 3 cm in the thalamus. In cerebellar hemorrhages, decreased level of consciousness is strongly associated with higher mortality (98). Intraventricular hemorrhage is associated with higher rates of death and disability as compared to intracerebral hemorrhage without ventricular extension (63).

Several prognostic models have been developed to estimate mortality and functional outcomes after intracerebral hemorrhage, including the ICH Score, which predicts 30-day mortality, and the FUNC Score, which predicts the likelihood of functional independence (48; 115). These tools are useful for risk stratification but should be applied cautiously and not be used in isolation to guide decisions regarding early withdrawal of life-sustaining treatment (42).

Recurrence of intracerebral hemorrhage. The recurrence rate of hypertensive intracerebral hemorrhage is lower than that of hemorrhage caused by cerebral amyloid angiopathy but remains clinically significant. Among survivors of hypertensive intracerebral hemorrhage, recurrence rates are estimated at approximately 1% to 2% per year (71). Poorly controlled hypertension is the strongest modifiable risk factor for recurrent hemorrhage, and sustained blood pressure reduction substantially lowers recurrence risk (08). Recurrent hypertensive hemorrhages most commonly occur in deep brain structures, including the basal ganglia, thalamus, pons, and cerebellum, reflecting the underlying small vessel arteriolosclerosis associated with chronic hypertension. Risk prediction tools developed for anticoagulation-associated bleeding, such as the HAS-BLED score, have limited utility in predicting recurrence of hypertensive intracerebral hemorrhage and should not be used for this purpose in isolation (21; 22).

Biological basis

	• Uncontrolled hypertension is the most common cause of spontaneous intracerebral hemorrhage.
	• Chronic hypertension may be distinguished from stress hypertension by physical examination and ancillary tests.

Etiology and pathogenesis

Etiology. Hypertensive intracerebral hemorrhage results from chronic hypertension-induced pathologic causes in the small vessels of the brain. Many patients have a documented history of hypertension; however, some may have previously undiagnosed hypertension, underscoring the importance of routine blood pressure screening for primary prevention. Clues to chronic hypertension can be gathered from other markers, including cardiomegaly on chest x-ray, left ventricular hypertrophy on electrocardiogram or echocardiogram, renal dysfunction, or hypertensive retinopathy on funduscopic examination.

In a large population-based study, hypertension was associated with a 3.9 relative risk for intracerebral hemorrhage (14). For the combination of hypertension by history, left ventricular hypertrophy, and cardiomegaly, the relative risk was 5.4. Among Black patients with a history of hypertension, the relative risk was 8.2 and increased to 13.3 when left ventricular hypertrophy and cardiomegaly were also present. Extreme work overload, defined as overtime above 100 hours/month, has also been associated with the risk of hypertensive intracerebral hemorrhage compared with lower overtime exposures (less than 60 hours/month) (88).

Genetic susceptibility to hypertension may also contribute to intracerebral hemorrhage risk. Multiple single-nucleotide polymorphisms (SNPs) have been found to be related to blood pressure. Although individual SNPs have not been strongly associated with intracerebral hemorrhage or pre-hemorrhage hypertension, composite genetic risk scores based on blood pressure variants have been associated with deep but not lobar intracerebral hemorrhage (34).

Pathology. Hypertensive intracerebral hemorrhage results from pathologic changes in the small penetrating arteries of the brain caused by chronic hypertension. The most common abnormalities include lipohyalinosis and microaneurysm formation (sometimes referred to as miliary or Charcot-Bouchard aneurysms).

Lipohyalinosis is considered the primary pathologic process underlying hypertensive intracerebral hemorrhages. It can be characterized by deposition of hyaline material within the blood vessel wall, which can lead to disruption of the smooth muscle, vessel wall thickening, reduced compliance, and progressive weakening, ultimately making the vessel more prone to rupture (101).

The association between parenchymal hemorrhage and miliary aneurysms of the small intracerebral arteries was first described by Charcot and Bouchard in 1868 (23) and later supported by other investigators (117; 27). Postmortem angiography revealed an association between hypertension and miliary aneurysms in the small vessels (100 to 300 µm in diameter) of the basal ganglia, internal capsule, thalamus, and, less commonly, centrum semiovale and cortical gray matter (117; 27). This distribution corresponds to the typical location of most hypertensive hemorrhages in the deep structures: putamen (40% to 50% of cases), subcortical white matter-lobar (20%), thalamus (15%), cerebellum (8%), pons (8%), and caudate nucleus (8%) (19). However, more recent pathologic studies suggest that miliary aneurysms may be a marker of more advanced cerebrovascular disease rather than the main direct cause of rupture (80).

After rupture of a small penetrating artery, the hematoma may continue to expand, most commonly within the first 6 hours, but may persist up to 24 hours, especially in those with a coagulopathy (147). Within hours of onset, accumulation of serum proteins resulting from blood clot retraction leads to formation of perihematoma edema (138). Typically, perihematomal edema increases over several days, often peaking around 3 to 7 days, and may persist for several weeks (149).

After 2 to 4 days, inflammatory cell infiltration begins with activation of microglial cells and recruitment of macrophages. Hemosiderin-laden macrophages and extracellular deposits of hematoidin become prominent within several weeks. The level of CD163, a scavenger receptor involved in hemoglobin clearance, has been associated with perihematoma edema severity and may be a potential prognostic biomarker (116).

