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Ventilation- perfusion alterations after smoke inhalation injury in an ovine model. J. Appl. PhysioL. 81(5): A 2250-2259, 1996. To study the pathophysiological mechanism of progressive hypoxemia after smoke inhalation injury, alterations in ventilation-perfusion ratio (VA/Q) were studied in an ovine model by using the multiple inert gas elimination technique. Because ethane was detected in expired gas of some sheep, we replaced ethane with krypton, which was a unique application of the multiple inert gas elimination technique when one of the experimental gases is present in the inspirate. Severity-related changes were studied 24 h after injury in control and mild, moderate, and severe inhalation injury groups., Pub. in Jnl. of Applied Physiology, v81 n5, p2250-2259, 1996.

The objective of this report is to observe the effect of 4 and 40 micro A direct current (DC) on edema formation after burn injury in rats. Silver-nylon wound dressings were used as either anodes (-) or cathodes (+) on 20% total body surface area full-thickness scalds in anesthetized male Sprague-Dawley rats. Untreated burned rats and rats treated with silver-nylon dressings without current were used as controls.

Infection is a major cause of morbidity and mortality in hospitalized burned patients. We have previously estimated the added risk for mortality due to infection in a population of more than 5500 admissions for burns and demonstrated that bacteremia was associated with a 21% increase of mortality above that predicted by logistic regression analysis of injury severity and age. When the bacteremic population was subdivided by pathogen, gram-negative opportunists were found to be the principal cause of the observed increase in mortality. Mortality in the group of patients with gram- negative bacterernia (GNB) was more than 50% greater than that predicted for patients without bacterernia. The clinical significance of gram - negative pathogens in burned patients became obvious after the introduction of newer generations of penicillin and arninoglycosides in the early 1960s. Pseudomonas domonas aerginosa and members of the Enterobacteriaceae family became predominant and, during the subsequent 20 years, caused several endemics .4.5 Distinguishing features of these endernics were multiple antimicrobial resistance and consistent biotypes within causative strains.

We have recently developed a new burn-specific equation that satisfactorily estimates initial caloric requirements for thermally injured patients. In the present study, we compared these estimates with resting energy expenditures (REE) (n = 141) measured weekly by indirect calorimetry in 20 patients between postburn days 3 and 348. In this group, mean initial burn size was 46.7% (range, 21-88) and mean age 31.3 years (range, 19-61). Serial measurements were continued until the burn wounds were closed or the patient was discharged. Multiple regression analysis indicated a relationship between REE, initial burn size, and postburn day in these patients (r = 0.65). This analysis indicated a general trend of decline in REE toward normal values 100 to 150 days postburn in patients with smaller burns (20%-40%) and roughly 250 days postinjury in those with larger burns (>75%). The initial predictive equation appeared adequate for estimating caloric needs during the first postburn month, but beyond 30 days postburn indirect calorimetric measurements became necessary for accurate estimation of caloric requirements.

In the course of developing a model of inhalation injury, the relationship between the severity of pulmonary injury and specific techniques and doses of smoke exposure was examined in pairs of rabbits simultaneously exposed to smoke. In group I (5 pairs), one animal in each pair was exposed to smoke with a breath hold (BH) at the end of each exposure; the second animal received an exposure producing the same level of carboxyhemoglobin without BH. in group II (6 pairs), both animals were exposed to 25 units of smoke simultaneously, with BH. In group III (3 pairs), one animal received a 20-unit exposure and the other a 25-unit exposure, both with BH. In group IV, 9 animals received 25-unit exposures with BH and were observed for 4 days. Groups V and VI served as controls. Smoke exposure with BH regularly produced severe injury in terms of decreased PaO2 and histopathologic changes. while exposure without BH did not, despite high levels of carboxyhemoglobin after smoke inhalation. The mean differences in percent residual PaO2 (PaO2 at 48 hours x 100/pre-injury PaO2) and in extravascular lung water (EVLW) at 48 hours within pairs of animals receiving 25 units with BH were 12.3% +/5.33%, and 0.271 +/- 0.157 mL/g, respectively. Histologic findings such as necrotic tracheobronchitis with pseudomembrane were consistently present. No differences were observed between animals receiving exposures of 20 and 25 units.

