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Summary Table

Category	Details
Risk Factors	Young adults (20-30 years), history of head trauma (assault, falls, motor vehicle accidents, sports injuries), temporal bone fracture, anticoagulant use
Etiology	Rupture of the middle meningeal artery (most common, ~85%), less commonly middle meningeal vein or dural venous sinuses
Patient Presentation	Post-traumatic headache with a "lucid interval" followed by rapid neurological decline: worsening headache, vomiting, progressive drowsiness, contralateral hemiparesis
Classic Physical Exam	Ipsilateral fixed and dilated pupil (CN III compression from uncal herniation), contralateral hemiparesis, Cushing triad (hypertension, bradycardia, irregular respirations) in late stages
Key Diagnostic Results	Non-contrast CT head: biconvex (lens-shaped) hyperdense collection that does NOT cross suture lines; skull X-ray may show temporal bone fracture
Management	Emergent surgical evacuation via craniotomy; if small and asymptomatic, serial CT with close observation in a neurosurgical ICU
Keywords	"Lucid interval," "lens-shaped," "biconvex," "temporal bone fracture," "middle meningeal artery," "does not cross suture lines," "fixed dilated pupil"

1. Pathophysiology

Epidural hematoma (EDH) occurs when blood accumulates in the potential space between the dura mater and the inner periosteum of the skull. This space does not exist under normal conditions because the dura is tightly adherent to the bone, meaning that significant force is required to separate them.

The most common mechanism is a traumatic rupture of the middle meningeal artery, which runs through a groove on the inner surface of the temporal bone. The temporal bone is the thinnest part of the skull, making it the most vulnerable to fracture. When the bone fractures, it lacerates the artery, and arterial blood under high pressure rapidly dissects the dura away from the skull, forming an expanding hematoma.

This arterial origin explains the clinical hallmark of the lucid interval. At the moment of impact, the patient may be briefly stunned or lose consciousness from the concussive force itself. They then "wake up" and appear neurologically intact because the hematoma has not yet reached a critical volume. However, because arterial bleeding is under high pressure, the clot expands relentlessly. Within minutes to hours, the enlarging hematoma raises intracranial pressure (ICP), compresses the underlying temporal lobe, and pushes the uncus of the temporal lobe over the edge of the tentorium cerebelli. This is called transtentorial (uncal) herniation.

Uncal herniation compresses the ipsilateral oculomotor nerve (CN III), producing a fixed and dilated ("blown") pupil on the same side as the hematoma. Continued expansion compresses the ipsilateral cerebral peduncle, causing contralateral hemiparesis (since the corticospinal tract has not yet crossed at the pyramidal decussation). In a minority of cases, the contralateral cerebral peduncle is pushed against the opposite tentorial edge (Kernohan notch phenomenon), causing paradoxical ipsilateral hemiparesis, which is a well-known exam distractor.

If the herniation progresses further, the brainstem becomes compressed, triggering the Cushing reflex: systemic hypertension (the brain's attempt to maintain perfusion against rising ICP), reflex bradycardia (baroreceptor-mediated), and irregular respirations. This triad signals imminent brainstem failure and death without intervention.

A smaller proportion of EDHs (~15%) are venous in origin, arising from dural venous sinuses or meningeal veins. These tend to accumulate more slowly, present with a more insidious course, and are more common in the posterior fossa of children.

2. Classification and Clinical Manifestation

By Location

Location	Artery/Source Involved	Clinical Notes
Temporal (most common)	Middle meningeal artery	Classic presentation with lucid interval; highest risk of uncal herniation
Frontal	Anterior meningeal artery or anterior ethmoidal artery	Less common; may present with personality changes or frontal signs
Posterior fossa	Transverse or sigmoid venous sinus	More common in children; risk of cerebellar tonsillar herniation and rapid respiratory arrest; often venous
Vertex	Superior sagittal sinus	Rare; venous origin; may present with bilateral leg weakness

By Volume and Clinical Severity

Category	Volume	Clinical Features	Management Approach
Small / Asymptomatic	< 30 mL, thickness < 15 mm, midline shift < 5 mm	Alert, no focal deficits, GCS 14-15	Non-operative: serial CT every 6-8 hours, neurosurgical ICU observation
Large / Symptomatic	> 30 mL, thickness > 15 mm, or midline shift > 5 mm	Declining GCS, focal neurological deficits, anisocoria	Emergent surgical evacuation (craniotomy)

Classic Temporal Progression

Phase	Timing	Clinical Picture
Initial impact	Time of injury	Brief loss of consciousness or concussive symptoms from the primary injury
Lucid interval	Minutes to hours post-injury	Patient appears awake, oriented, and neurologically intact
Rapid deterioration	Hours after injury (variable)	Severe headache, vomiting, contralateral hemiparesis, ipsilateral pupil dilation, declining consciousness
Herniation / Terminal	Late	Bilateral fixed dilated pupils, decerebrate posturing, Cushing triad, cardiorespiratory arrest