Astrocytic proliferation occurs in the neighboring parenchyma as part of the repair process. Apoptosis plays a major role in cell death after intracerebral hemorrhage and is associated with activation of nuclear factor-kB (NF-kB), ICAM-1, and IL-1B (140). In the chronic stage, the hematoma resolves, leaving a cavity lined by gliosis and hemosiderin-laden macrophages.

There have been various pathological classification approaches for intracerebral hemorrhage. For example, the SMASH-U classification is an algorithm that uses successive elimination to assign hemorrhage etiology into six categories: structural vascular lesions (S), medication (M), amyloid angiopathy (A), systemic disease (S), hypertension (H), or undetermined (U). Structural lesions, such as cavernomas and arteriovenous malformations, account for 5% of hemorrhages. Approximately 14% of cases were caused by anticoagulation and 5% by systemic disease. Amyloid angiopathy and hypertensive angiopathy were the most common causes at 20% and 35%, respectively. Despite thorough evaluation, etiology remained undetermined in 21% of cases (84). Other classification systems, such as the H-ATOMIC and CLAS-ICH, examine possible associations among multiple etiologies to determine the most likely etiology (82; 108). Although these classification systems are primarily used in research settings to standardize etiologic categorization, they may be useful in clinical practice to guide diagnostic evaluation and secondary prevention strategies.

Hypertensive intracerebral hematoma (autopsy specimen)

Axial section showing a large hematoma, originating in the left thalamus. The hemorrhage has dissected into the lateral ventricles. (Contributed by Dr. Sherman Stein.)

Epidemiology

	• Globally, stroke was the third leading cause of death in 2021, accounting for more than 3 million deaths annually.
	• Intracerebral hemorrhage makes up 28.8% of incident strokes worldwide.
	• Since 1990, the age-standardized incidence of intracerebral hemorrhage has decreased, although reductions have been smaller in regions with lower socio-demographics.
	• Hypertension is the leading cause of intracerebral hemorrhage and the primary modifiable risk factor.

According to the World Stroke Organization, intracerebral hemorrhage accounts for approximately 28.8% of incident strokes worldwide (100). Although intracerebral hemorrhage occurs half as frequently as ischemic stroke, it results in similar deaths and contributes disproportionately to disability-adjusted life years. Intracerebral hemorrhage is more common with older age, in men, and in countries with a lower socio-demographic index. Overall, the incidence of intracerebral hemorrhage has been decreasing globally, although reductions have been slower in countries with lower socio-demographic indices.

Elevated systolic blood pressure is the leading risk factor for intracerebral hemorrhage. Other top-ten contributing risk factors include ambient particulate matter pollution, household air pollution from solid fuels, smoking, a high-sodium diet, a diet lower in fruits, impaired kidney function, lead exposure, alcohol use, and high fasting plasma glucose (100). Public health initiatives targeting these risks are critical to reduce the burden of intracerebral hemorrhage. Coagulopathies are also associated with intracerebral hemorrhage, including the use of antithrombotic agents and primary hematologic disorders. This is especially relevant with the increasing prescription of oral anticoagulants for ischemic stroke protection in atrial fibrillation.

The absolute incidence of intracerebral hemorrhage increases with age, but 56% of all intracerebral hemorrhage cases occur in patients younger than 70 years old, and 18% occur in adults between the ages of 15 and 49 years (100). Geographically, most intracerebral hemorrhage burden occurs in Southeast Asia, East Asia, and Oceania, which together account for half of the global burden (100). One study conducted in the United States found that Black and Hispanic patients present with intracerebral hemorrhage at a younger age, with more than half of these cases being associated with untreated hypertension (65). Black and Hispanic patients were also much less likely to have health insurance, reflecting ongoing health care disparities (65).

Although no seasonal variation has been identified, the risk of intracerebral hemorrhage increases significantly between 8:00 am and 4:00 pm (96). In a small study, a drop in atmospheric pressure 2 days before ictus was associated with deep but not lobar intracerebral hemorrhage, suggesting a link to hypertensive etiology (55).s

Differential diagnosis

Confusing conditions

Because the clinical presentations of ischemic and hemorrhagic stroke often overlap, CT imaging is used to rapidly and reliably differentiate between ischemic and hemorrhagic stroke and the location of intracranial hemorrhage. Intracranial hemorrhage can be classified by the anatomic compartment involved and includes bleeding into the epidural, subdural, subarachnoid, intracerebral, and intraventricular spaces. Intracerebral hemorrhage is further subdivided into primary (spontaneous), resulting from intrinsic vessel wall disease, such as hypertensive arteriolosclerosis or cerebral amyloid angiopathy, and secondary hemorrhage due to underlying structural lesions, such as vascular malformations or tumors. Determining the underlying etiology of intracerebral hemorrhage is based on clinical risk factors and the location and imaging features of the hemorrhage on CT and MRI.

Cerebral amyloid angiopathy. Cerebral amyloid angiopathy is a cerebral small vessel disease that most commonly occurs in patients older than 50 years old and is an important cause of spontaneous lobar intracerebral hemorrhage. It most commonly occurs in the occipital lobes but may occur in any cortical region. In addition to lobar hemorrhage, cerebral amyloid angiopathy can cause convexity subarachnoid hemorrhage, cerebral microbleeds, microinfarcts, and progressive cognitive impairments and dementia. The underlying pathology involves deposition of beta-amyloid protein in the cortical and leptomeningeal arteries, leading to vessel wall fragility, rupture, and intracerebral hemorrhage.

