Although commonly arising from poorly controlled hypertension, spontaneous intracerebral hemorrhage may occur secondary to several other etiologies. Clinical presentation to the emergency department ranges from headache with vomiting to coma. In addition to managing the ABCs, the crux of emergency management lies in stopping hematoma expansion and other complications to prevent clinical deterioration. This may be achieved primarily through anticoagulation reversal, blood pressure, empiric management of intracranial pressure, and early neurosurgical consultation for posterior fossa hemorrhage. Patients must be admitted to intensive care. The effects of intracerebral hemorrhage are potentially devastating with very poor prognoses for functional outcome and mortality.
Key points
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Poorly controlled hypertension is the most common risk factor for spontaneous intracerebral hemorrhage (ICH).
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Patients with spontaneous ICH may present with headache and vomiting, but are at risk for early deterioration including loss of consciousness, coma, and death.
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The location, appearance, and size of the hemorrhage on computed tomography scan, in conjunction with the clinical picture, can help point toward its etiology and prognosis.
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Once hemorrhage has occurred, management focuses on prevention of hematoma expansion, perihematoma edema, obstructive hydrocephalus, and brain herniation.
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Primary emergency management focuses on blood pressure and empiric intracranial pressure management, reversal of existing coagulopathies, and identification of indications for early neurosurgical intervention.
Introduction
Spontaneous intracerebral hemorrhage (ICH) is a medical emergency with potentially devastating morbidity and mortality. After ischemic stroke, ICH represents the second most common type of stroke (15%). Bleeding within the brain can arise from multiple different etiologies ( Box 1 ), each of which can be considered its own separate disease.
Hypertension
Amyloidopathy
Vascular malformation
Hemorrhagic brain tumor
Hemorrhagic conversion from prior ischemic stroke
Cerebral venous sinus thrombosis
Introduction
Spontaneous intracerebral hemorrhage (ICH) is a medical emergency with potentially devastating morbidity and mortality. After ischemic stroke, ICH represents the second most common type of stroke (15%). Bleeding within the brain can arise from multiple different etiologies ( Box 1 ), each of which can be considered its own separate disease.
Hypertension
Amyloidopathy
Vascular malformation
Hemorrhagic brain tumor
Hemorrhagic conversion from prior ischemic stroke
Cerebral venous sinus thrombosis
Risk factors and pathophysiology
Although several other risk factors exist, by far the greatest risk factor for spontaneous ICH is hypertension ( Box 2 ). Over the course of time, chronic stress on the vascular walls leads to the fragmentation, degeneration, and eventual rupture of small penetrating vessels within the brain parenchyma. Hypertensive hemorrhages tend to occur in specific locations, including the deep structures of the basal ganglia and thalamus, as well as the pons, midbrain, and cerebellum.
Hypertension
Cigarette smoking
Antithrombotic therapy
African American
Diabetes
Older age
Heavy alcohol intake
Chronic kidney disease
Male sex
Poor diet
Complications from ICH occur in part owing to the limited space within the skull that is filled by brain tissue, blood, and cerebrospinal fluid. Increasing intracranial pressure (ICP) leads to decreased cerebral perfusion, as well as mechanical compression of brain contents that may ultimately lead to brain herniation. Blood may also leak into the cerebrospinal fluid drainage system and cause obstructive hydrocephalus.
Clinical presentation
Patients may present to the emergency department (ED) in a variety of ways, from those arriving on their own complaining of headache and vomiting, to those found obtunded and brought in by emergency medical services personnel. Even if focal neurologic deficits are not present immediately, a worsening level of alertness and potential loss of consciousness may develop quickly as the hematoma expands and causes compression of the surrounding brain parenchyma. The specific location of the ICH (ie, putamen, thalamus, caudate, lobes, cerebellum, pons) may correspond with particular neurologic signs and symptoms. For instance, thalamic hemorrhages may be associated with hallucinations or confusion, cortical hemorrhages with aphasia or neglect, and those in the posterior fossa with cerebellar or brainstem deficits. Early seizures in the first few days may also occur (14% incidence), more commonly with lobar hemorrhages.
Diagnostic considerations
Clinical Assessment Scores
As part of the initial evaluation of patients with suspected ICH, the emergency physician should obtain a baseline severity score based on physical examination. The National Institutes of Health Stroke Scale may be used to achieve this purpose and is preferred over the Glasgow Coma Scale. The benefit of scoring systems lies in the ability to communicate effectively about a patient’s dynamic medical condition over time to other medical providers. These providers, whether in the ED or an intensive care unit (ICU), can subsequently repeat the physical examination and identify changes.
