Adrenal hemorrhage in a pediatric burn patient.

Adrenal hemorrhage with subsequent insufficiency is a rare complication in the burn patient. The case of a previously healthy 3-year-old Latin American male who was a victim of child abuse is presented. He suffered a submersion injury in hot water leading to a 45% total body surface area burn. An acute deterioration on the 7th post burn day was unresponsive to standard inotropic support and cardiopulmonary resuscitation. Post mortem examination revealed bilateral adrenal hemorrhage that had not been present 2 days earlier. To the authors' knowledge, this is the first reported case in a pediatric burn patient. The clinical manifestations of adrenal insufficiency vary widely and can be easily confused with sepsis. High index of suspicion is necessary for early diagnosis and treatment. Serum cortisol level should be checked and steroid therapy implemented if sepsis syndrome is unresponsive to standard therapy in this setting. This early intervention may be the key to improved survival of the burn patient with a sudden unexplained deterioration resistant to well established resuscitation methods.

The effects of infection of thermal injury by Pseudomonas aeruginosa PAO1 on the murine cytokine response.

Pseudomonas aeruginosa infection, one of the major complications of burn wounds, may lead to sepsis and death. Using the Multi-Probe Template/RNase protection assay, we have compared the expression of different cytokine genes within the skin and livers of thermally injured mice infected with P. aeruginosa PAO1. Thermal injury alone enhanced or up-regulated certain cytokines, including macrophage colony-stimulating factor (M-CSF), interleukin 1 (IL-1)RI, IL-1 beta, macrophage inflammatory protein (MIP)-1 beta and MIP-2; while PAO1 challenge alone up-regulated tumour necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta) expression. The combination of thermal injury plus PAO1 infection enhanced the expression of several pro-inflammatory and haematopoietic cytokines [stem cell factor (SCF), leukocyte inhibitory factor (LIF), IL-6 and TNF-alpha]; induced the expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) and G-CSF by 5 h and the expression of additional cytokines, including TGF-beta, TNF-beta, lymphotoxin beta (LT-beta), interferon gamma (IFN-gamma), and IFN-beta by 40 h post-burn/infection. While the most intense cytokine expression occurred in the skin, the majority of cytokines tested were also expressed in the liver by 40 h post-burn/infection. These results suggest that in P. aeruginosa infection of burn wounds: (1) up-regulation of the expression of different cytokines, locally and within the livers of burned mice, is an indication of P. aeruginosa -induced sepsis; and (2) IL-6 and G-CSF play an important role in the host response mechanism.

A novel hemoglobin-adenosine-glutathione based blood substitute: evaluation of its effects on human blood ex vivo.

Chemically modified hemoglobin (Hb) solutions are under current investigation as potential red cell substitutes. Researchers at Texas Tech University have developed a novel free Hb based blood substitute product. This blood substitute is composed of purified bovine Hb cross-linked intramolecularly with o-adenosine-5'-triphosphate and intermolecularly with o-adenosine, and conjugated with reduced glutathione (GSH). In this study, we compared the effects of our novel blood substitute and unmodified (U) Hb, by using allogenic plasma as the control, on human blood components: red blood cells (RBCs), platelets, monocytes (Mo), and low-density lipoproteins (LDLs). The pro-oxidant potential of both Hb solutions on RBCs was examined by the measurement of osmotic and mechanical fragility, conjugated dienes (CD), lipid hydroperoxides (LOOH), thiobarbituric acid reactants (TBAR-S), isoprostanes (8-iso PGF2alpha) and intracellular GSH. The oxidative modification of LDLs was assessed by CD, LOOH, and TBAR-S, and the degree of apolipoprotein (apo) B cross-linking. The effects of Hb on platelets have been studied by monitoring their responses to the aggregation agonists: collagen, ADP, epinephrine, and arachidonic acid. Monocytes were cultured with Hb solutions or plasma and tested for TNF-alpha and IL-1beta release, then examined by electron microscopy. Results indicate that native UHb initiates oxidative stress of many blood components and aggravates inflammatory responses of Mo. It also caused an increase in RBC osmotic and mechanical fragility (p < 0.001). While the level of GSH was slightly changed, the lipid peroxidation of RBC increased (p < 0.001). UHb was found to be a stimulator of 8-iso PGF2alpha synthesis, a potent modulator of LDLs, and an effective potentiator of agonist induced platelet aggregation. Contrarily, our novel blood substitute did not seem to induce oxidative stress nor to increase Mo inflammatory reactions. The osmotic and mechanical fragility of RBCs was similar to that of the control. Such modified Hb failed to alter LDLs, increase the production of 8-iso PGF2alpha, but markedly inhibited platelet aggregation. The effect of this novel blood substitute can be linked with the cytoprotective and anti-inflammatory properties of adenosine, which is used as a cross-linker and surface modifier, and a modification procedure that lowers the hemoglobin pro-oxidant potential.