Cerebral amyloid angiopathy can be differentiated from hypertensive intracerebral hemorrhage by location: hypertensive intracerebral hemorrhages most commonly occur in non-lobar locations, such as the basal ganglia, thalamus, and pons. However, in more severe cases, it can occur in lobar locations. In contrast, cerebral amyloid angiopathy occurs only in lobar locations.

The Boston 2.0 criteria provide a validated framework for premortem diagnosis of cerebral amyloid angiopathy using clinical features, and hemorrhagic and white matter MRI features (24). Hemorrhagic features include lobar intracerebral hemorrhage, lobar cerebral microbleeds, convexity subarachnoid hemorrhage, and cortical superficial siderosis on susceptibility-weighted MRI sequences. Supportive MRI white matter features include more than 20 enlarged perivascular spaces in the centrum semiovale or white matter hyperintensities in a multispot pattern. In contrast, hypertensive small-vessel disease is associated with enlarged perivascular spaces and cerebral microbleeds in the deep grey matter and white matter hypertensities more localized to the periventricular white matter. As hypertensive arteriopathy progresses, white matter changes can become more diffuse.

Vascular malformation. Intracerebral hemorrhage can be due to an underlying intracranial vascular lesion, including arteriovenous malformation, dural arteriovenous fistulae, cavernous malformation, and aneurysm. For this reason, the American Heart Association recommends cerebral blood vessel imaging in patients with intracerebral hemorrhage when a vascular lesion is suspected (42). CT angiography of the head is recommended as the first-line screening modality given its ease of use and accessibility. It should be strongly considered in patients younger than 70 years old with spontaneous lobar intracerebral hemorrhage, in patients younger than 45 years old with deep or posterior fossa intracerebral hemorrhage, and in patients aged 45 to 70 years old with deep or posterior fossa intracerebral hemorrhage without a history of hypertension (42). If CT angiography is negative but suspicion remains high, MRI or digital subtraction angiography should be considered. Repeat or delayed vascular imaging may reveal lesions initially obscured by mass effect or compression of the hematoma.

Cerebral venous sinus thrombosis. Thrombosis of the cerebral venous sinuses or cortical veins can increase venous pressure, leading to venous infarction and secondary intracerebral hemorrhages. These hemorrhages often occur in more atypical locations, particularly the parasagittal region, and are frequently associated with edema disproportionate to the hematoma size. Venous imaging, such as CT or MR venography, should be performed in patients with risk factors for thrombosis or imaging features suggestive of a venous etiology.

Brain tumor. Intracerebral hemorrhage may occur due to primary or metastatic brain tumors. Among primary brain tumors, glioblastoma is the most common cause of tumor-related intracerebral hemorrhage (76). However, brain metastases are the most common intracranial neoplasm in adults and are a more frequent cause of hemorrhagic intracerebral lesions than primary brain tumors. Brain metastases from choriocarcinoma, melanoma, renal cell carcinoma, thyroid carcinoma, and lung carcinoma have a high propensity for hemorrhage. An underlying tumor should be considered when imaging demonstrates a contrast-enhanced lesion surrounded by vasogenic edema on CT or MRI, disproportionate edema relative to hematoma size, or persistent enhancement on follow-up imaging after the hematoma resolves.

Hemorrhagic transformation of an ischemic stroke. Hemorrhagic transformation occurs in approximately 27% of ischemic strokes and ranges from asymptomatic petechial hemorrhage to large hematomas that result in mass effect, cerebral edema, and neurological worsening (56). This process most commonly results from reperfusion of infarcted brain tissue with disruption of the blood-brain barrier. It is more likely to occur with anticoagulation use, administration of intravenous thrombolysis, higher stroke severity score, and larger infarcts (56). Imaging features that suggest hemorrhagic transformation include hemorrhage confined to a known arterial vascular territory, co-existence of surrounding infarcted tissue, and evolution of an ischemic infarct to later have hemorrhage.

Illicit drug-related intracerebral hemorrhage. Sympathomimetic drugs and other stimulants are associated with intracerebral hemorrhage, including amphetamine, methamphetamine, cocaine, phencyclidine, phenylpropanolamine, ephedrine, and methylphenidate (95; 18; 50). These substances can increase the risk of hemorrhage through sudden increases in blood pressure, vasospasm, and direct vascular toxicity. The diagnosis is supported by a history of recent drug use and a positive toxicology screen, although a negative drug screen does not exclude exposure if testing is delayed or a limited toxicology panel is ordered.

Hematological disorders. Hematologic disorders that impair coagulation or platelet function can increase the risk of intracerebral hemorrhage. Examples included inherited bleeding disorders, such as hemophilia, acquired conditions, such as drug-induced thrombocytopenia, and hematologic malignancies, such as leukemia. These disorders may result in spontaneous hemorrhage or increase the susceptibility to hemorrhage following minor vascular injury.

Unusual causes of intracerebral hemorrhage. Several uncommon conditions have been associated with intracerebral hemorrhage, often in the setting of an acute rise in blood pressure or blood flow. These include exposure to cold weather, dental pain or manipulation, manipulation of the trigeminal nerve, carotid endarterectomy, and correction of congenital heart defects and cardiac transplantation in the young (19). The location of the hematomas in these conditions is similar to the distribution seen in hypertensive intracerebral hemorrhage, suggesting rupture of the vulnerable small penetrating deep arteries.

