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Subdural hematoma

Last updated: April 30, 2021

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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.

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

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

Epidemiological data refers to the US, unless otherwise specified.

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.

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]

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]

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.

Approach

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.

General TBI management approach

Concurrent medical management

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