J.M. Domínguez-Roldán

Role of early cell-free DNA levels decrease as a predictive marker of fatal outcome after severe traumatic brain injury.

INTRODUCTION Circulating cell-free DNA levels are increased after trauma injury. This increase is higher since the first hours after trauma and may be related with primary outcome. A sensitive and reliable biomarker for patients at higher risk is needed to identify these patients to initiate early intervention. In this way, circulating DNA may be a possible biological marker after severe TBI. MATERIALS AND METHODS We investigated DNA plasma concentrations after severe traumatic brain injury and during the next 96 h in the Intensive Care Unit (ICU) by real time PCR. 65 patients suffering severe TBI were included in the study. RESULTS Cell-free DNA levels were considerably higher in patients samples compared with voluntary control ones. After the following four days we observed a 51% decrease during the first 24h and a 71% fall from 48 h. TBI population was stratified for the primary outcome (survivors/non-survivor) and DNA levels decrease ratio was calculated for the first 48 h. A higher decrease in the survivors from 0 h to 24h compared with the non-survivors was found. A cut-off point of 1.95 ratio was established for the detection of the highest proportions of patients after the TBI that will not survive after the injury with a sensitivity of 70% and specificity of 66%. CONCLUSIONS In summary we showed that severe TBI is associated with elevated cf-DNA levels and we propose that cf-DNA decrease during the first 24h may predict patient outcome.

Clinical Variables and Neuromonitoring Information (Intracranial Pressure and Brain Tissue Oxygenation) as Predictors of Brain-Death Development After Severe Traumatic Brain Injury

BACKGROUND AND PURPOSE The aim of this study was to ascertain the role of clinical variables and neuromonitoring data as predictors of brain death (BD) after severe traumatic brain injury (TBI). PATIENTS AND METHODS This prospective observational study involved severe TBI patients admitted to the intensive care unit between October 2009 and May 2011. The following variables were recorded: gender, age, reference Glasgow Coma Scale after resuscitation, pupillary reactivity, prehospital hypotension and desaturation, injury severity score, computed tomography (CT) findings, intracranial hypertension, and low brain tissue oxygenation (Pti02) levels (<16 mm Hg), as well as the final result of BD. RESULTS Among 61 patients (86.9% males) who met the inclusion criteria, the average age was 37.69 ± 16.44 years. Traffic accidents were the main cause of TBI (62.3%). The patients at risk of progressing to BD (14.8% of the entire cohort) were those with a mass lesion on CT (odds ratio [OR] 33.6; 95% confidence interval [CI]: 3.75-300.30; P = .002), altered pupillary reaction at admission (OR 25.5; 95% CI: 2.27-285.65; P = .009), as well low Pti02 levels on admission (OR 20.41; 95% CI: 3.52-118.33; P < .001) and during the first 24 hours of neuromonitoring (OR 20; 95% CI: 2.90-137.83; P < .001). Multivariate logistic regression showed that a low Pti02 level on admission was the best independent predictor for BD (OR 20.41; 95% CI: 3.53-118.33; P = .001). CONCLUSIONS Clinical variables and neuromonitoring information may identify TBI patients at risk of deterioration to BD.

Risk factors associated with diabetes insipidus in brain dead patients.

POLYURIA is one pathophysiological phenomena frequently associated with brain death. Hypothermia and diabetes insipidus are the primary mechanisms producing this sign. Polyuria is an important event, not only to its clinical significance suggesting severe dysfunction of hypohalamic-hypophysal tract due to severe brain impairment but also due to the difficulty in maintaining homeostasis until the donor is ready for organ removal. This study investigates whether clinical factors related to mechanisms producing brain death are associated with or even predict the subsequent development of diabetes insipidus.