http://emedicine.Medscape.

com/article/1137065

Epidural Hematoma
Author: David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology
Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program,
Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
Contributor Information and Disclosures
Updated: Mar 10, 2009

Introduction

Background
Epidural hematoma (ie, accumulation of blood in the potential space between dura and bone) may
be intracranial (EDH) or spinal (SEDH). Intracranial epidural hematoma occurs in approximately
2% of patients with head injuries and 5-15% of patients with fatal head injuries. Intracranial
epidural hematoma is considered to be the most serious complication of head injury, requiring
immediate diagnosis and surgical intervention. Intracranial epidural hematoma may be acute
(58%), subacute (31%), or chronic (11%). Spinal epidural hematoma may also be traumatic,
though it may occur spontaneously.

This MRI demonstrates spinal epidural hematoma.

Pathophysiology
Epidural hematoma usually results from a brief linear contact force to the calvaria that causes
separation of the periosteal dura from bone and disruption of interposed vessels due to shearing
stress. Skull fractures occur in 85-95% of adult cases, but they are much less common in children
because of the plasticity of the immature calvaria. Arterial or venous structures may be
compromised, causing rapid expansion of the hematoma; however, chronic or delayed
manifestations may occur when venous sources are involved. Extension of the hematoma usually
is limited by suture lines owing to the tight attachment of the dura at these locations. Recent
analyses have revealed that epidural hematomas may actually traverse suture lines in a minority of
cases.1

The temporoparietal region and the middle meningeal artery are involved most commonly (66%),
although the anterior ethmoidal artery may be involved in frontal injuries, the transverse or sigmoid
sinus in occipital injuries, and the superior sagittal sinus in trauma to the vertex. Bilateral epidural
hematomas account for 2-10% of all acute epidural hematomas in adults but are exceedingly rare
in children. Posterior fossa epidural hematomas represent 5% of all cases of epidural hematomas.

Spinal epidural hematoma may be spontaneous or may follow minor trauma, such as lumbar
puncture or epidural anesthesia. Spontaneous spinal epidural hematoma may be associated with
anticoagulation, thrombolysis, blood dyscrasias, coagulopathies, thrombocytopenia, neoplasms, or
vascular malformations. The peridural venous plexus usually is involved, though arterial sources of
hemorrhage also occur. The dorsal aspect of the thoracic or lumbar region is involved most
commonly, with expansion limited to a few vertebral levels.

Frequency
United States

Epidural hematoma complicates 2% of cases of head trauma (approximately 40,000 cases per
year). Spinal epidural hematoma affects 1 per 1,000,000 people annually. Alcohol and other forms
of intoxication have been associated with a higher incidence of epidural hematoma.

International

International frequency is unknown, though it is likely to parallel the frequency in the United States.

Mortality/Morbidity
Mortality rate associated with epidural hematoma has been estimated to be 5-50%.

The level of consciousness prior to surgery has been correlated with mortality rate: 0% for
awake patients, 9% for obtunded patients, and 20% for comatose patients.
Bilateral intracranial epidural hematoma has a mortality rate of 15-20%.
Posterior fossa epidural hematoma has a mortality rate of 26%.

Race
No racial predilection has been reported.

Sex
Intracranial and spinal epidural hematomas are more frequent in men, with a male-to-female ratio
of 4:1.

Age
Intracranial epidural hematoma is rare in individuals younger than 2 years.
Intracranial epidural hematoma is also rare in individuals older than 60 years because the
dura is tightly adherent to the calvaria.
Spinal epidural hematoma has a bimodal distribution with peaks during childhood and
during the fifth and sixth decades of life. Increasing age has been noted as a risk factor for
postoperative spinal epidural hematoma.

Clinical

History
Epidural hematoma should be suspected in any individual who sustains head trauma. Although
classically associated with a lucid interval between the initial loss of consciousness at the time of
impact and a delayed decline in mental status (10-33% of cases), alterations in the level of
consciousness may have a variable presentation. Posterior fossa epidural hematoma may exhibit
a rapid and delayed progression from minimal symptoms to even death within minutes.

