Stroke & Vascular Disorders
Stroke associated with cerebral angiography
Mar. 10, 2026
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Basal ganglia hemorrhage …
- Updated 01.20.2026
- Released 03.28.1995
- Expires For CME 01.20.2029
Basal ganglia hemorrhage
Introduction
Overview
Basal ganglia hemorrhage is one of the most severe strokes. This update highlights important clinical trial results on the treatment of intracerebral hemorrhage, including blood pressure management and surgery.
Key points
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• Intracerebral hemorrhage is an emergency requiring immediate evaluation and treatment. | |
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• The most common cause of basal ganglia hemorrhage is hypertension. | |
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• The risk of hematoma expansion and neurologic deterioration is highest within the first few hours from onset. | |
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• Outcome depends on volume, location, age, level of consciousness, intraventricular extension, and warfarin use. | |
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• Coagulopathy, if present, should be corrected. | |
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• A bundle of care consisting of rapid blood pressure control, anticoagulant reversal, and treatment of hyperglycemia and hyperthermia improves patients’ clinical outcomes. | |
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• Surgical treatment has a limited role in the treatment of intracerebral hemorrhage. External ventricular drainage may be necessary in patients with intraventricular hemorrhage or hydrocephalus. | |
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• New endoscopic, minimally invasive surgical techniques may reduce mortality and shorten ICU stays in basal ganglia hemorrhage, without clear benefit in functional outcomes. |
Historical note and terminology
Intracerebral hemorrhage was described for the first time in 1658 by Wepfer in his treatise on apoplexy (58). He described both intracerebral hemorrhage and subarachnoid hemorrhage. Through the years, intracerebral hemorrhage has also been termed "cerebral hemorrhage," "intracranial hemorrhage," “hemorrhagic stroke,” and "cerebral bleed." The advent of head CT and brain MRI have greatly improved the detection, localization, and characterization of brain hemorrhages. Intracranial hemorrhage refers to any bleeding within the cranial vault, including subdural and epidural hematomas and subarachnoid hemorrhage. Intracerebral hemorrhage refers specifically to bleeding within the brain parenchyma. The term “hemorrhagic stroke” is best avoided as it is vague.
Clinical manifestations
Presentation and course
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• Most patients with basal ganglia hemorrhage have hypertension. | |
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• The neurologic deficits depend on the location, size, and expansion of the hematoma. | |
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• The small hemorrhages may resemble lacunar infarctions, whereas the large ones may present as coma. |
The clinical presentation depends on the size, location, and rate of expansion of the bleed. Symptoms can evolve over several minutes to hours due to hematoma expansion. Almost a third of hemorrhages expand within the first few hours after presentation, with an additional 12% expanding in the next 20 hours (25). A large hematoma may present as obtundation or even coma, whereas a small hemorrhage may be clinically confused with lacunar infarction (99).
The typical clinical features include focal neurologic signs, headache, nausea, vomiting, and decreased level of consciousness (76; 92). Elevated blood pressure is found in over 90% of patients acutely, even in absence of history of hypertension (137).
The most common location for a basal ganglia hemorrhage is the putamen (137; 92). Putaminal hemorrhage in the dominant hemisphere may cause aphasia, contralateral hemiparesis, hemisensory loss, visual field defects, and gaze deviation towards the bleed. In the nondominant hemisphere, putaminal hemorrhage may cause neglect or apraxia. Uncal herniation may cause palsy of the ipsilateral third nerve. Other symptoms include auditory agnosia (189), cortical deafness (11), amnesia and acalculia (177), persistent lightheadedness (105), memory impairment (33; 181), or supernumerary phantom limb (98).
Caudate bleeding accounts for 5% to 7% of all intracerebral hemorrhages (181). Rupture into the ventricular system may cause nuchal rigidity, headache, nausea, vomiting, and decreased consciousness. Contralateral hemiparesis may also occur (181; 92).
A systematic review of all prospective studies that followed patients longitudinally after an intracerebral hemorrhage found a recurrence rate of 2.1% per patient-year in those patients who initially had a deep hemorrhage, compared to 4.4% per patient-year after a first lobar hemorrhage (15).
Prognosis and complications
Complications of intracerebral hemorrhage are direct and indirect.
Direct complications. Direct effects are caused by the local mass effect of hematoma and the surrounding edema. These include transfalcine and uncal herniation as well as midbrain compression. Hydrocephalus results from obstruction of the foramen of Monro or cerebral aqueduct or from a massive intraventricular hemorrhage.
Intracerebral hemorrhage is associated with higher mortality and more severe disability compared to ischemic stroke (17). The in-hospital mortality is between 30% and 50%. The outcome depends on hematoma size, location, expansion, intraventricular extension, age, African American ethnicity, prior use of warfarin, and coma (43; 158; 168; 120; 166; 165; 41; 54). The volume cutoff for poor outcome also depends on location (109). Globus pallidus and putamen lesions are associated with worse disability and mortality (49). Fever is an independent predictor of poor prognosis (174). Involvement of the posterior limb of the internal capsule has been related to worse functional outcomes (67).
