Article 1
Implementation of an evidence-based accelerated pathway: can hospital length of stay for children with blunt solid organ injury be safely decreased? Stokes SC, Brown EG, Jackson JE, Leshikar DE, Stephenson JT. Pediatr Surg Int. 2021 Jun;37(6):695-704.
Blunt solid organ injury occurs in 10-15% of pediatric trauma patients. Traditional non-operative management recommended grade + 1 day of bedrest leading to extended hospital observation. More recently, the American Pediatric Surgical Association revised their guidelines toward more abbreviated hospitalization and management based on hemodynamics. The authors sought to assess the safety and efficacy of an accelerated protocol for blunt solid organ injury management at a combined adult and pediatric trauma center.
Pediatric patients (<15years) who underwent non-operative management of blunt hepatic or splenic injuries were identified at a single Level 1 pediatric trauma center from 2014-2020. Children that were dead on arrival, had a concurrent traumatic brain injury or underwent initial operative management (within 6 hours of arrival) were excluded. The cohort was divided into before or after implementation of a “blunt solid organ injury accelerated protocol” in 2018. Primary outcome was total hospital length of stay (LOS), with ICU LOS, number of CBCs drawn, hospital cost, readmissions, delayed operative intervention and mortality as secondary outcomes.
Sixty-seven children pre-protocol were compared to 63 post-implementation. Baseline demographics, vital signs, ISS and grade of solid organ injuries were not different between cohorts. Median hospital LOS was significantly shorter post-protocol 2 vs. 4 days (p=0.015), which held for both ISS≥15 and ISS<15 subgroups. ICU LOS was not different. Fewer CBCs were obtained after the accelerated protocol, median 6 vs. 8 (p=0.006), which remained significant only in the ISS≥15 subset (7 vs. 10, p=0.014). Median hospital costs and charges were significantly less after implementation of the protocol. There were no significant differences between groups in delayed operative intervention, ER visits, readmission and mortality.
In summary, implementation of an accelerated protocol for management of children with blunt solid organ injuries reduced hospital LOS and costs without increasing rates of delayed intervention or return to hospital. Limitations of this work include it retrospective design and relatively low patient numbers, which may underpower this study to detect differences in rare events. This study suggests accelerated management of pediatric blunt solid organ injuries is safe, though larger, multicenter evaluation is needed to better define the nuances of this care plan.
Article 2
Injury Severity, Arrival Physiology, Coagulopathy, and Outcomes Among the Youngest Trauma Patients.
Gupta VS, Liras IN, Allukian M, Cotton BA, Cox CS Jr, Harting MT. J Surg Res. 2021 Apr 7;264:236-241.
Trauma-induced coagulopathy is a known predictor of mortality and poor outcomes. Rapid thromboelastography (rTEG) offers timely evaluation of the coagulation cascade for targeted intervention. Less is known regarding trauma-induced coagulopathy and rTEG usage in the youngest trauma patients. The purpose of this study was to evaluate rTEG and other physiologic variables associated with mortality in young pediatric patients.
This is a retrospective review of children under 5 years presenting as the highest level trauma activation to a single children’s hospital from 2010 through 2016. Children with >20% TBSA burns or expired within 30 minutes were excluded. Pre-hospital and initial clinical/physiologic variables were collected in addition to rTEG and laboratory values. Primary outcome was in-hospital mortality. Data was used to construct a multivariate logistic regression model with in-hospital mortality as the dependent variable.
The study population included 356 children, 311 survivors and 45 (13%) non-survivors. The primary mechanism of injury was blunt trauma (84%) with a median ISS of 16. Cause of death was hemorrhage in 4 (9%) and head injury in 41 (91%). On rTEG, non-survivors had significantly longer activated clotting time (152 vs. 121, p<0.001) and k-time (speed of clot formation, 2.6 vs. 1.2, p<0.001); with decreased mA (platelet contribution to clot strength, 49 vs. 66, p=0.009). Non-survivors also had significant differences on conventional laboratory analysis including higher INR (1.55 vs. 1.12, p<0.001) and lower platelet counts (197 vs. 317, p<0.001). Hypotension, hypothermia and tachycardia were more common in non-survivors. rTEG was not an independent predictor of mortality on regression analysis. Independent predictors of mortality were head injury severity (AIS, OR 3.65), arrival temperature (OR 0.58) and base deficit (OR 1.36).
Though this is the largest series of rTEG in young pediatric trauma patients, it is limited by the retrospective, single center methodology; the unknown impact of receiving pre-hospital procoagulant therapies or blood products and the lack of rTEG data available for those dying within 30 minutes. In summary, trauma-induced coagulopathy is associated with, but not independently predictive of in-hospital with mortality in young trauma patients. Factors independently associated with mortality were head injury severity, hypothermia and base deficit on arrival.