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You are in:eMedicine Specialties >Emergency Medicine >Trauma AndOrthopedics

Epidural Hematoma

Last Updated:March 8, 2006

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Synonyms and related keywords:EDH, head injury, blunt trauma,hemorrhage, extradural hemorrhage, blood between the skull anddura mater, epidural hematoma

AUTHOR INFORMATIONSection 1 of 11

Author InformationIntroductionClinicalDifferentialsWorkupTreatmentMedicationFollow-upMiscellaneousPicturesBibliography

Author:Daniel D Price, MD,Director, EmergencyUltrasound Fellowship, Attending Faculty, Department ofEmergency Medicine,Alameda County Medical Center -Highland Campus

Coauthor(s):Sharon R Wilson, MD,Assistant Professorof Emergency Medicine, Department of EmergencyMedicine,University of California at Davis Medical Center

Daniel D Price, MD, is a member of the following medicalsocieties:American College of Emergency Physicians,andSociety for Academic Emergency Medicine

Editor(s): Robert M McNamara, MD, FAAEM, Professorof Emergency Medicine, Temple University; Chief,Department of Internal Medicine, Section of EmergencyMedicine, Temple University Hospital; Francisco Talavera,PharmD, PhD, Senior Pharmacy Editor, eMedicine; EricLegome, MD, Assistant Professor of Emergency Medicine,New York University Medical School; Consulting Staff,

Department of Emergency Medicine, Bellevue Hospital

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Center, New York University Hospital, Manhattan VAHospital; John Halamka, MD, Chief Information Officer,CareGroup Healthcare System, Assistant Professor ofMedicine, Department of Emergency Medicine, BethIsrael Deaconess Medical Center; Assistant Professor ofMedicine, Harvard Medical School; and Rick Kulkarni,MD, Assistant Professor of Medicine, David Geffen UCLASchool of Medicine; Director of Informatics, Department ofEmergency Medicine, UCLA/Olive View-UCLA MedicalCenter

Disclosure

INTRODUCTION Section 2 of 11


Background: Epidural hematoma (EDH) is a traumaticaccumulation of blood between the inner table of the skull

and the stripped-off dural membrane. The inciting eventoften is a focused blow to the head, such as that producedby a hammer or baseball bat. In 85-95% of patients, thistype of trauma results in an overlying fracture of the skull.Blood vessels in close proximity to the fracture are thesources of the hemorrhage in the formation of an EDH.Because the underlying brain has usually been minimallyinjured, prognosis is excellent if treated aggressively.Outcome from surgical decompression and repair isrelated directly to patient's preoperative neurologiccondition.

Pathophysiology:Approximately 70-80% of EDHs arelocated in the temporoparietal region where skull fracturescross the path of the middle meningeal artery or its duralbranches. Frontal and occipital EDHs each constituteabout 10%, with the latter occasionally extending aboveand below the tentorium. Association of hematoma andskull fracture is less common in young children because ofcalvarial plasticity.

EDHs are usually arterial in origin but result from venous
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bleeding in one third of patients. Occasionally, torn venoussinuses cause EDH, particularly in the parietal-occipitalregion or posterior fossa. These injuries tend to be smallerand associated with a more benign course. Usually,venous EDHs only form with a depressed skull fracture,which strips the dura from the bone and, thus, creates aspace for blood to accumulate. In certain patients,especially those with delayed presentations, venous EDHsare treated nonsurgically.

Expanding high-volume EDHs can produce a midline shiftand subfalcine herniation of the brain. Compressedcerebral tissue can impinge on the third cranial nerve,resulting in ipsilateral pupillary dilation and contralateral

hemiparesis or extensor motor response.

EDHs are usually stable, attaining maximum size withinminutes of injury; however, Borovich demonstratedprogression of EDH in 9% of patients during the first 24hours. Rebleeding or continuous oozing presumablycauses this progression. An EDH can occasionally run amore chronic course and is detected only days after injury.

Frequency:

In the US: EDH occurs in 1-2% of all head traumacases and in about 10% of patients who presentwith traumatic coma.

Mortality/Morbidity:

Reported mortality rates range from 5-43%.