The mortality rate continues to increase from 50% at 30 days to 62% at 1 year according to the Oxfordshire Community Stroke Project (16).
The “ICH Score" predicts mortality at 1 month (73). The ICH Score is the sum of individual points assigned as follows:
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Glasgow coma score of 3 to 4 |
2 points |
The mortality rate at 30 days for intracerebral hemorrhage scores of 0, 1, 2, 3, 4, and 5 or greater were 0%, 13%, 26%, 72%, 97%, and 100%, respectively. The score has been externally validated and has been shown to predict 12-month survival (34; 74).
Premature do-not-resuscitate orders are an independent risk factor for poor prognosis, as it may lead to a self-fulfilling prophecy (18; 75). A modified intracerebral hemorrhage (MICH) score at 72 hours from onset is more predictive of poor functional outcome and death than on admission day, supporting the approach to delay discussions about withdrawal of care for a few days (122). The Neurocritical Care Society provides guidelines regarding prognostication in critically ill adults with intracerebral hemorrhage. Consensus recommendations include deferring neuroprognostication for at least 48 to 72 hours of admission. No clinical variable alone or prognostic scales were considered reliable by itself to predict functional outcome or mortality (82).
Retrospective studies have suggested an increased risk of dependency and death with higher initial mean arterial blood pressure and blood sugar levels (42; 148; 198).
Diffusion tensor imaging, which uses the mean fractional anisotropy as a measure of neuronal destruction, may improve recovery prediction (133; 175). Machine learning models using deep neural networks and support vector machines are likely better at predicting outcome than the clinical scores (118).
Clinical seizures occur rarely after basal ganglia hemorrhage (149). However, 20% to 30% of patients with intracerebral hemorrhage, including those with basal ganglia hemorrhage, had subclinical electrographic seizures. Although these patients experienced progressive midline shift and neurologic deterioration, their outcome was not affected (192).
Indirect complications. Indirect complications of basal ganglia hemorrhage include pneumonia, urinary tract infection, sepsis, deep venous thrombosis, and pulmonary embolism. These complications may prolong hospitalization and worsen the outcome. In a study of hospital records from 1979 to 2003, 1,606,000 patients had hemorrhagic stroke. Pulmonary embolism occurred in 11,000 (0.68%) and deep venous thrombosis occurred in 22,000 (1.37%). These rates did not change over 25 years of observation (178).
Recurrence of hemorrhage after frameless stereotactic blood aspiration was associated with early use of antiplatelet medication, history of diabetes mellitus, midline shift on admission, and presence of intraventricular hemorrhage (179; 159).
Chronic intracerebral hematoma is rarely associated with uncontrolled hypertension, trauma, or coagulopathy (203). There are two histological types of hematomas: encapsulated, caused by a vascular anomaly, and liquefied caused by hypertension (153). In a small retrospective study of 112 patients with intracerebral hemorrhage, four patients (4.9%) developed chronically expanding intracerebral hematoma. Only the layer sign was significantly associated with it (176).
Clinical vignette
A 56-year-old man was brought to the emergency room after collapsing at home. He complained of a severe left-sided headache. Several minutes later, he developed slurred speech and weakness of the right arm and leg. He went to bed hoping that the symptoms would resolve. His wife tried to awaken him in 1 hour and found him difficult to arouse. When he was moved from the bed, he appeared to be confused and had trouble walking. When placed in a chair, he collapsed to the floor and was then taken to the emergency room.
His past medical history was significant for hypertension for 15 years. He was not compliant with the antihypertensive medications. He smoked a pack of cigarettes per day for 30 years and drank five beers per day.
On examination he was stuporous, with a blood pressure of 200/105, pulse 66, respirations 20, without fever. He was intubated to protect his airway. His neck was somewhat stiff. Neurologic examination showed no response to verbal stimulation. His pupils were 4 mm and reactive. Eyes were deviated to the left, with a normal response to doll's eyes maneuver. Corneal reflexes were intact. The right side of his face was weak, as was the gag reflex. Motor exam showed flicker movement on the right to deep pain but purposeful withdrawal on the left. Deep tendon reflexes were increased on the right.
Head CT scan showed a 40 ml intracerebral hemorrhage in the left putamen, with blood extending into both lateral ventricles. Mild left-to-right midline shift was also seen. Laboratory studies, including platelet count and coagulation profile, were normal.
The patient was admitted to a neurologic intensive care unit. His head was elevated to 30 degrees, and his neurologic status was closely watched. He was ventilated to normocarbia. The elevated blood pressure was treated with intravenous nicardipine with a goal of systolic blood pressure below 140 mmHg. A ventriculostomy was placed to drain blood and cerebrospinal fluid. His intracranial pressure was initially 21 mm Hg but decreased quickly and then remained normal. Three days later, the ventriculostomy was removed and he was extubated on hospital day 7. Two weeks after admission, he was discharged to an acute rehabilitation facility.
