Subdural hematoma

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

• Incidence
  • Nontraumatic acute SDH: unknown ^[4]
  • Traumatic acute SDH: seen in approx. 30% of patients with severe traumatic brain injury (TBI) ^[5][6]
  • Chronic SDH: 2–13 individuals per 100,000 population ^[4]
• Sex: ♂ > ♀ (3:1) ^[2][7]
• Age
  • SDH is common in infants and toddlers. ^[2][8]
  • Acute SDH: more common in younger adults (30–50 years of age) ^[3]
  • Chronic SDH: more common in the elderly, especially individuals older than 70 years of age ^[3]

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]

• Most common cause: blunt head trauma (high-energy impact due to motor vehicle accidents) ^[9]
• Nonaccidental trauma, e.g., shaken baby syndrome
• Acceleration-deceleration injury ^[10]

Chronic SDH ^[3][8]

Traumatic chronic SDH

• In adults: mild trauma secondary to falls (e.g., due to old age, alcohol use disorder, epilepsy, hyponatremia)
• In infants ^[11]
  • Nonaccidental trauma, e.g., shaken baby syndrome
  • Birth trauma

Nontraumatic chronic SDH

• In adults: cerebral atrophy ; ^[12]
  • Advanced age
  • Alcohol use disorder ^[13]
  • Neurodegenerative disease, such as:
    • Alzheimer disease
    • Dementia (including HIV dementia, vascular dementia)
  • Chronic diabetes mellitus ^[14][15]
  • Previous traumatic brain injury
  • Cerebral irradiation ^[16]
• In infants and young children: meningitis ^[11]
• In both
  • Increased risk of hemorrhage due to:
    • Antithrombotic therapy or coagulopathy ^[4]
    • Intracranial aneurysm
    • Intracranial arteriovenous malformation
    • Intracranial tumors
    • Hypertension
    • Arteriosclerosis
    • Hemodialysis ^[17]
  • Iatrogenic (e.g., after neurosurgical procedures)
  • Spontaneous intracranial hypotension (rare) ^[18]

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.

• Rupture of bridging veins → low-pressure venous bleeding into the subdural space → 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]

• Symptom onset
  • Typically immediately after (or within 3 days of) the inciting event ^[19]
  • A lucid interval between head injury and onset of neurological symptoms is present in 12–40% of patients. ^[9]
• Progression
  • Rapid
  • Can progress to cerebral herniation and death
• Clinical features
  • Impaired consciousness and confusion, rapidly deteriorating to coma ^[2]
  • Focal neurological signs, such as:
    • Contralateral hemiparesis and UMN signs
    • Ipsilateral hemiparesis due to Kernohan syndrome (false localizing sign; uncommon)
    • Cranial nerve palsies, manifesting as:
      • Diplopia
      • Blurred vision
      • Unequal pupils
      • Anosmia
    • Slurred and/or disorganized speech
  • Pupillary abnormalities (e.g., anisocoria, unilateral or bilateral fixed dilated pupils)
  • Manifestations of ↑ ICP, such as:
    • Headache
    • Vomiting
    • Cushing triad
  • Signs of cerebral herniation syndromes
  • Abnormal posturing (e.g., decorticate posturing, decerebrate posturing)
  • Seizures
  • See ''Clinical features of traumatic brain injury'' for more information.

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]

• Symptom onset
  • Insidious
  • ≥ 3 weeks after the inciting event
• Progression: typically gradual
• Clinical features
  • Altered mental state that can progress to coma, characterized by:
    • Confusion
    • Delirium
    • Excessive drowsiness
  • Recurrent headaches
  • Cognitive deficits
    • Impaired memory
    • Dementia ^[22]
  • Focal neurological signs
    • Contralateral hemiparesis (most common) that can progress to hemiplegia
    • Incontinence
  • Ataxia and recurrent falls
  • Changes in personality ^[23]
  • Seizures (rare)

Important considerations ^[5][6]

• Immediate initiation of neuroprotective measures takes precedence over diagnostics in patients with acutely symptomatic SDH.
• Traumatic acute SDH: Follow trauma protocols, i.e., primary survey in TBI.
• Diagnostics should not delay the transfer of a patient to a neurocritical care unit if needed.