The role of quorum sensing in the in vivo virulence of Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an opportunistic pathogen that causes a wide variety of infections. The cell-density-dependent signaling mechanisms known as quorum sensing play a role in several of these infections including corneal, lung and burn wound infections. In addition, the quorum-sensing systems contribute to the ability of P. aeruginosa to form biofilms on medically important devices. The quorum-sensing systems accomplish their effect by controlling the production of different virulence factors and by manipulating the host immune response.

Pseudomonas aeruginosa strains obtained from patients with tracheal, urinary tract and wound infection: variations in virulence factors and virulence genes.

Pseudomonas aeruginosa produces several virulence factors including exotoxin A, exoenzyme S and elastase. In previous reports we have analysed several clinical isolates for the production of these three virulence factors and for possible heterogeneity within the genes that code for these factors (toxA, lasB and the exoS genes). The isolates were obtained from three specific sites (trachea, urinary tract and wounds). Although the isolates produced variable levels of these factors, isolates that were obtained specifically from urinary tract and wound infections produced increased levels of exotoxin A and exoenzyme S. In addition, a prolonged infection with P. aeruginosa appears to enhance exoenzyme S production. Restriction site polymorphism was very limited within the toxA, lasB, and exoS structural genes; however, the upstream region of toxA showed restriction site polymorphisms between the different isolates. The observed polymorphisms did not correlate with any variations in the levels of the virulence factors. In this article, we provide a short review of these studies.

Contribution of quorum sensing to the virulence of Pseudomonas aeruginosa in burn wound infections.

The Pseudomonas aeruginosa quorum-sensing systems, las and rhl, control the production of numerous virulence factors. In this study, we have used the burned-mouse model to examine the contribution of quorum-sensing systems to the pathogenesis of P. aeruginosa infections in burn wounds. Different quorum-sensing mutants of P. aeruginosa PAO1 that were defective in the lasR, lasI, or rhlI gene or both the lasI and rhlI genes were utilized. The following parameters of the P. aeruginosa infection were examined: (i) lethality to the burned mouse, (ii) dissemination of the P. aeruginosa strain within the body of the infected mouse (by determining the numbers of CFU of P. aeruginosa within the liver and spleen), and (iii) spread of the P. aeruginosa strain within the burned skin (by determining the numbers of CFU of P. aeruginosa at the inoculation site and at a site about 15 mm from the inoculation site [distant site]). In comparison with that of PAO1, the in vivo virulence of lasI, lasR, and rhlI mutants was significantly reduced. However, the most significant reduction in in vivo virulence was seen with the lasI rhlI mutant. The numbers of CFU that were recovered from the livers, spleens, and skin of mice infected with different mutants were significantly lower than those of PAO1. At 8 and 16 h post burn infection, comparable numbers of CFU of PAO1 and lasI and rhlI mutants were obtained from both the inoculation and distant sites of the burned skin of infected mice. In contrast, CFU of the lasR mutant and the lasI rhlI double mutant were recovered only from the inoculation site of infected mice at 8 and 16 h post burn infection. The ability of a plasmid carrying either the lasI or rhlI gene or the lasI and rhlI genes to complement the defect of the lasI rhlI double mutant was also examined. The presence of any of these plasmids within the lasI rhlI double mutant significantly enhanced its in vivo virulence, as well as its ability to spread within the burned skin. These results suggest that the quorum-sensing systems play an important role in the horizontal spread of P. aeruginosa within burned skin and in the dissemination of P. aeruginosa within the bodies of burned-and-infected mice and contributed to the overall virulence of P. aeruginosa in this animal model.

