Intracerebral Hemorrhage¶
Chapter 439 | Part 13: Neurologic Disorders
KEY CLINICAL POINTS¶
- Intracerebral hemorrhage (ICH) is a form of stroke, accounting for ~10% of all strokes with ~35–45% mortality within the first month.
- ICH is classified as primary (hypertensive, coagulopathy, drug-induced) or secondary (aneurysm, AVM, tumors, vascular malformations).
- CT imaging is the gold standard for diagnosis, with key features including location (putamen, thalamus, cerebellum) and hematoma expansion risk.
- Acute management prioritizes blood pressure control (target SBP 130–150 mmHg), coagulopathy reversal, and surgical intervention for large hematomas.
- ICH Score (Table 439-2) is a validated tool for mortality risk stratification based on age, hematoma volume, and clinical status.
1. DEFINITION & OVERVIEW¶
Intracerebral hemorrhage (ICH) is spontaneous bleeding into the brain parenchyma, distinct from subarachnoid hemorrhage. It is classified as primary (hypertensive, coagulopathy, drug-induced) or secondary (aneurysm, AVM, tumors). CT imaging is the primary diagnostic tool, with key features including location (putamen, thalamus, cerebellum) and hematoma expansion risk. ICH accounts for ~10% of all strokes, with ~35–45% mortality within the first month.
Table 439-1 Causes of Intracerebral Hemorrhage (ICH)¶
| CAUSE | LOCATION | COMMENTS |
|---|---|---|
| Cerebral amyloid angiopathy | Lobar | Degenerative disease of intracranial vessels; associated with dementia, rare in patients <60 years |
| Coagulopathy | Any | Risk for hematoma expansion |
| Drug | Any, lobar, subarachnoid | Cocaine, amphetamine |
| Hypertension | Putamen, globus pallidus, thalamus, cerebellar hemisphere, pons | Chronic hypertension produces hemorrhage from small (~30–100 mm) vessels |
| Aneurysm | Subarachnoid, intraparenchymal, rarely subdural | Mycotic and nonmycotic forms of aneurysms |
| Capillary telangiectasias | Usually brainstem | Rare cause of hemorrhage |
| Dural arteriovenous fistula | Lobar, subarachnoid | Produces bleeding from venous hypertension |
| CAUSE | LOCATION | COMMENTS |
|---|---|---|
| Metastatic or primary brain tumors | Lobar | Lung, choriocarcinoma, melanoma, renal cell carcinoma, thyroid, hepatocellular carcinoma, and pilocytic astrocytoma are more commonly associated with bleeding complications |
| Transformation | Basal ganglion, subcortical regions, lobar | Occurs in a significant proportion of prior ischemic subcortical regions, lobar of ischemic strokes, more infarction commonly in large hemispheric infarctions; is symptomatic in 3–9% of patients undergoing acute intervention |
1.1 Classification¶
Primary ICH: Hypertensive (most common), coagulopathy, drug-induced (e.g., anticoagulants, cocaine). Secondary ICH: Aneurysm rupture, AVM, tumors, vascular malformations, or trauma.
1.2 Diagnostic Imaging¶
Noncontrast CT is the gold standard for acute ICH detection, with high sensitivity and specificity. MRI may be used for subacute/chronic hemorrhage or to detect underlying vascular abnormalities.
2. EPIDEMIOLOGY¶
ICH incidence is highest in Asian and Black populations. Hypertension, coagulopathy, sympathomimetic drugs (cocaine, methamphetamine), and cerebral amyloid angiopathy (CAA) are leading risk factors. Advanced age, heavy alcohol use, and low-dose aspirin in patients without cardiovascular disease increase ICH risk. Cocaine/methamphetamine use is a major cause in young patients (<45 years).
2.1 Demographics¶
Incidence rates are particularly high in Asian and Black patient groups. Mortality is ~35–45% within the first month. Hypertension is the leading cause of primary ICH.
2.2 Risk Factors¶
Hypertension, coagulopathy, sympathomimetic drugs (cocaine, methamphetamine), cerebral amyloid angiopathy (CAA), advanced age, heavy alcohol use, and low-dose aspirin in patients without cardiovascular disease.
3. ETIOLOGY & PATHOPHYSIOLOGY¶
Hypertensive ICH results from rupture of small penetrating arteries, most commonly in the basal ganglia (putamen), thalamus, cerebellum, and pons. Coagulopathy, anticoagulant use, and vascular anomalies (e.g., AVMs, CAA) contribute to secondary ICH. Hemorrhage expansion is influenced by blood pressure, coagulopathy, and hematoma location.
3.1 Hypertensive ICH¶
Spontaneous rupture of small penetrating arteries in the basal ganglia, thalamus, cerebellum, and pons. Chronic hypertension leads to vessel wall degeneration and hemorrhage.
3.2 Coagulopathy and Anticoagulants¶
Drug-induced ICH (e.g., anticoagulants, antiplatelet agents) increases hematoma expansion risk. Warfarin use is associated with higher mortality compared to aspirin in ICH.
3.3 Vascular Anomalies¶
Arteriovenous malformations (AVMs), aneurysms, and cerebral amyloid angiopathy (CAA) are major causes of secondary ICH. CAA is a disease of the elderly with amyloid deposition in cerebral arteries.
4. CLINICAL FEATURES¶
ICH presents with abrupt focal neurologic deficits (e.g., hemiparesis, aphasia), headache, vomiting, and signs of increased ICP (e.g., papilledema, decerebrate rigidity). Large hematomas may cause brainstem compression, hydrocephalus, or herniation. Seizures occur in 6–15% of patients within 3 days.
