Resuscitation of severe thermal injury with hypertonic saline dextran: effects on peripheral and visceral edema in sheep.

BACKGROUND: Edema of tissue not directly injured by heat is a common complication after resuscitation of burn shock. Hypertonic 7.5% NaCl 6% dextran (HSD) infusion reduces early fluid requirements in burn shock, but the effects of HSD on peripheral and visceral tissue edema are not well-defined. METHODS: We measured the microcirculatory absorptive pressures of burned and nonburned skin and tissue water content of skin and other tissues in anesthetized sheep after 70% to 85% total body surface area scald and resuscitation. Fluid infusion was initiated 30 minutes after injury using 10 mL/kg HSD (n = 11) or lactated Ringer's (LR) (n = 12), with infusion rates titrated to restore and maintain preburn oxygen delivery (DO2). Thereafter, both groups received LR infusions as needed to maintain DO2 until the study's end at 8 hours. Colloid osmotic pressure was measured in plasma, and combined interstitial colloid osmotic and hydrostatic pressures were measured in skin. RESULTS: Both treatments successfully restored DO2, but fluid requirements were less with the HSD group than with the LR group (43+/-19 mL/kg vs. 194+/-38 mL/kg, respectively, p < 0.05). The peripheral and visceral tissue water contents at 8 hours postinjury until the end of the study in both burn groups were significantly higher than in nonburn controls. However, HSD-treated sheep had significantly less water content in the colon (less 28%), liver (less 9%), pancreas (less 55%), skeletal muscle (less 21%), and nonburned skin (less 12%) compared with LR-treated sheep (p < 0.05 for each). HSD-treated sheep maintained significantly higher (3 to 5 mm Hg) plasma colloid osmotic pressure than LR-treated sheep. CONCLUSION: There were no observed differences in edema in burn skin between the two treatment groups. The early volume-sparing effect of HSD and reduction in tissue edema are likely attributed to an increased extracellular osmolarity and a better maintenance of the plasma oncotic pressure.

Effect of cutaneous burn injury and resuscitation on the cerebral circulation in an ovine model.

The aim of our study was to evaluate the effects of a large cutaneous burn injury on the cerebral circulation. Anesthetized sheep (n = 8) were prepared with vascular catheters, a urinary catheter and a Richmond bolt for intracranial pressure monitoring. A scald injury was inflicted on 70 percent of total body surface area with hot water. Resuscitation was started 30 min after scald with Ringer's lactate to restore and maintain baseline oxygen delivery. Resuscitation maintained blood pressure, cardiac output and urine output at normal levels. Brain blood flow was measured with colored microspheres. During resuscitation intracranial pressure rose slowly from 10.6 +/- 1.5 to 17.0 +/- 4.0 mmHg (P < 0.05) and cerebral perfusion pressure was reduced from 86.4 +/- 6.8 to 64.1 +/- 2.8 mmHg (P < 0.05). During early resuscitation cerebrovascular resistance declined to maintain brain blood flow and oxygen delivery at baseline or better. After 6 h, mean cerebrovascular resistance was inappropriately increased during a period of reduced cerebral perfusion pressure which resulted in brain blood flow reductions of half the baseline levels. These data suggest that autoregulation maintains brain blood flow immediately after burn shock and early resuscitation, but the autoregulation may be less effective as burn resuscitation proceeds.

The role of interstitial starling forces in the pathogenesis of burn edema.

The formation and sustainability of burn edema require substantial change in net microvascular forces. We directly measured interstitial hydrostatic pressure (Pi) and total interstitial absorptive pressure (Pi + IIi), in dermis of anesthetized sheep, before and after a 70% to 85% total body surface area scald and during fluid resuscitation. The most rapid change occurred in Pi in the burn wound, which rapidly decreased from its baseline value of approximately -2 mm Hg to -11 mm Hg in the first 5 minutes, and thereafter increased but remained approximately -4 mm Hg through 4 hours of resuscitation. Pi in nonburned skin slowly increased from its preburn level -2 mm Hg, to become positive +1 mm Hg after 4 hours of resuscitation. The total interstitial absorptive pressure, Pi + IIi, slowly declined similarly from 15 to 16 mm Hg to approximately 10 to 11 mm Hg over 6 hours of resuscitation in both burned and nonburned dermis. Taken together, these data suggest that the rapid formation of burn edema is the result of development of a negative Pi in the burn wound, and its sustainability is the result of a large increase in interstitial compliance. Edema in nonburned skin did not start until after fluid resuscitation was initiated, and then developed as the plasma oncotic pressure declined from 21 to 10 mm Hg.

