How do you differentiate and manage a cerebral infarct (infarction) versus a cerebral bleed (hemorrhage) in a patient with impaired neurological function?

Differentiating and Managing Cerebral Infarct versus Cerebral Hemorrhage

Obtain an emergent noncontrast CT scan of the brain immediately—this is the gold standard first-line imaging modality that accurately identifies intracranial hemorrhage and distinguishes it from ischemic infarction, allowing for time-sensitive treatment decisions. 1

Initial Diagnostic Approach

Immediate Imaging Protocol

• Noncontrast head CT is the primary diagnostic study and should be performed emergently in all patients presenting with acute neurological deficits 1
• CT accurately identifies most cases of intracranial hemorrhage and helps discriminate nonvascular causes such as brain tumor 1
• MRI is more sensitive than CT for detecting acute infarction, particularly small cortical, subcortical, and posterior fossa infarcts, but CT remains the initial study of choice due to speed and availability 1
• The ACR Appropriateness Criteria rate noncontrast head CT as "usually appropriate" (rating 8/9) for new focal neurologic deficits 1

Key Imaging Distinctions

Hemorrhage on CT:

• Appears as hyperdense (bright white) signal acutely 1, 2
• Immediate visualization within minutes of symptom onset 2, 3
• May show mass effect with midline shift in larger bleeds 4

Infarction on CT:

• Often appears normal in first 6-12 hours 1, 5
• Early infarct signs include loss of gray-white differentiation, sulcal effacement, and hyperdense vessel sign 1
• Becomes hypodense (dark) after 12-24 hours 1
• CT is relatively insensitive for acute infarction, missing up to 50% of cases in the first 6 hours 1

Critical Pitfall: Hemorrhagic Transformation of Infarction

A major diagnostic challenge is that cerebral infarcts can undergo hemorrhagic transformation, appearing as blood on subsequent imaging despite initially being ischemic. 4, 5, 6, 7

Timing and Characteristics

• Hemorrhagic transformation occurs in approximately 5% of infarcts during life (far less than autopsy studies suggested) 4
• Most hemorrhagic transformations occur between 12-48 hours after stroke onset, though can occur up to 11 days later 6, 7
• Early spontaneous intra-infarct hematoma (ESIH) can develop within 18 hours, potentially leading to misdiagnosis as primary hemorrhage 5
• If initial CT is nonhemorrhagic but patient deteriorates, repeat CT is mandatory to detect hemorrhagic transformation 5, 6

Risk Factors for Hemorrhagic Transformation

• Large infarct size (82% of hemorrhagic transformations occur with large infarcts) 6
• Severe neurological deficit and decreased consciousness 7
• Mass effect with midline shift 4
• Cortical involvement 7
• Cardiac embolism as stroke etiology 5, 6, 7
• Anticoagulation therapy, especially with excessive dosing or acute hypertension 6

Distinguishing Primary Hemorrhage from Hemorrhagic Infarction

Clinical clues favoring hemorrhagic infarction over primary hemorrhage:

• Prior transient ischemic attacks 5
• Silent infarcts on CT 5
• Potential cardiac source of embolism 5, 7
• Distal arterial occlusions on vascular imaging 5
• Heterogeneous hemorrhage pattern rather than homogeneous hematoma 7

Management Based on Imaging Findings

If Hemorrhage is Identified

Blood Pressure Management:

• For systolic BP 150-220 mmHg, acutely lower to 140 mmHg—this is safe and improves functional outcomes 3, 8
• Assess BP every 15 minutes until stabilized 3, 8
• Avoid cerebral vasodilators like sodium nitroprusside if elevated intracranial pressure suspected 3

Coagulopathy Reversal:

• Immediately reverse anticoagulation if patient on warfarin: withhold medication, give vitamin K-dependent factor replacement, correct INR, and administer IV vitamin K 2, 3, 8
• Administer platelets if severe thrombocytopenia or platelet dysfunction 2, 8

Surgical Considerations:

• Patients with cerebellar hemorrhage who are deteriorating neurologically or have brainstem compression/hydrocephalus require immediate surgical evacuation 2, 3, 8
• For supratentorial hemorrhage, routine surgery is not recommended, but consider for superficial hematomas <1 cm from cortical surface 8

Monitoring:

• Admit to intensive care unit or dedicated stroke unit 3
• Monitor neurological status hourly for first 24 hours using validated scales 3
• Initiate intermittent pneumatic compression for VTE prophylaxis immediately 3, 8

If Infarction is Identified (No Hemorrhage)

Thrombolysis Eligibility:

• Intravenous thrombolysis can be administered if <4.5 hours from symptom onset and no contraindications 3
• Consider endovascular treatment for large vessel occlusions 3

Anticoagulation Decisions:

• For large embolic infarcts, delay anticoagulation several days to reduce risk of hemorrhagic transformation 6
• Avoid large bolus doses of heparin 6
• Prevent excessive anticoagulation and hypertension 6
• Contraindications to immediate anticoagulation include: CT-confirmed hemorrhagic infarction, midline shift, and decreased consciousness 4

Repeat Imaging:

• Obtain repeat CT if patient deteriorates clinically, as this may indicate hemorrhagic transformation 5, 6
• Consider repeat imaging at 24-48 hours for large infarcts at high risk for transformation 6, 7

Advanced Imaging Considerations

When MRI is Appropriate:

• MRI without contrast is rated equally appropriate (8/9) as CT for new neurologic deficits 1
• MRI with diffusion-weighted imaging is superior for detecting acute infarction, especially in posterior fossa 1
• MRI can detect hemorrhage using gradient echo or susceptibility-weighted sequences 1
• Do not delay treatment to obtain MRI if CT is immediately available 1

Vascular Imaging:

• CTA or MRA of head and neck should be obtained to identify arterial occlusions and guide endovascular therapy 1
• Can be performed immediately after noncontrast CT 1

Monitoring for Deterioration

Signs of worsening in supratentorial infarction:

• Ipsilateral pupillary dysfunction and mydriasis 1
• Progressive decrease in motor function to extensor posturing 1
• Contralateral Babinski sign from brainstem compression 1
• Abnormal respiratory patterns (late finding) 1

Signs of worsening in cerebellar infarction/hemorrhage:

• Brainstem compression signs 1
• Glasgow Coma Scale <12 or decline ≥2 points 1
• Pupillary anisocoria or pinpoint pupils 1
• Loss of oculocephalic responses 1