Biological basis
Etiology and pathogenesis
Although intracerebral hemorrhage may be due to a vascular malformation, cerebral venous sinus thrombosis, bleeding into a tumor, or trauma, this discussion will be limited to spontaneous hemorrhage, which is not associated with these factors. Although the risk factors for intracerebral hemorrhage are well documented, the triggers that precede the event are less known.
Hypertension. Hypertension is the most important risk factor for spontaneous, deep intracerebral hemorrhage.
Differences in method explain the variability in reports of hypertension as the cause of intracerebral hemorrhage, ranging from 56% to 89% (137; 57; 26; 173). One large study using older criteria for hypertension (systolic blood pressure more than 160 mmHg or diastolic blood pressure more than 90 mmHg) found that 73% of patients with deep intracerebral hemorrhage were hypertensive (23).
Hypertension is a greater risk factor for cerebral hemorrhage in Asians than in whites (206).
The distribution of small vessel disease helps predict the cause of the basal ganglia hemorrhage; lobar lacunes are associated with cerebral amyloid angiopathy, whereas deep lacunes are associated with hypertension (147). Perivascular spaces in both basal ganglia and center semiovale are associated with transient ischemic attack or ischemic stroke, but not with intracerebral hemorrhage (108). In a study of 1678 participants, MRI burden of dilated perivascular spaces in basal ganglia was independently associated with a higher risk of any stroke and intracerebral hemorrhage (47). The number of perforators seen on 7T brain MRI was lower in patients with deep intracerebral hemorrhage (P = 0.02) than in controls. At the same time, the pulsatility index in the basal ganglia was higher in patients with deep intracerebral hemorrhage (1.02±0.11, P = 0.11) than in controls (60).
The risk factors for cerebral hemorrhage are diabetes mellitus, renal and liver failure, male gender, cigarette smoking, and alcohol intake of two or more units daily (141; 56; 84; 37; 10; 104; 160; 85).
The cholesterol level is less clearly associated with intracerebral hemorrhage. In a large population-based study from Japan, the risk of death from intracranial hemorrhage was three times higher in hypertensive men with serum cholesterol levels under 160 mg/dL compared to those with higher levels (86). In contrast, a large study in South Korea found no such association (183). The Pravastatin Pooling Project reported no effect of pravastatin 40 mg on the risk of intracerebral hemorrhage in two large trials (29). Subsequently, a post hoc analysis of the SPARCL trial reported a slight increase in the incidence of intracerebral hemorrhage among the patients randomized to atorvastatin 80 mg who had prior hemorrhage, older age, stage 2 hypertension, and male gender (63). This association was independent of reduction in LDL levels (04). Moreover, the longitudinal prospective community-based cohort study that included 10,333 original participants and their descendants enrolled in the Framingham Study between 1948 to 2016 found that in addition to hypertension, statin use was associated with deep intracerebral hemorrhage (119).
Warfarin increases the risk of intracerebral hemorrhage, especially in the elderly and those with supratherapeutic levels (83; 51). The incidence of intracerebral hemorrhage is significantly increased with the use of warfarin (53). Aspirin use also increases the relative risk of intracerebral hemorrhage by 40%, although the absolute increased risk is small, approximately 0.15% per year (70). Clopidogrel appears to be associated with a similar risk. The combination of aspirin and clopidogrel may increase the risk of intracerebral hemorrhage in an additive fashion (204). Overall, about 10% of all intracerebral hemorrhages are related to the use of antithrombotic agents (70). Thrombolytic therapy also increases the risk of intracerebral hemorrhage (44).
The sympathomimetic agent phenylpropanolamine, which is used as an appetite suppressant and in cold and cough medications and is currently banned from market, also caused intracerebral stroke (96). Similarly, cocaine, amphetamine, or amphetamine derivatives may cause intracerebral hemorrhage (114). In an autopsy series of 17 young patients with fatal intracranial hemorrhages, all five patients with basal ganglionic hemorrhages were cocaine positive (142). Cannabis has been associated with basal ganglia hemorrhage in only three cases so far (13).
COL4A1 mutations that impair COL4A1 secretion are associated with sporadic intracerebral hemorrhage (197). The apolipoprotein epsilon 2 and epsilon 4 alleles increase the risk of lobar intracerebral hemorrhage whereas the epsilon 4 allele also increases the risk of deep intracerebral hemorrhage (19).
Several triggers precede the intracerebral hemorrhage. These include caffeine consumption, lifting weights greater than 25 kg, sexual activity, straining during defecation, vigorous exercise, and flu-like disease or fever (191).
