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Biomedical subjects

W G Cioffi

Publications and source records attributed to W G Cioffi.

At least 73 records · Page 4Linked to original sources

Resuscitation after uncontrolled venous hemorrhage: Does increased resuscitation volume improve regional perfusion?

BACKGROUND: Recent studies have questioned the use of aggressive fluid resuscitation after uncontrolled arterial hemorrhage until the bleeding is controlled. However, it remains unknown whether resuscitation after hemorrhage from a venous origin (usually nonaccessible to surgical intervention) has any beneficial or deleterious effects on regional perfusion. The aim of this study, therefore, was to determine whether increased volume of fluid resuscitation after uncontrolled venous hemorrhage improves hemodynamic profile and regional perfusion in various tissues. MATERIALS AND METHODS: After methoxyflurane anesthesia and midline laparotomy, both lumbar veins in the rat were severed, which resulted in lowering the mean arterial blood pressure to approximately 40 mm Hg. This pressure was maintained for 45 minutes by allowing further bleeding from the lumbar veins. The abdominal incision was then closed in layers and the animals received either 0, 10, or 30 mL of lactated Ringer's solution intravenously over a period of 60 minutes. Cardiac output and regional blood flow were determined by radioactive microspheres immediately or at 1.5 hours after the completion of resuscitation. RESULTS: Fluid resuscitation with 10 or 30 mL lactated Ringer's solution increased mean arterial blood pressure and cardiac output immediately after resuscitation compared with the nonresuscitated animals. At both time points, regional perfusion in the heart, kidney and intestines remained significantly decreased compared with the sham values, irrespective of the volume of fluid resuscitation. Moreover, no further improvements in hemodynamics or regional perfusion occurred when volume resuscitation was increased from 10 mL to 30 mL. Total hepatic blood flow, however, increased with 10 mL lactated Ringer's solution compared with the other hemorrhage groups and the increase was evident even at 1.5 hours after resuscitation. CONCLUSIONS: Fluid resuscitation after uncontrolled venous bleeding transiently increased cardiac output and mean arterial blood pressure compared with nonresuscitated animals. Moderate fluid administration, i.e., 10 mL, however, did increase total hepatic blood flow. In contrast, increasing the resuscitation volume to 30 mL did not improve hemodynamic parameters or regional perfusion. Thus moderate instead of no resuscitation or larger volume of resuscitation is recommended in an uncontrolled model of venous hemorrhage.

Aged↗

Up-regulation of a novel potent vasodilatory peptide adrenomedullin during polymicrobial sepsis.

A large number of studies have been and are being carried out to examine the role of nitric oxide in the hyperdynamic and hypodynamic stages of sepsis. It remains unknown, however, whether adrenomedullin (ADM), a novel potent vasodilatory peptide, is up-regulated during hyperdynamic sepsis and, if so, whether its production is sustained during hypodynamic sepsis. To determine this, rats were subjected to sepsis by cecal ligation and puncture (CLP), followed by administration of 3 mL/100 g body weight normal saline to these and sham-operated animals. Blood samples were taken at 1, 1.5, 2, 5, and 10 h (2-10 h post-CLP represents the hyperdynamic stage of sepsis) or at 20 and 30 h after CLP (i.e., the hypodynamic stage). Plasma levels of ADM were measured by radioimmunoassay. Adrenomedullin gene expression in various tissues was examined at 2, 10, or 20 h after CLP by reverse transcription-polymerase chain reaction (RT-PCR). The results indicated that plasma levels of ADM did not increase at 1 and 1.5 h after CLP but increased significantly at 2 h after the onset of sepsis. Moreover, circulating ADM increased progressively at 5-20 h and remained elevated at 30 h after CLP. The increased levels of plasma ADM during sepsis were correlated with up-regulation of ADM mRNA in the small intestine, left ventricle, and thoracic aorta. In contrast, ADM gene expression in renal and hepatic tissues was not significantly altered following the onset of sepsis. The association between the up-regulated ADM and the occurrence of hyperdynamic circulation during the early stage of sepsis (both occur at 2 h after CLP) may indicate a possible cause and effect relationship between the two events. Since we have previously shown that ADM-induced vascular relaxation decreased at 20 h after CLP, it appears that the down-regulation of ADM receptors may be responsible for the transition from the hyperdynamic stage to the hypodynamic stage of sepsis.

