Abstract
Background Paroxysmal Sympathetic Hyperactivity (PSH) occurs with high prevalence among critically ill Traumatic Brain Injury (TBI) patients and is associated with worse outcomes. The PSH-Assessment Measure (PSH-AM) consists of a Clinical Features Scale (CFS) and a Diagnosis Likelihood Tool (DLT), intended to quantify the severity of sympathetically-mediated symptoms and likelihood that they are due to PSH, respectively, on a daily basis. Here, we aim to identify and explore the value of dynamic trends in the evolution of sympathetic hyperactivity following acute TBI using elements of the PSH-AM.Methods We performed an observational cohort study of 221 acute critically ill TBI patients for whom daily PSH-AM scores were calculated over the first 14 days of hospitalization. A principled group-based trajectory modeling approach using unsupervised K-means clustering was used to identify distinct patterns of CFS evolution within the cohort. We also evaluated the relationships between trajectory group membership and PSH diagnosis, as well as PSH DLT score, hospital discharge GCS, ICU and hospital length of stay, duration of mechanical ventilation, and mortality. Baseline clinical and demographic features predictive of trajectory group membership were analyzed using univariate screening and multivariate multinomial logistic regression.Results We identified four distinct trajectory groups. Trajectory group membership was significantly associated with clinical outcomes including PSH diagnosis and DLT score, ICU length of stay, and duration of mechanical ventilation. Baseline features independently predictive of trajectory group membership included age and post-resuscitation motor GCS.Conclusions This study adds to the sparse research characterizing the heterogeneous temporal trends of sympathetic nervous system activation during the acute phase following TBI. This may open avenues for early identification of at-risk patients to receive tailored interventions to limit secondary brain injury associated with autonomic dysfunction and thereby improve TBI patient outcomes.