Basal ganglia hemorrhage was thought to occur when small artery aneurysms, formed mostly due to chronic hypertension, rupture (167; 35). Later, Fisher suggested that intracerebral hemorrhage may be caused by lipohyalinosis in the absence of aneurysms (52). Electron microscopy reveals severe arterial arteriosclerotic changes, including degeneration of the media and fragmentation and atrophy of the smooth muscle, without aneurysms, usually at the middle and distal portions of perforating arteries (186).
Cerebral amyloid angiopathy causes many cases of lobar hemorrhages, especially in the elderly (195; 161). In a pathologic study of 129 brains of patients with hypertension, the authors also found a weak association between amyloid angiopathy and deep intracerebral hemorrhage (161).
Hereditary intracerebral hemorrhage occurs among Dutch and Icelandic populations (89; 68). The mechanism is a mutation in the amyloid precursor protein gene or the cystatin gene, respectively (116; 115). A search for these mutations in patients with sporadic intracerebral hemorrhage was negative (64).
Bleeding triggers a cascade of events leading to secondary neuronal injury. Infiltration with leukocytes, activation of resident microglia, and release of cytokines, including TNF-alpha and matrix metalloproteinases, contribute to neuronal death (130; 02; 80; 200). Edema develops over hours to days due to clot retraction followed by breakdown of the blood-brain barrier and leukocyte trafficking into the brain (194; 202; 27; 121; 171). The triggers and mechanisms of injury likely include thrombin (112; 199), activation of Toll-like receptor 4 (171), and iron and hemoglobin degradation products released from the red blood cells (81; 78). In animal models, iron-mediated damage is prevented by deferoxamine, an iron chelator (79; 144).
Epidemiology
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• The incidence of intracerebral hemorrhage has decreased over several decades. | |
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• Men, lower socioeconomic status, increasing age, and certain racial groups have a higher incidence of intracerebral hemorrhage. | |
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• There is a projected increase in the incidence of intracerebral hemorrhage due to demographic changes. |
The incidence of spontaneous intracerebral hemorrhage is 37,000 to 52,000 cases per year in the United States (21). The incidence is associated with male gender, increasing age, and lower socioeconomic status (87; 10; 106). The incidence decreased from 1950 to 1979, most likely because of hypertension control (57). However, aging and shifts in racial demographics will likely increase the incidence by the year 2050 (188).
Several racial groups have an increased risk of intracerebral hemorrhage. In northern Manhattan, the relative risk for deep intracerebral hemorrhage was 4.8 in Black people compared to whites and 3.7 in Hispanics compared to whites (106). In the Cincinnati area, the annual incidence rates of intracerebral hemorrhage per 100,000 adults were 48.9 in Black people and 26.6 in whites. For deep intracerebral hemorrhage only, the annual incidence rate per 100,000 was 25.7 in Black people compared to 13.0 in whites (55). The highest disparity between intracerebral hemorrhage rates of Black people and whites occurred at younger ages (102). Worldwide, the Japanese have a higher rate of intracerebral hemorrhage, with an incidence of 55 per 100,000 (184).
Prevention
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• Improved treatment of hypertension has decreased the incidence and mortality of intracerebral hemorrhage. | |
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• Lifestyle modifications may also significantly decrease the risk of hemorrhage. |
Improved treatment of hypertension has decreased the incidence and mortality of intracerebral hemorrhage (57). In patients with prior stroke, the combination of a thiazide diuretic and an angiotensin-converting-enzyme inhibitor reduced the risk of intracerebral hemorrhage by 50% (31).
Reduction of diastolic blood pressure has decreased the recurrence of intracerebral hemorrhage from 10.0% per patient-year in patients with diastolic BP greater than 90 mm Hg to less than 1.5% in those with lower diastolic BP (p less than 0.001). No patients with diastolic BP less than 70 mm Hg experienced rebleeding (09).
Moderate and elevated levels of exercise appear to reduce the risk of cerebral hemorrhage (111). Reduction of alcohol intake and cigarette smoking is also reasonable.
The TRIDENT trial was presented at the 2025 World Stroke Congress, showing a reduction in the risk of recurrent intracerebral hemorrhage using a triple blood pressure therapy comprising telmisartan 20 mg, amlodipine 2.5 mg, and indapamide 1.25 mg (07).
Differential diagnosis
The differential diagnosis for abrupt neurologic deterioration due to intracerebral hemorrhage includes ischemic stroke, migraine, seizure, encephalitis, and tumor. Noncontrast head CT scan can quickly detect hemorrhage and rule out most of these diagnoses.
Intracerebral hemorrhage should also be differentiated from hemorrhagic transformation of an ischemic stroke, bleeding from a tumor, vascular malformation, aneurysm (mycotic, saccular), abscess or other infectious lesions, trauma, vasculitis or vasculopathy (including amyloid angiopathy and moyamoya disease), hypertensive encephalopathy, cerebral venous sinus thrombosis with hemorrhagic venous infarction, and acute hemorrhagic leukoencephalopathy (20; 93; 92; 187). Among these, unsuspected arteriovenous malformation was the most common lesion found after angiography (69).
