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This study investigates the hypothesis that indomethacin's 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-1alpha (IL-1alpha), IL-1beta, tumor necrosis factor-alpha (TNF-alpha) 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-1alpha 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-1beta, TNF-alpha 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-1alpha and IL-6.

Introduction: Rats with burn injury to > or = 50% of the BSA demonstrate a significant increase in body temperature (T(B)) during light hours, and decrease of circadian variation in T(B). This study investigated the hypothesis that part or all of the signal for increased T(B) in rats with burn injury is transmitted to the central nervous system by way of afferent vagal fibers., Methods: Four groups of animals were studied: Burn-Sham Vagotomy; Control-Sham Vagotomy; Burn-Vagotomy and Control-Vagotomy. Anesthetized animals had bilateral subdiaphragmatic vagotomy (VagX) or sham VagX performed, and AM radio transmitters were implanted in the peritoneal cavity for the purpose of recording T(B) and activity index (AI). Following a one week recovery period, burn animals received scald burns equal to 50.3 +/- 2.5% BSA., Results: The main effect of VagX upon T(B) was a small but significant reduction in T(B) during dark hours. At least 87% of this decrease in post-burn T(B) was also present for the control vagotomy group. Vagotomy had no effect on the increase in T(B) for the burn groups during light hours. During dark hours, VagX significantly reduced T(B) in burns and controls, and burn injury significantly reduced activity., Conclusions: One may speculate that afferent vagal signals are partially responsible for maintenance of T(B), with or without burn injury, and that the major signal for increase in T(B) for animals with burn injury is not a neural one via afferent vagal pathways.

This study investigates the hypothesis that continuous administration of indomethacin (a cyclo-oxygenase inhibitor) will chronically reduce body temperature (TB) in burned rats (i.e., modulate "true" fever). Male Sprague-Dawley rats had radio transmitters and osmotic pumps (containing indomethacin) placed in the peritoneal cavity, and 7 days later large full-thickness scald burns were produced. Activity and TB were continually recorded through the 14th postburn day (PBD). There were 4 experimental groups: burn + indomethacin (B-In), n = 9; burn + polyethylene glycol (B-Peg), n = 6; control + indomethacin (C-In), n = 9; and control + polyethylene glycol (C-Peg), n = 6. From PBD 5 through PBD 10, the B-Peg group had consistently and significantly higher TB during light hours than the B-In, C-In, and C-Peg groups. From PBD 7 through PBD 12, the B-In group had an average TB during light hours significantly lower or not different than the C-In and C-Peg groups. These results support the hypothesis that in this burned-rat model chronically increased TB during the light hours may be "fever" (rather than hyperthermia) and that the final effector link could be a prostanoid because changes in activity do not explain the changes in body temperature.

Hypothesis: IL-10 will reduce morbidity and mortality in murine MODS. Introduction. Intraperitoneal (ip) zymosan causes a triphasic inflammatory process leading to MODS. Phase I is an acute systemic inflammatory response to sterile peritonitis. Phase II is the recovery phase. Phase III is characterized by recurrent illness, progressive organ dysfunction, and elevated proinflammatory cytokines., Methods: Male ICR mice were randomized (on Experiment Day 0, time = 0 h) into four initial groups (A-D): Control Group A received no zymosan and no IL-10. Group B received zymosan (1 mg/g mouse BW, t = 0) and no IL-10. Group C received no zymosan and IL-10 at t = 2 h. Group D received zymosan and IL-10 at t = 2 h. On Experiment Day 4, mice in Groups B-D were randomized into six further treatment groups (B1 and B2, C1 and C2, D1 and D2). Group B1 received no treatment. Group B2 received IL-10 when clinical signs of recurrent illness developed (Phase III, 12-18 days after zymosan treatment). Mice were sacrificed when they were preterminal (clinical signs of shaking, shivering, or paralysis) or on Experiment Day 28 (survivors). Plasma total bilirubin and creatinine levels were measures of organ function. Terminal pulmonary compliance was measured in situ through a physiologic range of tidal volumes., Results: Mice entering Phase III consistently progressed to MODS characterized by elevated bilirubin and hemorrhagic lungs which, if left untreated, was lethal. Mice treated with IL-10 (Group B2) when they entered Phase III had lower mortality (28.6% vs 100%, P < 0.02), longer survival (25 vs 18 days, P < 0.05), and improved lung pulmonary compliance (slope beta1 = 0.082 ml/mm Hg vs 0.059 ml/mm Hg, P < 0.001) compared to untreated (Group B1) mice in Phase III., Conclusions: IL-10 improves survival even when given after clinical signs of illness are present., (Copyright 1998 Academic Press.)

