Intracerebral Hemorrhage¶
Chapter 439 | Neurologic Disorders · Part 13 – Neurologic Disorders · Chapter 439
Key Clinical Points¶
- Intracerebral hemorrhage (ICH) accounts for approximately 10% of all strokes; mortality is high, with 35–45% of patients dying within the first month.
- Hypertension is the leading cause of primary ICH, typically involving deep structures such as the putamen, thalamus, cerebellum, and pons.
- Cerebral amyloid angiopathy (CAA) is the most common cause of lobar hemorrhage in elderly patients.
- The 'spot sign' on CT angiography indicates ongoing bleeding and is associated with increased risk of hematoma expansion, higher mortality, and poorer functional outcomes.
- Target systolic blood pressure (SBP) for spontaneous ICH is 130–150 mmHg to avoid hypoperfusion, based on INTERACT2 and ATACH2 trials.
- Rapid reversal of coagulopathy is critical: Prothrombin complex concentrates (PCCs) for Vitamin K antagonists, Idarucizumab for dabigatran, and andexanet alfa for oral factor Xa inhibitors.
- Putamen hemorrhage presents with contralateral hemiparesis as the sentinel sign; thalamic hemorrhage features prominent sensory deficits and aphasia.
- Pontine hemorrhage typically results in deep coma, quadriplegia, and 1 mm pinpoint pupils that react to light.
- Cerebellar hemorrhages usually develop over several hours and are characterized by occipital headache, repeated vomiting, and ataxia of gait.
- The ENRICH trial showed benefit for surgical removal of lobar hematomas within 24 hours (volume 30–80 mL; GCS 5–14); the STICH trial found no benefit in early surgery for supratentorial ICH.
DEFINITION & OVERVIEW¶
• Definition: Spontaneous hemorrhage directly into the brain parenchyma. • Scope: Includes intracranial vascular anomalies such as arteriovenous malformations (AVMs). • Mortality: 35–45% of patients die within the first month. • Epidemiology: ◦ Higher incidence in Asian and Black patient groups. ◦ Risk factors include advanced age, heavy alcohol use, and low-dose aspirin use in those without symptomatic cardiovascular disease. ◦ Cocaine or methamphetamine use is a major cause of ICH in young patients (age <45 years). • Classification: ◦ Primary ICH: Spontaneous hemorrhage directly into the brain parenchyma. ◦ Secondary ICH: Includes bleeding into subarachnoid, subdural, or epidural spaces (usually trauma), and subarachnoid hemorrhage due to trauma or rupture of an intracranial aneurysm.
ETIOLOGY & PATHOPHYSIOLOGY¶
• Hypertension: Leading cause of primary ICH; results from rupture of small penetrating arteries (30–100 μm) in deep brain structures. ◦ Common sites: Putamen, globus pallidus, thalamus, cerebellar hemisphere, and pons. • Cerebral Amyloid Angiopathy (CAA): ◦ Disease of the elderly with arteriolar degeneration and amyloid deposition. ◦ Most common cause of lobar hemorrhage in patients ≥60 years. ◦ Associated with \epsilon2 and \epsilon4 apolipoprotein E gene variations. • Drug Use: Cocaine and methamphetamine are frequent causes in young patients; associated with acute, severe hypertension. • Vascular Anomalies: ◦ Arteriovenous Malformations (AVM): Tangle of abnormal vessels; risk of bleeding is 2–4% per year if previously unruptured. ◦ Capillary telangiectasias: Rare cause, usually in the brainstem. ◦ Cavernous angioma: Linked to mutations in KRIT1, CCM2, and PDCD10 genes. ◦ Dural arteriovenous fistula (DAVF): Produces bleeding from venous hypertension. • Tumors: ◦ Lobar location; common types include lung, choriocarcinoma, melanoma, renal cell carcinoma, thyroid, hepatocellular carcinoma, and pilocytic astrocytoma. • Other Causes: ◦ Vasculitis: e.g., polyarteritis nodosa or lupus erythematosus. ◦ Sepsis: Can cause small petechial hemorrhages in white matter. ◦ Moyamoya disease: Occasionally produces ICH. ◦ Transformation: Occurs in 3–9% of patients undergoing acute intervention for ischemic stroke.
Table 439-1: Causes of Intracerebral Hemorrhage (ICH)¶
• Hypertension: Putamen, globus pallidus, thalamus, cerebellar hemisphere, pons; involves small (30–100 μm) vessels. • CAA: Lobar; associated with dementia; rare in patients <60 years. • Drug: Any, lobar, subarachnoid; Cocaine, amphetamine. • Aneurysm: Subarachnoid, intraparenchymal, rarely subdural; Mycotic and nonmycotic forms. • AVM: Lobar, intraventricular, subarachnoid. • Capillary telangiectasias: Usually brainstem. • Cavernous angioma: Intraparenchymal; linked to KRIT1, CCM2, and PDCD10 mutations. • Dural arteriovenous fistula: Lobar, subarachnoid; produces bleeding from venous hypertension. • Dural sinus thrombosis: Along sagittal sinus, posterior temporal/inferior parietal. • Tumors: Lung, choriocarcinoma, melanoma, renal cell carcinoma, thyroid, hepatocellular carcinoma, and pilocytic astrocytoma. • Transformation: Basal ganglion, subcortical regions, lobar; occurs in 3–9% of patients undergoing acute intervention.
