Acute Subdural Hematoma in the ED

Updated: Oct 27, 2016
  • Author: Alex Koyfman, MD; Chief Editor: Trevor John Mills, MD, MPH  more...
  • Print


Because acute subdural hematoma (SDH) is not only the most common type of intracranial mass lesion, occurring in about one third of those with severe head injuries (Glasgow Coma Scale [GCS] score <9), but also associated with high mortality and morbidity rates, the emergent management of acute SDH is critical. See the Glasgow Coma Scale calculator. [1, 2, 3]

Traumatic acute subdural hematoma has a high mortality despite intensive treatment. In a study of patients with traumatic acute subdural hematoma, a midline shift exceeding the thickness of the hematoma by 3 mm or more at the initial CT predicted mortality in all cases. Of 59 patients, 29 died, with median survival being 2 days (0–276). Of the  nonsurviving patients, 21 (70%) had an initial GCS score of 5 or less. [3]

An acute subdural hematoma is a rapidly clotting blood collection below the inner layer of the dura but external to the brain and arachnoid membrane (see the first image below). Two further stages, subacute and chronic, may develop with untreated acute SDH. Generally, the subacute phase begins 3-7 days after acute injury (surgical literature favors 3 days; radiologic literature favors 7days) (see the second image below). The chronic phase begins about 2-3 weeks after acute injury.

Acute subdural hematoma. Note the bright (white) i Acute subdural hematoma. Note the bright (white) image properties of the blood on this noncontrast cranial computed tomography (CT) scan. Note also the midline shift. Image courtesy of J. Stephen Huff, MD.
Subacute subdural hematoma. The crescent-shaped cl Subacute subdural hematoma. The crescent-shaped clot is less white than on the computed tomography (CT) scan of the acute subdural hematoma in the previous image. Despite the large clot volume, this patient was awake and ambulatory. Image courtesy of J. Stephen Huff, MD.

Delayed acute subdural hematoma is defined as an acute SDH that is not apparent on the initial CT scan but appears on a follow-up CT scan. Delayed acute SDH occurs. in about 0.5% of acute SDH patients treated with surgery. [4]  Delayed acute SDH occurs mainly in middle-aged and elderly persons who are either on anticoagulation or antiplatelet therapy. Neurologic deterioration occurs within the first 24 hours for 70% of the patients. [5]

See also Subdural Hematoma, Subdural Hematoma Surgery, Imaging in Subdural Hematoma, Closed Head Trauma, Head Injury, and Forensic Autopsy of Blunt Force Trauma.


Emergency Department Management

Consultation and/or transfer

Consult a neurosurgeon as soon as the diagnosis of subdural hematoma (SDH) is suspected.

If feasible, patients with head trauma should initially be transported to a hospital with a dedicated trauma team because this is associated with significantly better functional outcomes in survivors of SDH. [6] Initiate rapid transfer if another facility is required for diagnosis or management: Rapid transport to a trauma center with a promptly available neurosurgeon decreases mortality in patients with SDH. [1] Transfer may be emergent, with appropriate stabilization measures taken and with appropriately skilled personnel accompanying the patient.

Intubation and imaging

Consider endotracheal intubation when Glasgow Coma Score (GCS; see the Glasgow Coma Scale calculator) score is less than 12 or other indications are present; this guarantees airway protection during the diagnostic workup.

Obtain an immediate head computed tomography (CT) scan in patients with head trauma who experienced clear loss of consciousness (LOC), are symptomatic, are disoriented/amnestic, or have any focal neurologic signs. The presence of a focal neurologic sign following blunt head trauma is ominous.

Measurement of CT in Hounsfield units (HU) of white matter at the injury site may be useful as a predictor of outcome in patients with subdural hematoma with cerebral edema. A cut-off value of 31.5 for HU of white matter showed 80% sensitivity and 99.9% specificity for death in one study. [2]

Optimizing venous outflow and reducing ICP

Elevate the head of the bed to 30°, and make sure that the head and neck are maintained in a midline position to optimize venous outflow from the brain.

Hyperventilation to a target partial pressure of carbon dioxide (pCO2) of 30 mm Hg can reduce intracranial pressure (ICP) in the short term, although a pCO2 level less than 25 mm Hg is strongly discouraged.

Intravenous mannitol (0.25 g/kg) may be used to decrease ICP. However, glucocorticoids are not indicated for head trauma.


Rapid reversal of anticoagulation with warfarin is key and has been shown to reduce hemorrhage progression and mortality for intracranial hemorrhage (ICH). [7] However, the potential benefit of reversing anticoagulation must be weighed against the individual risk. [8] Options include vitamin K, fresh frozen plasma (FFP), prothrombin complex concentrate (PCC), and recombinant factor VII (rfVIIa).

Vitamin K should be administered at 5-10 mg infused at 1 mg/min. This should be administered in all patients with anticoagulant-related ICH because it boosts synthesis of clotting factors and prevents rebound coagulopathy after FFP, PCC, or rfVIIa. [8]

FFP's dosage is individualized; generally 10-15 mL/kg is needed for full reversal. Immediate transfusion of 2 units of universal donor FFP reduced mortality rate in one study. [7]

The dose of PCC is individualized. It contains factors II, VII, IX, X. A small volume is needed compared with FFP. PCC can correct INR within minutes. Recent data show use of PCC is associated with improved outcome in patients with ICH. [9]

rfVIIa is administered at 10-100 mcg/kg (lower dose preferred due to risk of thromboembolic event at higher dosing). It has rapid onset. Improvement in mortality or functional outcome has not been shown.

Heparin may be fully reversed with 1 mg protamine sulfate/100 units heparin. Treatment for low molecular weight heparin (LMWH) is the same, but only partial reversal can be achieved. For pentasaccharide anticoagulants such as fondaparinux, limited data support the use of rfVIIa. No specific reversal agents for direct thrombin inhibitors are noted; however, PCCs may have limited effectiveness in reversing rivaroxaban, and rfVIIa has theoretical potential in ICH patients on dabigatran. Data on antiplatelet reversal are lacking. [8]


Burr holes are a temporizing option when rapid demise is associated with severe head trauma, especially if a herniation syndrome is clinically evident. [10] Generally, because the lesion represents clotted blood, the burr hole is not curative, and emergent craniotomy is necessary. However, Burr holes can guide surgical therapy when head CT imaging is unavailable. Begin on the side of the (first) dilated pupil.


Neurosurgical Consultation

When a patient who experienced head trauma presents with a Glasgow Coma Score (GCS) score less than 12, consider immediate neurosurgical consultation while stabilizing the patient and while diagnostic maneuvers are in progress.

Small, asymptomatic, acute subdural hematomas (SDHs) may be managed by observation, serial examinations, and serial computed tomography (CT) scanning.

Operative intervention is required for patients with focal findings, neurologic worsening, hematoma greater than 1 cm thick, midline displacement or shift greater than 5 mm, or increased intracranial or posterior fossa pressure. [11]

The usual treatment for acute SDH is craniotomy and evacuation by a neurosurgeon, [12] who, after making a large cranial flap, opens the dura. Then, the clot is removed with suction, cup forceps, and/or irrigation. Bleeding sites are identified and controlled.