Coagulopathy Predicts Mortality in Pediatric Patients with Traumatic Brain Injury

Trauma is the leading cause of death in children ages 1 to 21 years of age. Traumatic brain injury (TBI) poses a high risk of both morbidity and mortality within the subset of pediatric trauma patients. Numerous adult studies have shown that coagulopathy is commonly observed in patients who have sustained trauma and that the incidence is higher when there is TBI. Previously, it was thought that coagulopathy related to trauma was dilutional (i.e. due to replacement of red cells and platelets without plasma) but more recent studies show that the coagulopathy in trauma is early and likely independent of transfusion therapy. Additionally, abnormal coagulation studies (PT, PTT, INR, platelet count, fibrinogen, and D-dimer) following TBI are associated with increased morbidity and mortality in adults.

Although coagulopathy after traumatic brain injury in adults is well documented, the pediatric literature is fairly sparse. A recent study by Hendrickson et al in 2008 demonstrated that coagulopathy is both underestimated and under-treated in pediatric trauma patients who required blood product replacements. Here we present the results of a retrospective pilot study designed to assess coagulopathy in the pediatric TBI population. We analyzed all children admitted to our facility with TBI from January 2012 to December 2013. Patients were excluded if they had underlying diseases of the hemostatic system. All patients had baseline characteristics measured including: age, sex, mechanism of injury, Glasgow Coma Scale (GCS), injury severity score (ISS), initial complete blood count, DIC profile, hematological treatments including transfusions, ICU and hospital length of stay, ventilator days and survival status. Coagulation studies were defined as "abnormal" when they fell outside the accepted reference range of the pediatric hospital laboratory (PT 12.6-15.9, PTT 23.6-42.1 seconds, fibrinogen < 180 mg/dL units, platelets < 185 10³/mL and hemoglobin < 11.5 g/dL). Survival was measured as survival at 30 days from admission or last known status at hospital discharge.

One hundred and twenty patients met the inclusion criteria of the study and all were included in outcome analysis. Twenty-three of the 120 patients died (19.2%). Logistic regression analysis was used to compare survivors and non-survivors and baseline demographic data showed no difference in age or weight between the two groups with p-values of 0.1635 and 0.1624, respectively. Non-survivors had a higher ISS (30.26 vs 20.92, p-value 0.0004) and lower GCS (3 vs 5.8, p-value 0.0002) compared to survivors. Univariate analysis of coagulation studies to mortality showed statistically significant odds-ratios for ISS (OR 1.09, 95% CI 1.04-1.15), PT (OR 5.91, 95% CI 1.86-18.73), PTT (OR 6.48, 95% CI 2.04-20.52) and platelets (OR 5.63, 95% CI 1.74 – 18.21). Abnormal fibrinogen levels were not predictive of mortality (OR 2.56, 95% CI 0.96-6.79). These results are summarized in Table 1.

Our results demonstrate that, consistent with adult studies, abnormal coagulation studies are also associated with increased mortality in pediatric patients. Higher injury severity scores and lower GCS scores are also predictive of mortality. Taken together, these results suggest that possible early correction of coagulopathy in severe pediatric TBI patients could improve outcomes for these patients.