case_images: PMC3556561_01
case_images: CT scan of the head on hospital day 1 demonstrates poor gray-white junction differentiation suggestive of diffuse cerebral edema. There are scattered areas of subarachnoid hemorrhage in multiple frontal and parietal sulci as well as scattered areas of hyperattenuation at the gray-white junction in the frontal and parietal lobes which may be related to contusions or diffuse axonal injury. Also seen is a large left parietal scalp hematoma.
case_images: fneur-04-00003-g001.jpg
case_images: PMC3556561_01_fneur-04-00003-g001.jpg
case_images: F1
case_images: CT scan of the head on hospital day 11 demonstrates expected evolution of the previously noted cortical contusions, subdural hematomas, and changes of diffuse axonal injury. No new hemorrhage, mass effect, hydrocephalus, or CT radiographic evidence of acute ischemic injury. Stable diffuse cerebral swelling with partial effacement of the suprasellar cistern.
case_images: fneur-04-00003-g002.jpg
case_images: PMC3556561_01_fneur-04-00003-g002.jpg
case_images: F2
case_images: A repeat CT scan on hospital day 11 (Figure 2) did not show significant cerebral edema to explain the persistent and refractory intracranial hypertension.
case_images: Intracranial pressure is plotted over time. The timing of morphine and fentanyl administration are shown. Rescue doses of hyperosmolar therapy are plotted at the bottom of the graph.
case_images: fneur-04-00003-g003.jpg
case_images: PMC3556561_01_fneur-04-00003-g003.jpg
case_images: F3
case_images: Permitting transient increases of ICPs up to 30 mmHg after stimulation, we were able to rapidly resume normothermia (36.5 C), discontinue neuromuscular paralysis, and transition from propofol to a low dose of midazolam without the need for rescue doses of hyperosmolar therapy (Figure 3).