Understanding Spontaneous Brain Bleeds: A Comprehensive Patient Guide

Table of Contents

• Introduction: What is Spontaneous Intracerebral Hemorrhage?
• Symptoms and Early Assessment
• How Common Are Brain Bleeds and Who Is At Risk?
• What Causes Brain Bleeds and Where They Occur
• Diagnostic Imaging for Brain Bleeds
• Severity Assessment Scales
• Treatment Approaches for Early Deterioration
• Secondary Prevention and Anticoagulation Decisions
• What We Still Don't Know
• Patient Recommendations and Action Steps
• Source Information

Introduction: What is Spontaneous Intracerebral Hemorrhage?

Spontaneous intracerebral hemorrhage refers to sudden bleeding within the brain that occurs without any traumatic injury. This condition represents approximately 10-15% of all strokes, making it a significant neurological emergency. Unlike other types of brain bleeding caused by trauma, aneurysms, or vascular malformations, spontaneous hemorrhage originates from within the brain tissue itself.

The condition has gained increasing attention because the annual incidence in the United States has doubled over the past two decades to approximately 80,000 cases per year. What makes this condition particularly concerning is its high mortality rate of 30-40%, and survivors often face significant disabilities, cognitive decline, and increased risk of recurrent strokes.

Symptoms and Early Assessment

Patients experiencing a spontaneous brain bleed typically develop sudden neurological symptoms that evolve over minutes rather than seconds. Unlike ischemic strokes (which involve blocked blood vessels), hemorrhagic strokes often present with additional symptoms including headache, nausea, vomiting, and frequently a depressed level of consciousness.

The specific symptoms vary depending on where in the brain the bleeding occurs:

• Basal ganglia hemorrhage: Causes weakness on the opposite side of the body and eyes that deviate toward the side of the bleeding
• Thalamic hemorrhage: Produces weakness plus unusual eye signs including downward and inward deviation, small pupils, and sometimes "wrong-way eyes" where gaze moves away from the side of the bleed
• Lobar hemorrhage (cerebral hemispheres): Symptoms correspond to the specific brain area affected and can include weakness, sensory loss, and gaze preference
• Brain stem hemorrhage: Usually located in the pons, causing impaired consciousness, cranial nerve palsies, pinpoint pupils, impaired eye movement, and facial weakness
• Cerebellar hemorrhage: Causes vertigo, vomiting, and coordination problems, particularly with walking

The distinction between hemorrhagic and ischemic stroke must be made through brain imaging, as the symptoms alone cannot reliably differentiate between these two types of stroke.

How Common Are Brain Bleeds and Who Is At Risk?

A comprehensive meta-analysis of studies from 21 countries conducted between 1983 and 2006 found an overall incidence of intracerebral hemorrhage of 24.6 cases per 100,000 person-years. The risk increases significantly with age and shows important racial and ethnic disparities.

Asian populations experience approximately twice the risk of White populations. In the United States, Black and Hispanic individuals have about 1.6 times higher risk compared to White individuals. The main risk factors identified include:

• Hypertension: The strongest attributable risk factor for most populations
• Cerebral amyloid angiopathy: Protein buildup in brain blood vessels
• Anticoagulation therapy: Blood thinners increase bleeding risk
• Advanced age: Risk increases significantly after age 60
• Genetic factors: Certain apolipoprotein genotypes (ApoE2 and ApoE4) confer 3-5 times higher risk

Important research from blood pressure control trials (PROGRESS and SPS3 trials) demonstrated that lowering blood pressure reduces the incidence of intracerebral hemorrhage. While the use of direct oral anticoagulants has reduced the risk compared to older vitamin K inhibitors, the risk remains significant.

What Causes Brain Bleeds and Where They Occur

Spontaneous intracerebral hemorrhage typically occurs in deep brain structures as a consequence of damage to the walls of small cerebral blood vessels. These small arteries and arterioles are usually branches of large vessels that supply critical areas including the basal ganglia, thalamus, pons, and deep cerebellum.