Adrenomedullin↗

Testosterone: the culprit for producing splenocyte immune depression after trauma hemorrhage.

Studies indicate that, whereas immune functions in males are depressed, they are enhanced in females after trauma hemorrhage. Moreover, castration of male mice (i.e., androgen depletion) before trauma hemorrhage prevented the depression of cell-mediated immunity. Nonetheless, it remains unknown whether or not testosterone per se is responsible for producing the immune depression. To study this, female C3H/HeN mice (n = 7 animals/group) were pretreated with 5-dihydrotestosterone (DHT) or vehicle for 19 days, then subjected to laparotomy (e.g., trauma) and hemorrhagic shock (blood pressure 35 +/- 5 mmHg for 90 min) followed by fluid resuscitation or sham operation. Nontreated males underwent either trauma hemorrhage or sham operation. Twenty-four hours thereafter, splenocyte immune functions as well as plasma DHT, estradiol, and corticosterone levels were measured. DHT-pretreated females had significantly (P < 0.05) increased DHT levels, comparable to those seen in males. Conversely, estradiol levels in such females were similar to control males. Splenocyte proliferation as well as interleukin-2 and interleukin-3 release were not depressed in vehicle-treated females, whereas it was in DHT-treated females after trauma hemorrhage, comparable to hemorrhaged males. Thus high testosterone and/or low estradiol levels appear to be responsible for producing splenocyte immune depression in males after trauma hemorrhage. Agents that block testosterone receptors or increase estradiol levels may therefore be helpful in improving depressed immune functions in male trauma patients.

Animals↗

Inhaled nitric oxide prevents left ventricular impairment during endotoxemia.

We evaluated the effect of long-term inhalation of nitric oxide (NO) on cardiac contractility after endotoxemia by using the end-systolic elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardial dimension transducers to measure LV volume and a micromanometer to measure LV pressure. One week later, the animals were divided into a control group (n = 6) or a NO group (n = 6). All animals received intravenous Escherichia coli endotoxin (10 micrograms. kg-1. h-1) and equivalent lactated Ringer solution. NO inhalation (20 parts/million) was begun 30 min after the initiation of endotoxemia and was continued for 24 h. In both groups, tachycardia, pulmonary hypertension, and systemic hyperdynamic changes were noted. The end-systolic elastance in the control group was significantly decreased beyond 7 h. NO inhalation maintained the end-systolic elastance at baseline levels and prevented its impairment. These findings indicate that NO exerts a protective effect on LV contractility in this model of endotoxemia.

Administration, Inhalation↗

L-arginine restores the depressed cardiac output and regional perfusion after trauma-hemorrhage.

BACKGROUND: Previous studies indicate that vascular endothelial cell dysfunction occurs early after trauma-hemorrhage and may contribute to further alteration in tissue perfusion and cellular function. Because endothelial cell dysfunction is characterized by the reduced release of nitric oxide (NO) by endothelial constitutive NO synthase (cNOS), we tested the hypothesis that administration of L-arginine (ie, the substrate for cNOS) after trauma and hemorrhage should have beneficial effects on depressed cardiac output and organ blood flow under those conditions. METHODS: Rats underwent a laparotomy (ie, trauma induced) and were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of maximal shed blood volume was returned in the form of Ringer's lactate solution. The animals were than resuscitated with 4 times the volume of the shed blood in the form of Ringer's lactate solution over 1 hour. L-arginine (300 mg/kg body wt) or saline solution was infused intravenously during the first 15 minutes of resuscitation. Cardiac output and organ blood flow were determined by 85Sr-microspheres at 1.5 and 4 hours after the completion of resuscitation. Plasma interleukin-6 (IL-6) was determined by bioassay at 4 hours after resuscitation. RESULTS: Cardiac output and blood flow in the kidneys, small intestine, and lungs decreased significantly after hemorrhage and resuscitation. In addition, portal blood flow and total hepatic perfusion were also significantly reduced. Administration of L-arginine at the onset of fluid resuscitation, however, restored the depressed cardiac output and tissue perfusion. Moreover, the up-regulated plasma levels of IL-6 were also attenuated by L-arginine administration. CONCLUSIONS: Because the adjuvant use of L-arginine restored the depressed cardiac output and organ blood flow and decreased plasma levels of IL-6, administration of this essential amino acid should be considered as a useful adjunct to fluid resuscitation for improving cardiovascular function in trauma victims.