A comparison of two different 2400 mOsm solutions for resuscitation of major burns.

The reduction of burn edema is a common goal in the resuscitation of patients with thermal injury. Initial infusion of a 2400 mOsm hypertonic 7.5% NaCl 6% dextran (HSD) has been shown to reduce volume needs, but elevated serum sodium levels limit the dose that can be safely used. This study tested the hypothesis that a 2400 mOsm solution of NaCl, amino acids, glucose, and 6% dextran (Isosal-D) would reduce similar volume requirements while maintaining normal plasma sodium levels. Hemodynamics, plasma sodium, fluid balance, and tissue water content were measured after an initial baseline period and during resuscitation of a large scald injury in 21 anesthetized sheep. Resuscitation was begun 30 minutes after the scald with infusion of 10 ml/kg of either lactated Ringer's (LR), Isosal-D, or HSD and was continued with LR to restore and maintain baseline oxygen delivery throughout the 8-hour period. Oxygen delivery, cardiac output, and mean arterial pressure were rapidly reestablished by all three solutions, although a persistent tachycardia was noted with Isosal-D. Net fluid requirements of both HSD (35 +/- 13 ml/kg) and Isosal-D (72 +/- 13 ml/kg) were significantly lower than in the LR group (203 +/- 39 ml/kg). Mean serum sodium increased 11 mEq with HSD to a peak after 4 hours of 152 +/- 5 mEq, whereas with LR sodium fell 7 mEq to 132 +/- 4. Isosal-treated animals had minimal change in serum sodium. HSD significantly decreased tissue water content in colon, liver, pancreas, and nonburned skin compared with LR, whereas Isosal-D reduced edema only in the colon. It is concluded that in this protocol Isosal-D was not as effective as HSD at reducing volume needs and edema and had unexpected chronotropic effects.

Burn resuscitation: crystalloid versus colloid versus hypertonic saline hyperoncotic colloid in sheep.

OBJECTIVES: The present study was undertaken to assess the fluid balance and hemodynamic effects during the first 8 hrs of resuscitation in animals with a large body surface area burn, using lactated Ringer's solution, 6% hetastarch, and hypertonic saline dextran. DESIGN: A prospective, blinded, controlled, terminal study, using anesthetized animals. The initial baseline period was followed by scald injury, and three different treatment regimens were administered from coded bags to achieve a physiologic end point. SETTING: University laboratory. SUBJECTS: Eighteen female sheep (35 to 45 kg) were anesthetized with isoflurane. INTERVENTIONS: Test solutions (10 mL/kg of either lactated Ringer's solution, hetastarch, or hypertonic saline dextran) were infused 30 mins after the scald injury at a rate to restore and maintain the baseline oxygen delivery (DO2) value. MEASUREMENTS AND MAIN RESULTS: Cardiovascular hemodynamics, plasma sodium concentration, plasma colloid osmotic pressure, and fluid balance were measured before and after scalding and resuscitation. After the initial 10-mL/kg test solution dose was given, lactated Ringer's solution was infused to achieve the same end point of baseline DO2 for the remainder of the 8 hrs. The scald caused an initial 30% reduction in cardiac output, a 20% reduction in mean arterial pressure, and 10% to 15% increase in hematocrit. All three test solutions restored and maintained baseline DO2 within 1 hr. However, hetastarch and hypertonic saline dextran reduced the net fluid volume over 8 hrs by 48% and 74%, respectively, compared with lactated Ringer's solution. Edema in the burn wound was not affected by treatment, while hypertonic saline dextran reduced edema in nonburned skin compared with both lactated Ringer's solution and hypertonic saline dextran. Plasma colloid osmotic pressure was significantly higher in the hetastarch and hypertonic saline dextran groups. A continuous decrease in plasma sodium concentrations from baseline values (140 to 145 mmol/L) was measured in the lactated Ringer's solution and hetastarch groups (130 to 133 mmol/L) over 8 hrs. Plasma sodium concentrations in the group receiving hypertonic saline dextran were increased (150 to 155 mmol/L) at 4 hrs, but returned toward baseline by 8 hrs. CONCLUSIONS: Net volume loading can be reduced markedly by initial resuscitation of large body surface area burn injury using a colloid (hetastarch), and can be further reduced by use of hypertonic saline colloid. Hyponatremia was apparent in the isotonic crystalloid- and colloid-treated animals, but not in those animals treated with hypertonic saline colloid.