Hypothesis: Clinical study can help determine the safety and cardiovascular
and systemic effects of an early infusion of 7.5% sodium chloride in 6% de
xtran-70 (hypertonic saline-dextran-70 [HSD]) given as an adjuvant to a sta
ndard resuscitation with lactated Ringer (RL) solution following severe the
rmal injury.
Design: Prospective clinical study.
Setting: Intensive care unit of tertiary referral burn care center.
Patients: Eighteen patients with thermal injury over more than 35% of the t
otal body surface area (TBSA) (range, 36%-71%) were studied.
Interventions: Eight patients (mean +/- SEM, 48.2% +/- 2% TBSA) received a
4-mL/kg HSD infusion approximately 3.5 hours (range, 1.5-5.0 hours) after t
hermal injury in addition to routine RL resuscitation. Ten patients (46.0%
+/- 6% TBSA) received RL resuscitation alone.
Main Outcome Measures: Pulmonary artery catheters were employed to monitor
cardiac function, while hemodynamic, metabolic, and biochemical measurement
s were taken for 24 hours.
Results: Serum troponin 1 levels, while detectable in all patients, were si
gnificantly lower after HSD compared with RL alone (mean +/- SEM, 0.45 +/-
0.32 vs 1.35 +/- 0.35 mu g/L at 8 hours, 0.88 +/- 0.55 vs 2.21 +/- 0.35 mu
g/L at 12 hours). While cardiac output increased proportionately between 4
and 24 hours in both groups (from 5.79 +/- 0.8 to 9.45 +/- 1.1 L/min [mean
+/- SEM] for HSD vs from 5.4 +/- 0.4 to 9.46 +/- 1.22 L/min for RL), fillin
g pressure (central venous pressure and pulmonary capillary wedge pressure)
remained low for 12 hours after HSD infusion (P =.048). Total fluid requir
ements at 8 hours (2.76 +/- 0.7 mL/kg per each 1% TBSA burned [mean +/- SEM
] for HSD vs 2.67 +/- 0.24 mL/kg per each 1% TBSA burned for eL) and 24 hou
rs (6.11 +/- 4.4 vs 6.76 +/- 0.75 mL/kg per each 1% TBSA burned) were simil
ar. Blood pressure remained unchanged, and serum sodium levels did not exce
ed 150 +/- 2 mmol/L (mean +/- SD) in either group.
Conclusions: The absence of deleterious hemodynamic or metabolic side effec
ts following HSD infusion in patients with major thermal injury confirms th
e safety of this resuscitation strategy. Postburn cardiac dysfunction was d
emonstrated in all burn patients through the use of cardiospecific serum ma
rkers and pulmonary artery catheter monitoring. Early administration of HSD
after a severe thermal injury may reduce burn-related cardiac dysfunction,
but it had no effect on the volume of resuscitation or serum biochemistry
values.