Symptoms of epidural hematoma include the following:

o Headache
o Nausea/vomiting
 o Seizures
o Focal neurologic deficits (eg, visual field cuts, aphasia, weakness, numbness)
Spinal epidural hematoma typically causes severe localized back pain with delayed
radicular radiation that may mimic disk herniation. Associated symptoms may include the
following:
o Weakness
o Numbness
o Urinary incontinence
o Fecal incontinence

Physical
The physical examination should include a thorough evaluation for evidence of traumatic
sequelae and associated neurological deficits, including the following:
o Bradycardia and/or hypertension indicative of elevated intracranial pressure
o Skull fractures, hematomas, or lacerations
o Cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with
disruption of the dura
o Hemotympanum
o Instability of the vertebral column
o Alteration in level of consciousness (ie, Glasgow Coma Scale score)
o Anisocoria (eg, ipsilateral dilation of the pupil due to uncal herniation with
compression of the oculomotor nerve)
o Facial nerve injury
o Weakness (eg, contralateral hemiparesis due to compression of the cerebral
peduncle)
o Other focal neurological deficits (eg, aphasia, visual field defects, numbness,
ataxia)
Spinal epidural hematoma may have variable findings on physical examination,
determined by the level of the lesion. The findings include the following:
o Weakness (unilateral or bilateral)
o Sensory deficits with radicular paresthesias (unilateral or bilateral)
o Various alterations in reflexes
o Alterations of bladder or anal sphincter tone

Causes
Trauma
Anticoagulation
Thrombolysis
Lumbar puncture
Epidural anesthesia
Coagulopathy or bleeding diathesis
Hepatic disease with portal hypertension
Cancer
Vascular malformation
Disk herniation
Paget disease of bone
Valsalva maneuver
Hypertension
Chiropractic manipulation2
Differential Diagnoses
Alcohol (Ethanol) Related Neuropathy Intracranial Hemorrhage
Anisocoria Posttraumatic Epilepsy
Ankylosing Spondylitis Spinal Cord Hemorrhage
Cervical Spondylosis: Diagnosis and Management Spinal Epidural Abscess
Foix-Alajouanine Syndrome
Head Injury
Intracranial Epidural Abscess
Other Problems to Be Considered
Back pain
Spinal Cord Disease

Workup

Laboratory Studies
Complete blood count (CBC) with platelets - To monitor for infection and assess
hematocrit and platelets for further hemorrhagic risk.
Prothrombin time (PT)/activated partial thromboplastin time (aPTT) - To identify bleeding
diathesis.
Serum chemistries, including electrolytes, blood urea nitrogen (BUN), creatinine, and
glucose - To characterize metabolic derangements that may complicate clinical course.
Toxicology screen and serum alcohol level - To identify associated causes of head trauma
and establish need for surveillance with regard to withdrawal symptoms.
Type and hold an appropriate amount of blood - To prepare for necessary transfusions
needed because of blood loss or anemia.

