Traumatic epidural and subdural hematomas and extensive brain infarcts in a patient with pial arteriovenous malformation: Mechanisms underlying clinical and radiological findings
A 40-year-old man was brought to the emergency department, having been found lying by the road side. He had abrasions on the left frontal and temporal regions of the scalp. On examination, his Glasgow Coma Score (GCS) was E1 M5 V2 (8/15). He had paucity of right-sided limb movements to painful stimuli; his left pupil was larger than the right and not reacting to light. This was clinically suggestive of left uncal herniation. The exact time of injury could not be ascertained. He was investigated with an urgent plain computed tomography (CT) scan of the head. The CT scan showed a large left temporoparietal epidural hematoma (EDH) causing significant mass effect on the lateral ventricles and a midline shift of 1.5 cm []. There was a linear fracture of the temporal bone []. There was an underlying acute subdural hematoma (acSDH) associated with severe cerebral edema with effacement of all the basal cisterns [].\nImmediate surgery was decided on and he was shifted to the operating room within 60 min of being brought to the hospital (an analysis of the records revealed that this was the time taken for doing the CT scan, drawing blood for cross-match, and an urgent head shave). He underwent emergency left frontotemporoparietal craniotomy. During surgery, a linear fracture of the temporal bone was noted. Upon elevating the bone flap, a thick EDH was encountered and was evacuated. The source of the bleed was a laceration of the posterior branch of the middle meningeal artery (MMA), which was coagulated. The artery did not appear to be unduly enlarged. After evacuation of the EDH, the dura remained tense and had a bluish discoloration. The dura was opened and a thick subdural clot was encountered; this was evacuated. After evacuating the SDH, it was found that the posterior frontal lobe and the temporal lobe were covered by numerous distended, arterialized veins. The veins of the Sylvian fissure were grossly distended and arterialized []. There was a pial laceration adjacent to the large Sylvian vein which was the source of the SDH. This bleeding was controlled with gelatin sponge tamponade.\nPostoperatively, the pupillary asymmetry reverted. However, he remained comatose, with a GCS of E2 M5 V2 (9/15). A postoperative contrast-enhanced CT (CECT) showed complete evacuation of the EDH and SDH with reversal of the midline shift []. However, cerebral edema persisted. Multiple infarcts were seen in the left medial temporal lobe and centrum semiovale [Figures and ]. These were distributed in the left middle cerebral artery (MCA) and anterior cerebral artery (ACA) territories. There was a small bleed in one of the infarcts, suggestive of hemorrhagic transformation []. CECT showed a nidus in the left superior frontal region []. Angiogram showed a left superior frontal AVM fed by branches of the left MCA and the left ACA draining into the Sylvian vein, and superior sagittal sinus []. External carotid artery (ECA) injection did not show any feeders to the AVM. The nidus measured 4.5 cm supero-inferiorly. The Spetzler-Martin grade was 3. Surgery was offered for excision of the AVM; however, since he continued to be in altered sensorium, the patient's relatives were not willing for any further treatment and he had to be discharged at request. No further follow-up data is available.