[Pathogenesis of heat inhalation injury in burn patients].
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Burns↗
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Results for “Burns, Inhalation”
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Prognostic implications of inhalation injury in burn patients in Tokyo.
Inhalation injury has recently emerged as the major cause of mortality in burn patients. However, the prognostic value of inhalation injury has not been thoroughly assessed in Japanese burn facilities. The aim of the present study was to evaluate the impact of inhalation injury on burn patients' mortality in Tokyo. Of 6416 patients admitted to 13 burn facilities of the Tokyo Burn Unit Association between 1984 and 2002; the 5560 eligible patients were included in this study (mean age, 40+/-20 years; male, 61.6%; mean partial- and full-thickness burn size, 10.7+/-13.0% and 9.6+/-20.5%). Of the 5560 patients, 1690 patients (30.4%) had experienced inhalation injury. The overall in-hospital mortality rate of the patients with inhalation injury was higher than that of those without inhalation injury (33.6% versus 8.1%, odds ratio, 5.72 [95% CI, 4.91-6.67]). The results of the multivariate analysis indicated that inhalation injury; full- and partial-thickness burn size, and age were independent predictors of outcome (relative risk, 2.58 [2.03-3.29], 1.10 [1.09-1.11], 1.06 [1.06-1.07], 1.05 [1.05-1.06], respectively). In conclusion, inhalation injury was the most important predictor of overall mortality among burned patients in Tokyo.
Adult↗
Adult respiratory distress syndrome after smoke inhalation from burning poison ivy.
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Adult↗
Inhalation injury with burns: a lethal combination.
Inhalation injury is known to add significant morbidity and mortality to patients with burns. Estimating the severity of inhalation injury is difficult, as signs of respiratory failure may occur hours or even days after the injury. We have reviewed 86 consecutive patients who were admitted to our Burn/Trauma Center with burns and evidence suggestive of smoke inhalation. Of these patients, 88% required endotracheal intubation. There was a 62% mortality. Admission chest x-rays studies, PAO2, and auscultation of the patient's lungs were normal in 90% of the study group. These factors could not be used to predict respiratory failure or death. Patients with as little as 15% total body surface burns with mild smoke inhalation are at significant risk of respiratory failure and the need for ventilatory support.
Adolescent↗
Pulmonary capillary dynamics and fluid distribution after burn and inhalation injury.
A non-linear macroscopic mathematical model is described for the simulation of the different mechanisms that regulate the pulmonary capillary dynamics in patients with thermal injury. The techniques used in the construction of the model are those of 'system's dynamics'. This model has been incorporated into a patient simulator, which makes it possible to analyse the fluid and protein exchanges in a burn patient. The regulating mechanisms involved are: the pulmonary circulation, the fluid and protein transfer between the plasma and the interstitial space at the pulmonary capillary level, and the pulmonary lymphatic system. As a result of the sensitivity analyses of the model we propose that, for the simulation of the effects of an inhalation injury at the pulmonary capillary level, the parameters to be altered will be the pulmonary capillary permeability coefficient for proteins and the pulmonary capillary surface damaged by the injury. To verify the validity and utility of the model, the clinical progress of a series of burn patients with lung injuries has been compared with the results obtained using simulation.
Burns↗
Oxidants and the pathophysiology of burn and smoke inhalation injury.
A skin burn is a common traumatic injury that results in both local tissue damage and a systemic mediator-induced response. There is evidence of both local and systemic oxidant changes manifested by lipid peroxidation in animal burn models and also in burned man. Both increased xanthine oxidase and neutrophil activation appear to be the oxidant sources. Animal studies have also demonstrated decreased burn edema, and also decreased distant organ dysfunction with the use of antioxidants, suggesting a cause-and-effect relationship, which needs to be tested in man. Smoke inhalation injury, a chemical injury to the airways caused by incomplete products of combustion, is frequently seen in conjunction with a body burn. Lipid peroxidation, both in lung and in distant organs, is also seen with this injury. The combined body burn and smoke inhalation injury lead to a marked increase in mortality rate and also an increase in the degree of generalized oxidant release and lipid peroxidation. Although data in man are limited, the available information, along with that from animal research on burns and smoke inhalation, indicates oxidants may well play a key role, and antioxidants may be of clinical therapeutic use.