Imaging Studies
Plain radiography of the head (skull radiography) may reveal skull fractures, though CT
scanning has largely replaced the use of skull radiography because the diagnostic
information is so much greater with CT. Cervical spine radiographs with anteroposterior,
lateral, and odontoid views are useful to identify associated traumatic fractures. Plain
radiographs of the vertebral column may identify a cavernous angioma.
Myelography outlines the epidural space and may illustrate a space-occupying mass. CT
myelography may be used when MRI is unavailable or if the patient cannot tolerate MRI.
Noncontrast CT scanning of the head not only visualizes skull fractures but also directly
images an epidural hematoma.
o Acute epidural hematoma may appear as a hyperdense lenticular-shaped mass
situated between the brain and the skull, though regions of hypodensity may be
seen with serum or fresh blood. On rare occasion, an acute epidural may appear
completely isointense with respect to brain. Planoconvex or crescent-shaped
epidural hematoma must be differentiated from subdural hemorrhage. Subacute
lesions are homogenously hyperdense.
 o Chronic epidural hematoma may have a heterogeneous appearance due to
neovascularization and granulation, with peripheral enhancement on contrast
administration.
o CT scanning may also depict air collections and displacement of brain
parenchyma.
o Clinical deterioration should prompt repeat imaging with CT scanning.
MRI also demonstrates the evolution of an epidural hematoma, though this imaging
modality may not be appropriate for patients in unstable condition.
o Spinal MRI may delineate the location of an epidural hematoma and identify an
associated vascular malformation.
o Spinal cord enhancement may be apparent and should be distinguished from
inflammation or neoplasia.
o Diffusion-weighted imaging with the use of periodically rotated overlapping
parallel lines with enhanced reconstruction (PROPELLER) MRI may be used for
improved detection of acute spinal epidural hematoma.3
o Gadolinium-enhanced magnetic resonance arteriography (MRA) may further
define the extent of an arteriovenous malformation.
Conventional angiography may be required to demonstrate definitively the presence of a
vascular malformation.

Other Tests
Functional studies of the spinal cord, such as somatosensory evoked potentials, may be used for
intraoperative monitoring or for prognostication following surgery.

Procedures
Emergent decompression with placement of a burr hole may be necessary when
neurosurgical consultation is unavailable. For patients showing rapid deterioration with
clinical signs of impending herniation, place a burr hole on the side of the dilating pupil. In
the absence of a CT scan, place the burr hole 2 finger widths anterior to the tragus of the
ear and 3 finger widths above the tragus of the ear. 4
Lumbar puncture provides little additional information and may exacerbate neurologic
damage.

Treatment

Medical Care
Initial resuscitation efforts should include assessment and stabilization of airway patency,
breathing, and circulation. A thorough trauma evaluation is mandatory, including inspection for skull
fractures and appreciation of the force and location of impact. Immobilization of the spine should
be followed by emergent transfer of the patient to the nearest level I trauma center supported with
neurosurgical consultation.

Triage and initial management of a patient with epidural hematoma may be tailored to the
degree of neurological impairment at presentation. Alert patients may be evaluated with a
CT scan following a brief neurologic examination.
A patient with a small epidural hematoma may be treated conservatively, though close
observation is advised, as delayed, yet sudden, neurological deterioration may occur.
 Trauma patients may require diagnostic peritoneal lavage and radiographs of the chest,
pelvis, and cervical spine.
While neurosurgical consultation is requested, administer intravenous fluids to maintain
euvolemia and to provide adequate cerebral perfusion pressure.
Patients with elevated intracranial pressure may be treated with osmotic diuretics and
hyperventilation, with elevation of the head of the bed at an angle of 30 degrees. Patients
who are intubated may be hyperventilated with intermittent mandatory ventilation at a rate
of 16-20 breaths per minute and tidal volume of 10-12 mL/kg. A carbon dioxide partial
pressure of 28-32 mm Hg is ideal, as severe hypocapnia (<25 mm Hg) may induce
cerebral vasoconstriction and ischemia.
Coagulopathy or persistent bleeding may require administration of vitamin K, protamine
sulfate, fresh frozen plasma, platelet transfusions, or clotting factor concentrates.

Surgical Care
Although several recent reports have described successful conservative management of epidural
hematoma, surgical evacuation constitutes definitive treatment of this condition. Craniotomy or
laminectomy is followed by evacuation of the hematoma, coagulation of bleeding sites, and
inspection of the dura. The dura is then tented to the bone and, occasionally, epidural drains are
employed for as long as 24 hours.

Minimally invasive surgical procedures, including the use of burr holes and negative
pressure drainage, may be used in selected cases.
Novel therapeutic approaches
o Endovascular embolization to minimize bleeding during the acute stage
o Thrombolytic evacuation using closed suction drain

CT scanning performed before and after surgical evacuation of an intracranial

epidural hematoma.