Associated or underlying disorders

Left ventricular hypertrophy. Left ventricular hypertrophy is a marker of chronic hypertension and is associated with an increased risk of intracerebral hemorrhage (99).

Hypothyroidism. Hypothyroidism is associated with endothelial dysfunction and accelerated atherosclerosis and has been reported more often in patients with intracranial hemorrhage (57). However, this relationship may be indirect and mediated by similar vascular risk factors.

Diagnostic workup

Laboratory testing. All patients with intracerebral hemorrhage should undergo laboratory evaluation, including coagulation parameters (prothrombin time, international normalized ratio, and partial thromboplastin time), complete blood count, blood chemistry panel, and troponin.

CT head. Noncontrast CT of the head is the first-line imaging modality for patients presenting with suspected intracerebral hemorrhage because of its high sensitivity for detecting acute blood products and rapid acquisition compared with MRI. CT can also be used serially to evaluate for hematoma expansion and its complications, including cerebral edema, hydrocephalus, and brain herniation (151). The spatial resolution of modern CT scanners is on the order of a few millimeters.

Acute intracerebral hemorrhage appears as a hyperdense lesion with attenuation values typically between 40 and 90 Hounsfield units (122). This increased attenuation reflects the high protein concentration and hemoglobin content of the extravasated blood (93). Perihematomal edema, primarily plasma-derived vasogenic edema, surrounds the acute hematoma and contributes to mass effect (17). After 7 to 10 days, the high-attenuation values of the hematoma begin to decrease, beginning at the peripheral and progressing centrally. The hematoma may become isodense relative to surrounding brain tissue within 2 to 3 weeks for small hemorrhages or withi 1 to 2 months for larger hemorrhages (93). The reduction in size and attenuation values of intracerebral hematoma occurs at rates of 0.65 mm and 1.4 Hounsfield units per day, respectively (33). In the chronic stages, the hematoma resolves, leaving a residual cavity or encephalomalacia.

Hypertensive intracerebral hematoma (CT)

This unenhanced image shows a large, deep, right-sided hematoma with mass effect and dissection into the lateral ventricles. (Contributed by Dr. Sherman Stein.)

Heterogenous intensities within the hematoma and irregular margins on noncontrast CT of the head (manifesting as hypodense regions, fluid levels, or specific imaging signs such as the swirl sign, black hole sign, island sign, or satellite sign) are associated with increased risk of hematoma expansion and poorer prognosis (90; 89). A repeat CT scan is recommended within the first 24 hours of onset or in patients with a low Glasgow Coma Score or neurologic deterioration (01; 78).

CT angiography of the head. CT angiography of the head is recommended in patients with intracerebral hemorrhage when an underlying vascular lesion is suspected. According to guidelines, CT angiography should strongly be considered in patients younger than 70 years with lobar spontaneous intracerebral hemorrhage, in patients younger than 45 years with deep or posterior fossa intracerebral hemorrhage, or in patients aged 45 to 70 years with deep or posterior fossa hemorrhage without a history of hypertension (42). CT venography can also be performed when cerebral venous sinus thrombosis is suspected.

Contrast extravasation within the hematoma on early CT angiography (known as the “spot sign”) reflects active bleeding and is a strong predictor of hematoma expansion or worse outcomes (41; 136). The Spot Sign Score (SSSc), which includes the number of spot signs, their maximum axial dimension, and attenuation, further stratifies the risk of hematoma expansion, severe disability, and mortality (113).

MRI brain and MR angiography. In addition to distinguishing hemorrhage from infarction, MRI provides insight into the evolution of the intracerebral hemorrhage by detecting biochemical changes in hemoglobin and its breakdown products. The evolution of hemorrhage on MRI has been classically delineated into five stages: (1) hyperacute (first 24 hours), (2) acute (1 to 3 days), (3) early subacute (3 to 7 days), (4) late subacute (7 to 14 days), and (5) chronic (greater than 14 days). The different stages of hemorrhage, the changes of hemoglobin, and the intensity on MRI are described in Table 2 (11). MRI is also very sensitive for identifying microbleeds, underlying structural lesions, and associated white matter disease.

Table 2. Stages of Hemorrhage

Stage	Hemoglobin	T1-Weighted	T2-Weighted
Hyperacute	Oxyhemoglobin	Dark	Bright
Acute	Deoxyhemoglobin	Dark	Very dark
Subacute
• Early • Late	Methemoglobin Methemoglobin	Bright Bright	Dark Bright
Chronic
• Center • Rim	Hemachrome Hemosiderin	Bright Dark	Bright Very dark

Using diffusion-weighted, T2-weighted, and susceptibility (T2*) -weighted MRI sequences, intracerebral hemorrhage can be detected within 6 hours of onset. Typically, the hemorrhage appears “target-like” (36), reflecting three distinct regions: (1) center: isointense to hyperintense signal on T2* - and T2-weighted images; (2) peripheral: hypointense (deoxyhemoglobin) mostly on T2*-weighted images; (3) rim: hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging, representing vasogenic edema surrounding the hematoma (75).

Susceptibility-weighted MRI sequences detect chronic microbleeds in more than half of the patients (54%) with primary intracerebral hemorrhage. Microbleeds appear as round, hypointense foci smaller than 5 mm due to the perivascular hemosiderin. They result either from hypertensive vasculopathy or from cerebral amyloid angiopathy (135). The microbleeds located in the basal ganglia and thalamus are more likely to be associated with primary hypertensive intracerebral hemorrhage, whereas microbleeds located in the lobar regions are more suggestive of cerebral amyloid angiopathy (114).