Tumors with a propensity to bleed include metastatic melanoma, bronchogenic carcinoma, choriocarcinoma, and renal cell carcinoma. Of the primary brain tumors, glioblastoma multiforme, followed by oligodendroglioma, are the most likely to bleed (134). In a series of 2514 evacuated hematomas, 110 were found to be due to a tumor (4.4%) (117).
Cerebral venous sinus thrombosis causes intracerebral hemorrhage by impairing venous drainage. The treatment, unlike for other causes of intracerebral hemorrhage, is anticoagulation. Clues to the presence of cerebral vein thrombosis include subacute onset of neurologic symptoms, especially headache and visual symptoms, young age, and presence of a known hypercoagulable state.
Diagnostic workup
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• Coagulation studies, toxicology screening, troponin level, and ECG should be performed to rule out causes and potential complications of hemorrhage. | |
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• Noncontrast head CT is the diagnostic test of choice for the diagnosis of intracerebral hemorrhage due to its sensitivity and availability. | |
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• CT angiography may predict the risk of hematoma expansion. | |
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• MRI brain with and without contrast improves the detection of an underlying lesion. | |
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• Catheter angiography is the test of choice for diagnosing vascular lesions. |
Complete blood count and coagulation studies should be performed to rule out bleeding diathesis. Additional tests include troponin level, ECG, toxicology, and inflammatory markers.
Brain imaging is crucial for diagnosis of intracerebral hemorrhage. Intracerebral hematoma appears as a high-density lesion on noncontrast head CT, the test of choice at most centers because of availability, cost, and speed of acquisition. MRI may also be used to identify acute hemorrhage, although MRI characteristics of intracerebral hemorrhage are more complex. Repeat head CT within the first 24 hours or as soon as clinical deterioration is noted may provide valuable information regarding hematoma expansion, brain edema, hydrocephalus, and herniation (66).
MRI is as good as CT in detecting acute hemorrhage and more sensitive in detecting chronic hemorrhages (97). The utility of early MRI/MRA depends on the age of the patient. In a retrospective analysis of 400 patients with intracerebral hemorrhage, structural abnormalities were detected in 12.5% of patients. The diagnostic yield of MRI/MRA was 0% in patients older than 65 years with basal ganglia or thalamic hemorrhages (30).
Microhemorrhages seen on gradient echo MRI have been associated with an increased risk of symptomatic cerebral hemorrhages (50). The location of the micro-bleeds may also be associated with the location of a symptomatic hemorrhage (113).
MRI-visible perivascular spaces seen predominantly in basal ganglia are associated more often with hypertension. However, hemorrhages seen in the centrum semiovale and associated with cortical surface siderosis are seen with lobar hemorrhages (32).
Contrast-enhanced CT or MRI and CT and MRI angiography help identify an underlying lesion like arteriovenous malformation, dural arterio-venous fistula, cerebral vein thrombosis, acute hemorrhagic leukoencephalitis, hemorrhagic transformation of infarction, or tumors. Advanced imaging studies, eg, 99mTc-MIBI SPECT, may also be helpful in determining the presence of underlying tumor (134).
The “spot sign,” a hyperdense area within the intracerebral hemorrhage due to contrast extravasation may predict hematoma expansion. In a prospective cohort of 39 patients imaged within 3 hours of hemorrhage onset, the positive predictive value of the spot sign for significant hemorrhage expansion was 77%, and the negative predictive value was 96% (193). In a retrospective cohort imaged at later time points, the spot sign had a much lower positive predictive value (24%) but maintained a significant negative predictive value of 98% (62). The clinical utility of using the CT angiography spot sign to predict expansion remains to be validated in a prospective trial. The “spot sign” was also demonstrated by extravasation of gadolinium during a cerebral MRI performed in one patient with rapidly expanding hematoma (03).
Catheter angiography is the gold standard for identifying underlying vascular lesions. The most common abnormalities seen with angiography are arteriovenous malformation and aneurysm (69). In a prospective study of 206 patients who underwent both CT scan and angiography, those with putaminal, thalamic, or posterior fossa intracerebral hemorrhage cases were divided into four groups according to age (45 years old or younger and over 45 years old) and whether they had preexisting hypertension. The angiographic yield was 48% in the younger normotensive group with putaminal, thalamic, or posterior fossa intracerebral hemorrhage, and 63% in those with lobar intracerebral hemorrhage. In older hypertensive patients, the yield was 0% with deep intracerebral hemorrhage and 10% with lobar intracerebral hemorrhage (207). Thus, older patients with a history of hypertension and basal ganglia hemorrhages do not usually need angiography.
In cases of a suspected tumor, a systemic workup to rule out metastasis from another source (lung, melanoma, renal cell, or other) is indicated.