Animals↗

Trauma-hemorrhage induces increased thymic apoptosis while decreasing IL-3 release and increasing GM-CSF.

Although the thymus is an important organ in the ontogeny of T lymphocytes, little is known about the effects of hemorrhage and/or trauma on this organ. The objective of this study was to determine whether trauma-hemorrhage induces increased thymic apoptosis and, if so, which mediators may be involved. Male C3H/HeN mice underwent either sham operation, hemorrhagic shock (mean artery blood pressure of 35 +/- 5 mmHg for 90 min, followed by blood and fluid resuscitation), fracture of the right tibia, or fracture plus hemorrhage, respectively. At 3 days after the procedure, total viable thymocyte yield, thymocyte apoptosis (flow cytometry), thymus-derived IL-3 (bioassay), and GM-CSF (ELISA) were determined. The results demonstrate that fracture alone induces no significant change in the parameters measured. However, (i) there was a significant decrease in total viable thymocyte yield and an increase in thymocyte apoptosis following hemorrhage or fracture plus hemorrhage; (ii) thymocyte IL-3 release was significantly reduced after hemorrhage as well as fracture plus hemorrhage; (iii) thymus-derived GM-CSF was significantly increased after fracture plus hemorrhage, but not with hemorrhage alone. In conclusion, severe hemorrhage alone or coupled with fracture can induce thymus atrophy via apoptosis. In addition, the decreased IL-3 release suggests that apoptotic thymic involution may be due to the lack of growth factor support. Such dyshomeostasis may contribute to inappropriate/inadequate T cell maturation leading to host immune suppression following trauma-hemorrhage. Increased thymus-derived GM-CSF might be in part responsible for the systemic inflammatory response following trauma-hemorrhage.

Animals↗

Testosterone receptor blockade after hemorrhage in males. Restoration of the depressed immune functions and improved survival following subsequent sepsis.

BACKGROUND: Recent studies suggest that androgen depletion by castration before hemorrhage has protective effects on cell-mediated immunity in male mice after soft tissue trauma and hemorrhagic shock. OBJECTIVE: To determine whether treatment with an androgen receptor blocker (eg, flutamide) after trauma-hemorrhage and sepsis has any salutary effects on cell-mediated immunity and on the survival of male animals under those conditions. DESIGN: Male C3H/HeN mice were either sham operated or subjected to hemorrhagic shock (mean [+/- SEM] blood pressure, 35 +/- 5 mm Hg for 90 minutes) followed by adequate fluid resuscitation (with shed blood and lactated Ringer solution). The animals then received either vehicle or 25-mg/kg body weight flutamide subcutaneously immediately after the resuscitation as well as 24 and 48 hours thereafter. At 48 hours after shock, sepsis was induced by cecal ligation and puncture. Sham-operated animals underwent laparotomy only. At 24 hours after cecal ligation and puncture, the animals were killed, blood was collected, and splenocytes and splenic macrophages were harvested to produce nonadherent and adherent cultures. Splenocytes were evaluated for splenocyte proliferation and interleukin 2 release, while interleukin 1 and interleukin 6 release were assayed in splenic macrophages. Plasma testosterone and corticosterone levels were also measured by radioimmunoassay. In a separate set of experiments, survival was measured over a period of 9 days after the induction of sepsis. RESULTS: Hemorrhage followed by sepsis produced a significant (P < .05) depression of splenocyte and macrophage functions in vehicle-treated animals. In contrast, animals treated with flutamide showed markedly improved immune functions, as evidenced by restoration of splenocyte proliferation, interleukin 2 release, splenic macrophage interleukin 1 release, and improvement of splenic macrophage interleukin 6 release. Plasma corticosterone levels were notably elevated while testosterone levels were depressed after hemorrhage and the induction of sepsis. The survival rate of the animals in the flutamide-treated group was also notably higher than the survival rate of animals in the vehicle-treated group subjected to hemorrhage and sepsis. CONCLUSION: The findings that flutamide not only markedly improves the depressed immune functions but also the survival of animals after hemorrhage and the induction of sepsis suggest that the short-term administration of androgen receptor blocker in males after trauma represents a safe and novel approach for preventing immune deficiency and decreasing the mortality rate from subsequent sepsis.

