Extradural hematoma and its management

By Dr. Arshad Ullah Khan, Karachi

Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull and the stripped-off dural membrane. The inciting event often is a focused blow to the head, such as that produced by a hammer or 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 the 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 patient’s preoperative neurologic condition.

PATHOPHYSIOLOGY

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 posterior fossa. These injuries tend to be smaller and associated with a more benign course. Usually, venous epidural hematomas only form with a depressed skull fracture, which strips the dura from the bone and, thus, creates a space for blood to accumulate. In certain patients, especially those with delayed presentations, venous epidural hematomas are treated nonsurgically.

Expanding high-volume epidural hematomas 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. Rebleeding or continuous oozing presumably causes this progression. An epidural hematoma can occasionally run a more chronic course and is detected only days after injury.

FREQUENCY

United States

Epidural hematoma occurs in 1-2% of all head trauma cases and in about 10% of patients who present with traumatic coma.

MORTALITY/MORBIDITY

• Reported mortality rates range from 5-43%.
• Higher rates are associated with the following:
  • Advanced age
  • Intradural lesions
  • Temporal location
  • Increased hematoma volume
  • Rapid clinical progression
  • Pupillary abnormalities
  • Increased intracranial pressure (ICP)
  • Lower Glasgow coma scale (GCS)

• Mortality rates are essentially nil for patients not in coma preoperatively and approximately 10% for obtunded patients and 20% for patients in deep coma.

AGE

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

CLINICAL HISTORY

• Fewer than 20% of patients demonstrate the classic presentation of a lucid interval between the initial trauma and subsequent neurological deterioration.
• 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.
• Following injury, the patient may or may not lose consciousness. If he or she becomes unconscious, the patient may awaken or remain unconscious.
• Severe headache
• Vomiting
• 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 apneic, comatose, and minutes from death.

PHYSICAL

• Cushing response, consisting of the following, can indicate increased ICP:
  • Hypertension
  • Bradycardia
  • Bradypnea
• 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.
• Classic triad indicating transtentorial herniation consists of the following:
  • Coma
  • Fixed and dilated pupil(s)
  • Decerebrate posturing

•  
  • Hemiplegia contralateral to injury with herniation may be observed.

Causes

•  
  • Epidural hematoma (EDH) results from traumatic head injury, usually with an associated skull fracture and arterial laceration.

DIFFERENTIAL DIAGNOSES

Subarachnoid Hemorrhage
Subdural Hematoma

Other Problems to Be Considered

Cerebral contusion
Diffuse axonal injury

WORKUP

Laboratory 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 a potent cause of disseminated intravascular coagulation (DIC).

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 extraaxial, smoothly marginated, lenticular, or biconvex homogenous 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.

Other Tests

• Cervical spine evaluation usually is necessary because of the risk of neck injury associated with EDH.

PROCEDURES

•  
  • Perform burr hole(s) if the following occur:
    • Patient is herniating
    • All other treatments prove insufficient
    • Neurosurgery is unavailable for urgent consultation
    • Trephination (or placement of a Burr hole) should ideally be performed if possible by the consulting neurosurgeon at the receiving trauma center
    • Air or ground medical transport is prolonged
  • Burr hole procedure includes the following:
    • Drill hole adjacent to, but not over, skull fracture or in the area located by CT scan.
    • In the absence of CT scan, place a burr hole on the side of the dilated pupil, 2 finger widths anterior to tragus of ear and 3 finger widths above.

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.
• 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 with patients intubated in the ED.
  • Bag-valve-mask ventilation with good technique may be of more benefit to brain injured patients than prehospital intubation.

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 head of the bed 30° after the spine is cleared, or use 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 clinical signs of increased ICP progress and 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.
• Several treatment guidelines on various aspects of traumatic brain injury are available from the Brain Trauma Foundation.

Consultations

• Consult a neurosurgeon immediately for EDH evacuation and repair.
• Consult a trauma surgeon for other life-threatening injuries.

MEDICATION

Use RSI when intubating to minimize rises in ICP and catecholamine release. Etomidate, when used as 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, 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

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.

• Dosing
• Interactions
• Contraindications
• Precautions

Adult

0.25-1 g/kg IV q30-60min

Pediatric

Administer by weight as in adults

Phenytoin (Dilantin)

DOC for seizure prophylaxis. Fosphenytoin allows more rapid infusion and fewer side effects. If actively seizing, coadminister benzodiazepine.

FOLLOW-UP

Further Inpatient Care

• Transfer to operating room (OR) for epidural hematoma (EDH) evacuation and repair.
• Admit to neurosurgical ICU after surgery or directly for monitoring. This will likely include ICP, partial pressure oxygen (PO2), or other intracranial 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; timely decompression 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 last hours to months (see Postconcussive Syndrome).
• Vegetative state
• Death

Prognosis

• Mortality rates are essentially nil for patients not in coma preoperatively and approximately 10% for obtunded patients and 20% for patients in deep coma.
• If treated early, prognosis usually is excellent, because the underlying brain injury generally is limited.

MISCELLANEOUS

Medicolegal Pitfalls

• Failure to consider diagnosis, especially in a conscious patient with normal pupils
• Failure to transfer expeditiously to a trauma center with a neurosurgeon (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 patients who are being observed rather than sent for CT scan

Special Concerns

• Pediatric patients
  • Pediatric patients may not fracture the skull.
  • Pediatric patients have lower mortality rates, except in infants.
  • Guidelines for managing pediatric traumatic brain injury were published in 2003. They reflect adult guidelines with the exceptions of age-appropriate blood pressures and cerebral perfusion pressure, and endorsement of the use of hypertonic saline for control of increased ICP.
• Geriatric patients
  • EDH is more likely to occur with a fall.
  • Overall, EDH is much less common in older patients.
  • Subdural hematoma (SDH) is more common than EDH in elderly patients with intracranial hematoma. Brain atrophy stretches bridging veins.
  • Elderly patients have higher mortality rates