LAUSR

A 76-year-old woman was admitted to the neurocritical care unit after experiencing the sudden onset of the worst headache of her life. Initial computed tomography (CT) revealed diffuse subarachnoid hemorrhage with intraventricular hemorrhage and hydrocephalus. Her Hunt-Hess classification was 2, and her modified Fisher score was 3. CT angiogram revealed a right anterior choroidal aneurysm. Her neurological exam on admission was completely intact, but she soon developed increasing lethargy. An external ventricular drain (EVD) was placed with opening pressure of 22 cm H20. She regained her alertness. The aneurysm was coil embolized. Her external ventricular drain was kept open at 15 cm H2O. She was ambulating in the hallways with physical therapy daily. Initial transthoracic echocardiogram (TTE) revealed an ejection fraction of 65% with no other abnormalities. The EVD was maintained open at 15 cm H20 with daily cerebrospinal fluid drainage decreasing from 186 mL in the first 24 h after insertion to 69 mL in the 24 h prior to clamp. Prior to clamping, intracranial pressures (ICPs) ranged from 0 to 10 mm Hg with a mean of 6 mm Hg. On the morning of post-bleed day (PBD) 6, her EVD was clamped. That evening, she began to complain of a worsening headache that was associated with increased lethargy and disorientation. CT revealed increased dilatation of the ventricles (Fig. 1a). Her ICPs while she was deteriorating ranged from 2 to 20 mm Hg with a mean of 7.8 mm Hg. The ICP waveform suggested poor compliance with P2 higher than P1. Her EVD was subsequently reopened at 15 cm H2O. Throughout the course of the evening, her mental status continued to decline. She was taken for CT angiography and perfusion imaging which showed no evidence of vasospasm or perfusion deficit. By the morning of PBD 7, she was deeply stuporous with a forced downward gaze and required intubated for airway protection. A repeat CT revealed progression of hydrocephalus. The EVD was lowered to 0 cm H20. She became hypotensive. An electrocardiogram (EKG) was concerning for acute coronary syndrome with 1 mm ST elevation in the inferolateral leads (Fig. 2a). The EKG was low voltage making the new 1 mm changes significant for possible myocardial infarction. Initial troponin was 5.97 with CK-MB of 21.4. She became increasingly more hypotensive, unresponsive to intravenous fluid, and requiring vasopressors. A repeat transthoracic echocardiogram showed an ejection fraction of 35% with distal anterior septum, distal anterior wall, distal inferior wall, and apex akinesis (Fig. 2b). Emergent cardiac catheterization revealed only mild, non-obstructive & Kamel Gharaibeh [email protected]