A brief review on extradural or epidural hematoma.
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Extradural hemorrhage Momen Ali Khan Neurosurgery Resident Department Of Neurosurgery Dhaka Medical College Hospital
Extradural hematoma General information Incidence of EDH: 1% of head trauma admissions Ratio of male: female = 4:1. Usually occurs in young adults Rare before age 2 yrs or after age 60 (perhaps because the dura is more adherent to the inner table in these groups). [Handbook of Neurosurgery 10 th Greenberg 1072]
Source of bleeding 85% = arterial bleeding (the middle meningeal artery is the most common source of middle fossa EDHs). Middle meningeal vein Dural sinus. [Handbook of Neurosurgery 10 th Greenberg 1072]
Site of bleeding 70% occur laterally over the hemispheres with their epicenter at the pterion Frontal (5–10%) Occipital (5–10%) Posterior fossa (5–10%). [Handbook of Neurosurgery 10 th Greenberg 1072]
Presentation Brief posttraumatic LOC Followed by a “lucid interval” for several hours Obtundation Headache Vomiting Seizure Mass effect impact from hematoma Contralateral hemiparesis Ipsilateral pupillary dilatation Hemi-hyperreflexia + unilateral Babinski sign Bradycardia is usually a late finding “Textbook” presentation (< 10%-27% have this classic presentation) [Handbook of Neurosurgery 10 th Greenberg 1072] Obtundation is mild to moderate alertness reduction (altered level of consciousness) with decreased interest in the environment and slower than normal reactivity to stimulation.
Kernohan’s phenomenon Shift of the brainstem away from the mass may produce compression of the opposite cerebral peduncle on tentorial notch which can produce ipsilateral hemiparesis (so called Kernohan’s phenomenon or Kernohan’s notch phenomenon) a false localizing sign . [Handbook of Neurosurgery 10 th Greenberg 1072]
Nice to know 60% of patients with EDH have a dilated pupil, 85% of which are ipsilateral. No initial loss of consciousness occurs in 60%. No lucid interval in 20%. [Handbook of Neurosurgery 10 th Greenberg 1072]
Differential diagnosis of EDH Subdural hematoma A posttraumatic disorder described by Denny-Brown consisting of a posttraumatic “lucid interval ” followed by bradycardia, brief periods of restlessness and vomiting, without intracranial hypertension or mass. Children especially may have H/A, and may become drowsy and confused. Theory: a form of vagal syncope. [Handbook of Neurosurgery 10 th Greenberg 1072]
CT scan in EDH Biconvex : “Classic” CT appearance occurs in 84% of cases: high density biconvex (lenticular) shape adjacent to the skull Straight : In 11% the side against the skull is convex and that along the brain is straight Crescent : In 5% it is crescent shaped (resembling subdural hematoma). [Handbook of Neurosurgery 10 th Greenberg 1073]
Epidural hematoma, left side. Image: coronal CT illustrating an EDH (yellow arrowheads) crossing the tentorium (white arrow), which in addition to its biconvex shape, helps distinguish this from a subdural hematoma (SDH).
Treatment of EDH General management of EDH Prepare for surgery if indications are met. Prompt surgery if signs of local mass effect, signs of herniation (increasing drowsiness, pupil changes, hemiparesis…) or cardiorespiratory abnormalities. Management includes- Admit to ICU (ideal) with q 1-hour neuro checks NPO, saline, Antibiotic, Anticonvulsant, Analgesic, PPI Reverse coagulopathies. [Handbook of Neurosurgery 10 th Greenberg 1074]
Medical management of EDH [Handbook of Neurosurgery 10 th Greenberg 1074] Nonsurgical management may be attempted in patients not meeting surgical indications below, which generally limited to: Small (≤ 1cm maximal thickness) subacute or chronic EDH Minimal neurological signs/symptoms (e.g., slight lethargy, mild H/A) without focal deficit and without evidence of herniation For persistent headache, a short course of steroids (1-3 days) may help, then taper.
Follow-up CT [Handbook of Neurosurgery 10 th Greenberg 1074] Early after admission (e.g., 6 hours) Then any time the patient becomes symptomatic, In 1-2 wks. if clinically stable. Repeat in 1–3 mos (to document resolution). In 50% of cases there will be a slight transient increase in size between days 5–16, and some patients required emergency craniotomy when signs of herniation occurred.
