Epidural Hematoma Management in the ED
Updated: Dec 10, 2021
Author: Daniel D Price, MD; Chief Editor: Trevor John Mills, MD, MPH
Overview
Practice Essentials
Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull and the stripped-off dural membrane. EDH results from traumatic head injury, usually with associated skull fracture and arterial laceration. This is a life-threatening condition that may require immediate intervention and can be associated with significant morbidity and mortality if left untreated.[1] Injuries suffered while participating in extreme sports account for numerous emergency department visits for EDH.[2] The inciting event often is a focused blow to the head, such as that produced by a hammer or a baseball bat. In 85-95% of patients, this type of trauma results in an overlying fracture of the skull. Blood vessels in close proximity to the fracture are the sources of hemorrhage in the formation of an epidural hematoma. Because the underlying brain has usually been minimally injured, prognosis is excellent if treated aggressively. Outcome from surgical decompression and repair is related directly to the patient's preoperative neurologic condition.[3, 4]
In a study of 41 patients with epidural hematoma at a level I trauma center, patient age, severity of traumatic brain injury, and neurologic status were the main factors influencing outcome. Two patients died within 24 hours, and 39 patients (95%) survived. Thirty-two patients (78%) showed good recovery at latest follow-up.[5]
In cases of rare bilateral extradural hematoma (0.5-10%), higher mortality has been reported. Approach to treatment depends on the volume of blood, the time of diagnosis, and the neurologic deficit level. Simultaneous drainage of bilateral hematomas has been demonstrated to be an effective technique.[6, 7] Consult a neurosurgeon immediately for EDH evacuation and repair. Consult a trauma surgeon for other life-threatening injuries.
The outcome for EDH is more favorable than decades ago, most probably reflecting a well-established chain of trauma care.[8] However, study results show that morbidity and mortality after EDH evacuation remain relatively high (with 14% remaining disabled and 6% dying).[9] Rapid diagnosis and evacuation are important for a good outcome.[10]
Complications include neurobehavioral changes (postconcussive syndrome can last hours to months; see Postconcussive Syndrome), vegetative state, and death.
Mortality rates are essentially nil for patients not in coma preoperatively and are approximately 10% for obtunded patients and 20% for patients in deep coma.
(See the images below.)
Right temporal epidural hematoma with midline shift. Patient should be taken immediately to the operating room for neurosurgery. This may require emergent transport to a trauma center or other facility with a neurosurgeon available.
Brain CT scan of 90-year-old man who slipped on a waxed floor. Witnesses reported loss of consciousness followed by a "lucid interval." Patient arrived to ED unconscious. CT scan indicates epidural hematoma. Image courtesy of Dr Dana Stearns, Massachusetts General Hospital.
Pathophysiology
Epidural hematoma is most often caused by rupture of the middle meningeal artery secondary to head trauma with fracture of the temporal bone. It is a potentially fatal condition that can lead to elevated intracranial pressure, herniation, and death within hours following the inciting traumatic incident, unless surgical evacuation is accomplished.[11]
Approximately 70-80% of epidural hematomas (EDHs) are located in the temporoparietal region, where skull fractures cross the path of the middle meningeal artery or its dural branches. Frontal and occipital epidural hematomas each constitute about 10%, with the latter occasionally extending above and below the tentorium. Association of hematoma and skull fracture is less common in young children because of calvarial plasticity.
Epidural hematomas are usually arterial in origin but result from venous bleeding in one third of patients. Occasionally, torn venous sinuses cause an epidural hematoma, particularly in the parietal-occipital region or the posterior fossa. These injuries tend to be smaller and associated with a more benign course. Usually, venous epidural hematoma forms only with a depressed skull fracture, which strips the dura from the bone and thus creates a space for blood to accumulate. For certain patients, especially those with delayed presentation, venous EDH is treated nonsurgically.
Expanding high-volume EDH can produce a midline shift and subfalcine herniation of the brain. Compressed cerebral tissue can impinge on the third cranial nerve, resulting in ipsilateral pupillary dilation and contralateral hemiparesis or extensor motor response.
Epidural hematomas are usually stable, attaining maximum size within minutes of injury; however, Borovich et al demonstrated progression of epidural hematoma in 9% of patients during the first 24 hours.[12] Rebleeding or continuous oozing presumably causes this progression. An epidural hematoma can occasionally run a more chronic course that is only detected days after injury.