4.1 Symptomatology¶
Abrupt focal neurologic deficits (hemiparesis, aphasia), headache, vomiting, and signs of increased ICP (papilledema, decerebrate rigidity). Seizures occur in 6–15% of patients within 3 days.
4.2 Hemorrhage Location¶
Putamen (most common), thalamus, cerebellum, pons, and lobar regions. Cerebellar hemorrhage presents with occipital headache, vomiting, and ataxia. Lobar hemorrhage may cause hemianopsia or aphasia.
5. DIFFERENTIAL DIAGNOSIS¶
Differential diagnosis includes subarachnoid hemorrhage (SAH), ischemic stroke, brain tumors, and intracranial hemorrhage from trauma. CT imaging is critical to distinguish ICH from other causes, particularly in patients with headache and no focal deficits.
5.1 Subarachnoid Hemorrhage¶
Differentiated by CT findings (subarachnoid blood) and clinical features (severe headache, neck stiffness).
5.2 Ischemic Stroke¶
Differentiated by absence of hemorrhage on CT and clinical presentation (gradual onset vs. abrupt neurologic deficits).
6. INVESTIGATIONS & DIAGNOSIS¶
Noncontrast CT is the gold standard for ICH diagnosis. MRI may be used for subacute/chronic hemorrhage or to detect underlying vascular abnormalities. Lumbar puncture is generally avoided due to risk of herniation. ICH Score (Table 439-2) is a validated tool for mortality risk stratification.
Table 439-2 The Intracerebral Hemorrhage Score¶
| CLINICAL OR IMAGING FACTOR | POINT SCORE |
|---|---|
| Age | 0 (if <80 years), 1 (‡80 years) |
| Hematoma Volume | 0 (<30 cc), 1 (‡30 cc) |
| Intraventricular Hemorrhage Present | 0 (No), 1 (Yes) |
| CLINICAL OR IMAGING FACTOR | POINT SCORE |
|---|---|
| Infratentorial Origin of Hemorrhage | 0 (No), 1 (Yes) |
| Glasgow Coma Scale Score | 0 (13–15), 1 (5–12), 2 (3–4) |
| Total Score | 0–6 (sum of each category) |
6.1 Imaging¶
Noncontrast CT is the gold standard for acute ICH detection. MRI is used for subacute/chronic hemorrhage or to detect vascular abnormalities. CT angiography (CTA) or MR angiography (MRA) may be used to identify underlying vascular causes.
6.2 Laboratory Tests¶
Complete blood count, coagulation profile (PT, aPTT, INR), and platelet count. Rapid reversal of coagulopathy is critical in patients on anticoagulants.
7. MANAGEMENT & TREATMENT¶
Acute management includes blood pressure control (target SBP 130–150 mmHg), coagulopathy reversal (PCC, vitamin K, idarucizumab), and surgical intervention for large hematomas. Medical management is preferred for mild ICH, while surgical evacuation may be considered for severe cases. Functional outcomes are improved with early intervention.
7.1 Blood Pressure Management¶
SBP target of 130–150 mmHg to avoid hypoperfusion. Aggressive lowering may reduce hematoma expansion but requires careful monitoring to prevent cerebral hypoperfusion.
7.2 Coagulopathy Reversal¶
Rapid reversal of anticoagulants (PCC, vitamin K, idarucizumab) and platelet transfusion for thrombocytopenia (<50,000/ µ L).
7.3 Surgical Intervention¶
Craniotomy or minimally invasive hematoma evacuation for large hematomas ( ≥ 30 mL) or progressive neurological deterioration. Functional outcomes improve with early surgical intervention.
8. PROGNOSIS & COMPLICATIONS¶
Approximately 40% of patients with hypertensive ICH die, but survivors may achieve good to complete recovery. Complications include hydrocephalus, herniation, and secondary infections. ICH Score (Table 439-2) is a validated tool for mortality risk stratification.
8.1 Mortality¶
40% mortality in hypertensive ICH; survivors may achieve good to complete recovery. Mortality is higher in patients with large hematomas, infratentorial origin, or poor GCS scores.
8.2 Complications¶
Hydrocephalus, herniation, secondary infections, and poor functional outcomes. Early intervention improves prognosis.
9. SPECIAL CONSIDERATIONS¶
In pregnancy, ICH is associated with higher maternal mortality and requires multidisciplinary management. In pediatrics, ICH is often due to trauma or vascular anomalies. In the elderly, hypertension and CAA are leading causes. Anticoagulation management is critical in patients with atrial fibrillation and recent ICH.
9.1 Pregnancy¶
Higher maternal mortality; requires multidisciplinary management. Anticoagulation reversal is critical to prevent fetal complications.
9.2 Pediatrics¶
ICH in children is often due to trauma or vascular anomalies (e.g., AVMs). Early imaging and surgical intervention are critical.
9.3 Elderly Patients¶
Hypertension and CAA are leading causes. Management includes careful blood pressure control and surgical intervention for large hematomas.
10. KEY POINTS & CLINICAL PEARLS¶
- CT is the gold standard for ICH diagnosis. 2. ICH Score (Table 439-2) is a validated tool for mortality risk stratification. 3. Blood pressure control (130–150 mmHg) is critical to prevent hematoma expansion. 4. Coagulopathy reversal is essential in patients on anticoagulants. 5. Surgical intervention may improve outcomes in severe ICH cases.