Enlarged perivascular spaces, also known as Virchow-Robin spaces, are another MRI marker of cerebral small vessel disease and are commonly observed in patients with intracerebral hemorrhage. Their anatomical distribution may help distinguish underlying hemorrhage etiologies. Prominent enlarged perivascular spaces in the centrum semiovale are more strongly associated with cerebral amyloid angiopathy, whereas enlarged perivascular spaces in the basal ganglia are more characteristic of hypertensive arteriopathy (25).

Catheter intra-arterial digital subtraction angiography. Digital subtraction arteriography is used in selected cases to diagnose and guide treatment for macrovascular causes of intracerebral hemorrhage, including arteriovenous malformations, dural arteriovenous fistulas, and aneurysms. Digital subtraction angiography should be considered in patients younger than 70 years with lobar intracerebral hemorrhage, in patients younger than 45 years with deep or posterior fossa intracerebral hemorrhage, and in patients aged 45 to 70 years with deep or posterior fossa intracerebral hemorrhage without hypertension and a negative CT or MR angiogram (150; 42). In patients without a clear cause and a negative initial angiogram, a repeat angiogram in 3 to 6 months may uncover small vascular malformations initially obscured by the hemorrhage (54).

Extension of the hemorrhage into the ventricular system is not strongly associated with vascular malformations, and the diagnostic yield of catheter angiography is relatively low in these cases (64). However, digital subtraction angiography should be considered in patients with isolated intraventricular hemorrhage or abnormal CTA or MRA suggestive of a macrovascular cause.

Management

Initial management priorities for intracerebral hemorrhage include:

	• Airway protection and maintenance of adequate ventilation and oxygenation
	• Blood pressure control
	• Correction of coagulopathy
	• Management of intracranial pressure and cerebral edema
	• Drainage of intraventricular blood when indicated
	• Surgical hematoma evaluation when indicated
	• Identification and treatment of seizures
	• Management of neurologic and systemic medical complications

The American Heart Association/American Stroke Association has published a comprehensive guideline for the treatment of spontaneous intracerebral hemorrhage in adults (42). Checklists have also been created to ensure timely and evidence-based implementation of these guidelines (91).

Airway. Maintenance of airway patency and adequate oxygen saturation are the first priority in patients with intracerebral hemorrhage. Endotracheal intubation is indicated if the patient has inadequate gas exchange. Intubation should also be considered in patients with decreased levels of consciousness, worsening neurologic examination, or impaired protective airway reflexes, even if gas exchange is adequate (42). Prolonged coma or pulmonary complications beyond 2 weeks may require elective tracheostomy.

Blood pressure control. Most patients with intracerebral hemorrhage present with elevated blood pressure. Higher systolic blood pressure is associated with increased morbidity and mortality, but clinical trials of intensive blood pressure control have not consistently demonstrated improved clinical outcomes or mortality (04; 61; 62; 105). Moreover, a meta-analysis of four studies including 3315 patients found that controlled blood pressure reduction was safe but did not significantly reduce unfavorable outcomes (132).

Excessively and too rapidly lowering blood pressure may impair cerebral perfusion in vulnerable brain regions. Case reports have demonstrated cerebral ischemia with marked blood pressure reduction (39). Moreover, in the ATACH-2 trial, patients with more intensive systolic blood pressure lowering below 140 mmHg within 2 hours and maintained for at least 2 hours had higher rates of neurologic and renal adverse events without clear improvements in functional outcomes (106). Another study of 286 patients found an association between systolic blood pressure below 120 mmHg and ischemic lesions (15).

Although the optimal blood pressure targets and timing of blood pressure reductions require more investigation, guidelines recommend careful blood pressure lowering with a goal of maintaining adequate cerebral perfusion pressure. In patients with mild to moderate severity spontaneous intracerebral hemorrhage presenting with a systolic blood pressure between 150 and 220 mmHg, lowering the blood pressure to a target of 140 mmHg (with a goal range of 130 to 150 mmHg) with minimal fluctuations is safe and may improve functional outcomes (42). Lowering the systolic blood pressure to less than 130 mmHg may be harmful and should be avoided (42). Blood pressure should be reduced promptly, ideally within 2 hours of symptom onset, using titratable intravenous antihypertensives. Large variability in systolic blood pressure should be avoided as it has been associated with hematoma expansion and worse outcomes (92).

The optimal management for patients presenting with severe, sustained systolic blood pressure greater than 220 mmHg and for those with large and severe intracerebral hemorrhage is less well defined, and treatment should be individualized with close monitoring of neurologic status and cerebral perfusion. Analysis of the MSTIE III trial data found that a large hematoma volume on admission, a drop in systolic blood pressure by more than 80 mmHg within 24 hours, and moderate to severe white matter disease were associated with diffusion-weighted imaging lesions on follow-up MRI, suggesting the need for cautious blood pressure lowering in these patients (111).

Intracranial pressure monitoring and control. Intracranial pressure may be elevated in patients with intracerebral hemorrhage due to mass effect of the hematoma, perihematomal edema, or associated hydrocephalus. Intracranial pressure can be monitored by invasive devices, including a skull-anchored device that allows insertion of a sensor into the brain parenchyma or via an external ventricular drain that allows both measuring of the intracranial pressure and drainage of the cerebrospinal fluid to maintain a set pressure. The latter is usually the preferred modality, as it allows both continuous intracranial pressure monitoring and therapeutic cerebral spinal fluid drainage to reduce intracranial pressure.