To study a cohort of patients treated at the same institution and to compare that patient population with that of a previous report documenting the comorbidity of inhalation injury and pneumonia. Specifically, we wanted to determine whether there had been an improvement in survival of patients suffering inhalation injury.

Buffering of intragastric pH is an accepted treatment modality for prophylaxis against the development of gastric stress ulcers. This method of prophylaxis is commonly based on the pH value acquired by measurement of gastric aspirate. Recent literature suggests pH measurement techniques that involve gastric aspirate specimens have many flaws. The purpose of this study was to compare gastric pH measurements with the use of a nasogastric sensor, meter system, and pH-sensitive test paper. Fifteen hundred paired serial measurements of intragastric pH were obtained on 19 thermally injured patients (16 men and three women, ages 23 to 79 years, total body surface area bum 25% to 80%). A double-lumen tube containing an antimony/graphite pH sensor incorporated into the tip of the tube was inserted with the use of a standard technique. Each tube was in place an average of 5.7 days (range 1 to 15 days). Patients were randomized into two groups. The first group (six patients) received non-acid- buffering prophylaxis therapy. The second group (13 patients) received standard antacid or antacid/H2 histamine-blocking agent combination prophylaxis therapy. Analysis of the 539 paired measurements for the non-acid-buffering revealed a correlation coefficient of r = 0.532. The 961 measurements from the group receiving gastric acid buffering revealed a correlation coefficient of r = 0. 569. Paired t test values for the sample showed a significant difference (18.52, p < 0.0000) between measurement techniques.

Estimations of total urinary nitrogen from measured urinary urea nitrogen are commonly used in calculating nitrogen balance. Recently published studies suggest the urinary urea nitrogen/total urinary nitrogen relationship is in constant and total urinary nitrogen must be directly measured in burned patients. This study addresses the relationship of urinary urea nitrogen to total urinary nitrogen after thermal injury. Two hundred random 24-hour urine collections obtained from 45 thermally injured patients (mean bum size 59 +/ 28%, mean age 40.5 +/- 17.2 years) between 1 and 354 days postburn were analyzed for total urinary nitrogen and urinary urea nitrogen. Regression analysis relating total urinary nitrogen to estimated total urinary nitrogen (urinary urea nitrogen x 1.25) revealed a linear relationship (r = .936, P < .001).

Nitric oxide is biosynthesized from the amino acid l-arginine by the enzyme nitric oxide synthase. Nitric oxide is a vasodilator, a neurotransmitter, and may modulate immune function. The experiments presented here were performed to determine whether the synthesis of nitric oxide is increased following experimental burn injury in rats. After a 30% total body surface area burn in 300-g Lewis rats, the urinary output of nitrate, a stable metabolite of nitric oxide, was significantly increased for 8 days postburn compared with that in sham-burned control rats. The origin of the urinary nitrate from L-arginine was demonstrated by administering the stable isotope 15 N2-guanido-arginine to burned and sham-burned rats and observing an immediate enrichment of 15 N in nitrate.

Several fluorescent substances are present in the supernatants of acid precipitated whole blood or plasma from burned patients. Perchloric acid supernatants of sera from infected, but not uninfected, burned rats contained a fluorescent substance with maximum emission at 420 nm at 355-nm excitation (355 ex/420 em). In this study of serum from burned human patients, several fluorescent substances were resolved by reverse-phase high-pressure liquid chromatography. One of these fluorescent components had an high-pressure liquid chromatography retention time and fluorescent characteristics identical to those of neopterin. The identification of this component as neopterin was verified by thermospray mass spectrometry. Serum neopterin concentrations were then determined in supernatants of patient serum samples having various levels of 355 ex/420 em fluorescence. A correlation was found between the concentrations of neopterin determined by high-pressure liquid chromatography and the presence of bacteremia in burned patients. These findings suggest that neopterin, which is a useful indicator of infection In other clinical settings, may also be an indicator of infection in bumed patients.

