Intracerebral hemorrhage

Refers to bleeding directly into the brain parenchyma.

The annual incidence of intracerebral hemorrhage in the US is double to approximately 80,000 per year and deaths from IH is estimated to occur in 30 to 40% of cases.

The main causes of IH in adults are hypertension, cerebral amyloid angiopathy, and anticoagulation.

Hypertension is the strongest attributable risk factor.

Lowering blood pressure decreases the incidence of intracerebral hemorrhage.

Older age is associated with increased frequency of IH, owing in  part to association with cerebral amyloid angiopathy and with atrial fibrillation resulting in exposure to anticoagulation therapy.

Meta-analysis studies showed overall incidence of intracerebral hemorrhage of 24.6 per hundred thousand persons years between 1983 and 2006.

The risk of IH increases with age and is approximately twice as high in Asian populations as in white populations.

In the US the risk of intracerebral hemorrhage is approximately 1.6 times as high among Black persons and Hispanic persons as among white persons.

Survivors of intracerebral hemorrhage have neurologic disabilities, are at risk for recurrent stroke, cognitive decline, and systemic vascular disorders.

Often classified as primary, unrelated to congenital or acquired disease, secondary, directly related to a congenital or acquired process, and/or spontaneous, not secondary to trauma or surgery.

Patients with intracerebral hemorrhage present with focal neurologic findings that are abrupt in onset, but not instantaneous: there is an evolution that typically occurs over minutes.

Spontaneous intracerebral hemorrhage occurs in deep brain structures as a consequence of damage to the walls of small cerebral blood vessels that traverse these areas.

Small arteries and arterioles,  which are in most cases branches of larger vessels of the circle of Willis that supply the basal ganglia, thalamus, pons, and deep portions of the cerebellum.

Hypertensive cerebral vascularopathy and cerebral  amyloid angiopathy preferentially are involved in vessels of this size.

Intracerebral hemorrhage can be associated with headache, nausea, vomiting and, in many cases,  a depressed level of consciousness.

Lobar intracerebral hemorrhage located in the white matter of the frontal, parietal, temporal, or occipital lobe is more common in recent studies then deep cerebral hemorrhage.

Chronic hypertension and anticoagulation and rupture of AV malformations account for a larger portion of lobar hemorrhages than of basal ganglia hemorrhages.

Cerebral amyloid angiopathy is predominantly associated with lobar intracerebral hemorrhage or hemorrhage into the cerebellum.

ApoE2 and ApoE4 are associated with beta amyloid vascular deposition and confer is 3 to 5 times higher risk than in persons with more common APO E3.

In cases of cerebral hemorrhage from amyloid angiopathy, MRI may show multiple tiny asymptomatic hemorrhages of different ages.

The distinction between hemorrhagic and ischemic stroke is definitively made by imaging.

CT and MRI are sensitive and specific for the diagnosis of acute intracerebral hemorrhage, and they can establish the location and volume of the clot.

CT angiogram may detect an aneurysm or vascular malformation that underlies intracerebral hemorrhage.

CT angiograph studies are considered in patients who are younger than 70 years of age and have a lobar intracerebral hemorrhage, and in those who are younger than 45 years of age and have a deeper posterior fossa intracerebral hemorrhage, and those who are 45 to 70 years of age and have no history of hypertension.

A depressed level of consciousness usually indicates compression of the arousal nuclei and pathways of the upper brain stem.

Intraventricular hemorrhage with hydrocephalus can cause stupor.

Hemorrhage in the basal ganglia causes contralateral hemiplegia and a gaze preference to the side of the bleeding owing to transaction of the adjacent internal capsule.

Thalamic hemorrhage causes hemiplegia along with peculiar eye signs, including downward and inward deviation, miotic pupils, and occasionally a gaze preference to the side of the lesion.

In awake patient’s hemisensory loss may be detected.

The focal neurologic deficits with IH correspond to the location of the hemorrhage and its transection of white matter tracts and include hemiparesis, hemisensory loss, gaze preference and simulate ischemic stroke.

IH in the brainstem is usually located in the pons and impairs consciousness, causes cranial nerve palsies and causes pinpoint pupils, absent or impaired horizontal gaze, or ocular bobbing and facial weakness.

Dysarthria may be present in awake patients.

The disruption of the reticular activating system in the mid brain and upper pons can lead to coma.

A cerebeller intracerebral bleed it can be associated with vertigo, vomiting,  limb and gait ataxia.

The fourth ventricle can become obstructed by blood during a cerebeller bleed and may lead to hydrocephalus, stupor or coma.

The volume of the clot at the time of hospital admission is a predictor of the functional outcome at three months.

Hematoma expansion that causes worsening of clinical signs is particularly associated with poor functional outcome at three months.

Secondary brain injury occurs immediately caused by the clot, and perihematoma edema that is visible on imaging within hours of a intracerebral hemorrhage.

The edema surrounding the hematoma contributes to early neurologic deterioration beyond that caused by the mass of clot and the ultimate amount of edema may be larger than the initial hematoma.

10 to 20 cases per 100,000 population.

10-15% of all strokes.

10-20 cases per 100,000 population and increases with age.

More common in men than women, in blacks and Japanese.

Responsible for almost 30% of strokes in China.

Approximately 37-52,000 cases per year in the U.S.

Incidence in blacks 50 per 100,000 twice that of whites.

Acute intracerebral hemorrhage affects more than 1 million people worldwide annually.

Most commonly occurs in older individuals with history of hypertension or in patients on anticoagulants with warfarin.

As many as 80% of primary intracranial hemorrhages occur after small vessels are compromised by chronic hypertension.