Guidelines do not recommend routine intracranial pressure monitoring in all patients with intracerebral hemorrhage. However, intracranial pressure monitoring should be performed in patients with intracerebral or intraventricular hemorrhage and hydrocephalus contributing to decreased levels of consciousness and may be considered in patients with moderate to severe intracerebral hemorrhage with reduced level of consciousness (42).

Noninvasive methods of measuring intracranial pressure, such as transcranial Doppler ultrasonography or measurement of optic nerve sheath diameter, may serve as adjunctive information but should not replace invasive monitoring when precise intracranial pressure measurements and cerebrospinal fluid drainage are indicated (81; 20).

General measures. General measures for intracranial pressure reduction include elevation of the head of the bed to promote venous drainage, targeted sedation and analgesia to reduce metabolic demand and agitation, and avoidance of neck compression, such as tight endotracheal tube ties, that might impair the cerebral venous return (142).

Hyperosmolar therapy. Hyperosmolar therapy, including mannitol and hypertonic saline, can transiently reduce intracranial pressure by promoting osmotic movement of water from brain tissue. However, studies have not demonstrated clear mortality or functional benefit with use of either agent (07; 137; 110). Guidelines do not recommend prophylactic hyperosmolar therapy, but intermittent bolus hyperosmolar therapy can be considered as a temporizing measure (42).

There is no benefit to administering corticosteroids to treat elevated intracranial pressure, and corticosteroids are not recommended for this indication.

Decompressive craniectomy. In patients with intracerebral hemorrhage and refractory intracranial hypertension despite maximal medical management, decompressive craniectomy (with or without hematoma evacuation) may be considered to reduce mortality. However, the benefit of functional outcomes is not clear, and careful patient selection is recommended (42).

Intraventricular hemorrhage management. Intraventricular hemorrhage occurs in approximately 45% of patients with spontaneous intracerebral hemorrhage and is associated with increased mortality (45). A retrospective review demonstrated that external ventricular drain is associated with reduced mortality and improved short-term outcomes (51).

Intraventricular administration of thrombolytic agents has been investigated to accelerate thrombus reabsorption. The CLEAR-IVH trial showed that in patients with small intracerebral hemorrhage and large intraventricular hemorrhage, administration of low-dose tPA in the ventricular system to facilitate blood clot removal is safe; however, the impact on functional recovery was not demonstrated (87). The CLEAR III trial showed that although ventricular irrigation with alteplase was safe and improved clot removal, it did not improve functional outcomes at the mRS < 3 cutoff compared to saline (46). Guidelines state that intraventricular thrombolysis can be considered in patients with hydrocephalus who require an external ventricular drain, but it is not routinely recommended (42).

Seizure monitoring and management. A depressed level of consciousness that is disproportionate to the size or location of the hemorrhage should prompt continuous EEG monitoring to evaluate for nonconvulsive seizures. Clinical or electrographic seizures should be treated, but the use of anticonvulsants prophylactically in patients without documented seizures is not recommended (85; 42).

Hemostatic treatments. Platelet transfusions may be considered in emergency neurosurgery to reduce postoperative bleeding (74; 42). However, in patients not undergoing surgery, routine platelet transfusion has been associated with worse outcomes and is not recommended (05; 42).

In patients receiving anticoagulation, the anticoagulant should be discontinued immediately, and rapid reversal should be initiated using the appropriate reversal agent.

Recombinant activated factor VII (rFVIIa) has been shown to reduce hematoma expansion but did not improve functional outcomes or mortality and is not recommended for routine use (12; 35). Similarly, antifibrinolytic therapy with tranexamic acid has not been associated with clear improvements in functional outcomes (131).

Prevention and treatment of medical complications. Fluid status and electrolyte balance should be monitored, particularly if hyperosmolar agents and diuretics are used. Hyponatremia can occur from inappropriate antidiuretic hormone secretion or cerebral salt wasting. These disturbances can worsen cerebral edema and should be promptly recognized and treated.

Dysphagia. Dysphagia occurs in approximately 50% to 70% patients with intracerebral hemorrhage and is associated with an increased risk of aspiration pneumonia and worse outcomes (129). All patients should undergo formal dysphagia screening prior to oral intake, and patients should not eat or drink until safe swallowing is confirmed (53). If the patient cannot eat safely by mouth, alternative enteral access (such as a nasogastric tube) should be initiated, with consideration of longer-term enteral access (such as a percutaneous gastrotomy tube) if dysphagia persists.

Myocardial infarction. Acute myocardial infarction is uncommon after intracerebral hemorrhage (occuring in fewer than 1% of patients), but is associated with increased mortality (38). Baseline troponin and continuous telemetry in the acute phase after intracerebral hemorrhage should be considered to detect myocardial injury and arrhythmias (42).

Renal dysfunction. Renal dysfunction occurs in approximately 5% to 15% of patients with intracerebral hemorrhage. Excessive or overly rapid blood pressure reductions can lead to acute kidney injury. Importantly, CT angiography using iodinated contrast has not been associated with clinically meaningful acute kidney injury (97). Acute kidney injury is associated with higher rates of in-hospital mortality and worse functional outcomes at discharge (118). Chronic renal disease is associated with an increased burden of cerebral microbleeds in patients with intracerebral hemorrhage, likely reflecting a shared pathophysiology of small vessel disease (67).

