Subdural hematoma

Last updated: July 3, 2023

Summarytoggle arrow icon

Subdural hematoma (SDH) refers to bleeding into the intracranial subdural space that is typically caused by a rupture of the bridging veins. Trauma, including minor falls, cerebral atrophy, and conditions that increase the risk of bleeding (e.g., coagulopathy, hypertension) are common etiologies of SDH. According to the onset of symptoms, SDH can be classified into acute SDH, subacute SDH, and chronic SDH. Acutely symptomatic SDH typically manifests with altered mental status, focal neurological signs, and signs of increased ICP, and it can progress to brain herniation and death if not treated. Chronic SDH manifests gradually with cognitive deficits, impaired memory, personality changes, and focal neurological signs. Subacute SDH can manifest with features of acute and/or chronic SDH. In patients with acutely symptomatic SDH, neuroprotective measures to prevent secondary brain injury take precedence over diagnostics. Diagnosis is confirmed with a noncontrast head CT, which would show a crescent-shaped (concave) lesion that may cross cranial sutures typically located in the supratentorial region. Surgery is recommended in SDH that is symptomatic, ≥ 10 mm in size, or causing ≥ 5 mm shift in the midline. Conservative management can be considered for small asymptomatic SDHs in patients with no signs of increased ICP.

Definitiontoggle arrow icon

Subdural hematoma refers to a hemorrhage into the intracranial subdural space, which lies between the dura mater and the arachnoid mater. [1]

Classificationtoggle arrow icon

Depending on the length of time between the onset of symptoms and the inciting event, SDH can be classified into the following: [2][3]

  • Acute SDH: symptom onset within 3 days of the inciting event
  • Subacute SDH: symptom onset 4–20 days after the inciting event
  • Chronic SDH: symptom onset ≥ 21 days after the inciting event

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

SDH is caused by a rupture of the bridging veins, which can occur secondary to any of the following factors.

Acute SDH [3]

Chronic SDH [3][8]

Traumatic chronic SDH

Nontraumatic chronic SDH

SDH may occur after trivial trauma in patients with multiple risk factors.

Individuals at extremes of age (i.e., infants and the elderly) are at an increased risk of developing nontraumatic chronic SDH.

Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

Clinical features depend on the size and location of the hematoma and the length of time since the inciting event. In infants and young children unable to articulate symptoms, the presentation can be nonspecific (see shaken baby syndrome).

Acute SDH [2][3][9]

Traumatic acute SDH and acute EDH have similar clinical manifestations and are indistinguishable without neuroimaging.

Subacute SDH [20]

  • Symptom onset
    • 4–20 days after the inciting event
    • Can be acute or insidious
  • Progression: A rebleed can cause rapid neurological decline.
  • Clinical features: a combination of features of acute SDH and chronic SDH

Chronic SDH [3][21]

Diagnosticstoggle arrow icon

Important considerations [5][6]

Laboratory studies

  • Traumatic SDH: See ''Diagnostics'' in “TBI” for routine laboratory studies that should be obtained in all patients with TBI.
  • Nontraumatic SDH: Workup for the underlying cause (See “Etiology”)

Neuroimaging [24][25]

In trauma patients, findings of other injuries often accompany SDH, e.g., skull fractures, cerebral edema, and other types of TBI

CT head without IV contrast

MRI head [24][25]

Angiography [2][24]

Differential diagnosestoggle arrow icon

EDH is typically caused by arterial bleeding into the epidural space; SDH is typically caused by venous bleeding into the subdural space.

On neuroimaging, an EDH is biconvex (lentiform), does not cross cranial sutures, but can cross the midline; an SDH is concave, can cross cranial sutures but does not cross the midline.

The differential diagnoses listed here are not exhaustive.

Treatmenttoggle arrow icon


Specific treatment of SDH depends on the size of the hematoma, neurological status of the patient at presentation, and etiology (traumatic or nontraumatic). For patients with acute traumatic SDH, see also “Management approach for TBI”.

Neurosurgical interventions [4][9][26]

An SDH ≥ 10 mm in size or causing ≥ 5 mm midline shift should be surgically removed, even if the patient is asymptomatic. [1]

Conservative management

All conservatively managed patients should also receive supportive care, monitoring, secondary prevention measures for complications, and treatment of reversible underlying conditions.

Acute management checklist for acute traumatic SDHtoggle arrow icon

General TBI management approach

See also “Acute management checklist for moderate or severe TBI.”

Concurrent medical management

Prognosistoggle arrow icon

  • Acute SDH has a higher likelihood of an underlying parenchymal injury and is therefore associated with a worse prognosis than acute EDH. [29][44]
  • The prognosis of chronic SDH is better than that of acute SDH, however chronic SDH is associated with higher mortality with increasing age. [45]

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Referencestoggle arrow icon

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