Epidural/Extradural Hematoma

Extradural/Epidural hematoma

Definition

Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull (calvaria) and the stripped-off periosteal layer of dura membrane. It can also occur in the spinal cord (spinal epidural hematoma-SEDH).

Incidence and Prevalance

United States

Epidural hematoma complicates 2% of cases of head trauma

Mortality/Morbidity

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

Pathophysiology

Usually traumatic in nature; associated with calvarial fractures. 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.

Common arterial sources

70-80% of epidural hematomas (EDHs) are located in the temporoparietal region and the middle meningeal artery are involved most commonly (66%), although the anterior ethmoidal artery may be involved in frontal injuries.

Common venous sources

Usually, venous epidural hematomas only form with a depressed skull fracture.

Torn venous sinuses cause an epidural hematoma, particularly in the parietal-occipital region or posterior fossa (eg, transverse or sigmoid sinus). Hematoma in the posterior fossa represent only 5% of cases.. Disruption of the superior sagittal sinus may cause vertex EDH.

Etiology

· Traumatic

· Thrombolysis/anticoagulants

· Hypertension

Presentation

Symptoms of epidural hematoma include the following:

• Headache
• Nausea/vomiting
• Seizures
• Focal neurologic deficits (eg, visual field cuts, aphasia, weakness, numbness)

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
• Cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with disruption of the dura
• Hemotympanum
• 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)
• Facial nerve injury
• Weakness (eg, contralateral hemiparesis due to compression of the cerebral peduncle)
• Other focal neurological deficits (eg, aphasia - Aphasia is an acquired disorder of language due to brain damage., visual field defects, numbness, ataxia - Ataxia is defined as an inability to maintain normal posture and smoothness of movement.)

Investigation

Laboratory test

• 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. bleeding diathesis is an unusual susceptibility to bleeding
• 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 test

Plain radiography

CT scan. Advantage is that both fracture and the hematoma are visible.

Angiography – to visualise any lacerated vessels

MRI

Treatment and Management

Emergency care

 Establish IV access, administer oxygen, monitor, and administer IV crystalloids(normal saline) as necessary to maintain adequate blood pressure.

 Intubate using rapid sequence induction (RSI), to facilitate oxygenation, protect the airway, and allow for hyperventilation as needed.

 Elevate head of the bed 30° after the spine is cleared, to reduce ICP and increase venous drainage.

 Administer mannitol(Mannitol is used clinically to reduce acutely raised intracranial pressure until more definitive treatment can be applied). This reduces both ICP (by osmotically reducing brain edema) and blood viscosity, which increases cerebral perfusion.

 Hyperventilation to partial pressure of carbon dioxide (PCO₂) of 30-35 mm Hg treats signs of increasing ICP. 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.

Operative care

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.

Mininally invasive techniques involve the use of burr holes and drainage by negative pressure.

Burr holes procedure: The surgeon will make an incision, and reflect the scalp over the area of the hematoma. Then, an air powered drill is used to make a hole in the skull. The dura mater (tough covering of the brain) is then opened. The hematoma (blood clot) is now seen, and the surgeon will irrigate some of it out, and may pass a drain around the brain to provide post-operative drainage

References
www.emedicine.medscape.com