Changes on Continuous Transcranial Doppler During Treatment for Elevated Intracranial Pressure

A 53-year-old man with alcohol-related cirrhosis presented with acute peritonitis and esophageal variceal hemorrhage and developed septic and hemorrhagic shock and acute-on-chronic liver failure with ammonia of 497 μmol/L. He developed severe cerebral edema and convulsive status epilepticus requiring midazolam and ketamine infusions. Continuous transcranial Doppler (cTCD) monitoring of the left (not shown) and right middle cerebral arteries (MCAs) was performed at a depth of 52 mm before, during, and after treatment with 23.4% hypertonic saline (Panel 1A-D). Mean velocity (MV) and pulsatility index (PI) were graphed for both the left and right MCAs (Panel 2A and B). Monitoring with cTCD captured an initial high PI (Panels 1A and 2, Arrow 1) which initially rose while flows dropped (Panels 1B and 2, Arrow 2) in response to systemic hypotension. This suggested an intracranial vasodilatory response to systemic hypotension that contributed to elevated intracranial pressure and resultant higher resistance to flow. When the systemic hypotension resolved (Panels 1C and 2, Arrow 3), MV increased and PI began to drop. Approximately 15 minutes after the initiation of therapy for elevated intracranial pressure, MV and PI 1153671 JVUXXX10.1177/15443167231153671Journal for Vascular UltrasoundKleitsch et al research-article2023