Related Subjects:
|Subarachnoid Haemorrhage
|Perimesencephalic Subarachnoid haemorrhage
|Haemorrhagic stroke
|Cerebellar Haemorrhage
|Putaminal Haemorrhage
|Thalamic Haemorrhage
About
Hemorrhagic transformation is a common complication following an ischemic stroke (infarct), especially after thrombolytic therapy or anticoagulation. Understanding the classification of hemorrhagic changes is crucial for clinical management and prognosis. The most widely used classification divides hemorrhagic transformations into hemorrhagic infarctions (HI) and parenchymal hematomas (PH), each with subtypes based on imaging characteristics.
Hemorrhagic Infarction (HI)
Hemorrhagic infarction refers to the presence of petechial hemorrhages within the area of an ischemic infarct without significant mass effect. It is considered a benign form of hemorrhagic transformation and often does not require a change in therapeutic approach.
- HI1: Small petechiae along the margins of the infarcted area.
- HI2: More confluent petechiae within the infarcted area but without space-occupying effect.
Parenchymal Hematoma (PH)
Parenchymal hematoma is characterized by a homogeneous area of hemorrhage with mass effect, indicating a more severe hemorrhagic transformation. It is associated with worse clinical outcomes and may necessitate changes in management, such as reversing anticoagulation or surgical intervention.
- PH1: Hemorrhage occupying less than 30% of the infarcted area with mild space-occupying effect.
- PH2: Hemorrhage occupying more than 30% of the infarcted area with significant space-occupying effect, or a clot remote from the infarcted area.
Clinical Significance
- The differentiation between HI and PH is essential for clinical decision-making:
- HI (HI1 and HI2): Generally does not require changes in treatment and has a better prognosis. Anticoagulation or antiplatelet therapy may be continued cautiously.
- PH (PH1 and PH2): Associated with increased risk of neurological deterioration and poor outcomes. Immediate medical intervention is often required, which may include discontinuation of anticoagulants, administration of clotting factors, or surgical evacuation.
Imaging Features
Hemorrhagic transformations are diagnosed using imaging modalities such as computed tomography (CT) or magnetic resonance imaging (MRI):
- CT Scan: HI appears as heterogeneous hyperdensities within the infarcted area without mass effect. PH appears as a dense, homogeneous area of hyperdensity with associated mass effect.
- MRI: Susceptibility-weighted imaging (SWI) sequences can detect hemorrhagic components with high sensitivity.
Risk Factors
- Use of thrombolytic therapy (e.g., tPA) after ischemic stroke.
- Anticoagulant and antiplatelet therapy.
- Large infarct size.
- Hypertension.
- Blood-brain barrier disruption.
- Advanced age.
- Hyperglycemia.
Management
- Monitoring: Close neurological and imaging monitoring to detect early signs of deterioration.
- Blood Pressure Control: Maintain optimal blood pressure to reduce the risk of further hemorrhage.
- Medication Adjustment: Evaluate the need to discontinue or adjust anticoagulant or antiplatelet medications.
- Surgical Intervention: Consideration of decompressive craniectomy or hematoma evacuation in cases of significant mass effect and clinical deterioration.
- Supportive Care: Management in an intensive care unit for severe cases to support vital functions.
Prognosis: varies depending on the type of hemorrhagic transformation
- HI: Generally favorable prognosis with minimal impact on clinical outcome.
- PH: Associated with higher morbidity and mortality rates due to mass effect and increased intracranial pressure.
References
- Fiorelli M, Bastianello S, von Kummer R, et al. Hemorrhagic transformation within 36 hours of a cerebral infarct: relationships with early clinical deterioration and 3-month outcome in the European Cooperative Acute Stroke Study I (ECASS I) cohort. Stroke. 1999;30(11):2280-2284.
- Berger C, Fiorelli M, Steiner T, et al. Hemorrhagic transformation of ischemic brain tissue: asymptomatic or symptomatic? Stroke. 2001;32(6):1330-1335.
- Lansberg MG, Thijs VN, Bammer R, et al. Risk factors of symptomatic intracerebral hemorrhage after tPA therapy for acute stroke. Stroke. 2007;38(8):2275-2278.