Higher rates are associated with the following:o Advanced ageo Intradural lesionso Temporal locationo Increased hematoma volumeo Rapid clinical progressiono Pupillary abnormalitieso Increased intracranial pressure (ICP)o Lower Glasgow coma scale (GCS)

Mortality rates are essentially nil for patients not incoma preoperatively and approximately 10% forobtunded patients and 20% for patients in deepcoma.


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Age:

Patients younger than 5 years and older than 55years have an increased mortality rate.

Patients younger than 20 years account for 60% ofEDHs.

EDH is uncommon in elderly patients because thedura is strongly adhered to the inner table of theskull. In case series of EDH, fewer than 10% ofpatients are older than 50 years.

CLINICAL Section 3 of 11


History:

Fewer than 20% of patients demonstrate the classic

presentation of a lucid interval between the initialtrauma and subsequent neurological deterioration.

Following injury, the patient may or may not loseconsciousness. If he or she becomes unconscious,the patient may awaken or remain unconscious.

Severe headache

Vomiting

Seizure

Patients with posterior fossa EDH may have adramatic delayed deterioration. The patient can beconscious and talking and a minute later apneic,comatose, and minutes from death.

Physical:

Cushing response, consisting of the following, canindicate increased ICP:
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o Hypertension

o Bradycardia

o Bradypnea

Level of consciousness may be decreased, withdecreased or fluctuating GCS.

Contusion, laceration, or bony step-off may beobserved in the area of injury.

Dilated, sluggish, or fixed pupil(s), bilateral oripsilateral to injury, suggest increased ICP or

herniation.

Classic triad indicating transtentorial herniationconsists of the following:

o Coma

o Fixed and dilated pupil(s)

o Decerebrate posturing

Hemiplegia contralateral to injury with herniationmay be observed.

Causes:

EDH results from traumatic head injury, usually withan associated skull fracture and arterial laceration.

DIFFERENTIALSSection 4 of 11


Subarachnoid HemorrhageSubdural Hematoma

Other Problems to be Considered:

Cerebral contusionDiffuse axonal injury
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WORKUP Section 5 of 11


Lab Studies:

Perform appropriate laboratory work for associated trauma.

Coagulation abnormalities are a marker of severe head injury.Breakdown of the blood-brain barrier with exposed brain tissue is apotent cause of disseminated intravascular coagulation (DIC).

Imaging Studies:

Head CT scan

o Immediate unenhanced CT scan is the procedure of choicefor diagnosis.

o Head CT scan shows location, volume, effect, and otherpotential intracranial injuries.

o EDH forms an extraaxial, smoothly marginated, lenticular, orbiconvex homogenous density.

o EDH rarely crosses the suture line because the dura isattached more firmly to the skull at sutures.

o Focal isodense or hypodense zones within EDH indicateactive bleeding.

o Irregular hypodense swirling indicates active bleeding in themajority of patients.

o Air in acute EDH suggests fracture of sinuses or mastoid aircells.

o At surgery or autopsy, 20% of patients have blood in bothepidural and subdural spaces.

Other Tests:

Cervical spine evaluation usually is necessary because of the riskof neck injury associated with EDH.
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Procedures:

Perform burr hole(s) if the following occur:

o Patient is herniating

o All other treatments prove insufficient

o Neurosurgery is unavailable for urgent consultation

o Trephination (or placement of a Burr hole) should ideally beperformed if possible by the consulting neurosurgeon at thereceiving trauma center

o Air or ground medical transport is prolonged

Burr hole procedure includes the following:

o Drill hole adjacent to, but not over, skull fracture or in thearea located by CT scan.

o In the absence of CT scan, place a burr hole on the side ofthe dilated pupil, 2 finger widths anterior to tragus of ear and3 finger widths above.

TREATMENT Section 6 of 11


Prehospital Care:

Stabilize acute life-threatening conditions and initiate supportivetherapy. Airway control and blood pressure support are the mostimportant issues.

Establish IV access, administer oxygen, and monitor.

Administer IV crystalloids to maintain adequate blood pressure.