Bradykinin metabolism in perfused rat kidney.

The purpose of this study was to assess the capacity of perfused rat kidney to inactivate bradykinin (BK), and to compare the BK degrading capacity of rat kidney with the BK degrading capacities of rat lung, liver, and skeletal muscle, which was approximated by perfusion of rat hind limbs. Radioactively labeled BK, with the Pro2 and Pro3 residues having been tritiated, in an asanguinous salt solution was perfused through the kidney of the rat, over a concentration range of .0028-33 microM. Rat kidney had a large capacity to degrade BK and the system did not appear to approach saturation until perfusate BK concentrations reached 24 microM. A least-squares linear regression analysis and extrapolation to zero concentration was used to obtain values for amounts of BK degraded and BK fragments formed. The amount of BK cleaved was 99.9% of the administered dose. The major tritiated BK fragments formed, and the amount of each expressed as a percentage of the amount of BK degraded during transrenal passage, were the amino acid proline derived from the Pro2 and/or Pro3 residues of BK (Pro2,3), 60%; Pro-Pro (BK 2-3), 12%; Arg-Pro-Pro-Gly-Phe (BK 1-5), 14%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro (BK 1-7), 14%. The formation of BK 2-3 is indicative of initial aminopeptidase-P cleavage of BK to yield Arg, and des-Arg1-BK. Thus in rat kidney the aminopeptidase-P pathway is the major route for BK degradation, as is the case in rat liver.

Analysis of Pseudomonas aeruginosa clinical isolates for possible variations within the virulence genes exotoxin A and exoenzyme S.

We have previously characterized several Pseudomonas aeruginosa isolates that were obtained from patients with tracheal, urinary tract, or wound infections (A. H. Hamood, J. A. Griswold, and C. M. Duhan, 1996, J. Surg. Res. 61: 425). Analysis of additional isolates showed that regardless of the isolation site, some isolates produced significantly higher or significantly lower levels of either exotoxin A or exoenzyme S proteins. These variations did not correlate with the mucoid phenotype of the isolates. One aim of this study was to determine if the variations in the level of exotoxin A or exoenzyme S are due to DNA rearrangements within either the toxA or the exoS gene. This was accomplished by Southern blot hybridization experiments using a toxA internal probe, a toxA upstream probe, or an exoS internal probe. Hybridization with the toxA internal probe produced a 0.8-kb hybridizing fragment, whereas hybridization with the exoS internal probe produced either a 2.0- or a 2.3-kb hybridizing fragment. Hybridization with the toxA upstream probe, however, produced hybridizing fragments of varying sizes, regardless of their isolation site. Isolates that showed a similar hybridization fragment with either the toxA upstream probe or the exoS internal probe produced variable levels of exotoxin A or exoenzyme S. These results suggest that: [1] specific location within the host has no effect on either the mucoid phenotype of the isolate or the level of exotoxin A or exoenzyme S produced by the isolates; [2] although restriction polymorphism exists within the toxA upstream region, both the toxA and the exoS structural genes are relatively conserved; and [3] variations in the level of exoenzyme S and exotoxin A produced by different isolates do not correlate with either the observed heterogeneity within the toxA upstream region or the mucoid phenotype of the isolates.

Contribution of the regulatory gene lasR to the pathogenesis of Pseudomonas aeruginosa infection of burned mice.

Pseudomonas aeruginosa is a gram-negative opportunistic pathogen that causes severe infections in patients with burns. The P aeruginosa regulatory gene, lasR, regulates the expression of several virulence factors. The specific lasR isogenic mutant, PAO-R1, is defective in the synthesis of the 2 elastases (LasB and LasA) and produces low levels of exotoxin A and alkaline proteases. In this study, we used a burned mouse model to examine the role of lasR in the pathogenesis of P aeruginosa infections. We have examined the following aspects of P aeruginosa infections: 1) lethality to the burned mouse, 2) the dissemination within the body of the burned mouse, and 3) the local spread within the burned skin. In comparison with its parent strain, PAO1, PAO-R1 was less lethal. In addition, the numbers of PAO-R1 microorganisms recovered from the livers and spleens of the burned mice were less than those of PAO1. Furthermore, at 8 hours postinfection, equivalent numbers of PAO1 and PAO-R1 were detected at the inoculation site of the burned skin. However, only PAO1 microorganisms were detected at other sites of the burned skin. These results suggest that the lasR gene contributes (directly and indirectly) to the dissemination of P aeruginosa within the body of burned mice and its horizontal spread within the burned skin.