In previous studies, we established that circulating epinephrine (E) is not essential for a normal hypermetabolic response to burn injury in the rat, within the zone of thermal neutrality. In other studies, burned rats with adrenal medullectomy (AdxB) studied at 22 degrees C were unable to maintain rectal temperature (TR) after alpha-adrenergic blockage. These data suggest that norepinephrine (NE) is calorigenic in such animals without formal cold acclimation. These studies investigate the hypothesis that, contrary to the usual belief, norepinephrine might be calorigenic in rats without formal cold acclimation. Burned (B) and control (C) rats with adrenal medullectomies (Adx) and Sham (S) Adx (AdxB, SAdxB, AdxC, and SAdxC) were housed at either 22 degrees C or 28 degrees C. Calorimetry was performed during the eighth to eleventh days after the burn. For groups housed at 22 degrees C and studied at 28 degrees C, NE given intravenously (iv) produced an average 16.5%+/-3.3% increment in heat production (HP) for the four groups, which was significant for AdxB, SAdxB, and SAdxC. Intravenous administration of E produced an average increment in HP of 4.44%+/-4.1%, which was not significant. HP was significantly higher after NE than E in three cases. Studies with animals housed at 28 degrees C and studied at 28 degrees C produced intermediate but similar results. For groups housed at 28 degrees C and studied at 22 degrees C, iv administration of E and NE produced average decreases in He of 18%+/-6.7% for E and 10.75%+/-4.7% for NE. Except for the AdxC group, these differences were significant. These data suggest that chronic exposure to an ambient temperature of 22 degrees C produces an enhanced calorigenic response to NE in burn and control rats. Based on the data presented here, combined with earlier studies, NE must be considered as a facilitator for hypermetabolic response to burn injury in the rat. It is interesting to speculate whether NE is calorigenic for patients with large burn wounds, which are managed without dressings at ambient temperatures below thermal neutrality.

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.

Fractionation of alkaline phosphatase isoenzymes and isoforms by isoelectric focusing is a simple procedure that resolves up to 17 fractions having alkaline phosphatase activity. The fractions are stable at 4 degrees C, and undergo only slight changes during repeated freeze-thaw cycles. Pretreatment with phospholipase-C or sialidase changes the isoelectric focusing patterns of alkaline phosphatase in serum; we recommend they not be used owing to the loss of information. We found that the alkaline phosphatase fractions provide diagnostic information in addition to that given by the common liver-function tests in patients with chronic liver diseases. Primary biliary cirrhosis and primary sclerosing cholangitis showed similar biochemical changes, but they are very different from alcoholic cirrhosis based on the common liver-function tests and the alkaline phosphatase isoform patterns obtained by isoelectric focusing. Analysis of the laboratory data using neural networks has some limited use in distinguishing chronic and chronic-active hepatitis of any cause. We have confirmed the tissue assignments made by Griffiths (Prog Clin Biochem 1989; 8:63-74) for the alkaline phosphatase fractions in liver as obtained by isoelectric focusing: Fractions 1a and 1b show a strong correlation with biliary diseases, and fractions 2, 3, and 4 show consistent increases in patients with primary disorders of hepatocytes; these fractions have good sensitivity for hepatocyte injury, but their specificity is limited. Fraction 10 may be a marker of activated T-lymphocytes; it was abnormal in most of our patients suggesting that it is a sensitive but non-specific test. Analysis of alkaline phosphatase by isoelectric focusing deserves further evaluation, because it may facilitate the diagnosis of certain chronic liver disorders and could be a supplement to the biopsy.

