| Epidural Hematoma | | Counselor, Epidural hematoma (EDH) is the accumulation of blood in the potential space between brain dura and bone. EDH occurs in approximately 2% of patients with head injuries and 5- 15% of patients with fatal head injuries. EDH is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention. EDH may be acute (58%), subacute (31%), or chronic (11%). We value all your comments, so, if you have a suggestion for a newsletter subject but haven't submitted it yet, or if you have already submitted one but think of another, please take a minute to let us know by clicking on your "Reply" button and dropping us a note. To learn more about AMFS, Inc., the organization run by Physicians and Attorneys that provides medical experts and case review services nationwide, and has produced the following informational newsletter to aid you in understanding complex medical issues, please click here - www.medicalexperts.com. |
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|  Pathophysiology: Epidural hematoma usually results from a brief linear contact force that causes separation of the 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 skull. Arteries and veins may be compromised, causing rapid expansion of the hematoma; however, chronic or delayed manifestations may occur when veins are involved. Extension of the hematoma usually is limited by suture lines owing to the tight attachment of the dura at these locations. Bilateral epidural hematomas account for 2-10% of all acute epidural hematomas in adults but are exceedingly rare in children. The temporoparietal region and the middle meningeal artery are involved most commonly (66%). Epidural hematoma may also be spontaneous (SEDH) or may follow minor trauma, such as lumbar puncture or epidural anesthesia. SEDH may be associated with anticoagulation, thrombolysis, blood dyscrasias, coagulopathies, thrombocytopenia, neoplasms, or vascular malformations. |
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| Frequency/Mortality/Morbidity: Epidural hematoma complicates 2% of cases of head trauma (approximately 40,000 cases per year). SEDH affects 1 per 1,000,000 people annually. Alcohol and other forms of intoxication have been associated with a higher incidence of epidural hematoma. 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 EDH has a mortality rate of 15-20%. |
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| | 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 or delayed progression from minimal symptoms to even death within minutes. Symptoms of epidural hematoma include the following: headache, nausea/vomiting, seizures, and focal neurological deficits (eg, visual field cuts, aphasia, weakness, numbness). |
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| | Physical: The physical examination should include a thorough evaluation for evidence of traumatic sequelae and associated neurological deficits, including the following:Bradycardia and/ or hypertension indicative of elevated intracranial pressure, skull fractures, hematomas, or lacerations, cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with disruption of the dura, hemotympanum (blood behind the ear drum), fracture or instability of the vertebral column, alteration in level of consciousness (ie, Glasgow Coma Scale score), anisocoria (eg, ipsilateral dilation of the pupil due to uncal herniation with compression of the oculomotor nerve), and other focal neurological deficits (eg, aphasia, visual field defects, numbness, ataxia). |
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| | Lab 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. |
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| | 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. Noncontrast CT scanning of the head not only visualizes skull fractures but also directly images an epidural hematoma. 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. |
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| | 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. Lumbar puncture provides little additional information and may exacerbate neurological damage, therefore, it should not be done. |
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| | Medical Treatment: Initial resuscitation efforts should include assessment and stabilization of airway, 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. A patient with a small epidural hematoma may be treated conservatively, though close observation is advised, as delayed, yet sudden, neurological deterioration may occur. 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. |
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| | Surgical Treatment: 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. |
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| | Complications: Neurological deficits or death may occur with EDH. 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. |
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| | Medical/Legal Concerns: EDH must be considered in all patients who have experienced head injury. Alteration in the level of consciousness may be highly variable and unreliable as a clinical predictor. Failure to consider EDH in a completely lucid patient will result in delayed intervention and treatment, and is a major source of medical-legal concern. The absence of a skull fracture does not mean the absence of an intracranial bleed. Clinicians should have a low threshold for obtaining a CT scan in order to rule out EDH. Studies show that delayed transfer and triage may be the principal determinant of death. Therefore, it is imperative that the diagnosis be made quickly. Lastly, close neurologic observation is necessary to act quickly on sudden decompensation. |
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