Massive burn injury alters both the physical appearance and the functional ability of the child. The changed body necessitates concomitant alteration of the internal self-image, including feelings about the internal self or self-esteem. Six children of primary school age are being followed up in a prospective, longitudinal study to track their adaptation to burn disfigurement. Results of the first 5 1/2 years reveal that, initially, all children displayed pervasive developmental regression, accompanied by phobias, nightmares, and various other symptoms. Two years later, one half of the children had returned to the average range of development attainment. By the fifth year, five of the six children had returned to an average level of progressive personality development. The sixth child was progressing well considering cognitive and emotional deficits before the burn injury. A primary factor influencing adaptation appeared to be the role of the parent or parents in facilitating the acquisition of a positive self-image and in launching and maintaining active mastery in their children.
Background Factors contributing to mortality in burned children with acute renal failure have been identified; however, they have not been identified in thermally injured adults. Methods The records of 1,404 acutely burned adults admitted to the Blocker Burn Unit were reviewed. Seventy-six patients with acute renal dysfunction and burns covering more than 30% of their total body surface area with a full-thickness component greater than 10% total body surface area were identified. These patients were divided into those admitted from 1981 through 1989 (n = 35) and those admitted from 1990 to 1998 (n = 41). Results No significant differences could be shown in the incidence of acute renal dysfunction (5.4 vs. 5.1%) or mortality (88 vs. 87%) for the two time periods, respectively. Sixty-seven percent of the survivors were younger than 40 years of age, compared with only 25% of nonsurvivors (p < 0.02); sepsis was identified in 44 and 96% of survivors and nonsurvivors, respectively (p < 0.001). Fluid resuscitation was delayed in survivors by 1.7 +/- 1.0 hours compared with 4.4 +/- 2.1 hours in nonsurvivors (p < 0.001). Conclusion Early fluid resuscitation and the prevention of sepsis may reduce the incidence of acute renal dysfunction and mortality in burned adults.
Recombinant human growth hormone (rhGH) and hepatocyte growth factor (HGF) have both been shown to individually modulate hepatic acute phase reactant proteins and cytokine expression following trauma through different pathways. Recombinant hGH has also been shown to decrease serum and hepatic HGF concentrations after a thermal injury. We hypothesized that the combination of rhGH plus HGF improves the burn-induced acute phase response. Fifty-six male Sprague-Dawley rats received a 60% TBSA third-degree scald burn and were randomly divided to receive either rhGH (2.5 mg/kg/day sc.) plus HGF (200 microg/kg i.v. every 12 h) or placebo (saline). Rats were sacrificed on post-burn days 1, 2, 5, or 7 and serum constitutive and acute phase proteins, TNF-alpha, IL-1beta, IL-6 and liver total protein measured. Hepatic cytokine gene expression, triglyceride concentration, and hepatocyte proliferation were also measured. In rats receiving rhGH/HGF, serum albumin increased on days 5 and 7 and transferrin on day 7 after burn compared to placebo (P<0.05). Haptoglobin decreased 5 days after burn compared to placebo (P<0.05). RhGH/HGF increased serum TNF-alpha on day 2 after burn, while it decreased serum IL-1beta on day 1 after burn compared with placebo (P<0.05). RhGH/HGF had no effect on hepatic cytokine gene expression compared with placebo. Liver total protein content and hepatocyte proliferation increased on days 1, 2, 5, and 7 after burn with rhGH/HGF treatment (P<0.05). These findings indicate that rhGH in combination with HGF exert additive effects on constitutive hepatic proteins and partial inhibitory effects on acute phase protein and cytokine expression. RhGH/HGF has a strong mitogenic effect on hepatocytes.
The availability of donor sites is a limiting factor in autologous skin grafting and, therefore, the survival of patients with large total body surface area (TBSA) burns. Of 19 males admitted to our facilities with burns greater than 80% TBSA, eight had the scrotum spared injury. The remaining 11 patients served as a control population to study the efficacy of scrotal donor harvests. The scrotal skin was expanded using the Pitkin syringe and harvested at a depth of 5/1000 to 8/1000 in, with a mean yield of 73 +/- 8 sq cm. Expanded 4:1, this tissue covered an area of 280 +/- 33 sq cm. The scrotum was harvested 2 +/- 0.4 times, compared to 4 +/- 1 harvests of the other donor group. There were no statistical differences in the number of surgical procedures or the length of hospitalization between the two groups. The scrotal donor sites healed within the same length of time as other donor sites and were harvestable as frequently. Due to the natural expandability of scrotal skin, a large surface area of usable donor site is available and their harvest may be lifesaving in male patients with large TBSA burns.
