Mean Burn Size Research Articles

Visceral blood flow following thermal injury.

To determine if visceral blood flow was altered by thermal injury, effective renal blood flow (ERBF) was measured by para-aminohippurate clearance in five control subjects and 13 nonbacteremic burn patients (mean burn size: 50% total body surface, range: 24.5-83.5) 6-25 days after burn injury. Splanchnic blood flow (SBF) and cardiac output were determined in a matched group of ten patients by indocyanine green clearance and dilution techniques, respectively. Renal and splanchnic oxygen consumptions (VO2) were calculated from regional arteriovenous O2 differences and blood flows. ERBF was not significantly elevated in these patients (780 +/- 68 ml/min x m2, mean +/- SE, versus 552 +/- 37 in controls). SBF, at 1463 +/- 96 ml/min x m2, was twice normal and 19% of the cardiac index (7764 +/- 393 ml/min x m2). Individual variations in ERBF and SBF were unrelated to burn size or the time after injury, but ERBF varied with 24-hour sodium excretion. Renal and splanchnic VO2 were twice normal levels at 33 +/- 6 and 66 +/- 4 ml/min, respectively. These results indicate that an increase in ERBF is not an obligatory response to burn injury, but is dependent on sodium load and/or vascular volume. Conversely, SBF is consistently increased by thermal injury and contributes to the rise in cardiac output after injury. While the increase of SBF is appropriate for the rise in local VO2, the cause of the apparent splanchnic vasodilation is unknown.

Free T4, free T3, and reverse T3 in critically ill, thermally injured patients.

A prospective study of thyroid function was performed in 25 thermally injured patients. These patients are divided into two groups. The first group contains five patients with greater than 50% burn size studied longitudinally during the first 15 days following thermal injury. Significant suppression of serum concentrations of 3,5,3'-triiodothyronine (T3) and elevation of serum concentrations of 3,3',5'-triiodothyronine (rT3) were seen. The free thyroxine index and serum TSH concentrations remained within the normal range. To assess the clinical significance of these alterations in peripheral thyroid hormone concentrations, a second group of 20 patients was studied. We measured the free serum levels of T4 (FT4) and T3 (FT3) in ten patients, mean age 34 years, mean burn size 56%, studied during a period of clinical deterioration, and in ten patients of comparable age and burn size who were clinically stable. Both FT4 and T3 values were significantly lower in the unstable patients (p < 0.01). All FT3 values for the unstable patients (M +/- SE), 193 +/- 14 pg/dl, were below the normal range for FT3 of 230 to 669 pg/dl, and significantly lower than those observed in the stable patients (M +/- SE), 430 +/- 59 pg/dl (p < 0.001). This correlation of biochemical hypothyrodisim with clinical deterioration may have functional significance for the critically ill trauma patient.

Muscle blood flow following thermal injury.

Peripheral circulation is markedly increased during the hyperdynamic-hypermetabolic phase of thermal injury and appears to be directed primarily to the burn wound. To determine whether any portion of this extra blood flow reaches another major peripheral vascular bed, blood flow in the tibialis anterior muscle of the lower leg was measured by 133Xe clearance in ten hemodynamically stable, nonseptic burn patients (mean burn size = 42.5% total body surface) and five control subjects. Muscle blood flow was 3.52 +/- 0.26 ml/100 g.min (mean +/- S.E.M.) in these patients and 3.29 +/- 0.24 in controls, indicating that resting muscle perfusion was unaffected by the extent of total body surface injury, size of leg burn, or elevated rectal temperature (38.2 +/- 0.2 degrees C) of the patients. These results confirm the interpretations of previous studies suggesting that most of the increased peripheral blood flow following thermal injury is directed to the surface wound. Local and systemic factors responsible for the maintenance of muscle perfusion in the face of alterations in muscle metabolism following thermal injury are discussed.

Burn survival in a developing country

This paper presents survival rates among 533 burn patients admitted to the University of the Philippines-Philippines General Hospital Medical Center from 1969 to 1976. Mean burn size was 2357 per cent and the mean age was 1827 years. Survival in burns of less than 20 per cent has remained excellent, but in burns of 60 per cent and over survival has remained very poor. Comparison of survival rates with figures from the National Burn Information Exchange in the United States shows surprisingly similar results.

Wound Excision to Fascia in Burn Patients

All charts of burn patients admitted to the US Army Institute of Surgical Research over a four-year period were reviewed to determine the efficacy of excision of the burn wound to fascia as a therapeutic modality. Of 1,013 burn patients, 72 underwent this procedure. The patients who had excisions had a mean total burn size of 52% of body surface area (BSA) and a mean third-degree burn of 33%. We correlated survival with burn size, associated injuries, day of excision, wound coverage, and sepsis. Survival in the group who had excisions (57%) did not differ substantially from that of the other patients (38%) when broken down by burn size. Careful selection of patients for this procedure and criteria for selection are stressed.