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

• Indication: first-line imaging modality for suspected acute SDH
• Characteristic findings ^[24]
  • Crescent-shaped, concave, sharply demarcated extraaxial lesion
  • 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. ^[26]
  • Radiodensity of the lesion depends on the length of time since the inciting event.
    • Acute SDH: hyperdense
    • Subacute SDH: isodense ^[27]
    • Chronic SDH: hypodense
    • Acute-on-chronic SDH: hyperdense areas (recent hemorrhage) admixed with isodense or hypodense areas (older hematoma) ^[4][28]
  • Common locations
    • Supratentorial location (most common)
    • Posterior cranial fossa
    • Interhemispheric ^[24][29]
  • Radiographic signs of other concurrent TBIs can be present, e.g., EDH with SDH.

MRI head ^[24][25]

• Indications
  • Neurological features unexplained by CT findings ^[2]
  • Suspected subacute SDH or chronic SDH ^[24][25]
  • Evaluation for nontraumatic etiologies (e.g., AVM, dural metastases) ^[29][30]
• Characteristic findings ^[24][29]
  • Similar to those on CT scan
  • Intensity of the lesion on T2-weighting depends on the length of time since the inciting event.
    • Acute SDH: hypointense ^[29]
    • Subacute SDH: hyperintense ^[28][29]
    • Chronic SDH: hyperintense core with a hypointense rim ^[29]

Angiography ^[2][24]

• Indication: to determine the etiology of a nontraumatic SDH (e.g., ruptured aneurysm, vascular meningeal tumor, AVM)
• Modalities
  • CTA
  • MR angiography
  • DSA

• Other intracranial hemorrhages: See “Differential diagnosis of intracranial hemorrhage.”
• In addition, chronic SDH should be differentiated from:
  • Subdural hygroma ^[31]
    • Collection of CSF in the subdural space
    • Thought to be caused by a tear in the arachnoid membrane following head injury
    • Difficult to distinguish from a chronic SDH on CT scan
    • Surgical evacuation is recommended in symptomatic subdural hygroma.
  • Other causes of dementia (e.g., neurodegenerative diseases, ischemic stroke)

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”.

• 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
    • Neuroprotective measures
    • Empiric ICP management if there are signs of ↑ ICP
    • See also “Initial management of TBI.”
  • Surgical management: Hematoma evacuation (see “Neurosurgical interventions”)
  • Emergency temporizing measure: If there is rapid neurological decline (e.g., cerebral herniation syndrome) and surgery is delayed, consider immediate burr hole craniotomy, e.g., prior to interfacility transfer. ^[32][33]
• Asymptomatic SDH (acute, subacute, or chronic): urgent neurosurgery consult to determine surgical vs. conservative management and disposition.
• All patients
  • Supportive care, monitoring, and prevention of complications in brain injuries
    • Frequent neurological examinations
    • Prevention of secondary bleeding or hematoma expansion, e.g., discontinuing antithrombotics, anticoagulant reversal, possible platelet transfusion
    • Prevention of other complications as needed, e.g., VTE, seizures, CNS infections
  • Treatment of reversible underlying causes for spontaneous SDH (e.g., management of coagulopathy, hypertension, diabetes mellitus)
  • For patients with traumatic SDH see also “Management of trauma patients,” and “TBI.”