Bradykinin metabolism in rat hind limbs.

The purpose of this study was to assess the capacity of perfused rat hind limbs, the majority of which is skeletal muscle, to inactivate bradykinin (BK), and to compare the BK degrading capacity of rat hind limbs with the BK degrading capacities of rat lung and liver. BK, with tritiated Pro2 and Pro3 residues, in an asanguinous salt solution was perfused for a single passage through skeletal muscle and other tissues in the hind legs of the rat over a concentration range of .0029 to 49.3 microM. Rat hind limbs had a large capacity to degrade BK and the system did not approach saturation, even at 49.3 microM. A least-squares linear regression analysis and extrapolation to zero concentration was used to obtain values for amounts of BK degraded and BK fragments formed. The amount of BK cleaved was 95% of the administered dose. The major BK fragments formed, and the amount of each expressed as a percentage of the amount of BK degraded were Pro-Pro (BK 2-3), 8.6%; Arg-Pro-Pro-Gly-Phe (BK 1-5), 82%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro (BK 1-7), 6%. The BK 1-5 yield was reduced from 82% to one-fourth of that by angiotensin converting enzyme (ACE) inhibitors. BK 2-3 formation is indicative of initial aminopeptidase-P cleavage of BK to yield Arg, and des-Arg1-BK. ACE inhibitor sensitive formation of BK 1-5 is indicative of initial kininase-II, also known as ACE, cleavage of BK. Thus in rat hind limbs, the ACE pathway is the preponderant mechanism for BK degradation, which is in contrast to our previously published reports that in rat liver the amino-peptidase-P pathway predominates, and that in rat lung both the aminopeptidase-P pathway and the ACE pathway exhibit nearly equal capacities to degrade BK.

Bradykinin metabolism in the liver and lung of the rat.

Bradykinin (BK) in an asanguinous salt solution was perfused through intact rat liver. The perfusate was delivered through the portal vein and was collected from the inferior vena cava. BK concentrations varied from 0.0030 to 38.0 microm. The liver had a large capacity to degrade BK and the system did not approach saturation until perfusate BK concentrations reached 60 microm. The quantitatively predominant BK fragments formed and the amount of each formed, expressed as a percentage of the BK degraded during a single transhepatic passage, were Pro-Pro, 74%; Arg-Pro-Pro-Gly-Phe, 15%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro, 7%; the first is indicative of initial aminopeptidase-P cleavage of BK to yield Arg and des-Arg1-BK and the latter two are indicative of initial angiotension converting enzyme (ACE) cleavage of BK. On the other hand, while the perfused rat lung also had a large capacity to degrade BK, the quantitatively predominant BK fragments formed and the amount of each formed, again expressed as a percentage of BK metabolized during a single transpulmonary passage, were Pro-Pro, 47%; Arg-Pro-Pro-Gly-Phe, 35%; and Arg-Pro-Pro-Gly-Phe-Ser-Pro, 7%. Thus in rat liver the aminopeptidase-P pathway is the major route for BK degradation, whereas in rat lung the aminopeptidase-P and the ACE pathways exhibit nearly equal capacities to degrade BK.

Modulation of immune response in thermal injury by essential fatty acid-deficient diet.

This study was performed to determine the effects of essential fatty acid-deficient diet (EFAD) on immune parameters at 24 hours and 1 week after burn injury. Sprague Dawley rats were fed an EFAD diet or chow diet for 14 days. Twenty percent of the animals were put to death before the burn treatment (day 0), and the remainder were selected randomly to receive a scald or sham injury. Elevation in natural killer cell activity for EFAD-fed animals compared with rats fed the control diet was demonstrated at 100:1 effector:target (E:T) ratio on postburn day 1, and 25:1 E:T ratio on postburn day 7. EFAD-fed animals had significantly higher T-cell proliferation for all doses of phytohemagglutinin than did control animals before the burn injury. One week after the injury, EFAD-fed animals' T-cell activity was reduced to a level equivalent to that of control chow animals, whereas burned chow rats' lymphocyte activity was diminished significantly. EFAD diets enhanced T-cell proliferation and modestly improved natural killer cell response in both burned and control animals.