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.

Burn (B) and control (C) rats with and without adrenal medullectomy (Adx) 9-11 days postburn underwent warning and cooling of the preoptic anterior hypothalamus (POAH) during calorimetry at 22 degrees and 28 degrees C ambient. Blood was drawn for catecholamine assay during each displacement of the POAH temperature (Thy). The heat production (Hp) for the AdxB group at 22 degrees and 28 degrees C was not different from the Hp for the sham AdxB group (80 +/- 4 vs 86 +/- 8 at 22 degrees C, 58 +/- 8 vs 64 +/- 7 W/m2 at 28 degrees C) in spite of there being no detectable circulating epinephrine (E) for the AdxB groups. Cooling of the POAH of the AdxB 22 degrees C group, however, did not induce a further increment in Hp, in contrast to all other groups. Thy demonstrated good significant negative linear correlation with Hp for all groups. The resulting slopes were not significantly different from one another, indicating no difference in thermal sensitivity of the POAH between the groups. In four of eight groups plasma norepinephrine (NE) demonstrated positive correlation with Hp and in five of eight groups negative correlation with Thy, Plasma E values did not correlate with Hp and demonstrated negative correlation with Thy in two of four possible groups. These data show that postburn hypermetabolism is not dependent on E in the rat and suggest that NE may be calorigenic in burned rats.

This study in burned rats studied at two ambient temperatures (22 degrees and 28 degrees C) and housed at 28 degrees C was designed to investigate the role of catecholamines in the maintenance of thermal homeostasis following burn injury. Two weeks prior to burn or sham burn, animals underwent adrenal medullectomy or sham adrenal medullectomy. Between postburn days 9 and 13, simultaneous direct and indirect calorimetry was performed following administration of 2mg/kg of phentolamine (alpha adrenergic blocking agent) via a carotid arterial line. Following administration of phentolamine, heat production and body temperature decreased and heat loss increased immediately. The cooling slopes for the burn groups were significantly steeper than for the control groups, within ambient temperatures. Within ambient temperatures, the presence or absence of the adrenal medulla had no discernible effect on the cooling slope of the burns or the controls. The burned animals cooled 1.9-3.5 times faster at 22 degrees than at 28 degrees C, and controls cooled 2.0-3.9 times faster at 22 degrees than at 28 degrees C. Phentolamine produced a several-fold increase in serum concentrations of both norephinephrine (NE) and epinephrine (E), indicating a gross overlap in alpha and beta adrenergic receptor utilization for E and NE. The progressive cooling of the adrenal demedullated burn group at 22 degrees C following phentolamine administration seems to indicate that norepinephrine is calorigenic for rats under these experimental circumstances. These experimental results indicate a relatively non-essential role for catecholamines in the maintenance of thermal homeostasis within the thermal neutral zone in the rat.

Rats, with the preoptic anterior hypothalamus implanted with two thermodes and a thermocouple reentry tube, had simultaneous direct and indirect calorimetry performed [during the ninth to eleventh postburn day interval] at ambient temperatures of 22 degrees and 28 degrees C. During calorimetry, blood was drawn at baseline and near the end of each period of displacement of the preoptic anterior hypothalamus temperature for catecholamine assay. Cooling the preoptic anterior hypothalamus resulted in a significant increase in heat production and plasma epinephrine and norepinephrine concentrations for both burn and control groups at 22 degrees C and 28 degrees C (p < 0.05 for all comparisons). Heat production demonstrated consistent negative linear correlation with preoptic anterior hypothalamic temperature. Plasma epinephrine values correlated with preoptic anterior hypothalamic temperature for only the controls at 28 degrees C ambient, whereas norepinephrine had significant linear correlation with heat production for all groups and significant negative linear correlation with preoptic anterior hypothalamic temperature. These data indicate norepinephrine may be more important than epinephrine in the maintenance of postburn hypermetabolism in this rat burn model while demonstrating that the hypermetabolism is appropriately responsive to perturbation of preoptic anterior hypothalamic temperature.

