From the Guidelines
Atraumatic subdural bleed management should prioritize close neurological monitoring and neurosurgical consultation, with conservative management for small bleeds and surgical evacuation for larger bleeds causing significant mass effect or neurological deficits. The management of atraumatic subdural bleed involves a multidisciplinary approach, including neurology, neurosurgery, and critical care.
- For small bleeds with minimal symptoms, conservative management may be appropriate, including regular neurological checks and serial imaging (CT or MRI scans) 1.
- For larger bleeds causing significant mass effect or neurological deficits, surgical evacuation is often necessary, typically through burr hole drainage or craniotomy.
- Patients should receive supportive care including blood pressure control, seizure prophylaxis with levetiracetam (500-1000mg twice daily), and correction of any coagulopathy if present.
- Anticoagulant and antiplatelet medications should be temporarily discontinued if possible, as the risk of recurrent hemorrhage must be weighed against the risk of an ischemic cerebrovascular event 1.
- Common causes of atraumatic subdural bleed include coagulopathies, vascular malformations, intracranial hypotension, or metastatic tumors, so underlying etiology should be investigated.
- Prognosis depends on the size of the bleed, neurological status at presentation, patient age, and comorbidities.
- Follow-up imaging is essential to monitor for resolution or recurrence, typically at 4-6 weeks after initial diagnosis or sooner if symptoms worsen.
- The use of anticoagulation after intracranial hemorrhage is a complex issue, and the decision to restart anticoagulation should be made on a case-by-case basis, considering the risks and benefits of anticoagulation therapy 1.
- The presence of microbleeds on MRI may signify an underlying microangiopathy or the presence of cerebral amyloid angiopathy, and the risk of recurrent ICH is higher in patients with lobar ICH 1.
- In patients with compelling indications for early reinstitution of anticoagulation, intravenous heparin or low-molecular-weight heparin may be safer options for acute therapy than restarting oral warfarin 1.
From the Research
Atraumatic Subdural Bleed
- Atraumatic subdural bleed, also known as spontaneous subdural hematoma, is a condition where there is bleeding into the space between the brain and the skull without any apparent trauma 2.
- The incidence of subdural hematomas increases with age, and the use of antiplatelet agents or anticoagulation therapy is a significant risk factor for developing this condition 2, 3.
Management of Atraumatic Subdural Bleed
- The management of atraumatic subdural bleed involves medical and surgical interventions, with a focus on maintaining intracranial pressure (ICP) < 22 mmHg, cerebral perfusion pressure (CPP) > 60 mmHg, mean arterial pressure (MAP) 80-110 mmHg, and PaO2 > 60 mmHg 2.
- Patients with atraumatic subdural bleed may require anti-seizure medications, and their antiplatelet medications or anticoagulation may be reversed if neurosurgical interventions are anticipated, or until hemorrhage is stabilized on imaging 2.
Oral Anticoagulation Therapy and Atraumatic Subdural Bleed
- Oral anticoagulation therapy is a common prophylactic therapy for several diseases with a high thromboembolic risk, but it harbors a possible hemorrhage risk, with a special risk for subdural hematoma (SDH) 3, 4, 5.
- The safety and efficacy of resumption of oral anticoagulation versus long-term discontinuation has not been fully clarified in patients who experienced SDH while under treatment with oral anticoagulation 5.
Outcome and Prognosis
- The outcome and prognosis of patients with atraumatic subdural bleed depend on various factors, including the size and location of the hematoma, the patient's age and comorbidities, and the presence of oral anticoagulation therapy 3, 4, 6.
- Patients with atraumatic subdural bleed who are on oral anticoagulation therapy may have a higher risk of unfavorable outcome and mortality compared to those who are not on anticoagulation therapy 3, 4.