Definition and epidemiology
A subdural hematoma is bleeding into the subdural space, the potential space between the dura mater and the arachnoid mater, due to rupture of the bridging veins that cross this space to drain the cerebral cortex into the dural venous sinuses. Bridging veins are distinct from emissary veins, which connect extracranial veins to the dural sinuses through small skull foramina and are not the source of SDH.
SDH is one of the most common intracranial hemorrhages seen in clinical practice and a leading cause of trauma-related morbidity in older adults. It is classified by time course:
- Acute SDH: symptoms within 24-72 hours of injury
- Subacute SDH: symptoms over 3-14 days
- Chronic SDH: symptoms after 2-3 weeks, typically in elderly patients with brain atrophy
Incidence rises sharply with age; chronic SDH is particularly common in patients over 65, with brain atrophy increasing the length (and fragility) of bridging veins. Falls are the leading mechanism in older adults, while high-impact trauma (motor vehicle collisions, assaults) predominates in younger patients. In infants, SDH is a hallmark finding of abusive head trauma (shaken baby syndrome), coded separately as a birth/neonatal injury only when due to birth trauma (P10.0).
- Crescent-shaped hyperdensity crossing suture lines = SDH; lentiform shape not crossing sutures = epidural hematoma
- Caused by tearing of bridging veins, often with minimal trauma in elderly or anticoagulated patients
- Chronic SDH frequently mimics dementia, stroke, or depression in the elderly
- CT density evolves over time: hyperdense (acute) to isodense (subacute, easily missed) to hypodense (chronic)
- Ipsilateral fixed dilated pupil from uncal herniation compresses CN III on the side of the hematoma
- Kernohan's notch can cause ipsilateral hemiparesis, a classic exam trick
- Reverse anticoagulation promptly in any patient on warfarin or DOACs with suspected SDH
- Burr holes for chronic liquefied SDH; craniotomy for acute solid clot with mass effect
Etiology and risk factors
The underlying mechanism is shearing or stretching injury to bridging veins, which have thin walls and lack the structural support of arteries, making them vulnerable to acceleration-deceleration forces.
Risk factors
- Advanced age (brain atrophy increases traction on bridging veins)
- Chronic alcohol use (cerebral atrophy, coagulopathy, fall risk)
- Anticoagulant or antiplatelet therapy (warfarin, DOACs, aspirate/clopidogrel)
- Coagulopathy or thrombocytopenia
- History of falls or minor head trauma, often unwitnessed or forgotten
- Shunted hydrocephalus (brain collapse increases venous traction)
- Infancy, particularly in the setting of non-accidental trauma (shaking causes diffuse bridging vein tears)
- Dural metastases or coagulopathy from malignancy
In contrast to epidural hematoma, which almost always requires a significant traumatic force (often with skull fracture and middle meningeal artery injury), SDH can occur after trivial or no clear trauma, especially in the chronic form.
Pathophysiology
Trauma causes relative movement between the brain and skull, stretching and tearing the thin-walled bridging veins that traverse the subdural space. Because these are low-pressure veins (not arteries), bleeding is typically slower than in epidural hematoma, which explains the delayed presentation often seen in subacute and chronic SDH.
Blood spreads diffusely over the brain surface, unimpeded by dural attachments (unlike epidural hematoma, which is limited by suture lines). This produces the classic crescent (concave) shape on imaging.
In chronic SDH, the initial clot undergoes organization: fibroblasts form a neomembrane, and fragile, leaky capillaries within this membrane cause recurrent small bleeds, allowing the hematoma to gradually enlarge over weeks. Rebleeding and osmotic fluid shifts contribute to progressive mass effect.
As the hematoma expands, it compresses the underlying brain and can cause midline shift. Large or rapidly expanding SDH can lead to transtentorial (uncal) herniation, which compresses the ipsilateral oculomotor nerve (CN III), producing a fixed, dilated pupil on the side of the lesion, and compresses the contralateral cerebral peduncle, which can paradoxically cause ipsilateral hemiparesis (Kernohan's notch phenomenon).
