Subdural hemorrhage: Difference between revisions
(Major expansion: acute vs chronic features, anticoagulation reversal, surgical indications, peer-reviewed references) |
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*Bleeding between the dura mater and arachnoid membrane, typically from bridging vein rupture | *Bleeding between the dura mater and arachnoid membrane, typically from bridging vein rupture | ||
*Three types by timing: | *Three types by timing: | ||
** | **Acute (<3 days) — hyperdense (white) on CT | ||
** | **Subacute (3-21 days) — isodense (may be difficult to see) | ||
** | **Chronic (>21 days) — hypodense (dark) on CT | ||
*Most common in elderly and anticoagulated patients<ref name="karibe">Karibe H, et al. Surgical management of traumatic acute subdural hematoma in adults. ''Neurol Med Chir (Tokyo)''. 2014;54(11):887-894. PMID 25367584.</ref> | *Most common in elderly and anticoagulated patients<ref name="karibe">Karibe H, et al. Surgical management of traumatic acute subdural hematoma in adults. ''Neurol Med Chir (Tokyo)''. 2014;54(11):887-894. PMID 25367584.</ref> | ||
*Acute SDH mortality: 50-90% (highest of all traumatic intracranial lesions) | *Acute SDH mortality: 50-90% (highest of all traumatic intracranial lesions) | ||
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==Evaluation== | ==Evaluation== | ||
* | *Non-contrast CT head — test of choice<ref name="bullock2">Bullock MR, et al. Surgical management of acute subdural hematomas. ''Neurosurgery''. 2006;58(3 Suppl):S16-24. PMID 16710968.</ref> | ||
**Acute: hyperdense, crescent-shaped collection crossing suture lines | **Acute: hyperdense, crescent-shaped collection crossing suture lines | ||
**Chronic: hypodense, crescent-shaped; may have mixed density if rebleeding | **Chronic: hypodense, crescent-shaped; may have mixed density if rebleeding | ||
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===Acute SDH=== | ===Acute SDH=== | ||
*'''ABCs''' — intubate if GCS <=8 | *'''ABCs''' — intubate if GCS <=8 | ||
* | *Emergent neurosurgical consultation | ||
*'''Reverse anticoagulation''' immediately: | *'''Reverse anticoagulation''' immediately: | ||
**Warfarin: | **Warfarin: 4-factor PCC (25-50 units/kg) + Vitamin K 10 mg IV | ||
**Dabigatran: | **Dabigatran: Idarucizumab 5 g IV | ||
**Rivaroxaban/Apixaban: | **Rivaroxaban/Apixaban: Andexanet alfa or 4-factor PCC | ||
**Antiplatelet agents: platelet transfusion if surgical candidate | **Antiplatelet agents: platelet transfusion if surgical candidate | ||
*ICP management: head of bed elevation, osmotherapy ([[Mannitol]] or [[Hypertonic saline]]) | *ICP management: head of bed elevation, osmotherapy ([[Mannitol]] or [[Hypertonic saline]]) | ||
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==Disposition== | ==Disposition== | ||
*All acute SDH: | *All acute SDH: admit, neurosurgical evaluation, ICU for operative or declining patients | ||
*Chronic SDH: admit if symptomatic, new, or enlarging; small stable chronic SDH may have outpatient neurosurgery follow-up | *Chronic SDH: admit if symptomatic, new, or enlarging; small stable chronic SDH may have outpatient neurosurgery follow-up | ||
Latest revision as of 09:26, 22 March 2026
Background
- Bleeding between the dura mater and arachnoid membrane, typically from bridging vein rupture
- Three types by timing:
- Acute (<3 days) — hyperdense (white) on CT
- Subacute (3-21 days) — isodense (may be difficult to see)
- Chronic (>21 days) — hypodense (dark) on CT
- Most common in elderly and anticoagulated patients[1]
- Acute SDH mortality: 50-90% (highest of all traumatic intracranial lesions)
- May occur with minimal or no trauma in the elderly and anticoagulated
Risk Factors
- Advanced age (cerebral atrophy stretches bridging veins)
- Anticoagulation / antiplatelet therapy
- Chronic alcohol use (cerebral atrophy, coagulopathy)
- Coagulopathy or thrombocytopenia
- Prior falls or head trauma (even minor)
- CSF shunt (overdrainage)
Clinical Features
Acute SDH
- Headache, altered mental status, decreasing GCS
- Ipsilateral fixed/dilated pupil (uncal herniation)
- Contralateral hemiparesis
- May present with coma from onset
- Associated with high-energy mechanism or fall in anticoagulated patients
Chronic SDH
- Insidious onset over weeks to months
- Headache, cognitive decline, confusion, personality changes
- Gait disturbance, falls
- Fluctuating neurologic symptoms (may mimic stroke or dementia)
- History of trauma often absent or trivial
Differential Diagnosis
- Epidural hemorrhage
- Subarachnoid hemorrhage
- Intracerebral hemorrhage
- Ischemic stroke
- Meningitis
- Dementia (chronic SDH)
Evaluation
- Non-contrast CT head — test of choice[2]
- Acute: hyperdense, crescent-shaped collection crossing suture lines
- Chronic: hypodense, crescent-shaped; may have mixed density if rebleeding
- Evaluate for midline shift, mass effect, herniation
- Labs: CBC, coagulation studies (PT/INR, PTT), type and screen
- If on anticoagulation: specific reversal levels (e.g., anti-Xa for DOACs)
Management
Acute SDH
- ABCs — intubate if GCS <=8
- Emergent neurosurgical consultation
- Reverse anticoagulation immediately:
- Warfarin: 4-factor PCC (25-50 units/kg) + Vitamin K 10 mg IV
- Dabigatran: Idarucizumab 5 g IV
- Rivaroxaban/Apixaban: Andexanet alfa or 4-factor PCC
- Antiplatelet agents: platelet transfusion if surgical candidate
- ICP management: head of bed elevation, osmotherapy (Mannitol or Hypertonic saline)
- Surgical indications: clot thickness >10 mm, midline shift >5 mm, GCS drop >=2 points
Chronic SDH
- Neurosurgical consultation for possible burr hole drainage
- Reverse anticoagulation
- Many small, asymptomatic chronic SDH may be observed with serial imaging
- Symptomatic chronic SDH: typically surgical (burr hole or craniotomy)
Disposition
- All acute SDH: admit, neurosurgical evaluation, ICU for operative or declining patients
- Chronic SDH: admit if symptomatic, new, or enlarging; small stable chronic SDH may have outpatient neurosurgery follow-up