This study was conducted to examine the guinea pig as a suitable model for the study of the postburn hypermetabolic response and the febrile response that accompanies burn injury in man. Thirty animals were randomly assigned to four groups: > 50% body surface area burn (n = 6); 45% to 50% body surface area burn (n = 10); < 45% body surface area burn (n = 6); and controls (n = 8). On postburn days 3, 7, 11, 13, and 15, sequential temperature measurements were made. On postburn days 7 to 15, the randomly selected burn group (n = 12) and the control group (n = 8) had calorimetry studies performed. Sequential rectal temperature data demonstrate that the guinea pig does not mount a prolonged or consistent febrile response after burn injury (p > 0.05 for burn group vs control group on postburn days 7 to 13; p < 0.05 for postburn days 3 and 15 only). However, the burned guinea pig is significantly hypermetabolic after burn injury, with significant increases in dry and evaporative heat loss. The hypermetabolic response was proportional to burn wound size. Guinea pigs are not an ideal model for the study of the postburn febrile response; however, this is an excellent model for the study of postburn hypermetabolism.

Burn injury in man is characterized by increased body temperature proportional to burn wound size and may represent fever and/or hyperthermia. A nonseptic animal model used to study this phenomena has not been described. To test the hypothesis that large burn injuries in rats would produce increased body temperature, the rectal, skin, and body temperatures were sequentially measured and were calculated for rats in the control group and rats with burn injuries covering 26% to 63% of the body surface area [< or = 35%, 36% to 45%, and > or = 46% body surface area]. The group with burns covering > or = 46% of the body surface area had significantly higher rectal temperatures than did at least one other group on postburn days 7, 9, 11, 13, 18, and 20. On postburn days 7 and 11 this increase was significantly higher than that of all burn and control groups. Animals did not demonstrate any overt evidence of wound infection. These data do not establish a cause for increased body temperature after burn injury but suggest that a reproducible animal model may be possible for the study of the cause of increased body temperature after burn injury.

We describe a common dystrophin gene polymorphism in the black population that alters both HindIII and BglII restriction sites.

This study was performed to establish the relative efficiency of occlusive dressings and variable ambient temperature (group I) versus no dressings and variable ambient temperature (group II) versus no dressings and electromagnetic heaters (group III) for controlling the postburn hypermetabolic response. Fifteen burn patients and five normal controls (group IV) were studied when subjectively comfortable using partitional calorimetry, after which each patient was cold stressed by sequentially decreasing external energy support, and repeating calorimetry studies and serial plasma catecholamine assays. The percentage increase in heat production above predicted normal values was significantly increased for all groups when cold (C) versus neutral (N) (group I: [N] 24 +/- 24 versus [C] 49 +/- 25%; group II: [N] 46 +/- 35 versus [C] 74 +/- 47%; group III: [N] 21 +/- 20 versus [C] 78 +/- 25%; group IV: [N] -9 +/- 12 versus [C] 16 +/- 10%, p less than 0.05 all comparisons). Plasma catecholamine values did not increase significantly when patients were subjectively cold. These studies do not support the role of catecholamines as the primary mediator in the cause of the postburn hypermetabolic response. Using the patients' subjective comfort status as a guide for external energy support, it is possible to greatly reduce but not to eliminate the hypermetabolic response to burn injury.

A group of 15 burned children and young adults with large burns (mean, 41% +/- 15% BSA) were administered ibuprofen (40 mg/kg for 3 days). Each patient served as his or her own control in this crossover study (with and without ibuprofen). Paired calorimetric and temperature studies and urinary nitrogen measurements were performed. No nitrogen-sparing effect was identified for this dose of ibuprofen. However, patients demonstrated a statistically significant reduction in average rectal temperature (0.67 degrees C decreases) (p less than 0.01) and in metabolic rate (11.4% decreases) (p less than 0.01) while taking ibuprofen. Linear regression analysis of the reduction in temperature versus the reduction in metabolic rate yielded a statistically significant correlation (p less than 0.01) with a slope of 13.6% reduction in metabolic rate per degree centigrade reduction in the 72-hour average rectal temperature. These results support the hypothesis that ibuprofen attenuates the hypermetabolic response to thermal injury by blunting the temperature elevation that is usually seen.