Surgical management of EDH Indications for surgery Glasgow Coma Scale (GCS) score 8 and anisocoria → operating room as soon as possible Hematoma volume ≥ 30 cm 3 Hematoma volume < 30 cm 3 but accompanied by: Thickness >15 mm Midline shift >5 mm GCS 8 or less Focal motor deficit Effaced cisterns Deteriorating neurologic status [Atlas of Emergency Neurosurgery: 02]
Nice To Know EDH in pediatric patients is riskier than adults since there is less room for clot. The threshold for surgery in pediatrics should be very low. Although medical management of p-fossa EDHs has been reported, these are more dangerous (see below) due to small volume of p-fossa and vulnerability of brainstem to compression by even modest hematoma expansion. Surgery is recommended Timing of surgery It is strongly recommended that patients with an acute EDH and GCS < 9 and anisocoria undergo surgical evacuation ASAP [Handbook of Neurosurgery 10 th Greenberg 1074]
Surgical technical issues Clot removal Hemostasis Prevent reaccumulation Apply bone wax to intra- diploic bleeders Dural tack-up sutures Perforating the bone flap with a drill Placing a subgaleal drain which is maintained for several days or until output is scant [Handbook of Neurosurgery 10 th Greenberg 1075]
Postoperative Management Monitoring The patient should be monitored in the post-anesthesia care unit ( recovery room ), progressive care unit, or intensive care unit with frequent neurologic checks, occurring at least hourly initially . Patients with severe injuries will likely have additional invasive neuromonitoring (an ICP, external vent ricular drain, brain tissue oxygen monitor, or a combination thereof) to guide management. Drains should be monitored for output every 4 hours for the first 8 hours and then every 8-hour shift . The incision and/or dressing should be monitored for bleeding initially, and for erythema, exudate, and/or edema subsequent to the initial postoperative period. [Atlas of Emergency Neurosurgery: 14]
Medication [Atlas of Emergency Neurosurgery: 14] Postoperative antibiotics are continued for 24 hours unless there was gross contamination present at the time of surgery, in which case this period may be extended. Seizure prophylaxis should be continued for a total of 7 days for patients with EDH or SDH. The presence of documented seizures may provide an indication to continue therapy beyond this window. Depending on the clinical picture - Hyperosmolar therapy —mannitol and/or hypertonic saline— may be indicated for ICP control Sedation and/or neuromuscular paralytics may be indicated to assist ICP control Pressor support may be necessary to maintain adequate cranial perfusion pressure Ongoing coagulopathy should be corrected with fresh frozen plasma or other appropriate blood products/factors.
Further Management [Atlas of Emergency Neurosurgery: 14] Drains are removed on the first postoperative day , provided input has slowed sufficiently. If there is significant output, removal may be delayed another 1 to 2 days. The dressing is removed and the wound is cleansed with warm water and mild soap or shampoo after 24 hours. Skin sutures or staples are removed on or about postoperative day 10 to 14.
Mortality with EDH Overall: 20–55% (higher rates in older series). Optimal diagnosis and treatment within a few hours results in 5–10% estimated mortality (12% in a recent CT era series). Mortality in patients without lucid interval is double that for patients with a lucid interval. Bilateral Babinski’s or decerebration pre-op → worse prognosis. Death is usually due to respiratory arrest from uncal herniation causing injury to the midbrain. 20% of patients with EDH on CT also have ASDH at autopsy or operation. Mortality with both lesions concurrently is higher, reported range: 25–90% [Handbook of Neurosurgery 10 th Greenberg 1075]
Delayed epidural hematoma (DEDH) Definition An EDH that is not present on the initial CT scan, but is found on subsequent CT. Comprise 9–10% of all EDHs in several series. Theoretical risk factors for DEDH include the following (NB: many of these risk factors may be incurred after the patient is admitted following a negative initial CT): Lowering ICP either medically (e.g., osmotic diuretics) and/or surgically (e.g., evacuating contralateral hematoma) which reduces temponading effect Rapidly correcting shock (hemodynamic “surge”) may cause DEDH18 Coagulopathies [Handbook of Neurosurgery 10 th Greenberg 1075-76]
Nice to Know: DEDH tend to occur in patients with severe head injury and associated systemic injuries. However, DEDH have also been infrequently reported in mild head injury (GCS > 12). Presence of a skull fracture has been identified as a common feature of DEDH. Key to diagnosis: High index of suspicion. Avoid a false sense of security imparted by an initial “nonsurgical” CT. May develop once an intracranial lesion is surgically treated, as occurred in 5 of 7 patients within 24 hrs of evacuation of another EDH. 6 of 7 patients had known skull fractures in the region where the delayed EDH developed [Handbook of Neurosurgery 10 th Greenberg 1075-76]
Posterior fossa epidural hematoma Comprise ≈ 5% of EDH More common in 1 st two decades of life. Although as many as 84% have occipital skull fractures, only ≈ 3% of children with occipital skull fractures develop p-fossa EDH. The source of bleeding is usually not found, but there is a high incidence of tears of the dural sinuses. Cerebellar signs are surprisingly lacking or subtle in most. Overall mortality is ≈ 26% (mortality was higher in patients with an associated intracranial lesion). [Handbook of Neurosurgery 10 th Greenberg 1076]