Venous thromboembolism. Nonambulatory patients with intracerebral hemorrhage are at increased risk of deep vein thrombosis and pulmonary embolism. Intermittent pneumatic compression devices can decrease the risk of venous thromboembolism and should be instituted on the day of diagnosis (49). Low-dose prophylactic anticoagulation with unfractionated heparin or low molecular weight heparin can also reduce the risk of venous thromboembolism and should be considered after 24 to 48 hours of intracerebral hemorrhage onset, once hematoma stability has been confirmed (42).

In patients with lower-extremity deep vein thrombosis and a contraindication to therapeutic anticoagulation, placement of a temporary inferior vena cava filter may serve as a bridge until anticoagulation can be safely initiated. Therapeutic anticoagulation is often delayed 1 to 2 weeks after hemorrhage onset, depending on hematoma severity and overall clinical risk (42).

Fever. Fever occurs frequently after intracerebral hemorrhage and is associated with worse outcomes (16). Elevated temperatures should be treated promptly with antipyretic medications and supportive measures (42). Infectious causes should be investigated and treated. Targeted temperature management has not been shown to improve outcomes; therefore, maintaining normothermia is recommended (31).

Hyperglycemia. Serum glucose should be monitored to detect both hypo- and hyperglycemia. It is recommended to treat hypoglycemia (lower than 40 to 60 mg/dL) and hyperglycemia (higher than 180 to 200 mg/dL) to reduce mortality (NICE-SUGAR Investigators 2009; 42).

Decisions for life-sustaining treatments. Prognostication is challenging in the acute setting after intracerebral hemorrhage, and early withdrawal of life-sustaining therapies (such as mechanical ventilation, artificial nutrition, and antibiotics) can lead to self-fulfilling prophecies of worse outcomes. Therefore, in patients without preexisting documentation of wishes surrounding life-sustaining treatments, aggressive supportive care and avoidance of early treatment limitations (including delaying new do-not-resuscitate orders) should be considered, as early withdrawal of care may worsen outcomes (148; 42). In patients with do-not-resuscitate orders, appropriate medical and surgical interventions should be offered, unless explicitly declined by the patient or surrogate decision maker (42). Shared decision-making models between the medical team and patient or surrogates should be utilized to ensure that the care provided aligns with the patient’s values.

Statin use. Statin use is common in patients with intracerebral hemorrhage, as many vascular risk factors that increase the risk for intracerebral hemorrhage also increase the risk for ischemic heart disease and stroke. One randomized control trial (Stroke Prevention by Aggressive Reduction in Cholesterol Levels; SPARCL) found that high-intensity atorvastatin use was associated with increased risk of intracerebral hemorrhage (03). Subsequent observational studies have generally not demonstrated this association (109). The potential risk of intracerebral hemorrhage with statin therapy may vary based on hemorrhage location, with lobar hemorrhage (often due to cerebral amyloid angiopathy) being at higher risk (141). Some observational studies also suggest the potential risk is based on statin lipophilicity, with lipophilic statins posing a higher risk than hydrophilic statins (128), among other factors. Given this uncertainty, the risk of statin use in those with a history of intracerebral hemorrhage should be individualized and weighed against the benefits of cardiovascular and ischemic cerebrovascular prevention (42).

Craniotomy for supratentorial hemorrhage. A large clinical trial, the International Surgical Trial for Intracerebral Hemorrhage (STICH), demonstrated that surgical evacuation within 24 hours of randomization is not superior to conservative management, although there was a trend towards benefit in those with superficial lobar hemorrhage (125). The STICH II trial that enrolled conscious patients with superficial lesions did not show a statistically significant overall benefit of early surgery, although there was a trend toward improved outcomes with early surgery (126).

A meta-analysis suggests that surgery for supratentorial hematomas may reduce death and disability, but the results are heterogenous and not robust (104). In comatose patients with a large hematoma, large midline shift, or elevated intracranial pressure refractory to medical management, craniectomy with or without hematoma evacuation may be considered, although its impact on long-term outcomes is uncertain (42).

Less is known about surgical intervention in patients with low Glasgow Coma Scale scores, and outcomes are generally poor regardless of intervention arm. Small retrospective series suggest very poor outcomes in patients with loss of upper brainstem reflexes and extensor posturing despite emergency craniotomy (107). For patients with a Glasgow Coma Scale score of less than 8, surgical intervention did not show benefit (125). Limited data suggest that decompressive hemicraniectomy without clot evacuation may be feasible in select patients with refractory elevations in intracranial pressure, but outcomes are variable (52).

Craniotomy for infratentorial hemorrhage. In patients with a cerebellar hematoma, urgent surgical decompression is recommended when the hematoma volume is greater than 15 mL or when there is neurologic worsening, hydrocephalus, or brainstem compression, as surgery may be lifesaving. However, the impact of craniotomy on long-term functional status is less clear (66; 42).

Minimally invasive surgery. Minimally invasive surgery with endoscopic or stereotactic aspiration aims at reducing the morbidity associated with conventional open craniectomy while achieving hematoma volume reduction. A systematic review and meta-analysis of five randomized controlled trials and prospective controlled studies suggested that minimally invasive surgery may be associated with improved outcomes compared with open craniectomy for patients with supratentorial intracerebral hemorrhage (144). A meta-analysis comparing endoscopic surgery, minimally invasive surgery with thrombolytics, open craniotomy, and standard medical management found that endoscopic surgery ranked most favorably for improving survival and minimizing disability, but head-to-head randomized controlled trial data remain limited (72). No adequately powered randomized trials have directly compared device types for minimally invasive surgery.

