Extracranial pressure (ECP) monitoring in severe traumatic brain injury (TBI): A prospective study validating intra-abdominal pressure (IAP) measurement for predicting intracranial pressure (ICP).

Background: Intracranial pressure (ICP)--guided therapy is the standard of care in the management of severe traumatic brain injury (TBI). Ideal ICP monitoring technique is not yet available, based on its risks associated with bleeding, infection, or its unavailability at major centers. Authors propose that ICP can be gauged based on measuring pressures of other anatomical cavities, for example, the abdominal cavity. Researchers explored the possibility of monitoring intra-abdominal pressure (IAP) to predict ICP in severe TBI patients.

Methods: We measured ICP and IAP in severe TBI patients. ICP was measured using standard right frontal external ventricular drain (EVD) insertion and connecting it to the transducer. IAP was measured using a well-established technique of vesical pressure measurement through a manometer.

Results: A total of 28 patients (n = 28) with an age range of 18-65 years (mean of 32.36 years ± 13.52 years [Standard deviation]) and the median age of 28.00 years with an interquartile range (21.00-42.00 years) were recruited in this prospective study. About 57.1% (n = 16) of these patients were in the age range of 18-30 years. About 92.9% (n = 26) of the patients were male. The most common mode of injury (78.6%) was road traffic accidents (n = 22) and the mean Glasgow Coma Scale at presentation was 4.04 (range 3-9). The mean ICP measured at the presentation of this patient cohort was 20.04 mmHg. This mean ICP (mmHg) decreased from a maximum of 20.04 at the 0 h' time point (at the time of insertion of EVD) to a minimum of 12.09 at the 96 hr time point. This change in mean ICP (from 0 h to 96 h) was found to be statistically significant (Friedman Test: χ² = 87.6, P ≤ 0.001). The mean IAP (cmH2O) decreased from a maximum of 16.71 at the 0 h' time point to a minimum of 9.68 at the 96 h' time point. This change was statistically significant (Friedman Test: χ² = 71.8, P ≤ 0.001). The per unit percentage change in IAP on per unit percentage change in ICP we observed was correlated to each other. The correlation coefficient between these variables varied from 0.71 to 0.89 at different time frames. It followed a trend in a directly proportional manner and was found to be statistically significant (P < 0.001) in each time frame of the study. The rise in one parameter followed the rise in another parameter and vice versa.

Conclusion: In this study, we established that the ICP of severe TBI patients correlates well with IAP at presentation. This correlation was strong and constant, irrespective of the timeframe during the treatment and monitoring. This study also established that draining cerebrospinal fluid to decrease ICP in severe TBI patients is reflected in IAP. The study validates that IAP is a strong proxy of ICP in severe TBI patients.