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.

The effect of early enteral feeding on the hypermetabolic response following burn injury in a rat burn model has been investigated. The rates of heat production and partitioned heat loss were determined on the fourteenth postburn day for five treatment groups: I) burn, fed rat chow ad libitum starting 2 hours postburn; II) burn, fed by gastrostomy beginning 2 hours postburn; III) burn, fed by gastrostomy, delayed until 72 hours postburn; IV) controls, fed by gastrostomy 2 hours post anesthesia; and V) controls, fed rat chow ad libitum 2 hours post anesthesia. Gastrostomy feedings delivered 175 kcal/kg.day. The mean rates of heat production and heat loss for the three burn groups did not differ significantly whether rats were fed chow ad libitum, or by gastrostomy early or late. Contrary to previous studies using a guinea pig model, method and timing of feeding in this burned rat model had no significant effect on the postburn increment in the rate of heat loss and the corresponding increment in the rate of heat production.

Twenty-six adults more than 60 years old with burns greater than or equal to 30% of the body surface area were resuscitated using hypertonic lactated saline (HLS). Hemodynamic parameters of resuscitation were measured in ten of the patients using a Swan-Ganz catheter. In spite of signs of hemodynamic stability, these patients demonstrated mean cardiac indices (CI) below their age-corrected norms and pulmonary capillary wedge pressures (PCWP) below 5 mm Hg through 24 hours, yet 92% of the patients produced normal or super-normal volumes of urine. Hemodynamic monitoring may be helpful for precise fluid replacement in extensively burned elderly patients; however, a normal CI and PCWP may not be the appropriate endpoint for resuscitation of the elderly when using HLS. This review supports the concept that HLS resuscitation of critically burned older patients is both safe and efficacious, leading to an 81% survival of this severely compromised group well past the resuscitation phase of injury.

Trace element deficiency in burns is an area which apparently has not been investigated. We recently encountered a severely burned patient with profound copper depletion. Neuropsychiatric symptoms and delayed healing may have been secondary to this deficiency. Further study is needed to clearly delineate the role of acquired copper deficiency in recovering burned patients.

A retrospective chart review was conducted of 5418 culture and sensitivity reports from 93 paediatric burn patients to determine profiles of wound flora and invasive organisms, trend analysis and patterns of antibiotic resistance. Coagulase-positive Staphylococcus was the predominant burn wound pathogenic isolate and the predominant invasive organism for burns less than 60 per cent BSA. Pseudomonads were the predominant invasive organism for burn wounds greater than or equal to 60 per cent BSA. Only 7 per cent of all pathogenic isolates were fungi. A significant association was demonstrated between increasing burn size and an increasing incidence of Gram-negative and invasive organisms. Silver sulphadiazine remains a very effective topical agent for the control of bacterial and fungal growth in burn wounds after 10 years of intensive use in this burn unit. Pseudomonad isolates were routinely multi-drug resistant. Pseudomonad isolates from wounds treated topically with a silver sulphadiazine-cerium nitrate mixture were frequently resistant to aminoglycosides, colistin and carbenicillin. It is concluded from this review that severe restrictions on antibiotic usage within burn units, and strict internal environmental control within burn units may help to decrease the incidence of nosocomial resistant strains and cross infection. Regular monitoring of burn wound flora, and the protocol for wound care used in treating these patients have been effective in preventing septic episodes and death due to sepsis.