Guidelines recommend consideration of minimally invasive hematoma evacuation, with or without thrombolytics, in select patients with supratentorial intracerebral hemorrhage, particularly those with hematomas greater than 20 to 30 mL volume and a Glasgow Coma Scale of 5 to 12 to reduce mortality (42). These recommendations mainly stem from the largest minimally invasive surgery for intracerebral hemorrhage evacuation trial (Minimally Invasive Surgery with Thrombolysis in Intracerebral Hemorrhage, MISTIE III), which showed likely mortality benefit but neutral results for functional benefit (47).

More recently, the Early Minimally Invasive Removal of Intracerebral Hemorrhage (ENRICH) trial showed improvements in 180-day functional outcomes with minimally invasive hematoma evacuation compared to medical management alone when performed within 24 hours of last seen well (103). A trans-sulcal parafascicular approach with sulcal access through a port directed along the axis of the white-matter tracts was used. Notably, this trial stratified hemorrhage by location (lobar versus deep), and the improvement in functional outcomes was driven by lobar hemorrhage, such that trial enrollment for deep hemorrhage was stopped early for futility. Based on these results, early minimally invasive hematoma evaluation can be considered for those with moderate-to-large lobar hemorrhage (30 to 80 ml) with good premorbid function.

Transfer to another facility. Patients with intracerebral hemorrhage benefit from specialized, multidisciplinary medical care, most commonly performed in a stroke or neurocritical care unit. In one study of 1175 patients, those transferred to a specialized care center had lower mortality than patients remaining at the referral hospital, even when surgical intervention was not performed (02). Accordingly, many patients with intracerebral hemorrhage should be considered for transfer to a center with specialized neurology, neurosurgery, and neurocritical care expertise. The airway and hemodynamics should be stabilized before transfer. Telemedicine can facilitate early specialist consultation and assist triaging transfer decisions.

Outcomes

Intracerebral hemorrhage is associated with high early mortality and significant long-term disability. A pooled analysis found a median case fatality of 40% at 1 month and only approximately 12% to 40% of survivors achieving long-term functional independence (133). Male sex, preexisting comorbidities, in-hospital complications, and low institutional surgical volume were associated with increased in-hospital mortality (102).

Prognostic models can be used to risk-stratify outcomes after intracerebral hemorrhage. The most widely used is the ICH score, which incorporates age, Glasgow Coma Scale, hematoma volume, infratentorial location, and presence of intraventricular hemorrhage (48). However, prognostic models may be confounded by early withdrawal of life-sustaining treatment, potentially leading to overestimated mortality, and should be applied cautiously. The Max-ICH score attempts to minimize confounding due to early care termination (121). Many of these scores incorporate similar clinical and imaging features, including patient demographics, location and size of the intracerebral hemorrhage, and neurologic examination. Although severity scores are useful for risk stratification and communication, they should not be used in isolation to determine prognosis and must be interpreted in the context of the patient’s clinical condition and the medical team’s judgment.

Multidisciplinary rehabilitation after the acute hospitalization is a critical component of recovery and is associated with improved functional outcomes and reduced morbidity and mortality. For mild-to-moderate severity intracerebral hemorrhage, early discharge from the hospital to rehabilitation in the community can increase the likelihood of patients living at home at 3 months (69; 42). In those with moderate-severity intracerebral hemorrhage, early rehabilitation (typically 24 to 48 hours after stability) may improve survival and functional outcomes at 6 months (77). Caregiver education is important and may increase patients’ functional status and quality of life (42).

Media

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Author

Alexis T Roy MD MSc

Dr. Roy of Brigham and Women's Hospital and Harvard Medical School has no relevant financial relationships to disclose.
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Steven R Levine MD

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.
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Former Authors

Te-Long Hwang MD
Adrian Marchidann MD

Patient Profile

Age range of presentation: 45 to 65+ years
Sex preponderance: male>female, >1:1
Heredity: none
Population groups selectively affected: African Americans
Occupation groups selectively affected: none selectively affected

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Hypertensive intracerebral hemorrhage

Associated Disorders

Chronic hypertension
Intracerebral hemorrhage

Differential Diagnosis

cerebral amyloid angiopathy
vascular malformation
cerebral venous sinus thrombosis
brain tumor
hemorrhagic transformation of an ischemic stroke
- illicit drug-related intracerebral hemorrhage
- hematological disorders
- unusual causes of intracerebral hemorrhage
- left ventricular hypertrophy
- hypothyroidism

	• Poorly controlled blood pressure after an intracerebral hemorrhage is associated with recurrent hemorrhage, ischemic stroke, and mortality.
	• Long-term treatment of hypertension is the most important preventive measure to reduce the risk of recurrent intracerebral hemorrhage.
	• Current guidelines recommend a targeted blood pressure of less than 130/80 mmHg for secondary prevention.

Hypertensive intracerebral hemorrhage

Cite this article

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Table 1. Signs of Intracerebral Hemorrhage at Various Sites

Prognosis and complications

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Table 2. Stages of Hemorrhage

Management

Outcomes

Special considerations

Pregnancy

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

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