Intracerebral hemorrhage

Hemorrhagic strokes comprise 10-20% of all strokes. About half of the hemorrhagic strokes manifests as subarachnoid hemorrhages, and the other half manifests as intracerebral hemorrhage. The incidence is ~15/100.000 cases-year.


Hypertension (most common cause of spontaneous intracerebral hemorrhage)
Amyloid angiopathy
Vascular malformations
Brain neoplasms
Miscellaneous (septic embolism, Moyamoya, drugs, venous sinus thrombosis)


The clinical presentation consists of one or more neurological deficits that occur acutely and get progressively worse as time passes. Headache is also a common symptom.

Change in mental status (confusion to coma) can occur, as well as nausea and vomiting in patients with intracranial hypertension.


As soon as the diagnosis of stroke is suspected (a history and/or physical examination compatible with one or more acute neurological deficits) the patient should be closely stabilized, monitored and investigated further.

The first and most important initial test to obtain is a CT scan of the head without contrast. This CT scan should be enough to show the bleeding (appears as a hyperdensity).

The volume of the hematoma can be calculated by ABC/2, where A = the greatest hemorrhage diameter; B = the largest diameter 90 degrees from A; and C is the number of slices with bleeding multiplied by slice thickness in cm.

MRI with contrast, MRA or CTA may be performed to evaluate the cause of bleeding.

Other tests include CBC, CMP, ECG, and coagulation studies.


The A-B-C-D-E should be promptly assessed and life support measures (e.g. intubation) should be provided as needed.

The patient should not receive anything by mouth (NPO) and swallowing function should be evaluated.

Blood pressure should be controlled but carefully (there is a risk of intracranial hypertension and acute reductions of BP can cause ischemia in patients with elevated ICP).

Hyperglycemia may be tolerated between 140-180mg/dL. Higher values should be treated with insulin. Hypoglycemia should also be avoided.

VTE prophylaxis should be provided with intermittent pneumatic compression.

If the patient has high seizure risk (e.g. large lobar hemorrhage), seizure prophylaxis may be provided.

All anticoagulant and antiplatelet drugs should be discontinued. Patients that are already anticoagulated should receive treatment to reverse the anticoagulation (e.g. vitamin K, prothrombin complex concentrate). The adequate moment to restart these therapies is not yet known, but it is probably safe to restart after 1-2 weeks in most patients.

If there is indication of elevated intracranial pressure, it should be managed.

Neurosurgical interventions may be necessary in some situations (e.g. cerebellar hemorrhage >3cm; intraventricular hemorrhage with risk for hydrocephalus).


  1. Morgenstern, Lewis B., et al. “Guidelines for the management of spontaneous intracerebral hemorrhage.” Stroke 41.9 (2010): 2108-129.
  2. Kidwell CS et al. Comparison of MRI and CT for Detection of Acute Intracerebral Hemorrhage. JAMA. 2004;292(15):1823-1830.
  3. Ariesen MJ et al. Risk Factors for Intracerebral Hemorrhage in the General Population: A Systematic Review. Stroke. 2003;34:2060-2065.
  4. Qureshi AI et al. SPONTANEOUS INTRACEREBRAL HEMORRHAGE. N Engl J Med, Vol. 344, No. 19 ยท May 10, 2001.
  5. Anderson CS et al. Rapid Blood-Pressure Lowering in Patients with Acute Intracerebral Hemorrhage. N Engl J Med 2013; 368:2355-2365.