The Lethal Lens: Mastering the Diagnosis and Management of Epidural Hemorrhage (EDH)

 

Epidural Hemorrhage (EDH), also known as an epidural hematoma, represents a critical and potentially devastating form of traumatic brain injury (TBI). It is characterized by the accumulation of blood in the potential space between the inner surface of the skull and the outermost layer of the brain's covering, the dura mater. This condition demands immediate recognition and neurosurgical intervention to prevent catastrophic neurological deficits or death. Understanding the pathophysiology, clinical presentation, and characteristic imaging features is paramount for all clinicians, particularly those managing acute trauma. 


Pathophysiology of Epidural Hemorrhage

The primary mechanism leading to EDH is a severe head injury, typically involving a skull fracture. The force of the trauma often causes a tear in the underlying vascular structures, most commonly the middle meningeal artery (MMA) or one of its branches, which traverses the temporal bone. While venous sources, such as dural sinuses, can also be implicated, arterial bleeding from the MMA is responsible for the majority of EDH cases, accounting for the rapid accumulation and life-threatening nature of the hematoma.

As arterial blood rapidly collects, it dissects the dura mater from the inner table of the skull, leading to the classic biconvex (lenticular or lens-shaped) hematoma. The dura mater is tightly adhered to the skull at the cranial sutures, which is why the hematoma typically does not cross suture lines—a key diagnostic feature on imaging.

The rapidly expanding hematoma creates a mass effect, progressively increasing the intracranial pressure (ICP). As ICP rises, it can lead to herniation of brain tissue (e.g., transtentorial herniation), causing compression of vital brainstem structures (like the oculomotor nerve, leading to ipsilateral fixed and dilated pupil) and, ultimately, brainstem failure and death if not urgently managed.


Epidemiology: Who is at Risk?

While EDH is relatively uncommon, accounting for approximately 1-3% of all head injuries, it is disproportionately represented in certain demographics:

  • Age: EDH is most frequent in young adults and adolescents, particularly those in their second and third decades of life (the 10-30 age range). The higher incidence in this group is often attributed to the greater elasticity and adherence of the dura mater in younger individuals, requiring more force to separate the dura from the bone, which in turn increases the likelihood of a major vessel tear like the MMA. The middle-aged and elderly tend to have more adherent dural attachments, making subdural hematoma (SDH) more common.
  • Sex: Males are affected more frequently than females, largely reflecting a higher incidence of high-impact trauma in this group.
  • Mechanism: The vast majority of cases (75-95%) are associated with a linear skull fracture that crosses the path of the MMA. Common etiologies include motor vehicle accidents, assaults (as seen in the presented case), and falls.

Clinical Presentation: The Classic Lucid Interval

The clinical presentation of EDH is highly variable and can evolve rapidly, but the classic finding is the "lucid interval".

  1. Initial Loss of Consciousness (LOC): The patient may momentarily lose consciousness immediately following the impact.
  2. Lucid Interval: Following the brief LOC, the patient may awaken and appear relatively normal (the lucid interval). This period can last minutes to hours. The case study describes a patient who initially lost consciousness for 5 minutes after being struck with a glass bottle but was later discharged, only to return with worsening symptoms two hours later.
  3. Rapid Deterioration: As the arterial hematoma rapidly expands, increasing the ICP, the patient's condition rapidly worsens. Symptoms include:
    • Severe Headache
    • Nausea and Vomiting
    • Decreasing Level of Consciousness (LOC): Progressing from confusion to stupor, and finally coma. While the patient in the case study was initially GCS 15, this is a crucial symptom of progression.
    • Focal Neurological Deficits: Often hemiparesis (weakness on one side of the body) contralateral to the hematoma.
    • Pupillary Changes: The classic sign of tentorial herniation is an ipsilateral, fixed, and dilated pupil due to compression of the third cranial nerve (oculomotor nerve).

Imaging Features: Computed Tomography (CT) Scan

Computed Tomography (CT) remains the gold standard for the rapid diagnosis of acute EDH. The key features are critical for distinguishing EDH from other forms of intracranial hemorrhage:

1. The Classic Lenticular Shape (Biconvex)

  • The hematoma appears as a hyperdense (white/bright) collection, indicating acute blood, that is shaped like a biconvex lens (or a lemon).
  • This shape is due to the arterial pressure stripping the dura from the skull, but the tight adherence of the dura to the sutures restricts the spread, causing the collection to bulge inward.

2. Does Not Cross Suture Lines

  • A definitive feature: the collection is restricted by the cranial sutures. This helps differentiate EDH from a Subdural Hemorrhage (SDH), which often crosses suture lines but respects the falx cerebri and tentorium.