Crystalloid solutions such as Ringer's lactate have become the standard for initial volume replacement after hemorrhage. Although the relative merits of blood, colloid, and crystalloid have been extensively studied, little attention has been directed toward determining the optimal composition of the crystalloid solution. Based on the beneficial properties of hypertonic lactated saline solution in burn resuscitation, we have extended its use to acute hemorrhage. Using an awake canine model analogous to the clinical situation, we compared hypertonic lactated saline solution with Ringer's lactate solution for resuscitation in the presence of acute blood loss. The hypertonic lactated saline solution group required less fluid to restore and maintain cardiac output and blood pressure while maintaining better urine output. Although the Ringer's lactate solution group had increased shunt function indicative of pulmonary dysfunction, the shunt function in the hypertonic lactated saline solution group did not differ from that in the control group. Serum sodium and osmolality values were higher in the hypertonic lactated saline solution group, but at no time did they approach toxic levels.

Minipigs were divided into four experimental groups: nonburned control (C); burn, minimal resuscitation (MR); burn, standard resuscitation (SR); and burn, rapid resuscitation (RR). Resuscitation was begun 30 minutes postburn and hemodynamics were measured through 24 hours postburn. At 30 minutes postburn, the three burn groups demonstrated a significant decrease in cardiac index % (CI%). At 1 1/2 hours postburn, the RR group CI% was significantly greater than for the SR group and not significantly different from that of controls. At 2 hours postburn, fluid was abruptly decreased in the RR group and the salutary effect on CI promptly dissipated. In this model, the early decrement in CI following thermal injury is responsive to rapid resuscitation, concluding that the etiology of decreased CI following thermal trauma is at least partially due to inadequate volumes of fluid administration in the early postburn period.

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 Ringer's 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.

The sequential metabolic studies of nine severely burned patients were examined retrospectively. Information analyzed included heat production (M), partitioned heat loss (HL), the percentage of the body surface area open wound (% open wound) and skin (TS) and rectal (TR) temperatures. The reduction in the hypermetabolic response correlated with the number of days postburn (DPB), % open wound, average body temperature (TB = 0.8TR + 0.2TS) and evaporative heat loss (EV) (r = 0.62, 0.55, 0.56, 0.63, respectively). However, decrements in metabolic rate between sequential studies correlated only with the change in % open wound and the change in EV (r = 0.41 and 0.49, respectively). While changes in heat loss are not capable of predicting all of the variation in metabolic rate, burned patients demonstrate an increase in heat production largely secondary to the inability to conserve heat effectively in the periphery. This response is compounded by an altered central thermoregulation.

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 organisms's 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.

We performed a 5-year retrospective case-control study of 232 patients undergoing femoropopliteal (n = 188) or femorotibial (n = 44) bypass to determine if serial noninvasive studies herald postoperative graft failure. We correlated serial ankle/arm pressure indices (API) with graft patency. An interval drop in API of greater than or equal to 0.20 was considered hemodynamically significant, but interventional therapy was carried out only for clinically symptomatic graft failure and an API less than 0.20 above the preoperative value. The cumulative 5-year limb salvage rate was 82% and the patient survival was 63%. A significant drop in API did not correlate with cumulative 5-year graft patency. The 5-year cumulative primary graft patency rates were 60% and 62% in patients with stable and interval drops in API, respectively (Z = 0.15, p = N.S.) These results suggest that a significant drop in postoperative API does not predict patients with impending femoropopliteal or femorotibial graft failure. We believe that routine noninvasive surveillance and prophylactic intervention on detected asymptomatic lesions in leg bypass grafts may not be justified.

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 Ringer's 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)

The effect of early enteral feeding upon postburn hypermetabolism was studied on the fourteenth postburn day using five groups of rats. Feeding methods and treatments for the groups were: I) rat chow ad libitum at 2 hours postburn (PB); II) fed early by gastrostomy at 2 hours PB; III) fed late by gastrostomy at 72 hours PB; IV) fed early by gastrostomy--shaved control; V) rat chow ad libitum--shaved control. Gastrostomy feedings delivered 175 kcal/kg.day. The rates of heat production and heat loss did not differ significantly between any of the burn groups, whether fed ad libitum, or early or late by way of gastrostomy. The burned rats fed ad libitum gained significantly more weight than the rats fed late by gastrostomy. Contrary to previous studies using a guinea pig model, method and timing of feeding had no demonstrable effect on the postburn increment in heat loss and the secondary increment in heat production following thermal injury in rats.