Blood Testing
A rapid fingerstick glucose value should be obtained immediately in case the patient’s condition is due to hypoglycemia. Intravenous access should also be obtained immediately upon the patient’s arrival. The following markers should be ordered: complete blood count, basic metabolic panel including electrolytes and creatinine, troponin, prothrombin time, International Normalized Ratio (INR), partial thromboplastin time, and type and screen.
Radiographic studies
Computed Tomography
The abrupt onset of focal neurologic symptoms should be presumed as an ischemic stroke until proven otherwise, because time-sensitive evidence-based treatments exist for this form of stroke. Rapid neuroimaging with noncontrast computed tomography (CT) scan or MRI should be obtained to distinguish ischemic stroke from ICH. CT scan is the preferred imaging choice owing to its more rapid availability and lower cost. Hemorrhage appears as a high-density lesion. Its size and location can be visualized, as can the presence of intraventricular extension, edema, and/or brain herniation.
Computed Tomography Assessment
In a large retrospective study, ICH hematoma volumes greater than 32 mL supratentorially or 21 mL infratentorially were shown to be significant predictors of 30-day mortality. To communicate hematoma size with neurosurgery and ICU consultants, this measurement can be calculated rapidly and easily using the ABC/2 method ( Fig. 1 ).
Additionally, the ICH score incorporates this volume to predict outcomes and assist with medical decision making. Higher scores are associated with increased risk of mortality and decreased likelihood of good functional outcome. In the initial study of 152 patients with acute ICH, scores of 1, 2, 3, and 4 corresponded with 30-day mortality rates of 13%, 26%, 72%, and 97%, respectively ( Table 1 ). Subsequent studies have supported this positive association with mortality.
| Component | Points |
|---|---|
| GCS score | |
| 3–4 | 2 |
| 5–12 | 1 |
| 13–15 | 0 |
| ICH volume (cm 3 ) | |
| ≥30 | 1 |
| <30 | 0 |
| Presence of IVH | |
| Yes | 1 |
| No | 0 |
| Infratentorial origin of ICH | |
| Yes | 1 |
| No | 0 |
| Age (y) | |
| ≥80 | 1 |
| <80 | 0 |
| Total ICH score | 0–6 |
Location Corresponds with Etiology
Varying etiologies of spontaneous ICH may exert their effect within characteristic areas of the brain ( Figs. 2–5 ). Accordingly, the location of the hemorrhage may help point to the underlying etiology. For instance, bleeding from hypertensive ICH occurs most commonly in the basal ganglia (40%–50%) and other deeper structures within the parenchyma (thalamus, cerebellum, pons). ICH owing to amyloid (almost exclusively in elderly patients) or arteriovenous malformation (AVM) tends to occur in the lobar regions. Those originating from mass lesions may demonstrate edema surrounding the tumor and be seen in the grey–white junctions. Hemorrhagic conversion of a prior ischemic stroke may show hypodensity and edema in the middle cerebral artery territory with hemorrhage within it. ICH from a cerebral venous sinus thrombosis commonly appear at the sagittal and transverse sinuses.
Advanced imaging techniques
Computed Tomography Angiography of the Brain
Follow-up brain imaging is less useful when hypertensive hemorrhage is suspected, such as in patients with a history of poorly controlled hypertension and a CT image showing a deep bleeding pattern. However, beyond the noncontrast CT scan, additional imaging modalities may provide important information about the underlying cause of an ICH. CT head angiography is performed routinely for patients in whom spontaneous ICH is suspected owing to secondary etiology, such as aneurysm, AVM, tumor, or cerebral venous thrombosis. Certain indicators for such bleeds include lobar ICH, young age, and absence of cardiovascular disease risk factors. Suggestive radiologic evidence for vascular abnormalities causing ICH includes subarachnoid hemorrhage, enlarged vessels or calcifications along hemorrhage margins, hyperattenuation within a dural venous sinus, unusual hematoma shape and/or location, edema out of proportion with the presumed onset time, and the presence of a mass.
Furthermore, CT angiographic studies may identify contrast extravasation that is predictive of hematoma growth and 30-day mortality. Extravasation is reflected by tiny enhancing foci within the acute hematoma called spot signs ( Fig. 6 ). Spot signs are associated with intraoperative bleeding, postoperative bleeding, and larger residual ICH volumes during surgical evacuation. Their number, diameter, and attenuation are used to calculate the Spot Sign Score, which has been shown to independently predict poor functional outcomes and in-hospital mortality. This diagnostic marker does not have a clear role in determining management.