Epidemiology
Epidural hematoma occurs in 1-2% of all head trauma cases and in about 10% of patients who present with traumatic coma. Reported mortality rates range from 5-43%. Higher rates are associated with the following:
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Advanced age
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Intradural lesions
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Temporal location
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Increased hematoma volume
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Rapid clinical progression
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Pupillary abnormalities
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Increased intracranial pressure (ICP)
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Lower Glasgow coma scale score (GCS; see the Glasgow Coma Scale calculator)
Patients younger than 5 years and older than 55 years have increased mortality. Patients younger than 20 years account for 60% of EDHs. EDH is uncommon in elderly patients because the dura is strongly adhered to the inner table of the skull. In case series of EDH, fewer than 10% of patients are older than 50 years. Study results suggest that combined treatments (endovascular embolization + drainage surgery + use of urokinase) can provide an alternative minimally invasive option for acute traumatic EDH, especially for elderly patients or for those with contraindications for general anesthesia.[13]
Presentation
History
Fewer than 20% of patients demonstrate the classic presentation of a lucid interval between the initial trauma and subsequent neurologic deterioration. Following injury, the patient may or may not lose consciousness. If he or she becomes unconscious, the patient may awaken or remain unconscious. Other symptoms include severe headache, vomiting, and seizure.
Patients with posterior fossa epidural hematoma (EDH) may have a dramatic delayed deterioration. The patient can be conscious and talking and a minute later can be apneic, comatose, and minutes from death. It is imperative that neurosurgeons closely monitor the patient’s state of consciousness, as a rapid decline serves as a key diagnostic indicator of the need for immediate surgery.[14]
(See the image below.
Brain CT scan of 90-year-old man who slipped on a waxed floor. Witnesses reported loss of consciousness followed by a "lucid interval." Patient arrived to ED unconscious. CT scan indicates epidural hematoma. Image courtesy of Dr Dana Stearns, Massachusetts General Hospital.
Physical
Cushing response, consisting of hypertension, bradycardia, and bradypnea, can indicate increased ICP. Level of consciousness may be decreased, with decreased or fluctuating GCS. Contusion, laceration, or bony step-off may be observed in the area of injury. Dilated, sluggish, or fixed pupil(s), bilateral or ipsilateral to injury, suggest increased ICP or herniation.
The classic triad indicating transtentorial herniation consists of the following:
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Coma
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Fixed and dilated pupil(s)
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Decerebrate posturing
Hemiplegia contralateral to injury with herniation may be observed.
DDx
Differential Diagnoses
Workup
Imaging Studies
Head CT scan
Immediate unenhanced CT scan is the procedure of choice for diagnosis. Head CT scan shows location, volume, effect, and other potential intracranial injuries. Epidural hematoma (EDH) forms an extra-axial, smoothly marginated, lenticular, or biconvex homogeneous density.
EDH rarely crosses the suture line because the dura is attached more firmly to the skull at sutures. Focal isodense or hypodense zones within EDH indicate active bleeding. Irregular hypodense swirling indicates active bleeding in the majority of patients. Air in acute EDH suggests fracture of sinuses or mastoid air cells. At surgery or autopsy, 20% of patients have blood in both epidural and subdural spaces.
A retrospective study of pediatric patients with diagnosed traumatic EDH was performed to evaluate CT imaging findings in patients whose condition was managed with observation alone versus surgical evacuation. Forty-seven cases of EDH were analyzed, and 62% were managed by observation alone. Mean initial EDH thickness and volume were 8.0 mm and 8.6 ml in the observed group and 15.5 mm and 35 ml in the surgery group. Repeat CT imaging was performed in 86% of observed patients and in all surgery patients. Repeat CT scan results led to surgery in only 1 patient, who was initially treated with observation.[15]
Computed tomography angiography (CTA) was able to identify middle meningeal artery (MMA) vascular lesions in patients with EDH. Of 11 patients with small acute EDH, 3 were diagnosed with MMA pseudoaneurysm, and CTA was able to diagnose all 3, with dimensions ranging from 1.5-2.8 mm. Conventional angiography confirmed the findings of CTA.[16]
Guidelines regarding the role of repeat head CT imaging in the nonoperative management of traumatic EDH do not exist. Consequently, some children and others may be exposed to unnecessary additional ionizing radiation. Reimaging rarely changes management. Limiting reimaging to patients with neurologic findings of concern or with mass effect on initial evaluation could reduce imaging by more than 50%.[17]
Other Tests
Cervical spine evaluation usually is necessary because of the risk of neck injury associated with EDH.
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 a potent cause of disseminated intravascular coagulation (DIC).
Procedures
Perform burr hole(s) if the following occur:
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Patient is herniating
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All other treatments prove insufficient
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Neurosurgery is unavailable for urgent consultation
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Air or ground medical transport is prolonged
Burr hole procedure includes the following:
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Drill hole adjacent to, but not over, skull fracture or in the area located by CT scan
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In the absence of CT scan, place a burr hole on the side of the dilated pupil, 2 finger widths anterior to the tragus of the ear and 3 finger widths above
Trephination (or placement of a Burr hole) should ideally be performed if possible by the consulting neurosurgeon at the receiving trauma center[16] .
