Hypothesis: Reticuloendothelial system function is altered in patients with
multiple trauma and organ failure.
Design: Prospective cohort study.
Setting: Surgical intensive case unit at a level I trauma center. patients:
Patients with multiple blunt trauma and injury severity scores greater than
20, with no referrals.
Interventions: Every second day reticuloendothelial system (RES) clearance
capacity and liver blood flow were determined by administering labeled huma
n albumin. Liver function was measured by enzymatic decay of indocyanine gr
een, and levels of plasma tumor necrosis factor alpha were evaluated.
Results: In nonsurviving patients with blunt trauma, RES function was alter
ed and was associated with organ dysfunction and infectious complications.
Of 61 patients, 42 survived and 19 did not. Sixteen patients (84%) died of
multiple organ failure. Significantly elevated RES activity (colloid cleara
nce rate) was present between day 5 and day 13 after trauma in nonsurvivors
(0.86 +/- 0.16 [mean +/- SD] on day 7, P = .003) compared with survivors (
0.48+/-0.08 on day 7) and 20 healthy volunteers (0.47 +/- 0.06); RES activi
ty then decreased to subnormal levels in nonsurvivors. Tumor necrosis facto
r alpha plasma levels were elevated early after injury only in nonsurvivors
ton day 1:nonsurvivors, 1.2 +/- 0.4 ng/mL [mean +/- SD]; survivors, 0.5 +/
- 0.2 ng/mL; P = .02). Indocyanine green half-life values increased late af
ter trauma, indicating late organ failure (on day 19: nonsurvivors, 111 +/-
29 minutes [mean +/- SD]; survivors, 12 +/- 4 minutes; P<.001).
Conclusions: Early after trauma, nonsurviving patients demonstrated increas
ed proinflammatory cytokine levels, followed by a state of pathological hyp
eractivation of the reticuloendothelial system prior to death. These result
s indicate that the stationary host defense system is involved in the mecha
nisms causing organ failure after severe trauma.