Prospective Trials of Dexamethasone and Aerosolized Gentamicin in the Treatment of Inhalation Injury in the Burned Patient

The addition of an inhalation injury to a cutaneous burn results in a significant increase in patient mortality rates, both from early pulmonary edema and, later, Gram-negative pneumonitis. Steroids have been shown to decrease mortality in an inhalation injury model. Aerosolization of gentamicin has been used successfully to treat severe bronchial infections. Therefore, a prospective, randomized trial was undertaken to evaluate both these drugs. Sixty burned patients, with inhalation injury confirmed by bronchoscopy and 133Xenon scan, were studied: 30 patients received either dexamethasone or saline placebo for 3 days; serial pulmonary functions were measured on those able to cooperate; another 30 patients received either aerosolized gentamicin or placebo for 10 days. Both drug-treated groups were comparable to their controls in age and mean burn size. Results of the steroid trial showed no major differences in mortality, pulmonary complications, or changes in pulmonary functions. Results of the gentamicin trial showed no major differences in mortality, time of death, or pulmonary and septic complications between treated and control groups.

THE EFFECT OF CENTRAL NERVOUS SYSTEM NARCOSIS ON THE SYMPATHETIC RESPONSE TO STRESS

Heat production at the end of three hours of cold exposure (14°C) in normal men was significantly lower during He-O2 inhalation when compared with room air (43.8 ± 3.2 kcal/m2hr vs 58.8 ± 5.5, P < 0.05) as was core temperature (36.5 ± 0.1 vs 36.7 ± 0.1, P < 0.02). No effects on metabolism were noted in eight thermal neutral nonstressed studies (metabolic rate 37.8 ± 1.5 vs 35.2 ± 3.0, air vs He-O2). In six studies in normals, metabolism was unchanged following epinephrine infusion while breathing He-O2 (47.2 ± 2.0 vs 48.3 ± 0.9), suggesting helium dampens CNS sympathetic outflow but does not act as a peripheral blocking agent. Four burn patients (mean burn size 47% total body surface) were studied while breathing He-O2 for two hours, two (mean burn size 38%) while breathing argon-O2, and five (mean burn size 74%) following intravenous morphine administration. Hypermetabolism did not decrease with inhalation of the inert gases in the burn patient. However, morphine administration (0.38 mg/kg/hr) signficantly decreased oxygen consumption (77.4 ± 5.9 vs 55.0 ± 3.7), pulse rate (115 ± 4 beats/min vs 104 ± 5), core temperature (38.2 ± 0.1°C vs 37.3 ± 0.1), and minute ventilation (21.5 ± 2.5 liter/min. vs. 12.0 ± 1.0) while blood pressure and blood gases remained unchanged. The CNS response to injury or cold exposure may be dampened by central narcosis. The effect produced varies with the extent of stress, and some agents that modify mild stress in normal men exert no detectable effects on the hypermetabolic response to injury.

The effect of central nervous system narcosis on the sympathetic response to stress

Heat production at the end of three hours of cold exposure (14°C) in normal men was significantly lower during He-O 2 inhalation when compared with room air (43.8 ± 3.2 kcal/m 2hr vs 58.8 ± 5.5, P < 0.05) as was core temperature (36.5 ± 0.1 vs 36.7 ± 0.1, P < 0.02). No effects on metabolism were noted in eight thermal neutral nonstressed studies (metabolic rate 37.8 ± 1.5 vs 35.2 ± 3.0, air vs He-O 2). In six studies in normals, metabolism was unchanged following epinephrine infusion while breathing He-O 2 (47.2 ± 2.0 vs 48.3 ± 0.9), suggesting helium dampens CNS sympathetic outflow but does not act as a peripheral blocking agent. Four burn patients (mean burn size 47% total body surface) were studied while breathing He-O 2 for two hours, two (mean burn size 38%) while breathing argon-O 2, and five (mean burn size 74%) following intravenous morphine administration. Hypermetabolism did not decrease with inhalation of the inert gases in the burn patient. However, morphine administration (0.38 mg/kg/hr) signficantly decreased oxygen consumption (77.4 ± 5.9 vs 55.0 ± 3.7), pulse rate (115 ± 4 beats/min vs 104 ± 5), core temperature (38.2 ± 0.1°C vs 37.3 ± 0.1), and minute ventilation (21.5 ± 2.5 liter/min. vs. 12.0 ± 1.0) while blood pressure and blood gases remained unchanged. The CNS response to injury or cold exposure may be dampened by central narcosis. The effect produced varies with the extent of stress, and some agents that modify mild stress in normal men exert no detectable effects on the hypermetabolic response to injury.

Acute liver disease after cutaneous thermal injury.

To better define the acute liver disease complicating thermal injury, 81 burn patients were evaluated for hepatic damage. Clinical and laboratory evidence of hepatocellular injury was present as early as 24 hours after burn in 47 patients (58%). Patients with liver disease had a larger mean burn size (p less than 0.01) and greater mortality than patients with normal liver studies. The magnitude of initial enzyme derangements did not distinguish the survivors, but jaundice was associated with a poor prognosis. Seventeen of the 19 jaundiced patients (90%) died. The early occurrence of hepatocellular injury suggested that acute hemodynamic alterations were important etiologically. Intrahepatic cholestasis and jaundice developed later in septic or hypoxic patients and was accentuated by hemolysis and blood transfusions. In these patients, liver histology showed a nonspecific hepatitis. An increased risk of septic complications could not be attributed to the presence of liver disease. Late emergence of conjugated hyperbilirubinemia suggested an underlying septic process.