Neurosurgical interventions ^[4][9][26]

• Indications ^[1][26]
  • Hematoma size ≥ 10 mm
  • Midline shift ≥ 5 mm
  • Signs of cerebral herniation syndromes (e.g., extensor posturing, anisocoria)
  • Rapid neurological deterioration (e.g., ≥ 2-point decrease in GCS score from the time of injury or symptom onset to ER transfer) ^[9]
  • Unilateral or bilateral fixed dilated pupils
  • ICP > 20 mm Hg ^[9]
  • Failure of conservative management ^[26]
  • Additional indications in chronic SDH include: ^[4]
    • Change in baseline neurological status
    • Evidence of mass effect
    • Increasing size of hematoma
• Timing
  • Acute SDH: preferably within ≤ 4 hours of the inciting event ^[9][19]
  • Subacute SDH or chronic SDH: as soon as possible ^[34]
• Options
  • Signs of cerebral herniation syndromes: emergency craniotomy or decompressive craniectomy; consider emergency temporizing burr hole craniotomy if definitive neurosurgical management is delayed (e.g., requires interfacility transfer) ^[19][35]
  • Acute SDH ^[9][19][26]
    • Craniotomy with evacuation of hematoma
    • Decompressive craniectomy
  • Subacute SDH and chronic SDH ^[26][34][36]
    • Definitive surgery: Craniotomy and clot evacuation (with/without drain placement) ^[21][37]
    • Elderly or high surgical risk: Consider minimally invasive or bedside interventions, e.g., twist drill craniostomy. ^[38]

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

• Indications (all of the following): ^[1][26][39]
  • Asymptomatic
  • Hematoma < 10 mm in size
  • Midline shift < 5 mm
  • Normal pupillary reflex and no signs of ↑ ICP, regardless of the GCS score
• Acute SDH ^[1][26]
  • Admit to neurocritical care unit.
  • Neuroprotective measures
  • ICP monitoring
  • Serial neurological examinations ^[19]
  • Serial neuroimaging
    • Neuroimaging should be repeated within the first 36 hours or earlier if there is neurological deterioration. ^[1]
    • Subsequent neuroimaging may be repeated as needed. ^[40]
  • Urgent surgery in patients with neurological deterioration and/or evidence of hematoma expansion on neuroimaging ^[19]
• Subacute SDH or chronic SDH
  • Disposition depends on the size and location of the hematoma and neurological examination findings. ^[4]
  • Corticosteroids may have a role in aiding spontaneous regression of the hematoma. ^[34][41]
  • Surgery may be required for patients who become symptomatic. ^[34]

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

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

• Follow ABCDE approach to evaluate, prioritize, and manage other injuries (e.g., C-spine precautions, fluid resuscitation).
• Perform rapid focused neurological examination (e.g., GCS, pupillary exam, screening for lateralizing signs).
• Intubate for airway protection if necessary (e.g., low GCS): See “Intubation of patients with high ICP.”
• Stabilize and obtain immediate neuroimaging.
• Urgent neurosurgery consult: for operative intervention and to determine disposition
  • Neurosurgery available on-site: Transfer to operating room, or admit directly to neurocritical care unit.
  • Neurosurgery not available on-site
    • Urgent interfacility transfer to a neurocritical care unit.
    • If signs of cerebral herniation syndrome, consider skull trephination prior to transfer.
  • Neurosurgery not indicated: conservative management only

Concurrent medical management

• Initiate neuroprotective measures (See “Acute management checklist for neuroprotective measures.”)
• ICP management if signs of ↑ ICP
• Prevention of secondary bleeding and hematoma expansion: See “Prevention of complications in brain injuries.”
  • Administer tranexamic acid if GCS is 9–13 and < 3 hours have elapsed since TBI.
  • Hold antithrombotic agents.
  • Anticoagulant reversal as needed.
  • Consider platelet transfusion ^[42][43]
• Serial neurological examination (e.g., GCS, pupillary examination)
• Continuous monitoring of vitals, pulse oximetry, and capnography

• 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]

• One-Minute Telegram 77-2023-1/3: The drill still fits the bill for chronic SDH

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