Discussion
death, fever, hydrocephalus, neurological damage, hyperthermia
EVENTS, PATHOGENESIS, HYDROCEPHALUS
In this study, mICP values were significantly correlated with P2/P1 derived from NICPW analysis in a heterogeneous population of brain-injured patients. Moreover, P2/P1 values had, as for elevated mICP, prognostic value for ED. The presence of DC did not influence overall results. Hence, we report additional findings to the previous studies, from de Moraes et al. [In experimental and clinical settings, the noninvasive P2/P1 ratio has been well correlated with ICP or applied as additional information to predict outcomes and assess shunting malfunctioning in children with hydrocephalus [The clinical interest of P2/P1 should be on the understanding of the brain tolerance to different ICP values; as an example, if a patient with an ICP of 18 mmHg could be considered as having mICP values within acceptable ranges, the concomitant presence of P2/P1 > 1.2 might suggest poor ICC, potentially requiring additional investigations and interventions. On the opposite, an mICP of 23 mmHg, which should deserve prompt therapy according to guidelines, could be further evaluated in its pathogenesis (i.e., hyperthermia, awakening, fever) if P2/P1 ratio remains within normal ranges. A prospective study including additional neuromonitoring tools to better understand cerebral physiology during ICP surges is required to respond to this hypothesis and may fulfill the gaps left by numerical thresholds [The classic studies of Marmarou et al. [ICPW is a well-known parameter for intensivists and neurosurgeons; however, clinical applicability of ICPW remains difficult because invasive systems do not routinely analyze P2/P1, being a clear recognition of the two peaks not always possible. The expansion of multimodal neuromonitoring could help to further understand how ICP values should be optimized in clinical practice. In particular, as the combination of ICP values with brain oxygenation [This study has several limitations to acknowledge. First, a single session monitoring of these variables is clearly narrow for the outcome determination since ICP and ICC are dynamic properties that will vary continuously. Therefore, the association of P2/P1 with early mortality does not imply that altered ICC could be the only explanation for death, rather, this could be explained by the neurological damage itself even considering that our three groups disclosed no overall severity admission differences. Indeed, a cohort design is more adequate to outcome assessment, justifying a wider follow-up and register of IHT events that a patient may present during hospitalization. Second, a single-center study might influence patients’ management and early outcome, so that generalizability of overall results could be biased. Third, our results need for external validation. Although DC did not appear to significantly influence the applicability of NICPW analysis, some caution should be considered in such patients, who will require dedicated investigations with such monitoring tools.