Androgen Antagonists↗

Mechanism of intestinal mucosal immune dysfunction following trauma-hemorrhage: increased apoptosis associated with elevated Fas expression in Peyer's patches.

Although intestinal mucosal immune dysfunction occurs after trauma and hemorrhage and appears to contribute to infectious complications, the mechanism is not known. In this regard, the inappropriate induction of immune cell apoptosis may contribute to the immune dysfunction following trauma and hemorrhage. To study this, we examined Peyer's patch cells for evidence of apoptosis and changes in Fas protein expression, as well as alterations in the relative lymphocyte subpopulations after trauma and hemorrhagic shock. Male C3H/HeN mice underwent sham operation, trauma (i.e., laparotomy), hemorrhagic shock (mean arterial blood pressure of 35 +/- 5 mmHg for 90 min, followed by adequate crystalloid resuscitation), or trauma plus hemorrhage. Peyer's patch cells were isolated at 24 and 72 hr after the procedure. The percentage of apoptotic cells, Fas protein expression, and cell percentage of phenotype were determined by flow cytometry. The results indicate that trauma alone induced no significant change in the measured parameters. However, (i) there were a significant decrease in total viable cell yield and an increased apoptosis in Peyer's patch cells at 24 and 72 hr following hemorrhage or trauma plus hemorrhage; (ii) the increased apoptosis in Peyer's patch was predominantly in cells of the B-cell lineage; (iii) the increased apoptosis was associated with an elevated Fas expression. In conclusion, hemorrhage alone or trauma plus hemorrhage can induce increased apoptosis in Peyer's patch cells, which is associated with the increased Fas expression. Thus, apoptotic involution may play an important role in the depression of intestinal mucosal immune function after trauma and hemorrhagic shock.

Animals↗

The use of perfluorocarbon-associated gas exchange to improve ventilation and decrease mortality after inhalation injury in a neonatal swine model.

Patients with tracheobronchial disease frequently require mechanical ventilation during therapy and experience iatrogenic complications such as barotrauma and volutrauma. The purpose of this study was to determine whether perfluorocarbon-associated gas exchange (PAGE) results in lower ventilatory pressures and more efficient ventilation than that provided by conventional ventilation after tracheobronchial mucosal injury caused by smoke inhalation in neonatal piglets. Ten piglets were used for this prospective, randomized study. After administration of a severe smoke inhalation injury, the piglets were randomly assigned to either the perfluorocarbon or control groups. Group 1 served as the control population and received standard (time-cycled, volume-limited) mechanical ventilation. Ventilator settings were adjusted to maintain physiological pH and PO2 at the lowest tidal volume, rate, and end-expiratory pressure possible throughout the study period. Group 2 was administered intratracheal perfluorocarbon as well as identical mechanical ventilation to attain the same physiological pH and PO2. Oxygenation index, peak and mean airway pressures, and arterial blood gas levels were measured throughout the study period and subjected to statistical analysis. Histological comparison of airway and parenchymal tissues confirmed identical patterns of smoke injury in both groups. Carbon monoxide levels were the same in both groups. There was significant barotrauma and volutrauma in the control group, but none in the PAGE group. All controls died from 13 to 17 hours after injury; one PAGE pig died at 23 hours with all others surviving past 24 hours (P = .0021). Peak, plateau, and mean airway pressures were all significantly higher (P < .05) past 12 hours after injury and continued to increase until death in the controls. Arterial blood gases showed significantly (P < .05) decreased pH, PO2, and elevated PcO2 levels in the control group past 12 hours after injury. The oxygenation index was significantly elevated (P < .05) in the control group past 12 hours after injury. PAGE shows potential for improving ventilation and survival immediately after severe smoke inhalation injury and may have clinical applications in other nonhomogeneous lung injuries.