Consultations
Neurosurgeon (for potential emergent evacuation of the hematoma)
Neurologist
Rehabilitation specialist

Diet
The hypermetabolic and catabolic phenomena associated with severe head injury necessitate
caloric supplementation. Initiate enteral feedings as soon as possible.

Activity
Patients who are treated conservatively should undergo close observation and should avoid
strenuous activity. Inpatients should remain on bedrest during the initial phase; this can be
followed by a progressive increase in activity.

Medication
Osmotic diuretics, such as mannitol or hypertonic saline, may be used to diminish intracranial
pressure. As hyperthermia may exacerbate neurological injury, acetaminophen may be given to
reduce fevers. Anticonvulsants are used routinely to avoid seizures that may be induced by cortical
damage. Patients with spinal epidural hematoma may require high-dose methylprednisolone when
spinal cord compression is involved. Immobilized patients may require heparin for prevention of
venous thrombosis, whereas vitamin K and protamine may be administered to restore normal
coagulation parameters. Antacids are used to prevent gastric ulcers associated with traumatic
brain injury and spinal cord damage.

Osmotic diuretics
These agents reverse the pressure gradient across the blood-brain barrier, reducing intracranial
pressure.

Mannitol (Osmitrol, Resectisol)

Reduces cerebral edema by osmotic forces and decreases blood viscosity, resulting in reflex
vasoconstriction and lowering of intracranial pressure.

Adult

0.75-1 g/kg IV, followed by 0.25-0.5 g/kg IV q3-5h to maintain serum hyperosmolarity
(approximately 320 mOsm/L)

Pediatric

Not established; dose is dependent on weight, clinical condition, and laboratory results

These agents are helpful in relieving the fever associated with the condition.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

Reduces fever and maintains normothermia. DOC for pain in patients with documented
hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Adult

650 mg PO/PR q4-6h; not to exceed maximum daily dosage of 4 g

Pediatric

<12 years: 10-15 mg/kg/dose PO/PR q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO/PR q4h; not to exceed 5 doses (2.6 g) in 24 h

These agents reduce frequency of early posttraumatic seizures from 14% to 4%, but they do not
prevent later seizures. If seizures are not experienced for 7-10 d, the drug may be discontinued.

Fosphenytoin (Cerebyx)

Converted to phenytoin, which modulates neuronal voltage-dependent sodium channels.

Adult

15-20 mg/kg IV loading dose, followed by 300 mg IV q24h

 Pediatric

Not established; weight-adjusted dosage similar to that in adults

Anti-inflammatory properties mitigate tissue damage in spinal cord compression.

Methylprednisolone (Adlone, Medrol, Solu-Medrol)

Reduces injury associated with spinal cord compression. Decreases inflammation by suppressing
migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Adult

30 mg/kg IV bolus, followed by 4 mg/kg IV infusion over next 23 h

Pediatric

Administer as in adults

These agents reverse some coagulopathies or bleeding diatheses.

Phytonadione; vitamin K (AquaMEPHYTON, Konakion, Mephyton)

Promotes hepatic synthesis of clotting factors that inhibit warfarin effects.

Adult

2.5-10 mg IM/SC; repeat administration q6-8h until PT normalized

Pediatric

Not established; suggested dose is as in adults

Protamine sulfate

Neutralizes effects of heparin.

Adult

Dosage adjusted to time interval since discontinuation of IV heparin

Immediately: 1-1.5 mg/100 U heparin
30-60 min from discontinuation of heparin: 0.5-0.75 mg/100 U heparin
>60 min from discontinuation of heparin: 0.25-0.375 mg/100 U heparin
If SC heparin used, give 1-1.5 mg/100 U heparin; not to exceed 50 mg IV over 10 min

Pediatric

Not established; suggested dose is as in adults

These agents provide prophylaxis of gastric ulcers.