This study tests the hypothesis that halothane-induced inhibition of the endothelium-derived relaxing factor/nitric oxide (EDRF/NO) pathway significantly contributes to cardiovascular performance and thus reduces the vasoconstrictor response to NO synthesis inhibitors in vivo. We determined the effects of the administration of the NO synthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in chronically instrumented, halothane-anesthetized sheep and in awake control animals. Six sheep underwent halothane anesthesia (1.5 vol%) with mechanical ventilation. Five sheep were studied in the awake state with spontaneous breathing. Both groups received a bolus of L-NAME (25 mg/kg), followed 4 h later by L-arginine (300 mg/kg) to reverse the effects of L-NAME. L-NAME administration caused a significant increase in pulmonary and systemic vascular resistance (P < 0.05) in both groups. However, L-NAME produced a sharp increase in mean arterial and pulmonary artery pressures only in the control group, whereas the pressor response in the halothane group was attenuated. Cardiac output, which was significantly lower after L-NAME administration in both groups, increased after L-arginine. The results suggest that halothane does not significantly alter the EDRF/NO-mediated effects on the vasculature but potentiates the cardiac depressant effect of L-NAME.
Formulas for estimating the caloric requirements of pediatric patients with burns have been suggested. However, the needs of infant patients with burns have not been specifically addressed. This study was undertaken to determine the caloric intake required to maintain weight in patients under 1 year of age who had burns covering more than 25% total body surface area. Thirty patients were studied, and a comparison was made between the actual intake required for weight maintenance and the suggested calorie levels provided by published pediatric caloric formulas. The results indicated that a new formula was needed. Multivariate regression analysis indicated that body surface area and burn surface area were significant predictors of caloric requirements, but body surface area was the more important predictor in this infant population. The equation resulting from the regression provides 2100 kcal/m2 body surface area/day plus 1000 kcal/m2 body surface area burned/day.
Objective To modulate the hepatic acute phase response after a thermal injury by the administration of insulinlike growth factor I (IGF-I) in combination with its principal binding protein 3 (IGFBP-3). Summary Background Data The hepatic acute phase response is a cascade of events initiated to restore homeostasis after trauma; however, a prolonged response contributes to multiorgan failure, hypermetabolism, complications, and death. Although IGF-1 has been shown to improve cell recovery and play a major role in liver regeneration, its effect on the hepatic acute phase response is not known. Methods Sprague-Dawley rats (56 males) received a 60% total body surface area third-degree scald burn and were randomly divided to receive either rhIGF-I/BP-3 (10 mg/kg/day given subcutaneously) or saline (control). Rats were killed on postburn days 1, 2, 5, and 7 and serum glucose, electrolytes, acute phase reactant proteins, tumor necrosis factor α, interleukin 1β, interleukin 6, and rat and human serum IGF-I and IGFBP-3 were measured. Hepatic protein concentrations, hepatocyte proliferation, and hepatocyte apoptosis were determined. Results No hypoglycemia or electrolyte imbalance could be shown in rats receiving the growth factor complex compared with saline. rhIGF-I/BP-3 increased serum protein on postburn days 2 and 7, albumin on days 5 and 7, and transferrin on days 1, 5, and 7, and decreased haptoglobin and α1-acid glycoprotein on postburn days 5 and 7 compared with controls. IGF-I/BP-3 had no effect on type II acute phase proteins. Rats receiving IGF-I/BP-3 had lower serum levels of interleukin 1β and tumor necrosis factor α on the first day after burn compared with controls, whereas serum levels of interleukin 6 did not change. rhIGF-I/BP-3 significantly increased total liver protein content on postburn days 1, 2, 5, and 7 compared with controls. IGF-I/BP-3 increased hepatocyte proliferation and decreased hepatocyte apoptosis versus controls. Conclusion In combination with its principal binding protein, rhIGF-I decreases the proinflammatory cytokines interleukin 1β and tumor necrosis factor α, followed by a decrease in type I acute phase proteins. IGF-I/BP-3 had no effect on interleukin 6 and type II acute phase proteins. Decreases in acute phase protein and proinflammatory cytokine synthesis were associated with increases in constitutive hepatic proteins, total liver protein content, and hepatocyte proliferation. IGF-I/BP-3 attenuates the hypermetabolic response after thermal injury and may improve the clinical outcome.
Burn injury and sepsis have been repeatedly demonstrated to impair the function of circulating (blood) neutrophils. As a result of the difficulty in harvesting and purifying neutrophils from the burn wound, there have been minimal investigations to date on the effect of burn injury and sepsis on the function of neutrophils which have reached the wound. We utilized a sponge matrix model in order to obtain neutrophils from burned and burned-infected rats. Despite having a higher concentration of neutrophils in the blood, both the burned and burned-infected rats were noted to have a decreased number of neutrophils infiltrating the sponge compared with the controls (1.91 ± 0.30 X 106, 2.31 ± 0.47 X 106, and 4.82 ± 0.64 X 106 neutrophils per sponge, respectively). Blood neutrophils from both the burned and burned-infected rats had a greater chemiluminescence capacity than neutrophils from the control group (p<0.0001). This enhanced capacity was not present with sponge neutrophils obtained from the burned-infected group. The diminished capacity may have been the result of a decreased concentration of prostaglandin E in the sponge fluid of the burned-infected rats compared with that of the burned or control rats (52 ± 9, 135 ± 15, and 114 ± 13 pg/mL of sponge fluid, respectively).