Alterations in granulocyte function after thermal injury have been described. We have serially studied the level of granulocyte cytosolic peroxidase activity in 23 thermally injured patients during the first 6 weeks after injury. The patients' mean age and burn size were 35.1 + or - 15.7 years and 41.6% + or - 16.8% (range, 18% to 88%), respectively. Fourteen patients had concomitant inhalation injury, and the overall mortality rate was 4.3%.

The role of platelet-activating factor (PAF) in inhalation injury was studied in sheep, using CV-3988, a PAF antagonist. Following smoke exposure, 15 sheep were divided into three groups of five. Group I animals were untreated; group 11 animals were treated with CV-3988 before and after exposure; group III animals were treated only after exposure. In group I, platelet and WBC counts were markedly changed within 6 hours (p < 0.05); in the treated groups, alteration of cell counts was not obvious. Blood malondialdehyde (MDA) levels were increased significantly only in group I. Blood PGE2 and TXB2 levels did not differ among the groups. Mean tissue MDA and mean bronchoalveolar lavage fluid (BALF) MDA concentrations were significantly increased in group I (p < 0.01); mean BALF TXB2 levels were significantly decreased in group I (p < 0.01). These data suggest that PAF affects inhalation injury through modulation of lipid oxygenation and that PAF antagonists may offer therapeutic benefit in the management of this injury.

The relationship between effective blood volume and related hormones in burn patients following resuscitation is not well understood. Previous reports have suggested that hormone secretion is altered by a resetting of neural control mechanisms. Serum and urine sodium, plasma renin activity, serum ADH, Cardiac index, effective renal plasma flow, and total blood volume were measured in seven burn patients (mean age, total burn size, and postburn day: 32 years, 56%, and 9 days, respectively). The same values (with the exception of cardiac index and blood volume) were measured in 10 control patients (mean age, 24 years). The blood volume of patients was measured by 51 chromium red blood cell (RBC) labeling and compared to normal predicted values based on body surface area and sex. Mean serum sodium and osmolality were 138 mmol/L (millimolar) and 286 mosm/kg, respectively, in both patients and control subjects.

Pulmonary injury resulting from inhalation of chemical and particulate products of incomplete combustion is one of the principal determinants of mortality following burn injury. In this study, the histopathology of inhalation injury was examined in sheep. Mild, moderate, or severe smoke injury was produced in anesthetized sheep by insufflation with various doses of ambient temperature smoke, generated by burning polyethylene, wood pulp, and nonwoven cellulose pads. A total of 64 sheep were exposed and evaluated at times ranging from 15 minutes to 4 weeks after exposure. Morphologic changes in the lungs were studied using light microscopy and both transmission and scanning electron microscopy. The primary, dose-responsive injury observed was acute cell membrane damage in the trachea and bronchi leading to edema, progressive necrotic tracheobronchitis with pseudomembrane formation, and airway obstruction. These inflammatory and occlusive effects were followed by congestion, alveolar space edema, atelectasis, and bronchopneumonia. Morphologic changes occurring in the alveolar epithelium following high smoke dosage included intracellular edema in type-I cells, changes in the membrane- bound vacuoles of type-11 cells, and septal thickening caused by interstitial edema. No capillary endothelial changes were observed.

Death and the incidence of pneumonia are significantly increased in burn patients with inhalation injury, despite application of conventional ventilatory support techniques. The effect of high-frequency percussive ventilation on mortality rate, incidence of pulmonary infection, and barotrauma were studied in 54 burn patients with documented inhalation injury admitted between March 1987 and September 1990 as compared to an historic cohort treated between 1980 and 1984. All patients satisfied clinical criteria for mechanical ventilation. High-frequency percussive ventilation was initiated within 24 hours of intubation. The patients' mean age and burn size were 32.2 years and 47.8%, respectively (ranges, 15 to 88 years; 0% to 90%).