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

Joseph T. Murphy, Jureta W. Horton, Gary F. Purdue, John L. Hunt

Research output: Contribution to journalArticle

25 Citations (Scopus)

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% dextran-70 (hypertonic saline-dextran-70 [HSD]) given as an adjuvant to a standard resuscitation with lactated Ringer (RL) solution following severe thermal injury. Design: Prospective clinical study. Selling: Intensive care unit of tertiary referral burn care center. Patients: Eighteen patients with thermal injury over more than 35% of the total 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 thermal 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 measurements were taken for 24 hours. Results: Serum troponin I levels, while detectable in all patients, were significantly lower after HSD compared with RL alone (mean ± SEM, 0.45 ± 0.32 vs 1.35 ± 0.35 μg/L at 8 hours, 0.88 ± 0.55 vs 2.21 ± 0.35 μg/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), filling pressure (central venous pressure and pulmonary capillary wedge pressure) remained low for 12 hours after HSD infusion (P= .048). Total fluid requirements at 8 hours (2.76 ± 0.7 mL/kg per each 1% TBSA burned [mean ± SEMI for HSD vs 2.67 ± 0.24 mL/kg per each 1% TBSA burned for RL) and 24 hours (6.11 ± 4.4 vs 6.76 ± 0.75 mL/kg per each 1% TBSA burned) were similar. Blood pressure remained unchanged, and serum sodium levels did not exceed 150 ± 2 mmol/L (mean ± SD) in either group. Conclusions: The absence of deleterious hemodynamic or metabolic side effects following HSD infusion in patients with major thermal injury confirms the safety of this resuscitation strategy. Postburn cardiac dysfunction was demonstrated in all burn patients through the use of cardiospecific serum markers 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.

Original languageEnglish (US)
Pages (from-to)1091-1097
Number of pages7
JournalArchives of Surgery
Volume134
Issue number10
DOIs
StatePublished - Oct 1999

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Dextrans
Sodium Chloride
Hot Temperature
Body Surface Area
Wounds and Injuries
Resuscitation
Pulmonary Artery
Catheters
Hemodynamics
Serum
Safety
Burn Units
Central Venous Pressure
Pulmonary Wedge Pressure
Troponin I
Burns
Cardiac Output
Biochemistry
Intensive Care Units
Referral and Consultation

ASJC Scopus subject areas

  • Surgery

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Cardiovascular effect of 7.5% sodium chloride-dextran infusion after thermal injury. / Murphy, Joseph T.; Horton, Jureta W.; Purdue, Gary F.; Hunt, John L.

In: Archives of Surgery, Vol. 134, No. 10, 10.1999, p. 1091-1097.

Research output: Contribution to journalArticle

Murphy, Joseph T. ; Horton, Jureta W. ; Purdue, Gary F. ; Hunt, John L. / Cardiovascular effect of 7.5% sodium chloride-dextran infusion after thermal injury. In: Archives of Surgery. 1999 ; Vol. 134, No. 10. pp. 1091-1097.
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title = "Cardiovascular effect of 7.5{\%} sodium chloride-dextran infusion after thermal injury",
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{\%} dextran-70 (hypertonic saline-dextran-70 [HSD]) given as an adjuvant to a standard resuscitation with lactated Ringer (RL) solution following severe thermal injury. Design: Prospective clinical study. Selling: Intensive care unit of tertiary referral burn care center. Patients: Eighteen patients with thermal injury over more than 35{\%} of the total 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 thermal 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 measurements were taken for 24 hours. Results: Serum troponin I levels, while detectable in all patients, were significantly lower after HSD compared with RL alone (mean ± SEM, 0.45 ± 0.32 vs 1.35 ± 0.35 μg/L at 8 hours, 0.88 ± 0.55 vs 2.21 ± 0.35 μg/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), filling pressure (central venous pressure and pulmonary capillary wedge pressure) remained low for 12 hours after HSD infusion (P= .048). Total fluid requirements at 8 hours (2.76 ± 0.7 mL/kg per each 1{\%} TBSA burned [mean ± SEMI for HSD vs 2.67 ± 0.24 mL/kg per each 1{\%} TBSA burned for RL) and 24 hours (6.11 ± 4.4 vs 6.76 ± 0.75 mL/kg per each 1{\%} TBSA burned) were similar. Blood pressure remained unchanged, and serum sodium levels did not exceed 150 ± 2 mmol/L (mean ± SD) in either group. Conclusions: The absence of deleterious hemodynamic or metabolic side effects following HSD infusion in patients with major thermal injury confirms the safety of this resuscitation strategy. Postburn cardiac dysfunction was demonstrated in all burn patients through the use of cardiospecific serum markers 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.",
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N2 - Hypothesis: Clinical study can help determine the safety and cardiovascular and systemic effects of an early infusion of 7.5% sodium chloride in 6% dextran-70 (hypertonic saline-dextran-70 [HSD]) given as an adjuvant to a standard resuscitation with lactated Ringer (RL) solution following severe thermal injury. Design: Prospective clinical study. Selling: Intensive care unit of tertiary referral burn care center. Patients: Eighteen patients with thermal injury over more than 35% of the total 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 thermal 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 measurements were taken for 24 hours. Results: Serum troponin I levels, while detectable in all patients, were significantly lower after HSD compared with RL alone (mean ± SEM, 0.45 ± 0.32 vs 1.35 ± 0.35 μg/L at 8 hours, 0.88 ± 0.55 vs 2.21 ± 0.35 μg/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), filling pressure (central venous pressure and pulmonary capillary wedge pressure) remained low for 12 hours after HSD infusion (P= .048). Total fluid requirements at 8 hours (2.76 ± 0.7 mL/kg per each 1% TBSA burned [mean ± SEMI for HSD vs 2.67 ± 0.24 mL/kg per each 1% TBSA burned for RL) and 24 hours (6.11 ± 4.4 vs 6.76 ± 0.75 mL/kg per each 1% TBSA burned) were similar. Blood pressure remained unchanged, and serum sodium levels did not exceed 150 ± 2 mmol/L (mean ± SD) in either group. Conclusions: The absence of deleterious hemodynamic or metabolic side effects following HSD infusion in patients with major thermal injury confirms the safety of this resuscitation strategy. Postburn cardiac dysfunction was demonstrated in all burn patients through the use of cardiospecific serum markers 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.

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