The r-TEG data was clinically superior to results from 5 CCTs. In addition, r-TEG identified patients with an increased risk of early RBC, plasma and platelet transfusions, and fibrinolysis. Admission CCTs can be replaced with r-TEG.

OBJECTIVE To determine if implementation of damage control resuscitation (DCR) in patients undergoing damage control laparotomy (DCL) translates into improved survival. SUMMARY BACKGROUND DATA DCR aims at preventing coagulopathy through permissive hypotension, limiting crystalloids and delivering higher ratios of plasma and platelets. Previous work has focused only on the impact of delivering higher ratios (1:1:1). METHODS A retrospective cohort study was performed on all DCL patients admitted between 01/2004–08/2010. Patients were divided into pre-DCR implementation and DCR groups, and were excluded if they died prior to completion of the initial laparotomy. The lethal triad was defined as immediate post-operative temperature <95° F, INR>1.5, or a pH<7.30. RESULTS 390 patients underwent DCL. Of these, 282 were pre-DCR and 108 were DCR. Groups were similar in demographics, injury severity, admission vitals and laboratory values. DCR patients received less crystalloids (median 14 L vs. 5 L), RBC (13 U vs. 7 U), plasma (11 U vs. 8 U) and platelets (6 U vs. 0 U) in 24-hr; all p<0.05. DCR patients had less evidence of the lethal triad upon ICU arrival (80% vs. 46%, p<0.001). 24-hour and 30-day survival were higher with DCR (88% vs. 97%, p=0.006 and 76% vs. 86%, p=0.03). Multivariate analysis controlling for age, injury severity, and ED variables, demonstrated DCR was associated with a significant increase in 30-day survival (O.R. 2.5, 95% C.I. 1.10–5.58, p=0.028). CONCLUSION In patients undergoing DCL, implementation of DCR reduces crystalloid and blood product administration. More importantly, DCR is associated with an improvement in 30-day survival.

No abstract

Prognostic study, level III.

Crystalloid-based resuscitation of severely injured trauma patients leads to intestinal edema. A potential mechanism of intestinal edema-induced ileus is a reduction of myosin light chain phosphorylation in intestinal smooth muscle. We sought to determine if the onset of edema initiated a measurable, early mechanotransductive signal and if hypertonic saline (HS) can modulate this early signal by changing intestinal fluid balance. An anesthetized rat model of acute interstitial intestinal edema was used. At laparotomy, the mesenteric lymphatic was cannulated to measure lymph flow and pressure, and a fluid-filled micropipette was placed in the intestinal submucosa to measure interstitial pressure. Rats were randomized into four groups (n=6 per group): sham, mesenteric venous hypertension+80 mL/kg 0.9% isotonic sodium chloride solution (ISCS 80), mesenteric venous hypertension+80 mL/kg 0.9% ISCS+4 mL/kg 7.5% saline (ISCS 80+HS), or 4 mL/kg 7.5% saline (HS alone) to receive the aforementioned intravenous fluid administered over 5 min. Measurements were made 30 min after completion of the preparation. Tissue water, lymph flow, and interstitial pressure were measured. Resultant applied volume induced stress on the smooth muscle (sigmaravi-muscularis) was calculated. Mesenteric venous hypertension and crystalloid resuscitation caused intestinal edema that was prevented by HS. Intestinal edema caused an early increase in intestinal interstitial pressure that was prevented by HS. Hypertonic saline did not augment lymphatic removal of intestinal edema. sigmaravi-muscularis was increased with onset of edema and prevented by HS, paralleling the interstitial pressure data. Intestinal edema causes an early increase in interstitial pressure that is prevented by HS. Prevention of the edema-induced increase in interstitial pressure serves to blunt the mechanotransductive signal of sigmaravi-muscularis.