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A prospective analysis of hypertonic lactated saline v. Ringer's lactate-colloid for the resuscitation of severely burned children

Children and young people ranging in age from 5 months to 21 years, with burns covering greater than or equal to 30 per cent of the body surface area, were entered into a prospective study comparing the resuscitative efficacy of hypertonic lactated saline (HLS) and Ringers lactate-colloid (RL-colloid). The 24- and 48-h fluid requirements of children resuscitated with the RL-colloid were significantly greater than those resuscitated with HLS (P less than 0.02); 2.37 +/- 0.91 ml/kg/per cent burn (HLS) v. 3.43 +/- 1.51 ml/kg/per cent burn (RL-colloid) at 24 h post-burn and 4.18 +/- 1.37 ml/kg/per cent burn (HLS) v. 6.32 +/- ml/kg/per cent burn (RL-colloid) at 48 h (P less than 0.01). The urine output between the two groups was not significantly different, and the haematocrits were equally maintained. Patients in the RL-colloid group gained significantly more weight at 48 h (P less than 0.05). The sodium requirements and resulting sodium balances were not significantly different. The desired and significant elevation (P less than 0.001) of serum sodium in the HLS group was maintained for the 5 days of the study. Colloid oncotic pressures, serum albumin and albumin/globulin (A/G) ratios were not significantly different between the two groups until 48 h post-burn. The RL-colloid group received plasmanate during the second 24-h period. The significant elevation in serum albumin, A/G ratio and colloid oncotic pressure persisted for only 2 days--by 96 h post-burn these values were no longer significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathogenesis of fever in a rat burn model : The role of cytokines and lipopolysaccharide

We investigated the possible causal relationship between interleukin-6 (IL-6) and increased body temperature (T(B)) in a rat burn model. Transmitters for measuring core temperature and estimating activity were implanted in the abdominal cavity. Animals in the burn group were clipped and received full-thickness scald burns to 45% to 55% of the body surface area, and control animals were clipped. T(B) and activity were measured continuously through the tenth postburn day. Carotid lines were placed, and serial blood samples obtained for lipopolysaccharide, IL-6, and tumor necrosis factor-alpha assay. From the third through the tenth postburn day, the burn group had a consistently significantly higher T(B) during light hours than the control group did (average, 0.45 degrees C +/- 10 degrees C, p = 0.0001). Differences in activity during light hours were not significant between the two groups, therefore, do not account for the observed significant difference in T(B). The average IL-6 serum levels were 3.5-fold higher for the burned animals. In this study, burn and control serum levels of IL-6 demonstrated positive correlation with T(B). These data suggest, but do not prove, a causal relationship between IL-6 and fever in the rat burn model, and make it unlikely that circulating systemic lipopolysaccharide is the cause.We investigated the possible causal relationship between interleukin-6 (IL-6) and increased body temperature (T(B)) in a rat burn model. Transmitters for measuring core temperature and estimating activity were implanted in the abdominal cavity. Animals in the burn group were clipped and received full-thickness scald burns to 45% to 55% of the body surface area, and control animals were clipped. T(B) and activity were measured continuously through the tenth postburn day. Carotid lines were placed, and serial blood samples obtained for lipopolysaccharide, IL-6, and tumor necrosis factor-alpha assay. From the third through the tenth postburn day, the burn group had a consistently significantly higher T(B) during light hours than the control group did (average, 0.45 degrees C +/- 10 degrees C, p = 0.0001). Differences in activity during light hours were not significant between the two groups, therefore, do not account for the observed significant difference in T(B). The average IL-6 serum levels were 3.5-fold higher for the burned animals. In this study, burn and control serum levels of IL-6 demonstrated positive correlation with T(B). These data suggest, but do not prove, a causal relationship between IL-6 and fever in the rat burn model, and make it unlikely that circulating systemic lipopolysaccharide is the cause.

Retrospective evaluation of admission criteria for paediatric electrical injuries

In the medical community, the practice of admitting all electrical burns for 24-48 h of observation, monitoring and laboratory evaluation is widespread. This retrospective review of paediatric electrical burns was conducted to determine which patients may safely be treated as outpatients. Retrospective analysis of all paediatric burns admitted between 1980 and 1991 identified 35 patients with electrical injuries. Patients were divided into two groups for analysis: those burned by exposure to household voltages (120-240 V; n = 26) and those exposed to high voltages, in excess of 1000 V (n = 9). The majority of household electrical injuries occurred secondary to contact with the household 120 V (21/26). Contact with an extremity accounted for the largest number of these injuries (18/26). The mouth was the second most frequent site of injury (7/26). Most of these patients (20/26) had < 1 per cent BSA burn. No patient in the household-voltage group had an arrythmia that required treatment, nor were there any identified examples of compartment syndrome or other vascular complications. Seven patients did require minimal skin grafting. No deaths occurred in either group. The patients in the household-voltage group were significantly younger. High-voltage electrical injuries occurred in an older patient population and required more aggressive care and surgical intervention. This was evident at the time of initial evaluation. Based on these data, healthy children with small partial-thickness electrical burns and no initial evidence of cardiac or neurovascular injury do not appear to need hospital admission.

