Urinary Cortisol and Catecholamine Excretion after Burn Injury in Children

Abstract

Introduction: A severe burn causes increased levels of urine cortisol and catecholamines. However, little is known about the magnitude of this increase or how and when the levels return to normal. The purpose of this study was to determine in a large clinical prospective trial the acute and long-term pattern of urine cortisol and catecholamine expression in severely burned children. Methods: Pediatric patients with burns greater than 40% total body surface area (TBSA), admitted to our unit over a 6-yr period, were included into the study. Clinical data including length of stay, number of operations, and duration and number of infections were determined. Patients had regular 24-h urine collections during their acute admission and reconstructive periods. Urine collections were analyzed for cortisol, epinephrine, and norepinephrine. Each urine cortisol was compared with age-adjusted reference ranges. Ninety-five percent confidence intervals and ANOVA analysis were used where appropriate. Results: Two hundred twelve patients were included in the study (75 females and 137 males), with a mean ± sem TBSA of 58 ± 1% (third-degree 45 ± 2%) and mean age of 9 ± 0.4 yr. Urinary cortisol levels were significantly increased (3- to 5-fold) up to 100 d after the burn and then approached normal levels (P < 0.05). The rise in urine cortisol was significantly higher in male than female patients (P < 0.05). Early hypercortisolemia was associated with increased duration of severe infection (P < 0.05). Persistent hypercortisolemia was associated with increases in both infection rates and duration of severe infection (P < 0.05). Urinary catecholamines showed a significant increase at 11–20 d after the burn (P < 0.05). Urinary norepinephrine levels were significantly increased up to 20 d and then returned to normal (P < 0.05). Conclusions: Urinary levels of cortisol, epinephrine, and norepinephrine are significantly increased after a major burn. Early hypercortisolemia is associated with increased duration of severe infection. Persistent hypercortisolemia is associated with increases in both infection rates and duration of severe infection.

The Hepatic Response to Thermal Injury: Is the Liver Important for Postburn Outcomes?

“…Counterregulatory hormones such as glucagon, cortisone, and so on, post severe thermal injury, vary in their concentration. While glucagon appears to be decreased, Norbury et al (63) and Gauglitz et al (91) have shown recently that cortisone levels are increased markedly up to 3 years post severe thermal injury. The major mechanisms by which thermal injury causes hyperglycemia is probably not due to the hormonal system, but rather is associated on a molecular level with impaired insulin receptor signaling (92).…”

“…These responses are present in all trauma, surgical, or critically ill patients, but the severity, length, and magnitude is unique for burn patients (7). Marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion are thought to initiate the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state (7,8,26,(61)(62)(63) (Figure 4). The cause of this complex response is not well understood.…”

Hypothalamic-pituitary-adrenal axis in lethal canine Staphylococcus aureus pneumonia

“…Therefore, neither basal nor ⌬cortisol in response to ACTH distinguished survivors from nonsurvivors at relatively early time points during septic shock. A lack of association between survival and acute cortisol/ACTH responses has been previously documented in coronary syndromes (18,48), major surgery (44), trauma (66), burns (28,46), and hemorrhage (29). Aldosterone regulation appeared to be largely independent of the HPA axis stress response.…”

The Hepatic Acute Phase Response to Thermal Injury

“…post severe thermal injury vary in their concentration. While glucagons appears to be decreased Norbury et al (63) and Gauglitz et al (91) have recently shown that cortisone levels are markedly increased up to three years post severe thermal injury. The major mechanisms by which thermal injury causes hyperglycemia is probably not due to the hormonal system but rather on a molecular level associated with impaired insulin receptor signaling (92).…”

“…These responses are present in all trauma, surgical, or critically ill patients, but the severity, length, and magnitude is unique for burn patients (7). Marked and sustained increases in catecholamine, glucocorticoid, glucagon, and dopamine secretion are thought to initiate the cascade of events leading to the acute hypermetabolic response with its ensuing catabolic state (7,8,26,(61)(62)(63). The cause of this complex response is not well understood.…”