Animals↗

Effects of burns on inhalation injury.

BACKGROUND: There are few studies of smoke injury combined with thermal burn. METHODS: Seven sheep (G1) received smoke injury alone; eight (G2) received a 40% full-thickness scald burn immediately after smoke injury. All animals were resuscitated with lactated Ringer's solution and killed 48 hours after injury. Cardiopulmonary variables and blood gases were measured serially. Ventilation perfusion distribution was analyzed using the multiple inert gas elimination technique. Lung wet to dry weight ratio and malondialdehyde levels were determined. RESULTS: G2 resulted in early significant hemodynamic changes. Serum total protein concentration was significantly lower and malondialdehyde significantly higher in G2. However, PaO2, lung wet to dry weight ratio, and ventilation perfusion mismatching in G2 did not differ from those in G1. CONCLUSIONS: Although the addition of burn injury exaggerated the lung lipid peroxidation and hypoproteinemia in the presence of more pronounced hemodynamic changes, the pulmonary dysfunction was not accentuated.

Animals↗

Prospective outcome analysis of a protocol for the surgical and rehabilitative management of burns to the hands.

Treatment protocols for the management of burned hands are essential for integrating team efforts and achieving optimal functional results. Standard protocols are especially useful during mass casualty incidents, when the admission of multiple patients with large burns and/or associated injuries may reduce the priority usually accorded the hands. We prospectively evaluated a surgical and rehabilitative treatment protocol for burned hands during a mass casualty incident, after which 43 burn patients with 82 burned hands were admitted to one burn center. Soft-tissue management was individualized to achieve, if possible, wound closure within 14 days, and included the use of topical antimicrobials, cutaneous debridement and/or tangential excision, biologic dressings, and split-thickness autografts. Range of motion therapy was based on daily measurement of active motion of the metacarpophalangealjoints. Static splinting alternating with continuous passive motion every 4 hours was utilized for sedated patients. Continuous passive motion alternating with active ranging and night splinting was utilized for metacarpophalangeal flexion <70 degrees. Active ranging and progressive resistance was utilized for metacarpophalangeal flexion > or =70 degrees. Sixty-four hands required excision and grafting, with 89 percent having at least one autografting procedure completed by postburn day 16. Total active motion of the hands treated averaged 220.6 degrees on discharge and 229.9 degrees at 3 months after injury. Mean hand grip strength was 60.8 pounds at discharge and 66.0 pounds at 3 months after injury. Adherence to a standard hand burn protocol resulted in timely wound coverage and recovery of hand function for a large group of patients treated at a single burn facility after a mass casualty incident.

Accidents, Aviation↗

Testosterone receptor blockade after trauma-hemorrhage improves cardiac and hepatic functions in males.

Although studies have shown that testosterone receptor blockade with flutamide after hemorrhage restores the depressed immune function, it remains unknown whether administration of flutamide following trauma and hemorrhage and resuscitation has any salutary effects on the depressed cardiovascular and hepatocellular functions. To study this, male rats underwent a laparotomy (representing trauma) and were then bled and maintained at a mean arterial pressure (MAP) of 40 mmHg until the animals could not maintain this pressure. Ringer lactate was given to maintain a MAP of 40 mmHg until 40% of the maximal shed blood volume was returned in the form of Ringer lactate. The rats were then resuscitated with four times the shed blood volume in the form of Ringer lactate over 60 min. Flutamide (25 mg/kg) or an equal volume of the vehicle propanediol was injected subcutaneously 15 min before the end of resuscitation. Various in vivo heart performance parameters (e.g., maximal rate of the pressure increase or decrease), cardiac output, and hepatocellular function (i.e., the maximum velocity and the overall efficiency of indocyanine green clearance) were determined at 20 h after resuscitation. Additionally, hepatic microvascular blood flow (HMBF) was determined using a laser Doppler flowmeter. The results indicate that left ventricular performance, cardiac output, HMBF, and hepatocellular function decreased significantly at 20 h after the completion of trauma, hemorrhage, and resuscitation. Administration of the testosterone receptor blocker flutamide, however, significantly improved cardiac performance, HMBF, and hepatocellular function. Thus flutamide appears to be a novel and useful adjunct for improving cardiovascular and hepatocellular functions in males following trauma and hemorrhagic shock.