Management
The goals of intracerebral hemorrhage therapy are as follows:
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• Prevention of hematoma expansion | |
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• Prevention of recurrent hemorrhage | |
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• Reduction of intracranial pressure to optimize cerebral perfusion | |
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• Preserve or improve neurologic function |
The treatment should follow the American Heart Association/American Stroke Association guidelines that are updated periodically (66).
Disposition. Admission to a neurologic intensive care unit reduces mortality compared to a general intensive care unit, and transferring patients to a center with a neurologic intensive care unit lowers the risk of death (46; 163; 01). Early decision to not resuscitate accounted for much of the observed difference. Data from a U.S. nationwide inpatient sample show that the in-hospital mortality of patients who underwent surgical treatment was 27.2% and the complication rate was 41%. Male gender, preoperative comorbidities, complications, and low surgery volume were associated with increased in-hospital mortality.
Hemostasis. Coagulopathy should be emergently reversed, keeping in mind the main side effect: thrombosis. For warfarin and other vitamin K antagonists, vitamin K 10 mg intravenously and prothrombin complex concentrates are preferred to fresh frozen plasma (182).
Although prothrombin complex concentrates correct the coagulopathy faster, the study was not powered enough to detect differences in clinical outcome. Vitamin K reverses the effect of warfarin within 24 to 48 hours. Fresh frozen plasma or prothrombin complex concentrate may be needed in major bleeding. Protamine sulfate reverses unfractionated heparin completely but only partially reverses low molecular weight heparin. Idarucizumab is the antidote for dabigatran, andexanet alpha for apixaban, and rivaroxaban and ciraparantag for edoxaban. In an indirect comparison, andexanet alfa was associated with improved hemostatic effectiveness and mortality compared to four-factor prothrombin complex concentrate in patients with intracerebral hemorrhage due to rivaroxaban and apixaban. Aripazine has shown promising results against low molecular weight heparin, fondaparinux, and direct oral anticoagulants (36; 08; 45; 151; 38).
In patients experiencing hemorrhagic transformation of an ischemic stroke following thrombolysis, fibrinogen level should be measured, and cryoprecipitate 10 units should be administered empirically. Further doses may be given to maintain a fibrinogen level above 150 mg/dL. Platelets may be transfused in the event of thrombocytopenia (201).
The hemostatic agent rFVIIa enhances thrombin generation on the surface of activated platelets but fails to improve the clinical outcome of intracerebral hemorrhage (129; 24; 128; 61). Tranexamic acid also does not improve the functional status after 90 days (180). Patients who used antiplatelet agents before the hemorrhage had increased odds of dependence and death after platelet transfusion (14).
Blood pressure control. Elevated blood pressure is common in acute intracerebral hemorrhage and worsens prognosis (42; 155). In some but not all studies, hypertension was associated with hematoma expansion (95; 143; 88). In another study, although none of the blood pressure variables were related to hematoma growth, the systolic blood pressure load defined as the proportion of readings greater than 180 mmHg was associated with hematoma growth (162).
The concern that aggressive blood pressure treatment causes perihematomal ischemia has not been confirmed. Local metabolism is reduced, cerebrovascular reactivity is preserved, and there is no perihemorrhagic ischemic penumbra (157; 152; 205; 172; 100).
Intensive decrease of systolic blood pressure within 6 hours from onset to values lower than 140 mmHg decreased hematoma growth without an improved clinical outcome at 90 days (06). The follow-up study failed to demonstrate decrease of death and severe disability; however, the functional outcome was better in the intensive therapy arm (05). Nevertheless, larger reductions of systolic blood pressure (greater than 20 mmHg) within the first hour lowered the risk of poor outcome (196). A meta-analysis of four studies including 3315 patients found that intensive blood pressure reduction is safe (190).
The ATACH open-label pilot trial attempted to define the optimal blood pressure target for intensive management within 6 hours from onset. Although safe, the neurologic deterioration, adverse events, and 3-month mortality were lower than expected (12). The ATACH-II trial was stopped prematurely because achieving the target systolic blood pressure of 110 to 139 mmHg failed to decrease mortality and disability compared to a less restrictive target of 140 to 179 mmHg (156). However, in the same study, intensive blood pressure reduction led to decreased perihematomal edema, which is associated with poor outcome if present in basal ganglia (110).
Guidelines recommend treatment based on the level of mean arterial pressure and intracranial pressure, with a goal of cerebral perfusion pressure greater than 60 mmHg. Acute lowering of systolic blood pressure to 140 mmHg for those patients presenting with a systolic blood pressure of 150 to 220 mmHg appears to be safe. Chronic hypertension tends to shift the cerebral circulation autoregulation curve to the right (150). Rapidly lowering the blood pressure below the level of autoregulation effectiveness may trigger ischemia in patients with chronic hypertension even at normal blood pressure levels, thus, negating the benefits of rapid blood pressure control. Those patients in whom systolic blood pressure was lowered below 130 mmHg had, on brain MRI, ischemic lesions in addition to intracerebral hemorrhage (28).