Intubation, sedation, and neuromuscular blockade per protocol.

o There is some suggestion of increased mortality withprehospital intubation in retrospective reviews of traumapatients with moderate-to-severe head injury compared withpatients intubated in the ED.

o Bag-valve-mask ventilation with good technique may be of

more benefit to brain injured patients than prehospital


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intubation.

Emergency Department Care:

Establish IV access, administer oxygen, monitor, and administer IVcrystalloids as necessary to maintain adequate blood pressure.

Intubate using rapid sequence induction (RSI), which generallyincludes premedication with lidocaine, a cerebroprotective sedatingagent (eg, etomidate), and a neuromuscular blocking agent.Lidocaine may have limited effect in this situation, yet it carriesvirtually no risk. Premedication with fentanyl may also help blunt arise in ICP. Intubate after a basic neurologic examination tofacilitate oxygenation, protect the airway, and allow forhyperventilation as needed.

Elevate head of the bed 30 after the spine is cleared, or usereverse Trendelenburg position to reduce ICP and increase venousdrainage.

Administer mannitol 0.25-1 g/kg IV after consulting a neurosurgeonif MAP is greater than 90 mm Hg with continued clinical signs ofincreased ICP. This reduces both ICP (by osmotically reducingbrain edema) and blood viscosity, which increases cerebral bloodflow and oxygen delivery. Fluids must be replaced and hypovolemia

avoided.

Hyperventilation to partial pressure of carbon dioxide (PCO2) of 30-35 mm Hg treats incipient herniation or signs of increasing ICP;however, this is controversial. Be careful not to lower PCO2too far(


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MEDICATION Section 7 of 11


Use RSI when intubating to minimize rises in ICP and catecholaminerelease. Etomidate, when used as RSI sedating agent, maintains bloodpressure, lowers ICP and brain metabolism, and has rapid onset and briefduration. Thiopental is not recommended because of its predictable effectin lowering blood pressure, the leading cause of secondary brain injury.Mannitol osmotically reduces ICP and improves blood flow. Phenytoinprovides prophylaxis against early posttraumatic seizure. Once the patienthas received adequate fluids, pressors such as norepinephrine can be

used to maintain MAP >90 mm Hg.

Drug Category: Osmotic diuretic-- Osmotically reduces brain edemaand ICP and reduces blood viscosity, improving cerebral blood flow andoxygen delivery. Prior to ICP monitoring, use only for signs of herniation orprogressive neurological deterioration. Hypovolemia should be avoided byreplacing fluids (urine monitoring with placement of a bladder catheter isessential). Intermittent boluses may be more effective than continuousinfusion.

Drug NameMannitol (Osmitrol) -- Keeps serum osmolality


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to avoid pseudoagglutination; do not administerelectrolyte-free mannitol solutions with blood

Drug Category:Antiepileptic-- Prevents early posttraumatic seizure,which can increase ICP and neurotransmitter release as well as alterblood pressure and oxygen delivery.

Drug Name

Phenytoin (Dilantin) -- DOC for seizureprophylaxis. Fosphenytoin allows more rapidinfusion and fewer side effects. If activelyseizing, coadminister benzodiazepine.

Adult Dose17 mg/kg IV; mix in NS (precipitates in D5W);infuse no faster than 50 mg/min

Pediatric Dose Administer by weight as in adults

Contraindications

Documented hypersensitivity; because ofeffects on ventricular automaticity, do not use insinoatrial block, sinus bradycardia, second- andthird-degree AV block, or in patients withAdams-Stokes syndrome

Interactions

Increased toxicity with amiodarone,benzodiazepines, chloramphenicol, cimetidine,fluconazole, isoniazid, metronidazole,miconazole, phenylbutazone, succinimides,

sulfonamides, omeprazole, phenacemide,disulfiram, ethanol (acute ingestion),trimethoprim, valproic acid; effects maydecrease when taken concurrently withbarbiturates, diazoxide, ethanol (chronicingestion), rifampin, antacids, charcoal,carbamazepine, theophylline, sucralfate; maydecrease effects of acetaminophen,corticosteroids, dicumarol, disopyramide,doxycycline, estrogens, haloperidol,amiodarone, carbamazepine, cardiac

glycosides, quinidine, theophylline, methadone,metyrapone, mexiletine, oral contraceptives,valproic acid