ALTERATIONS IN HYPOTHALAMIC FUNCTION FOLLOWING THERMAL INJURY

Nine burn patients with a mean burn size of 39% (range, 23-65%) and five normal individuals studied in an environmental chamber selected optimal comfort temperature by regulating a bedside temperature control unit. The normal individuals selected 27.8 degrees C plus or minus 0.6 (SE) as the comfort temperature and their mean skin temperature was 33.4 plus or minus 0.6 and core temperature 36.9 plus or minus 0.1 while in this environment. In contrast, the burn patients maintained a higher ambient comfort temperature (mean 30.4 plus or minus 0.7, p less than 0.05 when compared to controls) associated with an elevated core (38.4 plus or minus 0.3, p less than 0.01) and surface temperature (35.2 plus or minus 0.4, p less than 0.05). Human growth hormone response to insulin hypoglycemia and arginine infusion was measured in nine additional burn patients (mean burn size, 52%; range, 23-90%) and five normals. Fasting HGH was significantly elevated (1.7 plus or minus 0.2 ng/ml, n = 18, versus control of 0.9 plus or minus 0.1, n = 10, p less than 0.001), despite fasting hyperglycemia in the burn patients (123 plus or minus 5 mg/100 glycemia in the burn patients (123 plus or minus 5 mg/100 ml versus 91 plus or minus 2, p less than 0.001). HGH response to insulin hypoglycemia was diminished in the burn patients with peak HGH value in patients averaging 12.6 ng/ml compared to 27.8 in the recovered patients and 32.6 in the controls (p less than 0.01). Patients receiving an arginine infusion also demonstrated diminished HGH response following injury. The HGH response to known stimuli returned toward normal with time and recovery in the surviving patients. Alterations in comfort temperature, fasting blood glucose, and glucose-HGH interaction occur following thermal trauma. These changes taken together suggest that metabolic responses to injury may be the consequence of homeostatic readjustment within the hypothalamus.

Acute gastric disease after cutaneous thermal injury.

Diffuse erosive "gastritis" was discovered as early as five hours postinjury in 45 of 54 burn patients (83.5%) evaluated by gastroduodenoscopy. Acute ulcers were identified in 14 patients (26%); concomitant duodenal disease was present in 34 patients (76%). Microvascular fibrin thrombi were not demonstrated even though five patients had disseminated intravascular coagulation. Seven patients were examined before nasogastric intubation; four, with a mean burn size of 59.6% total body surface, had diffuse "gastritis." Low total serum protein levels were measured in 81% of tested patients, but were not predictive of mucosal disease. Hemorrhage followed the clinical deterioration of six patients (11.1%); one ulcer perforated. Whereas coagulation abnormalities, nasogastric intubation, and hypoproteinemia may augment mucosal injury, the morphologic and histologic examinations of the lesions suggested a primary ischemic cause resulting from the opening of submucosal shunts or local vasoconstriction.

Catecholamines

Hypermetabolism characterizes the metabolic response to thermal injury and the extent of energy production is positively related to the rate of urinary catecholamine excretion. Alpha and beta adrenergic blockade decreased metabolism from 69.6 +/- 5.3 Kcal/m(2)/hr to 57.4 +/- 5.2 (p < 0.01), and infusion of 6 microgm epinephrine/minute in normal man significantly increased metabolic rate. Twenty noninfected burned adults with a mean burn size of 45% total body surface (range 7-84%) and four normal controls were studied in an environmental chamber at two or more temperatures between 19 and 33 C with vapor pressure constant at 11.88 mm Hg. All burn patients were hypermetabolic at all temperatures studied and their core and mean skin temperatures were significantly elevated above control values. Between 25 and 33 C ambient, metabolism was unchanged in controls and burns of less than 40% total body surface (48.9 +/- 4.6 Kcal/m(2)/hr vs. 48.9 +/- 4.5), but metabolic rate decreased in larger burns in the warmer environment (72.0 +/- 1.9 vs. 65.8 +/- 1.7, p < 0.001). At 21 C, metabolism and catecholamines increased, except in four nonsurvivors who became hypothermic with decreased catechol elaboration. Metabolic rate in ten patients with bacteremia was below predicted levels while catecholamines were markedly elevated suggesting interference with tissue uptake of the neurohormonal transmitters. Feeding burn patients or administering glucose and insulin improved nitrogen retention and altered substrate flow but did not significantly reduce urinary catecholamines or metabolic rate. Burned patients are internally warm, not externally cold, and catecholamines appear to mediate their increased heat production. Hypermetabolism may be modified by ambient temperature, infection, and pharmacologic means. Alterations in hypothalamic function due to injury, resulting in increased catecholamine elaboration, would explain the metabolic response to thermal injury.