Treatment
Prehospital Care
Stabilize acute life-threatening conditions and initiate supportive therapy. Airway control and blood pressure support are the most important issues.
Establish IV access, administer oxygen, and monitor.
Administer IV crystalloids to maintain adequate blood pressure.
Perform intubation, sedation, and neuromuscular blockade per protocol. There is some suggestion of increased mortality with prehospital intubation in retrospective reviews of trauma patients with moderate-to-severe head injury compared to patients intubated in the ED. Bag-valve-mask ventilation with good technique may be of greater benefit than prehospital intubation for brain-injured patients.
Consult a neurosurgeon immediately for EDH evacuation and repair.
Consult a trauma surgeon for other life-threatening injuries.
Emergency Department Care
Establish IV access, administer oxygen, monitor, and administer IV crystalloids as necessary to maintain adequate blood pressure.
Intubate using rapid sequence induction (RSI), which generally includes premedication with lidocaine, a cerebroprotective sedating agent (eg, etomidate), and a neuromuscular blocking agent. Lidocaine may have limited effect in this situation, yet it carries virtually no risk. Premedication with fentanyl may also help blunt a rise in ICP. Intubate after a basic neurologic examination to facilitate oxygenation, protect the airway, and allow for hyperventilation as needed.
Elevate the head of the bed 30° after the spine is cleared, or use the reverse Trendelenburg position to reduce ICP and increase venous drainage.
Administer mannitol 0.25-1 g/kg IV after consulting a neurosurgeon if MAP is greater than 90 mm Hg with continued clinical signs of increased ICP. This reduces both ICP (by osmotically reducing brain edema) and blood viscosity, which increases cerebral blood flow 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 PCO2 too far (< 25 mm Hg). Perform hyperventilation if there are clinical signs of increased ICP progress and patients are refractory to sedation, paralysis, osmotic diuretics, and, if possible, CSF drainage. This procedure reduces ICP by hypocarbic vasoconstriction and reduces risks of hypoperfusion and death of injured cells.
Phenytoin reduces the incidence of early posttraumatic seizures, although it does not affect late-onset seizures or the development of a persistent seizure disorder.
In a small case series, ED skull trephination before transfer of patients with CT-proven epidural hematoma (EDH) and anisocoria resulted in uniformly good outcomes without complications.[18] Time to relief of intracranial pressure was significantly shorter with trephination than without.
Several treatment guidelines on various aspects of traumatic brain injury are available from the Brain Trauma Foundation.[19, 20, 21, 22, 23, 24, 25, 26]
Transfer to operating room (OR) for epidural hematoma (EDH) evacuation and repair.
Transfer to hospital with a CT scanner and a neurosurgeon.
Consider air transport if a trauma center is distant; timely decompression is critical for a good outcome.
Admit to the neurosurgical ICU after surgery or directly for monitoring. This will likely include ICP, partial pressure of oxygen (PO2), or other intracranial monitoring devices.
Medication
Medication Summary
Use rapid sequence induction (RSI) when intubating to minimize increases in ICP and catecholamine release. Etomidate, when used as an RSI sedating agent, maintains blood pressure, lowers ICP and brain metabolism, and has rapid onset and brief duration. Thiopental is not recommended because of its predictable effect in lowering blood pressure (elevated blood pressure is the leading cause of secondary brain injury). Mannitol osmotically reduces ICP and improves blood flow. Phenytoin provides prophylaxis against early posttraumatic seizure. Once the patient has received adequate fluids, pressors such as norepinephrine can be used to maintain MAP > 90 mm Hg.
Osmotic diuretic
Class Summary
Osmotically reduces brain edema and ICP and reduces blood viscosity, improving cerebral blood flow and oxygen delivery. Prior to ICP monitoring, use only for signs of herniation or progressive neurological deterioration. Hypovolemia should be avoided by replacing fluids (urine monitoring with placement of a bladder catheter is essential). Intermittent boluses may be more effective than continuous infusion.
Mannitol (Osmitrol)
Keeps serum osmolality < 320 mOsm to prevent renal failure. Maintain euvolemia with adequate IV fluid replacement. Foley catheter is essential.
Antiepileptic
Class Summary
Prevents early posttraumatic seizure, which can increase ICP and neurotransmitter release as well as alter blood pressure and oxygen delivery.
Phenytoin (Dilantin)
DOC for seizure prophylaxis. Fosphenytoin allows more rapid infusion and fewer side effects. If actively seizing, coadminister benzodiazepine.