3. Diagnostic Workup

Test	Role	Expected Finding
Non-contrast CT head	Best initial test AND confirmatory test	Biconvex (lens-shaped) hyperdense collection; does NOT cross suture lines
Skull X-ray	Supplementary (not required)	Temporal bone fracture (present in ~75-90% of adult EDH cases)
CT angiography	If active bleeding or vascular injury suspected	May show active extravasation from the middle meningeal artery
MRI brain	Rarely needed acutely; used for subacute or equivocal cases	Better soft tissue detail; can identify small posterior fossa EDH

The non-contrast CT of the head is both the best initial test and the test that confirms the diagnosis. In the setting of head trauma with neurological deterioration, CT is fast, widely available, and highly sensitive for acute hemorrhage. The classic finding is a biconvex (lenticular or lens-shaped), hyperdense collection along the inner table of the skull. The hematoma appears bright white on CT because acute blood is hyperdense.

The critical imaging discriminator is that an epidural hematoma does not cross suture lines. This is because the dura is firmly attached to the skull at the suture lines, and the blood cannot dissect past these attachment points. This feature distinguishes it from a subdural hematoma, which freely crosses suture lines because it lies beneath the dura. However, an EDH can cross the midline if it extends beneath the sagittal sinus area, which is a subtlety sometimes tested.

Look for midline shift on the CT, which indicates the degree of mass effect. A midline shift greater than 5 mm generally warrants surgical intervention regardless of the patient's clinical status, because it predicts impending herniation.

Skull X-ray is not routinely required but, if obtained, may reveal a temporal bone fracture overlying the middle meningeal artery groove. This finding in the clinical context is strongly suggestive of EDH even before CT is obtained.

MRI is rarely used in the acute setting because CT is faster and sufficient. MRI has a role when the CT is equivocal, in subacute presentations, or for posterior fossa EDH where CT can be limited by bone artifact.

Lumbar puncture is absolutely contraindicated if an epidural hematoma (or any space-occupying intracranial lesion) is suspected. Removing CSF from below while there is increased pressure above accelerates transtentorial herniation.

4. Management and Treatment

Clinical Scenario	Intervention	Details
ABCs and initial stabilization	Secure airway, maintain MAP	GCS ≤ 8: intubate for airway protection; target MAP to maintain cerebral perfusion pressure (CPP) > 60 mmHg
Raised ICP (temporizing)	Osmotic therapy	Mannitol 20%: 1-1.5 g/kg IV bolus, or Hypertonic saline 3%: 250 mL IV bolus; elevate head of bed 30 degrees
Large or symptomatic EDH	Emergent craniotomy	Surgical evacuation of the clot, ligation or cauterization of the middle meningeal artery
Small, asymptomatic EDH	Observation	Serial CT imaging (every 6-8 hours initially), neurosurgical ICU monitoring, neurological checks every 1-2 hours
Posterior fossa EDH	Lower threshold for surgery	Even small posterior fossa EDHs can cause rapid brainstem compression and respiratory arrest
Anticoagulated patient	Reversal of anticoagulation	Warfarin: IV Vitamin K + 4-factor PCC; DOACs: Idarucizumab (for dabigatran), Andexanet alfa (for factor Xa inhibitors)

The first priority in any trauma patient with suspected EDH is securing the airway and hemodynamic stabilization. Patients with a Glasgow Coma Scale (GCS) score of 8 or below require endotracheal intubation to protect the airway. Avoid hypotension aggressively, as even a single episode of systolic blood pressure below 90 mmHg in traumatic brain injury doubles mortality.

While awaiting surgical intervention, temporizing measures to reduce ICP should be initiated if the patient shows signs of herniation (declining consciousness, pupil asymmetry, posturing). Mannitol (an osmotic diuretic) at a dose of 1 to 1.5 g/kg IV bolus draws water out of brain parenchyma and into the intravascular space, reducing brain volume. An alternative is hypertonic saline (3%), given as a 250 mL IV bolus, which is preferred in hypotensive patients because it expands intravascular volume rather than depleting it (unlike mannitol, which causes diuresis). The head of bed should be elevated to 30 degrees to promote venous drainage from the brain.

Hyperventilation (targeting $PaCO_2$ of 30-35 mmHg) causes cerebral vasoconstriction and transiently reduces ICP. However, this is only a bridge measure for minutes while preparing for surgery, because prolonged hyperventilation causes cerebral ischemia.