Sequential excision and grafting of the burn injuries of 1507 patients treated between 1967 and 1986: end results and the determinants of death.

The development of a more aggressive approach to burn wound management, leading to complete excision within 72 hours after burn, has led some to conclude that total early excision is a major force behind improved survival rates. We have summarized the results of treatment of 1507 patients with burn injuries treated between 1967 and 1986. Wounds were managed with use of standard topical therapy, occlusive dressings, and staged excision and grafting of full-thickness injury or deep dermal injury (not healed by 21 days). Data were analyzed with use of a logistic-regression model because, with the exception of older patient cohorts, the data did not fit the probit model. The major determinants predicting death were the percentage of body surface area burned, age, smoke inhalation, and the percentage of full-thickness burn. Concordance was 97%. These data show that aggressive sequential wound excision and grafting produces end results comparable with those achieved with complete early burn wound excision for similar age ranges and injury. Early harvest of available donor sites in patients with large burns may be more important to survival than complete early wound excision.

The effect of wound management on the interaction of burn size, heat production, and rectal temperature.

Metabolic and temperature data were collected for 56 patients with burns managed with four wound care protocols. Group I (n = 7) treated with dressings and variable ambient temperature selected for patient subjective comfort; group II (n = 7) managed without dressings and variable ambient temperature for patient comfort; group III (n = 6) no dressings, ambient temperature of 25 degrees C and the output of electromagnetic heaters adjusted for patient comfort; group IV (n = 36) dressings and ambient temperature of 28 degrees C. All groups were cold challenged: groups I and II by sequentially lowering ambient temperature, group III by decreasing the electromagnetic heater output, and group IV by removing dressings with ambient temperature remaining at 28 degrees C. Only groups II and IV demonstrated correlation between percent body surface area burn and heat production. The slope of the regression for group IV neutral was significantly less than that for group IV cold and group II neutral and cold. The relationship between percent body surface area burn and rectal temperature for groups I, II, and III neutral was equal to .03 degrees C increase in rectal temperature per 1% body surface area burn (Y = 37 + 0.03; r = 0.74; df 18; p < 0.01) and was not significantly different when cold. This predicts a 1.5 degrees C increase in rectal temperature for a patient with a 50% body surface area burn who does not have sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)

The pharmacokinetics of ibuprofen after burn injury.

Ibuprofen is an effective antipyretic in the postburn period and produces associated decrements in the hypermetabolic response. Burn injury is capable of altering the kinetics of many drugs, making the predictable use of agents such as ibuprofen difficult. Ten patients with serious burns were studied after the administration of 10 mg/kg ibuprofen suspension. The half-life varied from 1.4 to 5.1 hours, depending on the site of administration and/or the presence of solid food. The reported half-life for ibuprofen suspension is 1.8 to 2 hours. Burn size did not alter ibuprofen half-life or area under the time-concentration curve. Maximum ibuprofen concentration varied greatly, depending on route of administration. Time to maximal temperature reduction was between 2 and 3 hours after drug administration. Although the precise level of ibuprofen needed for cyclooxygenase inhibition is unknown, enteral administration results in levels below the targeted 10 to 20 mcg/ml for much of the traditional 6-hour dosing interval. Future studies with ibuprofen in the burn population must standardize more than just total dose.

Fluid requirements of severely burned children up to 3 years old: hypertonic lactated saline vs. Ringer's lactate-colloid☆

Children with burns greater than or equal to 30 per cent of the body surface area were entered into a prospective fluid resuscitation protocol using hypertonic lactated saline (HLS) or Ringers lactate-colloid. The two resuscitation groups were subdivided into patients less than or equal to 3 years old and children greater than 3 years old. The children under 3 years old required significantly more fluid and sodium during the first 48 h when calculations were made using body weight as the indexing factor. When fluid and sodium needs of paediatric age groups were calculated using body surface area as the indexing factor, significant differences in fluid and sodium requirements were no longer present between age groups. This suggests that these observed differences may reflect the difference in surface area to mass ratio for these age groups. Children resuscitated with HLS require 23 per cent less fluid in the first 24 h. If body weight is used for estimating fluid needs, clinicians should be aware of the differences in fluid requirements for children less than or equal to 3 years old compared with older paediatric patients. Formulas for estimating fluid needs are presented.