In a small study, atenolol decreased mortality, systemic inflammatory response syndrome, and pneumonia compared to amlodipine (91). Insufficient data exist regarding treatment of severe, sustained systolic blood pressure higher than 220 mmHg or of hematomas that are large and severe enough to require decompressive surgery.
Nitrate-based drugs (nitroprusside, nitroglycerin) and nifedipine can increase the intracranial pressure and are best avoided (39; 72). Antihypertensives less likely to increase intracranial pressure include beta-blockers (labetalol, esmolol), angiotensin-converting-enzyme inhibitors (enalapril, captopril), and nicardipine. Fast-acting, titratable, intravenously administered agents are preferred.
Bundle of care. The INTERACT3 trial showed that implementing a bundle of care comprising blood pressure management (systolic blood pressure target < 140mmHg), strict glucose control (6.1–7.8 mmol/L for patients without diabetes and 7.8–10.0 mmol/L for diabetic patients), antipyretic therapy (temperature target ≤ 37.5°C), and rapid reversal of anticoagulation (INR < 1.5) improved outcomes of patients with acute intracerebral hemorrhage (123). The targets must be reached within 1 hour of treatment initiation and maintained for 7 days.
Medical complications. Fluid and electrolyte balance should be monitored, particularly for those treated with hyperosmolar agents and diuretics. Inappropriate antidiuretic hormone secretion can occur in patients with intracerebral hemorrhage. In general, patients should receive nothing by mouth for the first 24 to 48 hours, and normocaloric parenteral nutrition or enteral nutrition (via Dobbhoff tube) should be instituted within 48 hours.
Dysphagia was diagnosed in 68% of patients with intracerebral hemorrhage (185). All patients should undergo formal dysphagia screening to prevent aspiration pneumonia (77). Bedside examination, including surveying for coughing while swallowing 3 ounces of water, has a good sensitivity and specificity for risk of aspiration in patients with neurologic injury (126). Percutaneous endoscopic gastrostomy was needed in 25% of intracerebral hemorrhage cases (101).
Approximately 0.3% of patients with intracerebral hemorrhage develop acute myocardial infarction during the first 3 days of treatment. This association increased mortality at discharge from 2% to 14.5% (59). Elevated troponin was associated with increased in-hospital mortality in one study but not at 30 days if not associated with ECG changes (125; 170).
Neurogenic pulmonary edema developed in 35% of patients with intracerebral hemorrhage and is associated with 37% mortality at 1 year (90). Acute respiratory distress syndrome occurs in 27% of patients with intracerebral hemorrhage; it is common in patients ventilated with a high tidal volume and is associated with in-patient mortality (48). Low tidal volume ventilation with attention to avoid increased intracranial pressure or hypoxia is a reasonable strategy in these patients (124).
Renal failure occurred in 8% of patients with intracerebral hemorrhage and is not increased by CT angiography (145). Renal dysfunction is also associated with deep cerebral microbleeds in patients with intracerebral hemorrhage (107). Acute renal failure is associated with higher rates of in-hospital mortality and moderate to severe disability at discharge (169).
Glucose level should be measured, and both hypoglycemia and hyperglycemia should be avoided. It is reasonable to treat fever, but therapeutic cooling is still investigational.
Venous thromboembolism can be prevented by heparin (5000 IU subcutaneous injections every 12 hours) or low molecular weight heparin after 1 to 4 days of onset and intermittent pneumatic stockings (66). If deep venous thrombosis occurs, a vena cava filter should be considered, as anticoagulation is contraindicated.
Clinical seizures after deep intracerebral hemorrhage are rare. Prophylactic anticonvulsants do not decrease the incidence of seizures (149) and may be associated with worse outcome (132).
Aspiration pneumonia can be prevented by formal speech and swallow evaluations before oral intake in all stroke patients. Foley catheters use should be minimized to prevent urinary tract infections. Fever is an independent prognostic factor for poor outcome after intracerebral hemorrhage (174). It is reasonable to evaluate and treat fever with acetaminophen, ice packs, and cooling blankets, if needed.
In a small study of 30 patients with intracerebral hemorrhage, early administration of fluoxetine was safe and improved the Fugl-Meyer motor scale at 90 days compared with placebo (127).
Surgical treatment. Preoperative state of alertness and hematoma volume are the main determinants of outcome. A Glasgow Coma Scale score of less than 8 and a hematoma volume greater than 60 ml had a mortality rate of 91% (22). Intraventricular extension of hemorrhage is associated with worse outcome (131).
If neurosurgical treatment is contemplated, platelet transfusion may be considered in patients with prior use of aspirin (66).
