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.
Remote supratentorial hematoma soon after posterior fossa surgery for the removal of a space-occupying lesion is a rare but dramatic and dreaded complication, carrying significant morbidity and mortality 3) 4) 5) 6) 7) 8) 9) 10).
Kerr et al., present a rare case of intracerebral hemorrhage secondary to consumptive coagulopathy in relation to ongoing endoleak after thoracic endovascular aneurysm repair (TEVAR). A 68-year-old man underwent elective TEVAR for an 18 cm diameter Crawford type II thoracoabdominal aneurysm. He was subsequently shown to have a type 1b endoleak and a short episode of disseminated intravascularcoagulation (DIC) perioperatively. Two months after the procedure, he experienced a consumptive coagulopathy leading to intracerebral haemorrhage and ultimately his death. Endoleak-related DIC is an underappreciated phenomenon within the medical literature. Currently, management is reliant on general DIC principles and anecdotal experiences of others within the case report literature 11).