Trauma in pregnancy: the role of interpersonal violence.

OBJECTIVE: Our purpose was to determine what role interpersonal violence as intentional injury plays in the pregnant trauma victim. STUDY DESIGN: We performed a retrospective review of medical records. RESULTS: During a 9-year period in a single university medical and trauma center, 203 pregnant women were treated for a physically traumatic event. Sixty-four women (31.5%) were victims of intentional injury, in most cases by the husband or boyfriend. Although the mean Injury Severity Score was higher in women with fetal death than in women with successful pregnancy outcomes (7.25 vs 1.74, respectively; p < 0.01), 5 of the 8 women with fetal losses incurred these despite an apparent absence of physical injury (maternal Injury Severity Score = 0). CONCLUSIONS: Interpersonal violence during pregnancy is a frequent and increasingly common cause of maternal injury. The inconsistent relationship between Injury Severity Score and serious fetal injury or death is underscored by the loss of 5 fetuses despite an Injury Severity Score of 0.

PIP: The role of interpersonal violence as intentional injury in the pregnant trauma victim was investigated. Data were obtained from the medical records. Results showed that during the 9-year study interval, 203 pregnant women were admitted after a traumatic event. About 64 women (31.5%) in the study population were victims of intentional injury, particularly one inflicted by a husband or boyfriend. The maternal Injury Severity Score (ISS) averaged 7.25 in women with fetal loss versus a mean maternal ISS of 1.74 (p 0.001) in the 140 women having successful pregnancy outcomes. Moreover, 5 of the 8 women with a fetal death had no evidence of physical injury and an ISS = 0. Thus, interpersonal violence appears to be a marker for adverse maternal and fetal outcomes. In addition, physical findings could give clues to the role of interpersonal violence in trauma during pregnancy.

Production of extracellular virulence factors by Pseudomonas aeruginosa isolates obtained from tracheal, urinary tract, and wound infections.

This study was conducted to determine the effect of the local environment within the host on the ability of P. aeruginosa to produce different extracellular virulence factors (elastase, phospholipase C, toxin A, and exoenzyme S). A total of 105 P. aeruginosa isolates was obtained from patients with tracheal, urinary tract, and wound infections. Quantitative analysis of the virulence factors was done by growing the isolates in vitro in different defined media. Single colonies of each isolate were inoculated from the primary isolation plates into the defined medium. All four virulence factors were produced by most isolates. However, depending on the location of their isolation, the isolates varied in the level of virulence factors they produced. High levels of elastase and phospholipase C were produced by most isolates obtained from trachea, urinary tract, and wounds. A significantly higher level of toxin A was produced by wound isolates, while a significantly higher level of exoenzyme S was produced by wound and urinary tract isolates. Some P. aeruginosa strains were frequently isolated from the same site of infection (persistent infection isolates). Comparative analysis of virulence factors produced by these isolates showed that, regardless of the isolation site, subsequent isolates produced higher levels of exoenzyme S. These results suggest that: (1) elastase, phospholipase C, toxin A, and exoenzyme S are produced by P. aeruginosa isolates from different sites of infection; (2) the production of higher levels of elastase and phospholipase C is important in all types of infections, while the production of toxin A and exoenzyme S is important in wound infection; (3) persistent infection with P.aeruginosa may enhance exoenzyme S production.

The effect of smoke inhalation on bradykinin metabolism by the perfused and ventilated rat lung.

