A 30-year-old male, presented after an hour following trauma, with a Glasgow Coma Scale (GCS) score of 6/15 and symmetric and reacting pupils. Computed tomography (CT) scan of the brain showed an acute SDH in the right fronto-temporo-parietal region with mass effect and midline shift []. There were linear fractures of the ipsilateral parietal, temporal, and occipital bones with pneumocephalus, in the vicinity, of the right transverse sinus []. He underwent emergency craniotomy and evacuation of the SDH. A lax duroplasty, was done and the bone flap not replaced, as the brain was tense. He remained neurologically stable on ventilator support, with symmetric and reacting pupils. A routine follow-up CT scan of the brain after 24 h showed an ipsilateral EDH straddling the transverse sinus, causing mass effect and herniation of the brain through the craniectomy defect []. He underwent emergency craniotomy and evacuation of the hematoma. His extended glasgow outcome score (GOS-E) was 8 (upper good recovery), at 6 months.
We report a 19-year-old Caucasian male of Iranian Nationality with acute right-sided traumatic SDH (due to car accident) with presenting Glasgow Coma Scale score of 6/15 and CT evidence of severe brain swelling and associated midline shift and contralateral small fractural EDH in the temporoparietal region (). The patient was anisocoric (right sided mydriasis) at presentation. He underwent an emergent decompressive craniectomy and evacuation of the SDH. During surgery, the brain showed considerable swelling after hematoma evacuation and coagulation of the ruptured bridging vein causative of hematoma. Therefore, an augmentation duraplasty using free pericranial flap was performed. Regarding severe brain swelling during operation, a possible intracranial pathology amenable to surgery was suspected and immediate post-operative CT scan revealed expansion of the contralateral EDH. Due to mass effect of EDH, a second surgery was offered. The patient’s family declined second surgery for EDH evacuation. The patient was transferred to intensive care undergoing ICP monitoring. Despite all medical measures such as mannitol, high dose barbiturate therapy, and mild hypothermia, the patient's ICP remained high (about 25 mmHg). CPP was around 65 mmHg. Serial CT scans were performed the next days, showing right PCA territory infarct as well as expansion and spontaneous resolution of the EDH. The ICP remained relatively high (about 20 mmHg) in the following days. The patient was discharged 3 months after admission in persistent vegetative state.