Practice Essentials
Acute subdural hematoma (SDH) occurs most often after head injury and, despite rapid diagnosis and aggressive neurosurgical intervention, can result in high morbidity and mortality. [1, 2] Forensic pathologists often analyze cases of traumatic SDH due to road accidents, suicides, homicides, assaults, and domestic or on-the-job accidents. [3] Acute subdural hematoma (SDH) is the most common type of intracranial mass lesion, occurring in about one third of those with severe head injury (Glasgow Coma Scale [GCS] score < 9); emergent management of acute SDH is critical. [4, 5, 6] (See the Glasgow Coma Scale calculator.)
Acute SDH 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.
Traumatic acute SDH is associated with high mortality despite intensive treatment. In a study of patients with traumatic acute SDH, a midline shift exceeding the thickness of the hematoma by 3 mm or more at initial computed tomography (CT) predicted mortality in all cases. Of 59 patients, 29 died, with median survival of 2 days (0–276). Of the nonsurviving patients, 21 (70%) had an initial GCS score of 5 or less. [6]
Delayed acute SDH is defined as acute SDH that is not apparent on initial CT scan but appears on a follow-up CT scan. Delayed acute SDH occurs in about 0.5% of patients with acute SDH who are treated with surgery. [7] Delayed acute SDH occurs mainly in middle-aged and elderly persons who are receiving anticoagulation or antiplatelet therapy. Neurologic deterioration occurs within the first 24 hours for 70% of patients. [8]
When a patient who experienced head trauma presents with a GCS score less than 12, consider immediate neurosurgical consultation while stabilizing the patient and while diagnostic maneuvers are in progress.
Consider endotracheal intubation and obtain an immediate head 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.
Elevate the head of the bed to 30°, and make sure the head and neck are maintained in a midline position to optimize venous outflow from the brain. Rapid reversal of anticoagulation with warfarin is key and has been shown to reduce hemorrhage progression and mortality due to intracranial hemorrhage (ICH). Options for achieving hemostasis include vitamin K, fresh frozen plasma (FFP), prothrombin complex concentrate (PCC), and recombinant activated factor VII (rfVIIa).
Acute SDH is a serious traumatic disease, and predictive methods for hematoma growth are necessary to decide whether emergent operation is necessary. [9]
Small, asymptomatic, acute SDH may be managed by observation, serial examinations, and serial 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. [10]
The usual treatment for acute SDH is craniotomy and evacuation by a neurosurgeon, [11] 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.
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
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 approach is associated with significantly better functional outcomes among survivors of SDH. [10] If another facility is required for diagnosis or management, begin rapid transport to a trauma center with a promptly available neurosurgeon; this leads to decreased mortality among 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 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 SDH with cerebral edema. A cut-off value of 31.5 HU of white matter showed 80% sensitivity and 99.9% specificity for death in one study. [5]
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.
Hemostasis
Rapid reversal of anticoagulation with warfarin is key and has been shown to reduce hemorrhage progression and mortality due to intracranial hemorrhage (ICH). [11] However, the potential benefit of reversing anticoagulation must be weighed against the individual risk. [12] Options for achieving hemostasis 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. It 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. [12]
Dosage of FFP 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. [11]
The dose of PCC is individualized. It contains factors II, VII, IX, and X. A small volume is needed compared with FFP. PCC can correct international normalized ratio (INR) within minutes. Data show use of PCC is associated with improved outcomes in patients with ICH. [13]
rfVIIa is administered at 10-100 mcg/kg (lower dose is preferred due to risk of a thromboembolic event at higher dosing). Its effects are rapid, but improvement in mortality or functional outcome has not been shown.
Heparin may be fully reversed with 1 mg protamine sulfate/100 units heparin. Treatment with 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 for patients with ICH receiving dabigatran. Data on antiplatelet reversal are lacking. [12]
Surgery
Acute SDH is a serious traumatic disease, and predictive methods for hematoma growth are necessary to decide whether emergent operation is necessary. One study aimed to evaluate the incidence of "leakage" using computed tomography angiography (CTA) in patients with acute SDH and to identify its prognostic value. Results indicate that the leakage sign is a sensitive predictor of hematoma expansion and poor outcomes in acute SDH. If the hematoma is small but leakage sign-positive, strict observation is necessary and aggressive surgery may improve outcomes. [14]
Trephination
Burr holes are a temporizing option when rapid demise is associated with severe head trauma, especially if a herniation syndrome is clinically evident. [15] 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.
Craniotomy or decompressive craniectomy
A study by Ahmed et al evaluated in-hospital mortality of patients who presented with acute SDH and underwent emergency decompressive craniectomy (DC) or craniotomy (CO) within 4 hours of hospital arrival. Patients had severe head injury with an Abbreviated Injury Scale (AIS) score of 3 or greater and a GCS score of 8 or greater. Investigators reported that overall in-hospital mortality for emergency CO or DC for evacuation of SDH remains high, and preference for one operative procedure over the other did not impact overall mortality. [14]
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 hematoma (SDH) may be managed by observation, serial examinations, and serial 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. [16]
The usual treatment for acute SDH is craniotomy and evacuation by a neurosurgeon, [17] 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.
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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.
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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.
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Chronic subdural hematoma. The 3 cm, isodense crescent-shaped clot is resulting in midline shift.