The effect of smoke inhalation on bradykinin metabolism was studied in the rat lung perfused with Ringer's bicarbonate solution. After smoke (from cotton, polyester, or seat cushion material) inhalation, tritium-labeled bradykinin was added to the Ringer's bicarbonate solution, and then the lung perfusion effluent aliquots containing bradykinin and its metabolic fragments were collected after a single transpulmonary passage. For the 20 control rats without smoke inhalation, 91% of the bradykinin dose was metabolized, with Pro-Pro (I), 49%, and Arg-Pro-Pro-Gly-Phe (II), 32%, being the predominant bradykinin cleavage fragments. For 12 rats with smoke inhalation, 89% of the bradykinin dose was metabolized, with I (28%) and II (36%) being the major bradykinin cleavage fragments. The type of smoke did not significantly alter the capacity of the rat lung to metabolize bradykinin. Exposure to smoke from seat cushion material for more than 3 minutes caused pulmonary edema and thickening, and smoke exposure for more than 5 minutes caused loss of integrity at the lung alveolar-capillary interface. In contrast, exposure to cotton or polyester smoke did not cause any observable gross changes of the lung. Electron microscopic examination of lung exposed to seat cushion material smoke revealed considerable damage, with the type I epithelium existing as patches on the alveolar surface and capillary endothelium separated from the basement lamina. Thus in our model acute, short-term inhalation of smoke did not significantly alter the amount of bradykinin metabolized by the pulmonary endothelium so long as the integrity of the lung alveolar-capillary interface was maintained, although there seemed to be a moderate shift in the amount of major cleavage fragments from I to II.

A comparison of Xeroform and SkinTemp dressings in the healing of skin graft donor sites.

The best donor site dressing would minimize pain while it increased the rate of healing. This study compares a standard fine-mesh gauze dressing, Xeroform (Sherwood Medical Industries Ltd., Markham, Ontario, Canada), to a new collagen-based dressing, SkinTemp (BioCore Inc., Topeka, Kan.). Eight patients requiring two donor sites of equal size received Xeroform gauze on one site and SkinTemp on the other. The Xeroform was covered for 24 hours and was then allowed to air-dry. Healing was determined to be complete once the gauze peeled off and complete epithelialization was observed. The SkinTemp was covered for 7 days and inspected on days 3, 5, and 7. Pain was measured daily with a standard visual analog scale. Mean Xeroform donor site size was 224.75 cm2, and SkinTemp size was 319.87 cm2. Donor site thickness was 0.012 to 0.014 inches for both. Mean length of healing was 10.62 days for Xeroform and 7.75 days for SkinTemp. Mean pain rating was 22.28 mm for Xeroform and 15.29 mm for SkinTemp. The overall preference of the eight subjects yielded five choosing SkinTemp and three choosing Xeroform, and seven reported SkinTemp as less painful. SkinTemp dressing appears to be less painful and has a better healing rate compared with Xeroform.

The mangled lower extremity: can salvage be predicted?

The ability to predict amputation following combined orthopedic, vascular and soft tissue trauma to an extremity could eliminate prolonged attempts at salvage of a doomed limb. We reviewed our experience with 48 mangled lower extremities in 46 patients. Twenty-one penetrating wounds and 25 blunt injuries occurred in 37 men and nine women ranging in age from 3 to 59 years. Severity of injuries to muscle, skin, and major nerves were strongly interrelated (r = 0.49 to 0.74, P < 0.001), but there were no correlations between injuries to these tissues and severity of bone injury (r < 0.19, P > 0.20). Twenty-four limbs were salvaged, and 24 were amputated. Increased severity of soft tissue injury was associated with a greater probability of limb loss (P < 0.001), but limb salvage or amputation could not be predicted accurately by any variable or group of variables such as age, mechanism of injury, Injury Severity Score, presence of shock, level of injury, venous injury or repair, sequence of repair (vascular vs skeletal), time of fasciotomy, arteriography, blood requirement, or duration of ischemia. Amputation was best predicted by severity of injury to the sciatic or tibial nerves (P < 0.001), and by failure of arterial repair (P < 0.01). Severe extremity injuries require a coordinated approach and decisions regarding amputation require careful judgement. These decisions cannot always be made at the time of presentation or during the initial operation. If after revascularization and skeletal stabilization the extremity is clearly nonviable or remains insensate, then delayed amputation can be performed under more controlled circumstances.

The role of infection in outcome of Multiple Organ Failure.