The definitive treatment for a large or symptomatic EDH is emergent craniotomy with evacuation of the hematoma and direct hemostasis of the bleeding vessel (typically ligation or cauterization of the middle meningeal artery). Surgical indications include hematoma thickness greater than 15 mm, midline shift greater than 5 mm, or any neurological deterioration regardless of imaging findings.

For small EDHs (less than 30 mL, thickness under 15 mm, midline shift under 5 mm) in a neurologically intact patient (GCS 14-15 with no focal deficits), non-operative management with serial CT scanning and close observation in a neurosurgical ICU is appropriate. However, the patient must have immediate access to an operating room if deterioration occurs.

Posterior fossa EDHs deserve special emphasis. The posterior fossa is a tight, enclosed space, and even a small hematoma can compress the brainstem and fourth ventricle, causing obstructive hydrocephalus and respiratory arrest with very little warning. The threshold for surgical evacuation is therefore much lower for posterior fossa EDHs.

The prognosis for EDH is generally favorable compared to other traumatic intracranial hemorrhages, provided surgery is performed before irreversible herniation. Mortality drops to below 10% with timely evacuation but rises dramatically if the patient progresses to bilateral fixed dilated pupils before reaching the operating room.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Subdural hematoma (SDH)	Both present after head trauma with declining mental status and lateralizing signs	SDH appears crescent-shaped on CT and crosses suture lines; EDH is biconvex and does not cross suture lines. SDH is more common in the elderly and in patients on anticoagulants; EDH is more common in young patients with temporal bone fractures. SDH is caused by bridging vein rupture; EDH by arterial (middle meningeal artery) rupture.
Subarachnoid hemorrhage (SAH)	Both can present with sudden severe headache after trauma	SAH shows blood in the sulci and cisterns on CT (not a focal collection). Non-traumatic SAH classically presents with "thunderclap headache" and is caused by aneurysm rupture. There is no lucid interval pattern in SAH.
Intracerebral hemorrhage (ICH)	Both cause focal neurological deficits and raised ICP	ICH is an intraparenchymal bleed (within the brain tissue itself), not in the epidural space. CT shows a hyperdense lesion within the brain parenchyma. Most commonly caused by hypertension, not trauma in the typical tested scenario.
Concussion	Both follow head trauma; the initial presentation can overlap during the "lucid interval" phase	Concussion causes transient neurological dysfunction that improves. EDH causes progressive neurological decline after a lucid interval. CT is normal in concussion.
Brain abscess	Both can cause focal neurological deficits and increased ICP	Brain abscess presents with fever, subacute onset, and ring-enhancing lesion on contrast CT/MRI. There is no history of acute trauma.
Tension pneumocephalus	Both are post-traumatic conditions causing raised ICP and neurological decline	CT shows air (hypodense, black) in the cranial cavity, not blood (hyperdense, white). Look for a history of skull base fracture or recent neurosurgical procedure.

6. Traps and High-Yield Pearls

The single most tested concept around epidural hematoma is the lucid interval. Exam writers craft vignettes where a young patient sustains head trauma, seems perfectly fine for a period, and then suddenly deteriorates. Students who do not recognize this temporal pattern may incorrectly choose concussion (because the patient initially seemed well) or may delay ordering a CT because the patient "looks normal" at the time of evaluation. The exam is testing whether you understand that a normal-appearing patient after head trauma can harbor a rapidly expanding arterial bleed, and that the window for intervention is short.

A second common trap involves confusing the CT appearance of EDH and SDH. Both are extra-axial collections, and both are hyperdense on acute CT. The discriminator the exam expects you to apply is shape and relationship to suture lines: biconvex and confined by suture lines equals epidural; crescent-shaped and crossing suture lines equals subdural. If a vignette describes a crescent-shaped collection, do not pick epidural hematoma regardless of how "arterial" the clinical story sounds.

A third pitfall involves the Kernohan notch phenomenon. In the standard presentation, the hemiparesis is contralateral and the dilated pupil is ipsilateral to the hematoma. However, some vignettes may present ipsilateral hemiparesis (a false localizing sign), and students may be confused about the side of the lesion. The blown pupil is the more reliable lateralizing sign because it directly reflects uncal compression of CN III on the side of the hematoma.

Finally, never forget the contraindication of lumbar puncture in the presence of a suspected space-occupying intracranial lesion. If a vignette offers LP as an answer choice for a patient with post-traumatic headache and focal neurological findings, it is always wrong and is placed there to test whether you recognize the herniation risk.

The core competency being tested in epidural hematoma questions is pattern recognition: identifying the lucid interval, correctly interpreting CT morphology, understanding the herniation sequence, and knowing that emergent craniotomy is the definitive intervention.

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