CLINICAL FEATURES¶
• General Presentation: Abrupt onset of focal neurologic deficit; symptoms often worsen over 30–90 min. • Seizures: Uncommon at presentation but occur in 6–15% within the first 3 days. • Anatomical Site Specifics: ◦ Putamen: Contralateral hemiparesis (sentinel sign); face sags (5–30 min), slurred speech, limb weakness, and eyes deviating away from the side of hemiparesis. ◦ Thalamus: Prominent sensory deficit (all modalities); aphasia (often with preserved repetition); homonymous visual field defect; eye deviation downward/inward (looking at nose); skew deviation; ipsilateral Horner's syndrome. ◦ Pons: Deep coma, quadriplegia, and 1 mm pinpoint pupils that react to light; decerebrate rigidity; impaired doll's-head or oculocephalic maneuvers. ◦ Cerebellum: Develops over several hours; characterized by occipital headache, repeated vomiting, and ataxia of gait; parens of conjugate lateral gaze; skew deviation. ◦ Lobar: Symptoms depend on site: ◦ Occipital → hemianopsia. ◦ Left temporal → aphasia/confusion. ◦ Parietal → hemisensory loss. ◦ Frontal → arm weakness. • Complications: Edema may cause progression over 24–96 h; hydrocephalus from fourth ventricle compression may require external ventricular drainage.
INVESTIGATIONS & DIAGNOSIS¶
- Imaging Modalities: ◦ Noncontrast CT: Preferred for speed/availability; detects acute focal hemorrhages. ◦ MRI: More sensitive for delineating posterior fossa lesions. ◦ CTA/MRA: Used if patient is young, not hypertensive, or location is atypical. ◦ Spot Sign: Identified on CTA or post-contrast CT; indicates ongoing bleeding → higher risk of expansion and mortality.
- Laboratory Evaluation: ◦ Routine blood chemistry and hematologic studies (Platelet count, PT, PTT, INR) to identify coagulopathy.
- Prognostic Scoring (Table 439-2): • Age: ≥80 years → 1 point. • Hematoma Volume: ≥30 cc → 1 point. • Intraventricular Hemorrhage: Present → 1 point. • Infratentorial Origin: Yes → 1 point. • GCS Score: ◦ 5–12 → 1 point. ◦ 3–4 → 2 points. • Total Score: 0–6 sum of categories.
MANAGEMENT & TREATMENT¶
- Airway Management: Immediate attention due to potential for rapid deterioration in consciousness.
- Blood Pressure Control: ◦ Target SBP: 130–150 mmHg for spontaneous ICH (based on INTERACT2 and ATACH2).
- Coagulopathy Reversal: ◦ Vitamin K antagonists → Prothrombin complex concentrates (PCCs). ◦ Dabigatran → Idarucizumab. ◦ Oral factor Xa inhibitors → Andexanet alfa.
- Surgical Management: ◦ Lobar Hematomas: Surgical removal beneficial if within 24 hours of onset, volume 30–80 mL, and GCS 5–14 (ENRICH trial). ◦ Supratentorial ICH: No benefit in early surgery (STICH trial). ◦ Cerebellar Hematoma: Surgical evacuation required if hydrocephalus is present. ◦ Hydrocephalus: External ventricular drainage for fourth ventricle compression.
PROGNOSIS & COMPLICATIONS¶
• Mortality: High in first month (35–45%). • Expansion Risk: Increased by 'spot sign' and coagulopathy. • Long-term: Potential for Déjérine-Roussy syndrome (chronic contralateral pain) after thalamic hemorrhage.
KEY PEARLS & CLINICAL TRAPS¶
• Putamen = Hemiparesis; Thalamus = Sensory/Aphasia; Pons = Coma/Pinpoint Pupils. • Spot Sign: Indicates active bleeding → poor prognosis. • BP Target: 130–150 mmHg (specific target for spontaneous ICH). • Coagulopathy: Must be identified and reversed immediately to prevent expansion. • Cerebellar: Evacuate if hydrocephalus is present; use EVD for fourth ventricle compression.
Reference Tables¶
TABLE 439-1 Causes of Intracerebral Hemorrhage¶
Harrison's 22e, p.3453
| CAUSE | LOCATION | COMMENTS |
|---|---|---|
| Primary ICH | ||
| Cerebral amyloid angiopathy |
Lobar | Degenerative disease of intracranial vessels; associated with dementia, rare in patients <60 years |
| Any | ||
| Drug | Any, lobar, subarachnoid | Cocaine, amphetamine |
| Putamen, globus pallidus, thalamus, cerebellar hemisphere, pons |
||
| Secondary ICH | ||
| Aneurysm | Subarachnoid, intraparenchymal, rarely subdural |
Mycotic and nonmycotic forms of aneurysms |
| Lobar, intraventricular, subarachnoid |
||
| Capillary telangiectasias |
Usually brainstem | Rare cause of hemorrhage |
| Intraparenchymal | ||
| Dural arteriovenous fistula |
Lobar, subarachnoid | Produces bleeding from venous hypertension |
| Along sagittal sinus, posterior temporal/ inferior parietal |
||
| 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 |
| Basal ganglion, subcortical regions, lobar |
TABLE 439-2 The Intracerebral Hemorrhage Score¶
Harrison's 22e, p.3455
| CLINICAL OR IMAGING FACTOR | POINT SCORE |
|---|---|
| Age | |
| <80 years | 0 |
| ≥80 years | 1 |
| Hematoma Volume | |
| Intraventricular Hemorrhage Present | |
| No | 0 |
| Yes | 1 |
| Infratentorial Origin of Hemorrhage | |
| Glasgow Coma Scale Score | |
| 13–15 | 0 |
| 5–12 | 1 |
| 3–4 | 2 |
| Total Score | 0–6 Sum of each category above |