Epidural and Subdural Hematomas

Traumatic brain injuries (TBIs) are a significant cause of morbidity and mortality worldwide, with epidural and subdural hematomas representing two of the most severe forms. While both conditions involve bleeding within the intracranial space, their underlying pathophysiology and clinical presentations differ. This review provides a comprehensive overview of epidural and subdural hematomas, their complications, and the management strategies to preserve cerebral perfusion pressure, reduce metabolic demands, and prevent secondary injuries to the central nervous system (CNS).


Epidural Hematoma

Epidural hematomas occur when an artery, typically the middle meningeal artery, is injured, and arterial blood accumulates between the dura mater and the calvarium. This injury is often associated with a skull fracture. Epidural hematomas do not cross suture lines due to the tight adherence of the dura to the calvarium, resulting in a biconvex or elliptical appearance on imaging. These hematomas are frequently associated with a "lucid interval," during which the patient may initially appear conscious and normal, but the headache worsens, and mental status declines as ICP rises.

Subdural Hematoma

Subdural hematomas result from the tearing of bridging veins due to rapid or sudden changes in velocity. This injury leads to an accumulation of venous blood in the subdural space, below the dura mater but above the arachnoid membrane. Subdural hematomas can cross suture lines, giving them a crescent-shaped appearance on head computed tomography (CT). If left untreated, these hematomas can cause mass effects and lead to uncal and/or tonsillar herniation. Subdural hematomas are more common in elderly patients due to reduced brain volume and stretched bridging veins.


Increased ICP can result in four types of brain herniation: central, subfalcine, tonsillar, and uncal (or transtentorial) herniation. As ICP rises, cerebrospinal fluid (CSF) initially moves into the spinal canal, and ventricles and cisterns collapse. ICP can rapidly increase at this stage, causing a shift in brain parenchyma away from the accumulating blood. If swelling continues, the brain parenchyma will herniate through various spaces, with the final movement occurring through the foramen magnum, leading to brainstem compression and death.

Management Strategies

The primary goals of management are to maintain cerebral perfusion pressure, reduce metabolic demands, and avoid secondary injuries to the CNS. Management strategies include head elevation, mannitol or hypertonic saline, hyperventilation, administration of barbiturates or sedatives, anticonvulsant therapy, ventriculostomy, maintenance of normovolemia with intravenous (IV) fluids, and therapeutic hypothermia.

Elevation of the Head

Elevating the head of the bed to 30 degrees, maintaining the head and neck in a midline position, and avoiding tight-fitting cervical collars, unless medically necessary, can help reduce ICP. If the elevation of the head of the bed is contraindicated due to other injuries, placing the patient in reverse Trendelenburg position (i.e., elevating the entire bed and then lowering the leg portion to maintain the head higher than the level of the heart) can be considered.


Mannitol (0.5-1.0 mg/kg IV over 15 minutes) can be administered to reduce cerebral edema by creating an osmotic gradient between the vascular space and the brain's extracellular fluid. This gradient causes water to shift out of the brain and into the vascular space, reducing brain volume and ICP. Mannitol should not be used in hypotensive or hypovolemic patients, as it can decrease blood pressure and reduce cerebral perfusion pressure (CPP).

Hypertonic Saline

Administering hypertonic saline in varying concentrations (e.g., 3% NaCl) can help reduce ICP by creating an osmotic gradient similar to mannitol. The appropriate concentration and administration rate should be determined based on the patient's ICP level and other clinical factors.


Short-term hyperventilation to reduce the partial pressure of carbon dioxide (PCO2) to no less than 30-35 mm Hg can lower ICP in patients with evidence of brain herniation. This treatment should only be used temporarily to prepare for surgical intervention, as prolonged reduction of PCO2 to ≤ 25 mm Hg can significantly decrease cerebral blood flow and oxygen delivery.

Barbiturates or Sedatives

Barbiturates, such as pentobarbital, or sedatives, like etomidate, can be used to suppress neuronal activity and reduce ICP. The appropriate dosing and administration schedules should be determined based on the patient's clinical status and other factors, such as the risk of bradydysrhythmias, hypotension, and adrenal suppression.


Anticonvulsant medications, including fosphenytoin, phenytoin, and levetiracetam, are primarily used in patients with traumatic brain injuries, especially those with penetrating injuries or depressed skull fractures. The appropriate medication, dosing, and administration schedule should be determined based on the patient's clinical status and seizure risk.


Invasive removal of CSF via ventriculostomy performed by a neurosurgeon is one of the most effective treatments for lowering ICP. This procedure involves the insertion of a catheter into the ventricles of the brain to drain excess CSF and reduce ICP.

Intravenous Fluids

Maintaining normovolemia with appropriate IV fluid administration is essential to prevent hypotension, which can reduce CPP. Hypotonic fluids should be avoided, as they can encourage free water movement into brain tissue and exacerbate swelling.

Therapeutic Hypothermia

Therapeutic hypothermia is a controversial management strategy with conflicting data, and it is not universally recommended. However, preventing and treating fever is crucial in managing patients with epidural or subdural hematomas.

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