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Spontaneous intracerebral hemorrhage

Spontaneous intracerebral hemorrhage (ICH), is nontraumatic bleeding into the brain parenchyma.


Spontaneous intracerebral hemorrhage (ICH) is a global public health issue and accounts for 10–15% of all stroke cases 1).

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:

see Hypertensive intracerebral hemorrhage.

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.

see Spontaneous intracranial hematoma caused by neoplasm

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

see Intracerebral hemorrhage and anticoagulation

see Intracerebral hemorrhage and ruptured intracranial aneurysm.

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.

Posterior fossa surgery

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).


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.

see Intracerebral hemorrhage volume


Although several studies have been conducted in recent years, the optimal treatment for improving outcome in spontaneous ICH patients is still unclear 11) 12) 13) 14).

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 15).

The choice of surgical or conservative treatment for patients with spontaneous intracerebral hemorrhage (ICH) is controversial.

Blood pressure reduction

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 16).




Hematoma expansion is an important determinant of outcome in spontaneous intracerebral hemorrhage (ICH) due to small vessel disease (SVD).

Acute hydrocephalus

Case series

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 [11] years and 140 [55.1%] female) and 164 patients with deep ICH (mean [SD] age 67 [14] 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 17).

Case reports

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 18).


Qureshi AI, Mendelow AD, Hanley DF. Intracerebral haemorrhage. Lancet. 2009 May 9;373(9675):1632-44. doi: 10.1016/S0140-6736(09)60371-8. Review. PubMed PMID: 19427958; PubMed Central PMCID: PMC3138486.
Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hanley DF. Spontaneous intracerebral hemorrhage. N Engl J Med. 2001;14:1450–1460. doi: 10.1056/NEJM200105103441907.
Bucciero A, Quaglietta P, Vizioli L. Supratentorial intracerebral hemorrhage after posterior fossa surgery: Case report. J Neurosurg Sci. 1991;35:221–4.
Haines SJ, Maroon JC, Jannetta PJ. Supratentorial intracerebral hemorrhage following posterior fossa surgery. J Neurosurg. 1978;49:881–6.
Harders A, Gilsbach J, Weigel K. Supratentorial space occupying lesions following infratentorial surgery early diagnosis and treatment. Acta Neurochir (Wien) 1985;74:57–60.
Seiler RW, Zurbrugg HR. Supratentorial intracerebral hemorrhage after posterior fossa operation. Neurosurgery. 1986;18:472–4.
Tondon A, Mahapatra AK. Superatentorial intracerebral hemorrhage following infratentorial surgery. J Clin Neurosci. 2004;11:762–5.
Vrettou CS, Stavrinou LC, Halikias S, Kyriakopoulou M, Kollias S, Stranjalis G, et al. Factor XIII deficiency as a potential cause of supratentorial haemorrhage after posterior fossa surgery. Acta Neurochir (Wien) 2010;152:529–32.
Pandey P, Madhugiri VS, Sattur MG, Devi BI. Remote supratentorial extradural hematoma following posterior fossa surgery. Childs Nerv Syst. 2008;24:851–4.
Wolfsberger S, Gruber A, Czech T. Multiple supratentorial epidural haematomas after posterior fossa surgery. Neurosurg Rev. 2004;27:128–32.
