Subdural hematoma (SDH) refers to bleeding into the intracranial subdural space that is typically caused by a rupture of the . 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 . 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 .
Depending on the length of time between the onset of symptoms and the inciting event, SDH can be classified into the following: 
- Sex: ♂ > ♀ (3:1) 
Epidemiological data refers to the US, unless otherwise specified.
SDH is caused by a rupture of the , which can occur secondary to any of the following factors.
Acute SDH 
- Most common cause: blunt head trauma (high-energy impact due to motor vehicle accidents) 
- Nonaccidental trauma, e.g.,
- Acceleration-deceleration injury 
Chronic SDH 
Traumatic chronic SDH
- In adults: mild trauma secondary to falls (e.g., due to old age, alcohol use disorder, epilepsy, hyponatremia)
- In infants 
Nontraumatic chronic SDH
- In adults: cerebral atrophy 
- In infants and young children: meningitis 
- In both
SDH may occur after trivial trauma in patients with multiple risk factors.
- Rupture of → low-pressure venous bleeding into the 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 ).
Acute SDH 
- Typically immediately after (or within 3 days of) the inciting event 
- A head injury and onset of neurological symptoms is present in 12–40% of patients.  between
- Impaired consciousness and confusion, rapidly deteriorating to coma 
- Focal neurological signs, such as:
- Pupillary abnormalities (e.g., anisocoria, unilateral or bilateral fixed dilated pupils)
, such as:
- Signs of
- Abnormal posturing (e.g., decorticate posturing, decerebrate posturing)
- See '' '' for more information.
Subacute SDH 
- 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 weeks after the inciting event
- Progression: typically gradual
Altered mental state that can progress to coma, characterized by:
- Excessive drowsiness
- Recurrent headaches
- Cognitive deficits
- Focal neurological signs
- Ataxia and recurrent falls
- Changes in personality 
- Seizures (rare)
- Altered mental state that can progress to coma, characterized by:
Important considerations 
CT head without IV contrast
- Indication: first-line imaging modality for suspected acute SDH
Characteristic findings 
- Crescent-shaped, concave, sharply demarcated
- Can cross cranial suture lines
- Does not cross the midline
- A large unilateral SDH can cause midline shift to the contralateral side; midline shift may be absent or less significant in bilateral SDH. 
- Radiodensity of the lesion depends on the length of time since the inciting event.
- Common locations
MRI head 
- Characteristic findings 
- Other intracranial hemorrhages: See “ .”
- In addition, chronic SDH should be differentiated from:
- Subdural hygroma 
- Other causes of dementia (e.g., neurodegenerative diseases, ischemic stroke)
The differential diagnoses listed here are not exhaustive.
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”.
Symptomatic SDH (acute, subacute, or chronic)
- Immediate neurosurgery consult and/or transfer to a neurocritical care unit if expertise is not available on site
- Medical management
- Empiric if there are
- Surgical management: Hematoma evacuation (see “Neurosurgical interventions”)
- Emergency temporizing measure: If there is rapid neurological decline (e.g., ) and surgery is delayed, consider immediate , e.g., prior to interfacility transfer. 
- Asymptomatic SDH (acute, subacute, or chronic): urgent neurosurgery consult to determine surgical vs. conservative management and disposition.
- Supportive care, monitoring, and prevention of complications in brain injuries
- Treatment of reversible underlying causes for spontaneous SDH (e.g., management of coagulopathy, hypertension, diabetes mellitus)
Neurosurgical interventions 
- Hematoma size ≥ 10 mm
- Midline shift ≥ 5 mm
- Signs of extensor posturing, anisocoria) (e.g.,
- Rapid neurological deterioration (e.g., ≥ 2-point decrease in GCS score from the time of injury or symptom onset to ER transfer) 
- Unilateral or bilateral fixed dilated pupils
- ICP > 20 mm Hg 
- Failure of conservative management 
- Additional indications in chronic SDH include: 
- Signs of cerebral herniation syndromes: emergency or ; consider emergency temporizing if definitive neurosurgical management is delayed (e.g., requires interfacility transfer) 
Acute SDH 
- with evacuation of hematoma
Subacute SDH and chronic SDH 
- Definitive surgery: and clot evacuation (with/without drain placement) 
- Elderly or high surgical risk: Consider minimally invasive or bedside interventions, e.g., . 
An SDH ≥ 10 mm in size or causing ≥ 5 mm midline shift should be surgically removed, even if the patient is asymptomatic. 
- Indications (all of the following): 
Acute SDH 
- Admit to neurocritical care unit.
- ICP monitoring
- Serial neurological examinations 
- Serial neuroimaging
- Urgent surgery in patients with neurological deterioration and/or evidence of hematoma expansion on neuroimaging 
- Subacute SDH or chronic SDH
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
- Follow C-spine precautions, fluid resuscitation). to evaluate, prioritize, and manage other injuries (e.g.,
- Perform rapid focused neurological examination (e.g., GCS, pupillary exam, screening for ).
- Intubate for airway protection if necessary (e.g., low GCS): see “Airway management”
- Stabilize and obtain immediate neuroimaging.
- Urgent neurosurgery consult: for operative intervention and to determine disposition
Concurrent medical management
- Initiate Acute management checklist for neuroprotective measures”) (see “
- Prevention of secondary bleeding and hematoma expansion
- Serial neurological examination (e.g., GCS, pupillary examination)
- Continuous monitoring of vitals, pulse oximetry, and capnography