The large, multicenter International Surgical Trial for Intracerebral Hemorrhage (STICH) did not find benefit from surgery in patients with hemorrhage (131). Another randomized study of subcortical or putaminal intracerebral hemorrhage larger than 30 mL within 8 hours from ictus showed improved functional outcome compared to medical treatment but no benefit in overall survival (146).
The optimal timing of surgery for supratentorial hemorrhage is unknown. A meta-analysis of eight surgical trials (2816 cases) has shown improved outcome if randomization occurred within 8 hours of ictus (65). However, patients with basal ganglia hemorrhage did not benefit from early surgery. Ultra-early surgery, within 4 hours of onset, was associated with worse outcome (140).
Minimally invasive surgery plus rtPA for intracerebral hemorrhage evacuation reduced the clot size and edema but did not improve the clinical outcome in the MISTIE III trial (139; 135; 136). The ENRICH trial showed better functional outcomes in patients within 24 hours of acute intracerebral hematoma of 30 to 80 ml, a Glasgow Coma score between 5 and 15, and an NIHSS of more than 5 (154). This was an adaptive trial that initially included anterior basal ganglia hemorrhage, but due to ineffectiveness in this group, enrollment continued with only lobar hemorrhages. A single-center retrospective review of minimally invasive surgery for basal ganglia intracerebral hemorrhage of 10 to 50 ml suggested an improvement in mortality rates, length of stay, and cost-effectiveness, although there was no difference in functional outcomes according to treatment (94).
One potential alternative to tPA administration for clot lysis, still in the experimental stage, is transcranial MR-guided focused ultrasound (138). The success of the endoscopic hematoma evacuation is operator dependent. Renal failure on hemodialysis and liver cirrhosis were associated with poor removal rate (71). The impact on the clinical outcome of these interventions is not yet known, and more studies are needed before they can be recommended.
Large hemorrhages may increase intracranial pressure and impair consciousness. Reduction of increased intracranial pressure follows the same steps used in other conditions (164). Intracranial pressure monitors in patients with a Glasgow coma score of less than 9 may guide optimization of intracranial pressure and cerebral perfusion pressure when the neurologic examination is unreliable due to decreased level of consciousness. Supportive measures include maintaining a straight neck position and reducing agitation and pain. Ventriculostomy may be used to measure and adjust the intracranial pressure by removing cerebrospinal fluid (164).
The cerebral perfusion pressure, defined as the mean arterial blood pressure minus intracranial pressure, should be maintained above 50 to 60 mmHg. Hyperventilation to pCO2 30 to 35 mmHg and osmotic diuretics such as mannitol are useful temporizing measures but do not provide long-term reduction in intracranial pressure. The effectiveness of mannitol was evaluated in a trial of 141 patients with temporal lobe intracerebral hemorrhage and evidence of herniation (coma, enlarged pupil) who were going emergently to the operating room for hematoma evacuation. They were randomized to low-dose (0.7 g/kg) or high-dose (1.4 g/kg) mannitol. High-dose mannitol was associated with significantly better 6-month clinical outcomes (p < 0.005) (40). Hypertonic saline is another effective treatment for elevated intracranial pressure. Clinical outcomes have not been prospectively compared between the two treatments.
Outcomes
Diffusion tensor imaging may help predict outcome in basal ganglia hemorrhage (133).
Special considerations
Pregnancy
The Baltimore-Washington Cooperative Young Stroke Study found the risk of intracerebral hemorrhage during pregnancy was 2.5 times greater than for nonpregnant women of similar age and race. This relative risk was increased dramatically at 28.3 in the 6 weeks postpartum (103).
Anesthesia
No evidence exists to suggest that general anesthesia causes or precipitates intracerebral hemorrhage. Anesthetic agents that cause a significant increase in intracranial pressure or a dramatic fall in blood pressure may be harmful when given to patients with large intracerebral hemorrhages.
Media
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Contributors
All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.
Author
-
Eva Rocha MD PhD
Dr. Rocha of Universidade Federal de São Paulo has no relevant financial relationships to disclose.
See Profile
Editor
-
Steven R Levine MD
Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.
See Profile
Former Authors
- Mark J Alberts MD
- Brett Cucchiara MD
- Lauren H Sansing MD
- Adrian Marchidann MD
Patient Profile
- Age range of presentation
-
- 19 to 65+ years
- Sex preponderance
-
- male=female
- Heredity
-
- heredity may be a factor
- Population groups selectively affected
-
- African descent
- Asians
- Dutch
- Hispanics
- Icelandic
- Occupation groups selectively affected
-
- none
ICD & OMIM codes
- ICD-10
-
- Intracerebral haemorrhage in hemisphere, subcortical: I61.0
- Intracerebral haemorrhage in hemisphere, unspecified: I61.2
- ICD-11
-
- Intracerebral haemorrhage, site unspecified: 8B00.Z
- Deep hemispheric haemorrhage: 8B00.0
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