Pregnancy D - Unsafe in pregnancy

Precautions

Administer slowly (50 mg/min) to avoidhypotension; avoid extravasation; perform bloodcounts and urinalyses when initiating therapyand at monthly intervals for several mo tomonitor for blood dyscrasias; discontinue use ifskin rash appears and do not resume use if rash


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is exfoliative, bullous, or purpuric; after too-rapidIV administrations death from cardiac arrestmay occur, which is sometimes preceded bymarked QRS widening; administer cautiously topatients with acute intermittent porphyria;exercise caution with diabetes, as it may raiseblood sugar levels; discontinue drug if hepaticdysfunction occurs

FOLLOW-UP Section 8 of 11


Further Inpatient Care:

Transfer to operating room (OR) for EDH evacuation and repair.

Admit to neurosurgical ICU after surgery or directly for monitoring.This will likely include ICP, partial pressure oxygen (PO2), or otherintracranial monitoring devices.

Repeat CT scan in the event of clinical deterioration.

Transfer:

Transfer to hospital with a CT scanner and neurosurgeon.

Consider air transport if a trauma center is distant; timelydecompression is critical for a good outcome.

Deterrence/Prevention:

Encourage use of seat belts and car seats.

Advocate helmets for bicycling, skateboarding, snowboarding,rollerblading, and horse and motorcycle riding.

Complications:

Neurobehavioral changes: Postconcussive syndrome can lasthours to months (seePostconcussive Syndrome).

Vegetative state

Death

Prognosis:
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Mortality rates are essentially nil for patients not in comapreoperatively and approximately 10% for obtunded patients and20% for patients in deep coma.

If treated early, prognosis usually is excellent, because theunderlying brain injury generally is limited.

MISCELLANEOUS Section 9 of 11


Medical/Legal Pitfalls:

Failure to consider diagnosis, especially in a conscious patient with

normal pupils

Failure to transfer expeditiously to a trauma center with aneurosurgeon (air medical transport may be warranted)

Failure to diagnose EDH in a patient with altered mental status(instead naming alcohol or another intoxicant as the cause)

Failure to perform frequent routine neurologic checks in patientswho are being observed rather than sent for CT scan

Special Concerns:

Pediatric patients

o Pediatric patients may not fracture the skull.

o Pediatric patients have lower mortality rates, except ininfants.

o Guidelines for managing pediatric traumatic brain injury were

published in 2003. They reflect adult guidelines with theexceptions of age-appropriate blood pressures and cerebralperfusion pressure, and endorsement of the use ofhypertonic saline for control of increased ICP.

Geriatric patients

o EDH is more likely to occur with a fall.

o Overall, EDH is much less common in older patients.

o Subdural hematoma (SDH) is more common than EDH in


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elderly patients with intracranial hematoma. Brain atrophystretches bridging veins.

o Elderly patients have higher mortality rates.

PICTURES Section 10 of 11


Caption:Picture 1. Right temporal epidural hematoma with midline shift. Pshould be taken immediately to the operating room for neurosurgery. Thisrequire emergent transport to a trauma center or other facility with a neuroavailable.

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Picture Type:CT

Caption:Picture 2. Brain CT scan of 90-year-old man who slipped on a waWitnesses reported loss of consciousness followed by a "lucid interval." Paarrived to ED unconscious. CT scan indicates epidural hematoma. Imageof Dr Dana Stearns, Massachusetts General Hospital.

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BIBLIOGRAPHY Section 11 of 11


Adelson PD, Bratton SL, Carney NA, et al: Guidelines for the acute
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NOTE:

Medicine is a constantly changing science and not all therapies are clearly established. New research changes drugand treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to

provide information that is up-to-date and accurate and is generally accepted within medical standards at the time ofpublication. However, as medical science is constantly changing and human error is always possible, the authors,editors, and publisher or any other party involved with the publication of this article do not warrant the information inthis article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results ofusing this information. The reader should confirm the information in this article from other sources prior to use. Inparticular, all drug doses, indications, and contraindications should be confirmed in the package insert.FULLDISCLAIMER

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Hematoma Epidural.docx