Abstract
We aimed to investigate intracranial pressure (ICP) changes over time and the neurologic prognosis for out-of-hospital cardiac arrest (OHCA) survivors who received targeted temperature management (TTM). ICP was measured immediately after return of spontaneous circulation (ROSC) (day 1), then at 24 h (day 2), 48 h (day 3), and 72 h (day 4), through connecting a lumbar drain catheter to a manometer or a LiquoGuard machine. Neurological outcomes were determined at 3 months after ROSC, and a poor neurological outcome was defined as Cerebral Performance Category 3–5. Of the 91 patients in this study (males, n = 67, 74%), 51 (56%) had poor neurological outcomes. ICP was significantly higher in the poor outcome group at each time point except day 4. ICP elevation was highest between days 2 and 3 in the good outcome group, and between days 1 and 2 in the poor outcome group. However, there was no difference in total ICP elevation between the poor and good outcome groups (3.0 vs. 3.1; p = 0.476). All OHCA survivors who had received TTM had elevated ICP, regardless of neurologic prognosis. However, the changing pattern of ICP levels differed depending on the neurological outcome.
Highlights
Hypoxic-ischemic brain injury (HIBI), which often occurs after cardiac arrest (CA), increases the permeability of the blood–brain barrier’s (BBB) tight junctions due to microvascular damage induced through oxidative stress, which leads to BBB disruption and vasogenic edema and causes an elevation in intracranial pressure (ICP) [1,2,3]
We aimed to investigate the association between ICP levels and neurological outcomes for 3 days after the return of spontaneous circulation (ROSC) in patients with out-of-hospital CA (OHCA) treated with temperature management (TTM)
We excluded patients who had experienced a traumatic cardiac arrest or an interrupted TTM owing to transfer, those who were ineligible for lumbar puncture (LP), those who were receiving extracorporeal membrane oxygenation, and those who had no of kin to provide consent for an LP procedure
Summary
Hypoxic-ischemic brain injury (HIBI), which often occurs after cardiac arrest (CA), increases the permeability of the blood–brain barrier’s (BBB) tight junctions due to microvascular damage induced through oxidative stress, which leads to BBB disruption and vasogenic edema and causes an elevation in intracranial pressure (ICP) [1,2,3]. Increased ICP is a serious post-CA complication closely associated with poor neurological outcomes [4,5,6]. Some studies have reported that ICP control may play an important role in improving mortality and neurological prognosis in post-CA care [7,8,9]. Recently published international guidelines for post-CA care do not provide guidance concerning appropriate ICP levels and methods for reducing ICP [10].
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