Cardiovascular effect of 7.5% sodium chloride-dextran infusion after thermal injury

Citation
Jt. Murphy et al., Cardiovascular effect of 7.5% sodium chloride-dextran infusion after thermal injury, ARCH SURG, 134(10), 1999, pp. 1091-1097
Citations number
29
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
ARCHIVES OF SURGERY
ISSN journal
00040010 → ACNP
Volume
134
Issue
10
Year of publication
1999
Pages
1091 - 1097
Database
ISI
SICI code
0004-0010(199910)134:10<1091:CEO7SC>2.0.ZU;2-M
Abstract
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.