Alteration in temperature regulation induced by burn injury in the rat.

The preoptic anterior hypothalamus (POAH) of rats housed at three ambient temperatures was implanted with perfusion apparatuses. Response of heat production to displacement of POAH temperature was determined for control animals and animals with burns (31% +/- 3% total body surface area). At an ambient temperature of 22 degrees C there was a significant increase in thermosensitivity of the POAH for both control rats and rats with burns compared with thermosensitivity at 32 degrees C. Within ambient temperatures there was no effect on thermosensitivity detected for rats with burns compared with control rats. The threshold temperature for heat production was shifted significantly upward (p less than 0.05) both by a lower ambient temperature and by burn injury. The reference temperature for heat production was also shifted to the right by burn injury (p less than 0.05). The significant shifts to the right for threshold temperature and reference temperature for heat production enhance the organismss ability to meet the stress of the hypermetabolic response. At a warm ambient temperature (32 degrees C) there are no significant differences in thermoregulation detected in animals with burns or control animals.The preoptic anterior hypothalamus (POAH) of rats housed at three ambient temperatures was implanted with perfusion apparatuses. Response of heat production to displacement of POAH temperature was determined for control animals and animals with burns (31% +/- 3% total body surface area). At an ambient temperature of 22 degrees C there was a significant increase in thermosensitivity of the POAH for both control rats and rats with burns compared with thermosensitivity at 32 degrees C. Within ambient temperatures there was no effect on thermosensitivity detected for rats with burns compared with control rats. The threshold temperature for heat production was shifted significantly upward (p less than 0.05) both by a lower ambient temperature and by burn injury. The reference temperature for heat production was also shifted to the right by burn injury (p less than 0.05). The significant shifts to the right for threshold temperature and reference temperature for heat production enhance the organismss ability to meet the stress of the hypermetabolic response. At a warm ambient temperature (32 degrees C) there are no significant differences in thermoregulation detected in animals with burns or control animals.

The effect of indomethacin on the cytokine cascade and body temperature following burn injury in rats

Abstract This study investigates the hypothesis that indomethacins ability to prevent “fever” following burn injury in rats is mediated via decreased plasma concentrations of IL-6, the putative mediator of increased body temperature. Sprague–Dawley rats had radio transmitters and osmotic pumps containing indomethacin placed in the peritoneal cavity. Seven days later full thickness scald burns to 50% of the body surface area were produced. Following burn injuries, daily blood samples were obtained from a carotid catheter for assay of lipopolysaccharide (LPS), interleukin-1α (IL-1α), IL-1β, tumor necrosis factor-α (TNF-α) and IL-6. In addition, body temperature ( T B ) and activity index were obtained every five minutes by telemetry. There were four experimental groups: burn+indomethacin (B-In); burn+polyethylene glycol (Peg) (B-Peg); control+indomethacin (C-In); and control+Peg (C-Peg). Burned animals demonstrated a significant two-fold increase in plasma IL-1α levels ( p =0.004) and a seven-fold increment in IL-6 ( p =0.0001) through the 7th PBD, and indomethacin administration had no significant effect upon the cytokine plasma levels. There were no significant increases in IL-1β, TNF-α or LPS in any group. Indomethacin eliminated the chronic increase in T B following burn injury, and this effect was not produced by changes in plasma levels of the endogenous pyrogens IL-1α and IL-6.

The effect of ablation of the preoptic anterior hypothalamus on energy metabolism and plasma catecholamines after burn injury in the rat.

Rats with burn injuries demonstrate changes in thermoregulation including an upward shift of the set-point and reference temperatures with no change in sensitivity of the response in heat production to displacement of the temperature of the preoptic anterior hypothalamus. In the present studies, the response in plasma and urinary catecholamines to burn injury after destruction of the preoptic anterior hypothalamus was examined in the rat. Preoptic anterior hypothalamic lesioning impaired the hypermetabolic response to burn injury, and at 22 degrees C, burned lesioned rats were hypothermic. Furthermore, plasma levels and urinary excretion rates for catecholamines were not decreased in burned lesioned rats, but rather showed an inverse relationship with heat production. Burned lesioned rats were capable of maintaining body temperature at an ambient temperature of 28 degrees C. This suggests that a less precise thermoregulation is present in lesioned animals. Rats in which the preoptic anterior hypothalamus has been destroyed have reduced tolerance to burn injury.