Hanley DF, Thompson RE, Muschelli J, Rosenblum M, McBee N, Lane K, Bistran-Hall AJ, Mayo SW, Keyl P, Gandhi D, Morgan TC, Ullman N, Mould WA, Carhuapoma JR, Kase C, Ziai W, Thompson CB, Yenokyan G, Huang E, Broaddus WC, Graham RS, Aldrich EF, Dodd R, Wijman C, Caron JL, Huang J, Camarata P, Mendelow AD, Gregson B, Janis S, Vespa P, Martin N, Awad I, Zuccarello M; MISTIE Investigators. Safety and efficacy of minimally invasive surgery plus alteplase in intracerebral haemorrhage evacuation (MISTIE): a randomised, controlled, open-label, phase 2 trial. Lancet Neurol. 2016 Nov;15(12):1228-1237. doi: 10.1016/S1474-4422(16)30234-4. Epub 2016 Oct 11. PubMed PMID: 27751554; PubMed Central PMCID: PMC5154627.
Hanley DF, Lane K, McBee N, Ziai W, Tuhrim S, Lees KR, Dawson J, Gandhi D, Ullman N, Mould WA, Mayo SW, Mendelow AD, Gregson B, Butcher K, Vespa P, Wright DW, Kase CS, Carhuapoma JR, Keyl PM, Diener-West M, Muschelli J, Betz JF, Thompson CB, Sugar EA, Yenokyan G, Janis S, John S, Harnof S, Lopez GA, Aldrich EF, Harrigan MR, Ansari S, Jallo J, Caron JL, LeDoux D, Adeoye O, Zuccarello M, Adams HP Jr, Rosenblum M, Thompson RE, Awad IA; CLEAR III Investigators. Thrombolytic removal of intraventricular haemorrhage in treatment of severe stroke: results of the randomised, multicentre, multiregion, placebo-controlled CLEAR III trial. Lancet. 2017 Feb 11;389(10069):603-611. doi: 10.1016/S0140-6736(16)32410-2. Epub 2017 Jan 10. PubMed PMID: 28081952.
Vespa P, Hanley D, Betz J, Hoffer A, Engh J, Carter R, Nakaji P, Ogilvy C, Jallo J, Selman W, Bistran-Hall A, Lane K, McBee N, Saver J, Thompson RE, Martin N; ICES Investigators. ICES (Intraoperative Stereotactic Computed Tomography-Guided Endoscopic Surgery) for Brain Hemorrhage: A Multicenter Randomized Controlled Trial. Stroke. 2016 Nov;47(11):2749-2755. Epub 2016 Oct 6. PubMed PMID: 27758940.
Hemphill JC 3rd, Greenberg SM, Anderson CS, Becker K, Bendok BR, Cushman M, Fung GL, Goldstein JN, Macdonald RL, Mitchell PH, Scott PA, Selim MH, Woo D; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015 Jul;46(7):2032-60. doi: 10.1161/STR.0000000000000069. Epub 2015 May 28. PubMed PMID: 26022637.
de Oliveira Manoel AL, Goffi A, Zampieri FG, Turkel-Parrella D, Duggal A, Marotta TR, Macdonald RL, Abrahamson S. The critical care management of spontaneous intracranial hemorrhage: a contemporary review. Crit Care. 2016 Sep 18;20(1):272. Review. PubMed PMID: 27640182.
Wang X, Arima H, Heeley E, Delcourt C, Huang Y, Wang J, Stapf C, Robinson T, Woodward M, Chalmers J, Anderson CS. Magnitude of Blood Pressure Reduction and Clinical Outcomes in Acute Intracerebral Hemorrhage: Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial Study. Hypertension. 2015 Mar 23. pii: HYPERTENSIONAHA.114.05044. [Epub ahead of print] PubMed PMID: 25801872.
Boulouis G, van Etten ES, Charidimou A, Auriel E, Morotti A, Pasi M, Haley KE, Brouwers HB, Ayres AM, Vashkevich A, Jessel MJ, Schwab KM, Viswanathan A, Greenberg SM, Rosand J, Goldstein JN, Gurol ME. Association of Key Magnetic Resonance Imaging Markers of Cerebral Small Vessel Disease With Hematoma Volume and Expansion in Patients With Lobar and Deep Intracerebral Hemorrhage. JAMA Neurol. 2016 Oct 10. doi: 10.1001/jamaneurol.2016.2619. PubMed PMID: 27723863.
Kerr N, Kerr J, Faed JM, Krysa J. Spontaneous intracerebral haemorrhage: a rare complication of aortic aneurysm endoleak. BMJ Case Rep. 2018 Jun 23;2018. pii: bcr-2018-225249. doi: 10.1136/bcr-2018-225249. PubMed PMID: 29936448.
spontaneous_intracerebral_hemorrhage.txt · Last modified: 2018/06/25 17:02 by administrador