Case 36 History ---- The patient was a 20-year-old man with no prior medical history who developed a headache on June 27 while visiting family. On the morning of June 28, he awoke with acute confusion and agitation, prompting EMS activation. At an outside hospital, he was combative with a GCS of 10 and required sedation and intubation for airway protection. Initial head CT demonstrated a large left parieto-occipital intraparenchymal hemorrhage with intraventricular extension, surrounding edema, and approximately 8-9 mm midline shift with subfalcine herniation. Subsequent CTA demonstrated slight interval enlargement of the large left parietal parenchymal and intraventricular hemorrhage, measuring approximately 5.9 × 3.3 × 6.6 cm, with surrounding edema, diffuse supratentorial sulcal and cisternal effacement, dilation of the lateral ventricles (L>R) due to intraventricular blood products, and descending central herniation. The CT angiogram was markedly limited by poor contrast bolus timing and was inadequate to exclude an aneurysm or vascular malformation. Lack of opacification of the superior sagittal sinus relative to the transverse sinuses was suspicious for dural venous thrombosis. He was transferred the same day to a tertiary neurocritical care unit, where he experienced rapid neurologic decline with development of fixed, dilated pupils and clinical signs of herniation. On June 28 he underwent emergent left decompressive hemicraniectomy with clot evacuation and placement of an external ventricular drain. Postoperatively, imaging showed partial reduction in hematoma burden and ventricular decompression, but diffuse loss of gray-white differentiation consistent with severe cerebral edema and hypoxic-ischemic injury. Over June 28-29 his course was marked by refractory intracranial hypertension and multisystem complications, including neurogenic shock requiring vasopressors, acute respiratory failure requiring full ventilatory support, and diabetes insipidus with significant polyuria and hypernatremia treated with vasopressin and fluid management. Neurologic examinations progressively worsened, demonstrating loss of brainstem reflexes and absence of spontaneous respirations. On June 29 a brain perfusion study demonstrated absence of cerebral blood flow. Despite continued supportive care, his neurologic exam remained absent. On June 30 a second neurologic evaluation confirmed the findings, and formal apnea testing showed no respiratory drive, with arterial blood gas demonstrating pH 7.17 and pCO2 81 mm Hg.