Hypertension is associated with intracranial hemorrhage originating in the periventricular deep white matter, deep sub cortical structures, pons, and cerebellum.

In patients older than seventy years of age cerebral amyloid angiopathy is responsible for approximately 20% of intracranial hemorrhages.

Approximately 12-24% of cases related the warfarin anticoagulation.

Anticoagulation with warfarin increases risk 2-5 times related the intensity of anticoagulation.

Hypertension most important risk factor.

Other causes of intracranial hemorrhage including drug use, bleeding diatheses, malignant brain lesions, and congenital vascular abnormalities.

Primary intracerebral hemorrhage accounts for 78-88 percent of cases and originates from spontaneous rupture of small blood vessels damaged by chronic hypertension or amyloid angiopathy.

Associated with the highest mortality rate with 38% of affected patients surviving the first year.

Morbidity and mortality have remained unchanged over the past several decades.

Acute intracerebral hemorrhage is the least treatable form of stroke.

The outcome for acute intracerebral hemorrhage is determined by the volume and growth of the underlying hematoma.

The median one month fatality rate is 40%, and only 12-39% of patients achieve functional independence.

After intracerebral hemorrhage, blood pressure is often elevated and can reach very high levels, and is a predictor of that outcome.


The focus for treatment of a patient with an intracerebral hemorrhage is the prevention of secondary brain damage caused by clot, enlargement, secondary brain, edema, and intraventricular hemorrhage.

INTERACT 2 investigators found that intensive lowering of blood pressure does not result in a significant reduction in the rate of the primary outcome of death or severe disability in patients with acute intracerebral hemorrhage (Anderson CS et al).

In the above study early intensive lowering of blood pressure is not associated with any significant increase in adverse reactions.

A reasonable aim for blood pressure management is to lower the patient’s systolic blood pressure to 130 to 150 mmHg, particularly if the diastolic blood pressure exceeds 220 mm H.G. within two hours after intracerebral hemorrhage.

Secondary intracerebral hemorrhage occurs in association with vascular abnormalities such as arteriovenous malformations and aneurysms.

Intraventricular hemorrhage occurs in 30 to 50% of patients with IH.

Intraventricular hemorrhage can result in hydrocephalus with added volume of the ventricular space, obstruction of the CSF, and information, security secretions of the CSF leads to a decreased level of arousal and poor outcome.

Significant hydrocephalus symptoms are treated with the placement of an external ventricular drain.

Often occurs without known risk factors.

The standard of care is blood pressure control and ventilation, with the hope that hemorrhage will resolve spontaneously.

Craniotomy to remove a blood clot is a consideration for patients at imminent threat to life, but success in removing such clots has to be balanced with the potential loss of brain tissue as a result of the procedure.

Presently techniques are being developed for a minimally invasive burr hole to be placed and a catheter introduced to administer recombinant tissue type plasminogen activator (rtPA) directly into the clot, allowing for subsequent easier removal of such clot.

Utilizing activated Factor VII within 4 hours after the onset of symptoms results in a smaller increase in the volume of intracerebral hemorrhage than use of placebo.

Use of activated Factor VII results in improved functional outcome and decreased mortality rate at 3 months (29% to 18%).

Use of activated Factor VII result in 3 fold increase in severe arterial and venous thromboembolism at 90 days.

Neuronal injury due to direct tissue damage, inflammatory changes, edema, intraventricular extension of hemorrhage and hydrocephalus.

The incidence of oral anticoagulant related ICH is 0.3-1.8% of patients per year who are taking warfarin.

Anticoagulant related factors and ICH are intensity of anticoagulation , age, comorbidity, duration of treatment, race, and higher risk of primary brain hemorrhage.

The newer novel oral anticoagulants which include dabigatran, apixaban, and Rivaroxaban are safer with regard to incidence of ICH.

The treatment of intracerebral hemorrhage associated with antiplatelet agents with platelet transfusions is hazardous, and should not be given due to higher mortality and higher rates of disability.

There is no subset of patients in whom surgery to evacuate the hematoma is efficacious.

Patients with IH that is associated with anticoagulant use are at risk for hemorrhage expansion, neurologic deterioration, and poor outcomes at 3 to 6 times as high as the rates seen with intracerebral hemorrhage in the absence of anticoagulation.

The mass effect of an intracerebral clot and surrounding swelling can result in its most severe consequence, a transtentorial herniation.

Patients with ICH  associated with anticoagulants are at risk for hemorrhagic expansion, neurologic deterioration, and poor outcome 3 to 6 times as  high as  patients with ICH in the absence of anticoagulation.

Guidelines, recommend it intravenous vitamin K and prothrombin complex concentrate over fresh, frozen plasma if the INR is elevated over, owing to the use of vitamin K antagonists.

Reversal, agent, idarucizumab and anndexant anlpha are available for patients with intracerebral hemorrhage associated with direct oral anticoagulants in the form of direct thrombin and factor Xa an inhibitors.

In general, surgical removal of the clot to alleviate transtentorial herniation has been inconsistent or negative.

Surgical removal of a cerebellum intracerebral hemorrhage can be considered if clinical imaging signs of brainstem compression are present with a clot  volume is greater than 15 mL.

Among patients in whom surgery could be performed within 24 hours after acute intracerebral hemorrhage, minimally invasive, hematoma, evacuation, resulted in better functional outcomes at 180 days, then those with medical management: surgery benefit appears to  be attributable to intervention for lobar hemorrhages (ENRICH, trial investigators).

Osmotic therapy is used to treat acute neurologic, see relation, secondary to mass effect, or edema associated with IH, but the results have been uncertain.


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