Two main pathological processes damage these small vessels:

1. Hypertensive cerebral vasculopathy: Chronic high blood pressure causes what neurologist C.M. Fisher termed "lipohyalinotic change" - a combination of hyalinization and lipid deposition in vessel walls that weakens them
2. Cerebral amyloid angiopathy: β-amyloid protein deposition in arterioles and capillaries, predominantly associated with lobar hemorrhages or cerebellar hemorrhages

Interestingly, lobar intracerebral hemorrhage (located in the outer brain regions) has become more common in recent medical series than deep hemorrhages. While chronic hypertension remains a risk factor for lobar hemorrhage, anticoagulation and vascular malformations account for a larger proportion of these cases compared to deep hemorrhages.

For patients with cerebral amyloid angiopathy, MRI often reveals multiple tiny asymptomatic hemorrhages of different ages, dilated perivascular spaces, and superficial siderosis (iron deposition from previous bleeding episodes).

Diagnostic Imaging for Brain Bleeds

Computed tomography (CT) and magnetic resonance imaging (MRI) are both highly sensitive and specific for diagnosing acute intracerebral hemorrhage. These imaging techniques establish the exact location and volume of the blood clot, which is critical for treatment decisions.

American Heart Association guidelines recommend CT angiography for specific patient groups:

• Patients younger than 70 with lobar intracerebral hemorrhage
• Patients younger than 45 with deep or posterior fossa hemorrhage
• Patients aged 45-70 with no history of hypertension

This additional imaging can detect underlying aneurysms or vascular malformations that might have caused the bleeding, though these findings are uncommon when the clot is contained entirely within brain tissue.

The volume of the blood clot at hospital admission is a powerful predictor of functional outcome at 3 months. Approximately 25% of spontaneous cases show expansion of the hematoma between the first CT scan and a follow-up scan (usually within 6-24 hours). This expansion occurs even more frequently (30-40%) in cases associated with anticoagulant medications.

Severity Assessment Scales

Medical professionals use validated scales to quickly assess the severity of intracerebral hemorrhage. The most commonly used tool is the Intracerebral Hemorrhage (ICH) Score, which incorporates:

• Glasgow Coma Scale score (measure of consciousness level)
• Patient's age
• Presence of infratentorial hemorrhage (bleeding in lower brain areas)
• Presence of intraventricular hemorrhage (bleeding into brain ventricles)
• Clot volume

This scoring system helps estimate the risk of early death, death at 12 months, and functional outcomes. However, its primary purpose is for quality improvement and helping providers discuss clinical severity with families rather than determining individual treatment decisions.

Treatment Approaches for Early Deterioration

The primary focus after a brain bleed is preventing secondary brain damage. Three main elements attract clinical attention: clot enlargement, secondary brain edema, and intraventricular hemorrhage.

Managing Hematoma Expansion

Hematoma expansion typically occurs within the first 6 hours after symptom onset and causes additional tissue destruction. The FAST trial tested recombinant factor VIIa administered within 4 hours of symptom onset and found a 15 percentage point reduction in clot size expansion at 24 hours with the highest dose. However, this did not translate to differences in severe disability or death rates. The ongoing FASTEST trial is testing factor VIIa administration within 2 hours of symptoms.

For patients on anticoagulants, the risk of hemorrhage expansion is 3-6 times higher. Research shows that four-factor prothrombin complex concentrate works better than fresh frozen plasma for normalizing blood clotting in patients on vitamin K antagonists. Specific reversal agents (idarucizumab and andexanet alfa) are available for newer direct oral anticoagulants.

Interestingly, the PATCH trial found that platelet transfusions in patients on antiplatelet therapy actually doubled mortality and increased disability rates. Therefore, current guidelines recommend against platelet transfusions except in patients needing neurosurgical procedures.