Androgen Antagonists↗

Flutamide: a novel agent for restoring the depressed cell-mediated immunity following soft-tissue trauma and hemorrhagic shock.

Recent studies indicate beneficial effects of androgen depletion in male mice, before trauma-hemorrhage on cell-mediated immunity following soft-tissue trauma and hemorrhagic shock. Nonetheless, it remains unknown whether androgen receptor blockade following the insult has any salutary effects. To study this, male C3H/HeN mice were either sham-operated or subjected to soft-tissue trauma (i.e., 2.5 cm midline laparotomy) followed by hemorrhagic shock (blood pressure 35 +/- 5 mmHg for 90 min) and then adequately resuscitated (shed blood and lactated Ringer's). Immediately after the completion of resuscitation, as well as 24 and 48 h thereafter, the animals received either vehicle, 10 mg/kg body weight (BW) flutamide or 25 mg/kg BW flutamide subcutaneously. At 72 h after resuscitation, all animals were killed. The spleens and peritoneal macrophages (M phi) were then harvested and cultures established to determine IL-2 and IL-3 release, splenocyte proliferative capacity, as well as splenic and peritoneal M phi IL-1 release. Moreover, plasma testosterone and corticosterone levels were measured. Our results indicate that trauma-hemorrhage resulted in significant depression of splenocyte and M phi functions in vehicle-treated and animals receiving 10 mg/kg BW flutamide. Treatment with 25 mg/kg BW flutamide following trauma-hemorrhage, however, resulted in levels of cytokine release which were comparable with those found in sham-operated animals. No significant alterations in plasma corticosterone and testosterone levels were observed in any of the experimental groups. These findings indicate that short-term therapy of males with the androgen receptor blocker, flutamide at 25 mg/kg BW, following trauma-hemorrhage has protective effects on immune functions. This protective effect is dose dependent, since 10 mg/kg BW flutamide did not produce significant salutary effects. Thus, flutamide represents a novel and safe agent for improving the depressed functions in male trauma patients suffering severe blood loss.

Animals↗

Ventilatory support following burns and smoke-inhalation injury.

The first major improvement in the treatment of burn injury came with the recognition of the importance of fluid resuscitation to prevent shock and renal failure. Subsequently, the use of topical antibiotics to control burn-wound infection and prevent invasive burn-wound sepsis led to the next significant reduction in morbidity and mortality of burn patients. Although progress has been made in the treatment of inhalation injury, the pathophysiology of the injury is still incompletely defined. A better understanding of pathogenic mechanisms will lead to the development of therapeutic agents and treatment regimens that will modulate the cascades of humoral mediators of organ dysfunction and reduce the morbidity and mortality associated with inhalation injury. The recognition of ventilator-induced lung injury has led to adoption of alternative ventilatory techniques such as high-frequency percussive ventilation, which has been shown to substantially reduce the morbidity associated with inhalation injury.

Burns↗

Computed tomography in blunt hepatic trauma.