3. Associated Skull Fracture

  • A skull fracture is present in a high percentage of cases (up to 90%). High-resolution bone window CT is essential for visualizing the fracture.

4. Mass Effect

  • Large hematomas will cause significant mass effect, visible as effacement of the cortical sulci, compression of the ventricles, and midline shift of the brain tissue (as seen in the attached images). The red arrow in [Figure 1] points to the midline shift.

Case Study Imaging Analysis

The provided CT images clearly demonstrate the diagnostic features of EDH: 

[Figure 1] Axial brain window: Shows a large, hyperdense (acute blood), lenticular-shaped mass in the left temporoparietal region. Note the significant midline shift to the right, indicated by the red arrow. This shift is an indicator of dangerously high ICP. 

[Figure 2] Coronal brain window: Confirms the large, peripherally located, biconvex hematoma, characteristic of EDH.

[Figure 3] Axial bone window: Confirms the large, biconvex shape of the left Epidural Hemorrhage and its peripheral location, abutting the inner table of the skull.

[Figure 4] Axial brain window: An additional axial view confirming the extensive left-sided Epidural Hemorrhage and significant mass effect.


Differential Diagnosis: Distinguishing Intracranial Hemorrhages

The primary goal of the trauma physician is to distinguish EDH from other life-threatening intracranial hemorrhages.

Condition

Location

Classic Shape

Suture Line Crossing

Typical Mechanism

Epidural Hemorrhage (EDH)

Between skull and dura

Biconvex (Lens-shaped)

Does NOT cross sutures

Skull fracture, Arterial (MMA) tear

Subdural Hematoma (SDH)

Between dura and arachnoid

Crescent-shaped (Concave-convex)

Crosses sutures (but respects the falx)

Tearing of bridging veins (often in elderly/alcoholics)

Subarachnoid Hemorrhage (SAH)

Between arachnoid and pia

Fills cisterns and sulci

Follows brain contours

Aneurysm rupture (Traumatic SAH is also common)

Intraparenchymal Hemorrhage (ICH)

Within brain parenchyma

Irregular, within the brain tissue

N/A

Trauma, uncontrolled hypertension, AVM


Diagnosis and Treatment: The Race Against Time

Diagnosis

Diagnosis relies on a combination of clinical findings (history of trauma, LOC, the lucid interval, neurological deterioration) and rapid imaging. CT scan is the cornerstone, providing immediate confirmation of the hematoma and its size, location, and associated mass effect.

Treatment

EDH is a neurosurgical emergency. The goal is rapid decompression to relieve the mass effect and lower the ICP.

  1. Non-Surgical Management: Very small, stable EDHs (often < 30 ml volume, 15 mm thickness, GCS >= 8, no focal deficit) may be managed conservatively in a neuro-ICU with close neurological monitoring and ICP control.
  2. Surgical Evacuation: The definitive treatment for symptomatic or large EDHs is urgent burr hole placement and/or craniotomy for hematoma evacuation. This is often the first procedure in emergency settings to save the patient's life. The bleeding vessel (usually the MMA) is identified and cauterized or ligated to prevent re-bleeding.

Key Principle: Time is Brain. Immediate intervention is crucial to prevent further secondary brain injury and potentially fatal complications.


Prognosis and Prevention

Prognosis

The prognosis for EDH is directly tied to the speed of diagnosis and surgical intervention.

  • Patients who undergo surgery while conscious (GCS 13-15) often have an excellent prognosis, with a high chance of complete recovery.
  • Delay in treatment, progression to coma (GCS $\le 8$), or significant associated brain injury leads to a much poorer outcome, including severe disability or death.
  • Other factors include the size and location of the hematoma and the patient's age.

Prevention

Prevention primarily revolves around reducing head trauma. This includes:

  • Protective Equipment: Mandating and using helmets in high-risk activities (sports, cycling, construction).
  • Safety Measures: Promoting seatbelt use and enforcing driving safety laws.
  • Public Awareness: Educating the public and clinicians on the importance of immediate medical evaluation after any head injury, even if symptoms appear minor (recognizing the dangers of the lucid interval).


Quiz

Question 1: (Pathophysiology and Vascular Source) A 25-year-old male presents with a brief loss of consciousness after a blunt head trauma, followed by a "lucid interval." His neurological status then rapidly deteriorates. A CT scan confirms an Epidural Hemorrhage. What is the most common vascular structure injured in a typical EDH, and what anatomical finding on a non-contrast CT scan differentiates it from a Subdural Hematoma?

(A) Anterior cerebral artery; It is crescent-shaped and crosses suture lines.