Blood Pressure Management

Two major trials examined blood pressure control after intracerebral hemorrhage:

• ATACH-2 trial: 1000 patients received intensive (110-139 mm Hg) or standard (140-180 mm Hg) blood pressure control for 24 hours. Outcomes were similar at 90 days, but some intensive-treatment patients experienced kidney injury.
• INTERACT2 trial: 2783 patients received similar blood pressure targets for 7 days. Findings were neutral regarding death or severe disability at 90 days.

Based on these results, current practice often aims for systolic blood pressure of 130-150 mm Hg, especially if readings exceed 220 mm Hg within 2 hours of hemorrhage, with careful monitoring of kidney function.

Managing Intraventricular Hemorrhage and Mass Effect

Intraventricular hemorrhage (bleeding into brain ventricles) occurs in 30-50% of patients and often causes hydrocephalus (fluid buildup) that decreases consciousness. The CLEAR III trial tested alteplase administration to dissolve ventricular clots in 500 patients. While overall outcomes didn't differ, thrombolysis might improve survival.

Surgical clot removal has shown inconsistent results. The STICH II trial found similar outcomes between surgical and conservative treatment for most patients, though removal of superficial lobar clots might be beneficial. For cerebellar hemorrhages, surgical removal is typically performed when clinical or imaging signs of brainstem compression exist or when clot volume exceeds 15 ml.

Secondary Prevention and Anticoagulation Decisions

For survivors of intracerebral hemorrhage who need anticoagulation for other conditions (particularly atrial fibrillation), decisions about resuming blood thinners are complex. Ongoing clinical trials are addressing this critical question:

• ASPIRE trial (NCT03907046): Testing new oral anticoagulants versus aspirin in intracerebral hemorrhage survivors
• ENRICH-AF (NCT03950076): Evaluating edoxaban versus no treatment in atrial fibrillation patients with previous cerebral hemorrhages

These trials will help determine whether newer anticoagulants can provide stroke prevention with lower rates of recurrent brain bleeding compared to current options.

What We Still Don't Know

Despite significant research, important questions remain unanswered about intracerebral hemorrhage:

• The ideal blood pressure target, choice of medication, and duration of treatment after hemorrhage
• Whether intensive monitoring in specialized units improves outcomes
• The role of prophylactic antiseizure medications
• How to best predict outcomes without prematurely withdrawing life-sustaining treatments
• The safety of resuming anticoagulation in survivors who need it for other conditions

Current evidence suggests that withholding prognosis determinations in the first few days after hemorrhage is appropriate, as some patients who might otherwise survive may succumb if life-sustaining treatments are withdrawn too early.

Patient Recommendations and Action Steps

Based on the current evidence, patients can take several important steps:

1. Control blood pressure: This remains the most significant modifiable risk factor for preventing first and recurrent hemorrhages
2. Discuss anticoagulation risks: If taking blood thinners, have regular conversations with your doctor about bleeding risks versus benefits
3. Know the symptoms: Recognize the signs of intracerebral hemorrhage - sudden neurological symptoms, headache, nausea, vomiting, and decreased consciousness
4. Seek immediate care: If symptoms occur, seek emergency medical attention immediately as early treatment may limit damage
5. Participate in shared decision-making: For survivors, engage in thorough discussions with healthcare providers about treatment options and goals of care

For patients with cerebral amyloid angiopathy (often suggested by multiple small brain bleeds on MRI), particular caution with anticoagulant medications is warranted.

Source Information

Original Article Title: Spontaneous Intracerebral Hemorrhage
Authors: Kevin N. Sheth, M.D.
Publication: The New England Journal of Medicine, October 27, 2022; 387:1589-1596
DOI: 10.1056/NEJMra2201449

This patient-friendly article is based on peer-reviewed research from The New England Journal of Medicine. It preserves all significant data, statistics, and clinical findings from the original scientific review while making the information accessible to patients and caregivers.