BACKGROUND: Nonoperative management of blunt hepatic injury in hemodynamically stable trauma patients is now common. Recently, it has been proposed that the finding of hepatic periportal tracking (PPT) of blood on the initial computed tomographic (CT) scan is a sensitive marker of significant hepatic and subhepatic injury that might militate against nonoperative management. While CT scan is useful in diagnosing the injury, the utility of follow-up CT scans has not been elucidated. DESIGN: Retrospective chart review. SETTING: Regional trauma center. PATIENTS: The records of 58 hemodynamically stable patients with blunt hepatic trauma were reviewed and the following data recorded: age, outcome, Injury Severity Score (ISS), operative intervention, and complications. Computed tomographic scans were taken on admission and reviewed for the presence of PPT. The timing and radiographic appearance of follow-up CT scans was also recorded. RESULTS: Seventeen patients (29%) had radiographic evidence of PPT while 41 patients (71%) did not. Age, ISS, injury grade, overall success rate of nonoperative management, and incidence of complications were not statistically significant between the two groups. In no instance did a routine follow-up CT scan affect subsequent management of the patient. CONCLUSIONS: The finding of PPT on the admission CT scan is not clinically significant and does not preclude nonoperative management of patients with blunt hepatic injury. Furthermore, routine follow-up CT scans are not indicated, as treatment is not influenced by their results. Rather, follow-up CT scans should be obtained as dictated by the patient's clinical course. Extrapolation of these findings to all patients with blunt hepatic trauma in the United States would result in considerable savings of health care dollars, without negatively affecting patient care.

Adolescent↗

Prolonged alteration in gut permeability following nonthermal injury.

To assess the extent of intestinal permeability following nonthermal injury ratios of lactulose and mannitol (L-M) concentrations in urine following enteral administration were determined simultaneously by a gas-liquid chromatography assay on days 3, 5, 7, 10, and 13 in 15 patients with an Injury Severity Score > 20. Thirteen of 15 patients recovered uneventfully and two developed minor infections. L-M ratios were significantly increased on days 3-10 (P < 0.05 vs controls). The data are consistent with previous studies describing early changes in gut permeability following nonthermal injury and show that altered permeability can persist for up to 10 days in patients with uneventful recoveries.

Adolescent↗

Aeromonas bacteraemia in burn patients.

Human aeromonas infection is uncommon and is usually associated with immunosuppression, chronic disease or trauma in an aquatic setting. Burn injury may induce a state of immunosuppression, making the thermally injured patient a suitable host for aeromonas infection. We reviewed the experience of one burn centre with this pathogen. Retrospective examination of blood culture results from 8151 patients admitted between 1959 and 1994 disclosed eight patients with clinically relevant Aeromonas hydrophilia bacteraemia. Five were burned outside the USA. Aquatic exposure was known or suspected in only three cases. Five of the eight patients died. Aeromonas infection in burn patients is rare but may occur in the absence of aquatic exposure.

Adult↗

Effect of ambient temperature on metabolic rate after thermal injury.

OBJECTIVE: The authors describe the effect of ambient temperature on metabolic rate after thermal injury. SUMMARY BACKGROUND DATA: Thermal injury induces a hypermetabolic state, which is reported to increase with the extent of burn. The magnitude of this response is further influenced by ambient temperature. METHODS: The resting energy expenditure was measured by indirect calorimetry at ambient temperatures of 22, 28, 32, and 35 C. It was indexed to a calculated basal metabolic rate in normal volunteers and adult patients with burns involving at least 20% of the total body surface area who had no evidence of systemic infection. These measurements were performed between postburn days 6 and 21. RESULTS: The effect of ambient temperature on metabolic rate was measured in 44 burn patients and 8 normal volunteers. Burn size ranged from 20 to 97% total body surface area with a mean of 44 +/- 18.5% total body surface area. Metabolic rate did not change significantly in control subjects as ambient temperature was varied (p<0.05). Regression analysis showed that burn size and ambient temperature were significant determinants (p<0.01) of metabolic rate in the patients and that together these factors accounted for 55% of the variation observed (df adj. r(2)=0.55) across the range of ambient temperatures studied. Metabolic rate was independent of burn size at ambient temperatures of 32 and 35 C (p<0.02) and increased by a factor of 1.5 X basal metabolic rate. A further increase in metabolic rate, which was positively correlated with burn size, resulted from nonshivering thermogenesis at ambient temperatures 28 and 22 C. The magnitude of this response was greatest at 22 C. CONCLUSIONS: These findings suggest that the hypermetabolic response to thermal injury is maximal in burns as small as 20% total body surface area and that an additional burn size-dependent increase in metabolic rate results from heat loss at ambient temperatures below thermoneutrality.

Adult↗