(B) Superior sagittal sinus; It is biconvex and crosses the midline falx cerebri.

(C) Middle meningeal artery; It is biconvex (lenticular) and does NOT cross suture lines.

(D) Bridging veins; It is biconvex and is usually only seen in the elderly.

(E) Posterior cerebral artery; It is crescent-shaped and does NOT cross the tentorium. 

Answer & Explanation

Answer: (C)

Explanation: The vast majority of EDHs are caused by a tear in the Middle Meningeal Artery (MMA), often in association with a skull fracture. The arterial pressure causes the blood to rapidly strip the dura mater from the skull, creating a biconvex (lens-shaped) collection. Crucially, the tight adherence of the dura to the cranial sutures prevents the hematoma from crossing these lines, a feature that distinguishes it from the crescent-shaped Subdural Hematoma (SDH).

Question 2: (Clinical Presentation and The Lucid Interval) The 18-year-old patient in the case study was initially struck and lost consciousness for 5 minutes. He was later discharged, only to return 2 hours later with severe headache, nausea, and vomiting. This clinical course is classic for Epidural Hemorrhage. What is the most critical physiological reason for the rapid, severe deterioration following the lucid interval?

(A) Tearing of the subdural bridging veins, leading to a slow, chronic increase in blood volume.

(B) Venous bleeding from the superior sagittal sinus causing cerebral edema.

(C) Auto-regulation failure of cerebral blood flow due to an ischemic stroke.

(D) Rapid accumulation of arterial blood, creating a critical mass effect and leading to rapidly increasing Intracranial Pressure (ICP).

(E) A delayed inflammatory reaction to the traumatic impact. 

Answer & Explanation

Answer: (D)

Explanation: EDH is typically an arterial bleed (MMA). Arterial pressure is high, causing blood to accumulate rapidly. This rapid accumulation within the fixed volume of the skull creates a quickly expanding mass effect, leading to a catastrophic rise in Intracranial Pressure (ICP). The lucid interval ends abruptly when the ICP reaches a critical threshold, leading to brainstem compression and subsequent neurological decline.

Question 3: (Management and Prognosis) A patient is diagnosed with a large, symptomatic Epidural Hemorrhage with evidence of significant midline shift on CT (similar to Figure 1). What is the immediate, life-saving definitive management for this patient, and what factor most positively affects their long-term outcome?

(A) Administration of IV mannitol and close monitoring in a general ward.

(B) Emergency intubation and continuous hyperventilation to maintain pCO2 below 20 mmHg.

(C) Initiation of therapeutic hypothermia and anti-seizure medication.

(D) Urgent surgical evacuation via craniotomy; the best prognosis is achieved if the surgery is performed while the patient is still conscious (high GCS).

(E) Lumbar puncture to relieve pressure and antibiotics to prevent infection. 

Answer & Explanation

Answer: (D)

Explanation: Large, symptomatic EDHs are a neurosurgical emergency requiring urgent surgical evacuation (craniotomy or burr holes) to remove the hematoma and decompress the brain. Prognosis is highly dependent on the patient's neurological status at the time of surgery; patients who are operated on while conscious (GCS >= 13) have a significantly better prognosis than those operated on in a comatose state.


References

  1. Bullock, M. R., Chesnut, R., Ghajar, J., Gordon, D., Hartl, R., Newell, D. W., et al. (2006). Guidelines for the management of severe traumatic brain injury. Journal of Neurotrauma, 23(Suppl 1), S1-S86.
  2. Greenberg, M. S. (2020). Handbook of Neurosurgery (9th ed.). Thieme.
  3. Servadei, F., Compagnone, C., & Esente, S. (2018). Traumatic Extradural Hematoma: Management and Surgical Treatment. Acta Neurochirurgica, 160(8), 1693–1697.
  4. Gennarelli, T. A., & Graham, D. I. (2005). Neuropathology of Head Trauma. In D. J. Cooper, & V. D. A. D. V. D. G. N. M. B. V. D. A. D. M. T. P. J. C. K. G. S. (Eds.), Traumatic Brain Injury (pp. 165–186). Oxford University Press.
  5. Ko, T. I., Park, Y. S., Park, S. S., Lim, B. J., Kim, K. B., Kim, K. H., et al. (2022). Epidural Hematoma in Traumatic Brain Injury. Journal of Korean Neurosurgical Society, 65(1), 1-10.
  6. Smith, J. S., & Shiozawa, P. (2023). Epidural Hematoma. StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK518972/
  7. New England Journal of Medicine (NEJM). (2008). Epidural Hemorrhage. N Engl J Med, 358(15), e17.

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