Famotidine (Pepcid)
 Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric
acid secretion, gastric volume, and hydrogen concentrations. Minimizes development of gastric
ulcers.

Adult

20 mg IV/PO bid

Pediatric

Not established; suggested dose is as in adults

Dosing
Interactions
Contraindications
Precautions
Dosing
Interactions
Contraindications
Precautions
Dosing
Interactions
Contraindications
Precautions
Anticoagulants
These agents reduce risk of venous complications in immobilized patients.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not
actively lyse but is able to inhibit further thrombogenesis. Prevents re-accumulation of clot after
spontaneous fibrinolysis. Used for prophylaxis of deep venous thrombosis.

Adult

5000 U SC bid

Pediatric

Follow-up

Further Inpatient Care

Following initial management in the emergency department, the patient may be sent for emergent
neurosurgical evacuation of the hematoma or may be transferred to the ICU for further care.
Subsequent care generally includes the following:

Serial neurologic examinations

Treatment of elevated intracranial pressure
Avoidance of hypotension or hypertension (ie, maintain mean arterial pressure [MAP]
between 70-130 mm Hg)
Use of isotonic solutions, such as normal saline, to minimize cerebral edema
Avoidance of hyperthermia
 Treatment or prevention of posttraumatic seizures
Observation and potential repair of CSF leaks
Treatment of urinary tract infections
Prevention of venous thrombosis
Prophylaxis for gastric ulcers
Physical, occupational, and speech therapy
Repeat CT scan for clinical deterioration

Further Outpatient Care

After hospital discharge, continued physical, occupational, and speech therapy may be required.

Inpatient & Outpatient Medications

Mannitol or other osmotic diuretics for elevated intracranial pressure
Steroids for spinal cord compression
Acetaminophen for fever
Subcutaneous heparin for prevention of venous complications
Famotidine or other antacids for gastric ulcer prophylaxis
Fosphenytoin or other anticonvulsants for posttraumatic seizures
Anticholinergics for bladder complications
Baclofen, diazepam, or tizanidine for spasticity due to spinal cord damage
Amitriptyline, carbamazepine, or gabapentin for neuropathic pain

Transfer
Although emergent decompression of an epidural hematoma should not be delayed, trauma
patients should be transferred to centers with neurosurgical expertise.

Deterrence/Prevention
Educate the public regarding traumatic brain injury, including appropriate use of safety
equipment, precautions, and measures that may reduce the incidence of head injury.
Avoid lumbar puncture or epidural anesthesia in individuals on anticoagulation, following
thrombolysis, or when a bleeding diathesis is suspected.

Complications
Neurological deficits or death may occur.
Posttraumatic seizures due to cortical damage may develop 1-3 months after the initial
injury, with decreasing frequency over time. Alcoholism increases the risk of posttraumatic
seizures.
Delayed effects of an epidural hematoma include the postconcussion syndrome, which is
characterized by headaches, dizziness, vertigo, restlessness, emotional lability, inability to
concentrate, and fatigue.
Spinal epidural hematoma may cause spasticity, neuropathic pain, and urinary
complications.

Prognosis
Declines with advancing age
Deteriorates when associated with other intracranial injuries
Depends on the initial Glasgow Coma Scale score (0% mortality for awake patients, 40%
mortality for comatose individuals)
Worsens with delays between injury and surgical intervention
 In spinal epidural hematoma, the MRI appearance of T2-hyperintensity within the spinal
cord may portend a poor clinical outcome.5

Patient Education
Educate patients regarding prevention of traumatic brain injury, with particular emphasis on sports
injuries, use of safety precautions, and proper use of safety equipment.

Miscellaneous

Medicolegal Pitfalls
Consider epidural hematoma in all patients who have experienced head injury.
Alteration in the level of consciousness may be highly variable and unreliable as a clinical
predictor.
Obtain CT scan whenever possible.
Skull fractures are not always present, particularly in children.
Delayed transfer and triage may be the principal determinant of death.
Close observation requires frequent neurologic evaluations.