MRI
MRI takes longer to perform and is more expensive than CT imaging. Although much less frequently used, MRI may nevertheless be performed to evaluate for secondary causes of ICH, including hemorrhagic conversion of prior ischemic stroke. With high diagnostic accuracy, it may also detect AVMs, tumors, and cerebral venous thrombosis. MRI without contrast may be most useful in patients who are unable to receive intravenous (IV) contrast agents owing to allergy or renal disease.
Evaluation and management
Initial Assessment
Even before the patient is taken for CT imaging, the initial evaluation for any patient with suspected ICH begins with assessment of airway, breathing, and circulation (ABCs). Given the varying etiologies of ICH, it is also important for the emergency physician to obtain a focused yet detailed history from the patient, family members, and/or emergency medical services personnel ( Table 2 ). Although there is some overlap, the different etiologies call for certain focused management strategies, with the major difference being blood pressure control parameters.
| Components of Patient History to Obtain | ||
|---|---|---|
| Patient age | Time of symptom onset | History of prior stroke |
| Antiplatelet agents and/or anticoagulation | Hypertension | Liver disease |
| Bleeding diathesis | Drug use | Alcohol use |
Intervention Overview
Overall, treatment is generally supportive and aimed at preventing further injury to the brain by preventing the following complications: (1) hematoma expansion, (2) development of edema, (3) obstructive hydrocephalus, and (4) brain herniation. Some interventions must be taken immediately, whereas others may come secondarily ( Table 3 ).
| Primary Management | |||
| Reversal of anticoagulation | Blood pressure control | ICP control | Surgery as needed |
| Secondary goals | |||
| Seizure management | Glycemic control | Fever control | Intensive care disposition |
Rapid initiation of interventions may improve functional outcomes, because clinical deterioration may occur early. For instance, early hematoma expansion occurs in 18% to 38% of patients who receive repeat CT scan within 3 hours of onset. This has been shown to carry an association with poor clinical outcomes including an increased mortality rate of up to 30% to 55% at 30 days. These sobering statistics highlight the importance of mitigating ICH growth in the ED.
Reversal of anticoagulation
Antithrombotic Agents
Patients taking the vitamin K antagonist warfarin carry a 5- to 10-fold increased risk of suffering an ICH, and approximately 15% of cases are associated with its use. Once the ICH occurs, prolonged bleeding causes 27% to 54% of patients to develop early hematoma expansion that is associated with doubling of the mortality risk. These life-threatening risks are further exacerbated when coagulopathy is not corrected rapidly.
Current guidelines recommend administration of IV vitamin K (5–10 mg) by slow push over 10 minutes. Although long lasting, it takes 6 to 24 hours for vitamin K to achieve its reversal effects.
Fresh frozen plasma (FFP) contains factors I (fibrinogen), II, V, VII, IX, X, XI, XIII, and antithrombin. Relatively large volumes of FFP (10–15 mL/kg) are administered, which puts patients at risk for volume overload and pulmonary edema. Moreover, the INR of FFP itself is about 1.6, limiting the extent to which the coagulopathy can be reversed. Along with its required blood type matching, thawing time, and longer duration of administration, FFP takes several hours to achieve its INR reversal effects.
Prothrombin complex concentrate (PCC) contains vitamin K–dependent coagulation factors II, VII, IX, and X. Compared with FFP, the vials contain a higher concentration of clotting factors within a smaller volume and take only minutes to fully administer. PCC can normalize the INR completely within 10 minutes, although it brings a higher risk of disseminated intravascular coagulation. The INR needs to be checked within 30 minutes and redosed as needed.
Research shows that PCC should be the first-line reversal agent for most patients with therapeutic warfarin levels ( Table 4 ). Three randomized controlled trials comparing the two reversal agents found that PCC lowered the INR more rapidly than FFP and with no clear difference in thromboembolic risk. In terms of outcomes research supporting PCC, one prospective observational study showed a lower risk of death or severe disability at 3 months, whereas a retrospective study showed an increased 1-year survival. Another study comparing the two treatments for Warfarin reversal showed that in patients whose INR was corrected within 2 hours, there was no difference in hematoma growth incidence or extent. Even if it may not necessarily be the agent but rather the timing of coagulopathy reversal that imparts a greater effect, FFP takes longer than PCC to administer for the reasons mentioned.
| Pre-treatment INR | 2–4 | 4–6 | >6 |
|---|---|---|---|
| 4-Factor PCC dose (units of factor IX/kg) | 25 | 35 | 50 |
| Maximum dose (units of Factor IX) | 2500 | 3500 | 5000 |
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