It is widely assumed that infections are the principal cause and primary outcome determinant of the syndrome of Multiple Organ Failure (MOF) in critically ill patients. Infections are frequent in these patients, but the prevention and treatment of infections may not influence the course of MOF. This study tested the hypothesis that infections play a decisive role in the outcome of MOF. Data were gathered concurrently on all adult patients admitted over an 18-month period to a non-cardiac surgical ICU at a university hospital and recorded in a computer database. Sepsis was defined as a state characterized by at least three of the following: fever, tachycardia, leukocytosis or leukopenia, increased cardiac index, reduced systemic vascular resistance, and hypercatabolism manifested by nitrogen-wasting. The presence of an infection was not required for the diagnosis of sepsis. Mild sepsis was defined as the presence of three or four parameters. Severe sepsis was defined as the presence of five or six parameters. MOF was defined as the development of dysfunction of at least two of the following major organ systems: cardiac, gut, pulmonary, renal, cerebral, and hepatic. Of 749 admissions, 73 patients developed MOF. Thirty four (47%) had a documented source of infection, 37 (51%) had positive blood cultures, and all had sepsis. Hospital mortality was 66 percent (48 of 73 patients). Death could not be predicted by bacteremia (P > 0.25), nor by the presence of an infectious source (P = 1.0), but was strongly associated with severe sepsis (P < 0.0005).(ABSTRACT TRUNCATED AT 250 WORDS)

Computed tomography in the management of blunt thoracic trauma.

Computed tomographic (CT) scanning has proved to be valuable in evaluating the head and abdomen of victims of blunt trauma; CT scans of the thorax often are obtained on patients with blunt torso trauma, but their value for this purpose is unclear. We conducted a prospective study to evaluate the role of chest CT scanning in thoracic trauma. Hemodynamically stable patients at least 18 years old with an estimated Abbreviated Injury Scale--Thorax score of 2 or greater underwent a contrast-enhanced CT scan of the chest, usually in conjunction with CT scans of the head, abdomen, or both. Thirteen patients were dead on arrival, 14 required emergency surgical procedures, and 13 were too unstable to undergo chest CT scan. Thirty-three patients were not included because they refused to participate or the protocol was not followed. Forty-six men (69%) and 21 women with a mean age of 42.7 years completed the study. Sixty-one were injured in motor vehicle crashes, four were injured in falls, and one each was injured by assault and by crushing forces. Injury Severity Scores ranged from 4 to 45, with a mean of 20.5. Four patients died (6%), three from head injury and one from multiple organ dysfunction. Chest roentgenography (CXR) was superior to CT scanning in identifying rib fractures, but CT scanning was more sensitive than CXR for pneumothorax, fluid collections, and infiltrates (p < 0.001); CT scanning also was more specific for aortic injury. Despite this quantitative superiority, the abnormalities missed by CXR but identified by CT scanning infrequently led to a change in management.(ABSTRACT TRUNCATED AT 250 WORDS)

White blood cell response to burn injury.

Multiple sites of decreased immune response have been discovered, but the instigation of this diffuse immunosuppression remains a matter of much debate. Several investigators have observed immunosuppressive affects of low-molecular weight peptides found in the serum of burn and trauma patients. These substances have been termed suppressive active peptides (SAP). Current research is also focusing on the intricate connection between stress hormones and neurotransmitters, in which there exist a complex information channel between the immune, endocrine, and central nervous systems. It is becoming clear that immune homeostasis may require regulatory influence via immunocompetent cells, along with influences from the central nervous system and a balanced endocrine environment. In fact, macrophages, lymphocytes, and neutrophils contain receptors for many hormones including corticosteroids, insulin, growth hormone, catecholamines, acetylcholine, and endorphins. The dramatic alteration in the hormonal milieu after injury may play a significant role in immunocompetence. Attempts to modulate specific defects in the immune system have been unsuccessful to date. Our goal, to decrease the risk of infection in burn patients, therefore, is meticulous supportive care. This includes not only reducing the risk of invading bacteria, but also increasing the patient's resistance to overall infection. The cornerstone of this support is to restore mechanical barrier function to as near normal as possible. Immediately after injury, vigorous wound management includes several daily debridements combined with wound protection using an appropriate topical antimicrobial substance.(ABSTRACT TRUNCATED AT 250 WORDS)