Clinical features
Presentation varies widely by time course and patient age.
Acute SDH
- Often follows significant trauma
- Decreased level of consciousness, which may be immediate or evolve rapidly
- Headache, vomiting, confusion
- Focal neurologic deficits (hemiparesis) contralateral to the lesion
- Signs of herniation in severe cases: ipsilateral pupillary dilation, decerebrate posturing
Chronic SDH
- Insidious, nonspecific presentation often mistaken for dementia or stroke
- Progressive headache, confusion, gait disturbance, or personality change
- Mild hemiparesis or focal weakness
- History of a fall weeks earlier that may not be recalled
- Can mimic a wide range of neurologic and psychiatric conditions in the elderly
Lucid interval
Unlike epidural hematoma, a lucid interval is less classically described in SDH, though it can occur, especially in cases with concomitant cerebral contusion masking the evolving bleed.
Diagnosis
Noncontrast CT head is the first-line and most important diagnostic test.
CT findings
- Crescent-shaped (concave), hyperdense (acute), extra-axial collection
- Crosses suture lines (distinguishes from epidural hematoma)
- May cause midline shift and effacement of sulci/ventricles
- Density changes with age of bleed: hyperdense (acute, 0-7 days), isodense (subacute, 1-3 weeks, can be subtle and easily missed), hypodense (chronic, >3 weeks)
- Mixed density ("acute on chronic") suggests rebleeding into a pre-existing chronic SDH
Additional workup
- MRI is more sensitive for isodense/subacute SDH and for detecting small or bilateral collections
- Coagulation studies (PT/INR, PTT, platelet count) to assess bleeding risk and guide reversal
- Baseline neurologic exam and Glasgow Coma Scale (GCS) for severity grading and serial monitoring
| Feature | Subdural hematoma | Epidural hematoma |
|---|---|---|
| Shape on CT | Crescent, concave | Lentiform (biconvex) |
| Crosses sutures | Yes | No |
| Vessel | Bridging veins | Middle meningeal artery (usually) |
| Onset | Often delayed, variable | Rapid, classic lucid interval |
Differential diagnosis
- Epidural hematoma: lentiform shape, does not cross sutures, classic lucid interval, arterial source
- Ischemic stroke: focal deficit without trauma history, different CT/MRI appearance
- Subarachnoid hemorrhage: sudden severe headache ("thunderclap"), blood in sulci/cisterns rather than extra-axial crescent
- Dementia or delirium: chronic SDH in elderly patients can closely mimic cognitive decline; always consider imaging in new confusion with fall history
- Brain tumor or abscess: subacute presentation with focal deficits and mass effect, differentiated by contrast enhancement pattern on imaging
- Normal pressure hydrocephalus: gait disturbance, incontinence, and cognitive decline overlap with chronic SDH presentation in the elderly
Management
Management depends on hematoma size, symptoms, and rate of neurologic change, following consensus from major neurosurgical and trauma guidelines (e.g., Brain Trauma Foundation).
Initial stabilization
- ABCs, airway protection if GCS is low
- Reverse anticoagulation promptly if present (vitamin K antagonist reversal, specific DOAC reversal agents, or platelet transfusion as indicated)
- Frequent neurologic checks and ICP monitoring in severe cases
Conservative management
- Small, asymptomatic hematomas (generally less than 10 mm thickness, less than 5 mm midline shift) can be managed with serial clinical observation and repeat imaging
- Appropriate for many chronic SDH cases found incidentally with minimal symptoms
Surgical management
Indicated for significant mass effect, midline shift, or neurologic deterioration:
- Burr hole drainage / twist-drill craniostomy: preferred for chronic, liquefied SDH
- Craniotomy with hematoma evacuation: preferred for acute SDH with solid clot and significant mass effect
- Decompressive craniectomy: considered for refractory intracranial hypertension or large acute SDH with significant midline shift
- Subdural drains after evacuation reduce recurrence rates
Adjuncts
- Antiepileptic prophylaxis may be considered in select high-risk acute cases per local protocol, though evidence and guideline recommendations vary
- Hyperosmolar therapy (mannitol or hypertonic saline) for acutely elevated ICP as a bridge to definitive treatment
- Address and treat underlying coagulopathy or correct reversible risk factors
Complications and prognosis
Complications
- Herniation (uncal/transtentorial) with brainstem compression, which is life-threatening
- Recurrence after surgical drainage, especially in chronic SDH (occurs in a meaningful minority of cases)
- Seizures
- Persistent neurologic deficits or cognitive impairment
- Hydrocephalus
Prognosis
- Acute SDH carries significant mortality, particularly in elderly patients, those with low GCS at presentation, or large hematoma volume
- Chronic SDH generally has a better prognosis with appropriate drainage, though recurrence and the frail baseline health of many patients affect outcomes
- Early recognition and prompt intervention are the strongest modifiable determinants of outcome
SDH = Slow Development, bleeding from bridging veins builds up over time (Subacute/Chronic), unlike the rapid arterial bleed of epidural hematoma.
