It is the second most common subtype of stroke, with 5.3 million cases and over 3 million deaths reported worldwide in 2010.
In 2001 the annual incidence of 20–30 per 1,000,000 people 2).
The most important modifiable risk factor in spontaneous ICH is chronic arterial hypertension:
Besides hypertension, cerebrovascular amyloid deposition (i.e., cerebral amyloid angiopathy) is associated with ICH in older patients.
It is a common initial symptom of intracranial vascular malformations.
Coagulopathies (i.e., the use of antithrombotic or thrombolytic agents, congenital or acquired factor deficiencies) and systemic diseases, such as thrombocytopenia, are possible causes of ICH. The use of oral anticoagulants, especially vitamin K inhibitors (i.e., warfarin), has increased coagulopathy-associated ICH in recent years, accounting for more than 15 % of all cases
Psychosocial, ethnic, and economic factors play a role in the prevalence of cerebral hemorrhage, with ICH being twice as common in low-income and middle-income countries compared with high-income countries. Other identified risk factors for ICH include age (i.e., each decade from 50 years of age is associated with a 2-fold increase in the incidence of ICH) and an elevated alcohol intake.
Etiologies of ICH to always consider include: intracranial aneurysms (typically presenting as subarachnoid hemorrhage); arteriovenous malformations (ICH is the first presentation of AVMs in 60 % of cases); cerebral venous sinus thrombosis and venous infarction; brain tumors (<5 % of all ICH cases) including cerebral metastasis (e.g., lung cancer, melanoma, renal cell carcinoma, thyroid carcinoma, and choriocarcinoma) and primary CNS tumors (e.g., glioblastoma multiforme and oligodendrogliomas); and drugs of abuse (e.g., cocaine, amphetamines). Because of the differing etiologies of ICH, a rapid and accurate diagnosis of the underlying etiology of ICH is essential to direct appropriate management strategies.
cerebral venous sinus thrombosis and venous infarction.
Although CT remains important in the acute setting, MR imaging has proved invaluable for diagnosis and characterization of intracranial hemorrhage.
Hemorrhage volume is a powerful predictor of 30-day mortality after spontaneous intracerebral hemorrhage (ICH). Kothari et al., compared a bedside method of measuring CT ICH volume with measurements made by computer-assisted planimetric image analysis.
Recent clinical trials examining hemostatic therapy, blood pressure control, and hematoma evacuation have advanced our understanding of ICH management. Timely and aggressive management in the acute phase may mitigate secondary brain injury. The initial management should include: initial medical stabilization; rapid, accurate neuroimaging to establish the diagnosis and elucidate an etiology; standardized neurologic assessment to determine baseline severity; prevention of hematoma expansion (blood pressure management and reversal of coagulopathy); consideration of early surgical intervention; and prevention of secondary brain injury 7).
The choice of surgical or conservative treatment for patients with spontaneous intracerebral hemorrhage (ICH) is controversial.
The Second Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT 2) study, demonstrated better functional outcomes with no harm for patients with acute spontaneous intracerebral hemorrhage (ICH) within 6 h of onset who received target-driven, early intensive BP lowering (systolic BP target <140 mmHg within 1 h, continued for 7 days) and suggested that greater and faster reduction in BP might enhance the treatment effect by limiting hematoma growth.
Optimal recovery from intracerebral hemorrhage was observed in hypertensive patients who achieved the greatest SBP reductions (≥20 mm Hg) in the first hour and maintained for 7 days 8).
Case fatality is extremely high (reaching approximately 60 % at 1 year post event). Only 20 % of patients who survive are independent within 6 months.
418 consecutive patients admitted with primary lobar hemorrhage or deep ICH to a single tertiary care medical center between January 1, 2000, and October 1, 2012. Data were analyzed on March 4, 2016. Participants were consecutive patients with computed tomographic images allowing ICH volume calculation and MRI allowing imaging markers of small vessel disease (SVD).
The ICH volumes at baseline and within 48 hours after symptom onset were measured in 418 patients with spontaneous ICH without anticoagulant therapy, and hematoma expansion was calculated. Cerebral microbleeds, cortical superficial siderosis, and white matter hyperintensity volume were assessed on MRI. The associations between these SVD markers and ICH volume, as well as hematoma expansion, were investigated using multivariable models.
This study analyzed 254 patients with lobar ICH (mean [SD] age, 75  years and 140 [55.1%] female) and 164 patients with deep ICH (mean [SD] age 67  years and 71 [43.3%] female). The presence of cortical superficial siderosis was an independent variable associated with larger ICH volume in the lobar ICH group (odds ratio per quintile increase in final ICH volume, 1.49; 95% CI, 1.14-1.94; P = .004). In multivariable models, the absence of cerebral microbleeds was associated with larger ICH volume for both the lobar and deep ICH groups (odds ratios per quintile increase in final ICH volume, 1.41; 95% CI, 1.11-1.81; P = .006 and 1.43; 95% CI, 1.04-1.99; P = .03; respectively) and with hematoma expansion in the lobar ICH group (odds ratio, 1.70; 95% CI, 1.07-2.92; P = .04). The white matter hyperintensity volumes were not associated with either hematoma volume or expansion.
In patients admitted with primary lobar or deep ICH to a single tertiary care medical center, the presence of cortical superficial siderosis was an independent variable associated with larger lobar ICH volume, and the absence of cerebral microbleeds was associated with larger lobar and deep ICHs. The absence of cerebral microbleeds was independently associated with more frequent hematoma expansion in patients with lobar ICH. Boulouis et al., provide an analytical framework for future studies aimed at limiting hematoma expansion 13).