Practice questions
1. A 78-year-old man on warfarin is brought in by his daughter for 3 weeks of worsening confusion and unsteady gait. He fell at home about a month ago but did not seek care at the time. Noncontrast CT of the head shows a crescent-shaped hypodense collection over the left cerebral convexity with mild midline shift. Which vessel is most likely responsible for this finding?
2. A 24-year-old man is brought to the emergency department after a motorcycle collision. He was initially conscious but his GCS has dropped from 14 to 9 over the past hour. Exam shows a dilated, nonreactive pupil on the right and weakness of the right arm and leg. Which of the following best explains the right-sided hemiparesis in this patient?
3. A 45-year-old woman presents after a fall from a ladder with a brief loss of consciousness followed by return to baseline alertness. Two hours later she develops worsening headache and lethargy. CT shows a biconvex, hyperdense extra-axial collection that does not cross the coronal suture. What is the most likely source of bleeding?
Frequently asked questions
What causes a subdural hematoma?
A subdural hematoma is caused by tearing of the bridging veins that run between the brain surface and the dural venous sinuses, usually from head trauma or acceleration-deceleration forces. It is more common in the elderly, alcoholics, and patients on anticoagulants because brain atrophy and fragile vessels make bridging veins more susceptible to injury, sometimes after only minor or forgotten trauma.
What are the first symptoms of a subdural hematoma?
Early symptoms often include headache, confusion, and drowsiness, which can progress to focal weakness or decreased consciousness. In acute cases following major trauma, symptoms may appear within hours, while chronic subdural hematomas in older adults can present insidiously over weeks with gradual confusion, gait problems, or personality change that mimics dementia.
How is a subdural hematoma diagnosed?
Diagnosis is made with a noncontrast CT scan of the head, which shows a crescent-shaped collection of blood that crosses suture lines. MRI can help detect smaller or isodense subacute hematomas that are harder to see on CT, and coagulation studies are checked to assess bleeding risk and guide reversal of any anticoagulants.
Is a subdural hematoma curable?
Many subdural hematomas, especially small or chronic ones, can resolve or be effectively treated with surgical drainage, though outcomes depend heavily on size, patient age, and how quickly treatment is given. Large acute hematomas carry significant risk of death or lasting neurologic damage, while smaller chronic hematomas generally have a better prognosis after burr hole drainage.
Subdural hematoma vs epidural hematoma — what is the difference?
Subdural hematoma results from bridging vein injury and appears as a crescent shape that crosses suture lines, often with a slower, more variable onset. Epidural hematoma usually results from middle meningeal artery injury, appears as a lens-shaped (biconvex) collection confined by suture lines, and classically presents with a lucid interval followed by rapid deterioration.
Key drugs
Related conditions and differentials
Sources and further reading
StatPearls (NCBI Bookshelf)MedlinePlusWHO ICD-10: I62.0
Educational content for medical students, prepared by the WhiteCoat Pro editorial team with AI assistance; every page is reviewed by a second AI model for factual errors. It is not medical advice and does not replace the product label, local guidelines or a clinician.