Burns↗
Explosive burns during abusive inhalation of butane gas.
Explosion burns during abusive inhalation of butane gas rarely occurred in the past, but recently it has become a social problem among groups of teenagers. This cause constitutes 1.6% of admissions due to flame burn at the burn unit of Hallym Medical Center. A retrospective review during a five-year period identified 48 patients. The male to female ratio was 3:1. The mean age of patients was 16 years and 8 months. The places where the accidents occurred were commonly bedrooms or motel rooms. There were nine group settings of 27 patients at the time of the accident. Inhalation injury (n = 12) was noted on admission. The average burn size was 28.5 percent of the total body surface area. All patients sustained burn injury on the face, arms and hands and 24 patients among them had extended burn areas on the trunk and/or lower extremity. 22 patients (mean hospital stay; 51.6 d) required skin grafting and 12 patients (mean hospital stay; 22.3 d) were treated with conservative management. The mortality rate was 10.4 percent. Explosion burns during abusive inhalation of butane gas can result in mortality as well as major burn injuries.
Accidents↗
Ketorolac attenuates cardiopulmonary derangements in sheep with combined burn and smoke inhalation injury.
Massive cutaneous burn combined with smoke inhalation causes high mortality in fire victims. Cyclo-oxygenase (COX) and inducible nitric oxide (NO) synthase (iNOS) have been shown to be up-regulated in burn injury. Ketorolac, a non-steroidal, anti-inflammatory agent (NSAID), inhibits prostaglandin and thromboxane synthesis through inhibition of COX. NSAIDs have been shown to down-regulate iNOS. Thus we hypothesized that treatment with ketorolac would attenuate burn/smoke-related cardiopulmonary derangements. We conducted a fully controlled long-term laboratory investigation in an Intensive Care Unit setting. Eighteen female sheep were surgically prepared for chronic study. After a recovery period of 5 days, a tracheotomy was performed under ketamine/halothane anaesthesia. Sheep were given a 40% total body surface third-degree burn and insufflated with cotton smoke (48 breaths, <40 degrees C). Sheep were divided into three groups: sham (not injured and not treated; n =6), control (injured, but not treated; n =6) and treated (injured and administered ketorolac 60 mg/day; n =6). The sham group had stable cardiopulmonary and systemic haemodynamics. Control animals showed depressed cardiopulmonary function, decreased pulmonary gas exchange, increased pulmonary microvascular leakage and decreased left ventricle stroke work index with elevated left atrial pressure. Systemic vascular leak in control animals was evidenced by robust haemoconcentration (haematocrit and fluid net balance). Treatment with ketorolac prevented all of these morbidities. Post-treatment with ketorolac also resulted in significant inhibition of elevated plasma nitrite/nitrate levels in control animals. These results suggest that ketorolac may ameliorate cardiopulmonary morbidity, at least in part, by inhibiting excessive NO.
Animals↗
Role of nitric oxide in vascular permeability after combined burns and smoke inhalation injury.
Patients with severe burn and/or smoke inhalation injury suffer both systemic and pulmonary vascular hyperpermeability. We hypothesized that nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) plays a role in the changes in microvascular permeability seen with this injury. To test the hypothesis, we administered mercaptoethylguanidine (MEG), a selective iNOS inhibitor, to conscious sheep subjected to a combined smoke inhalation and third-degree burn injury to 40% of total body surface area. The sheep were surgically prepared for chronic study with lung and prefemoral lymph fistulas in order to estimate microvascular permeability. Both the groups and a control group of animals showed an increase in iNOS protein and message in their lungs. The control animals showed significant increases in either plasma or lymph NO2-/NO3- (NOx) concentration at 24 h after injury, with associated cardiac depression and hemoconcentration. The airway epithelium stained for nitrotyrosine. In the treatment group, NOx did not increase significantly in plasma or lymph throughout the experiment, there was no nitrotyrosine staining, hemodynamic depression was not observed, and the fluid requirement was significantly less than in the control group. Changes in pulmonary microvascular permeability were significantly suppressed by inhibition of iNOS. However, there was no significant difference between the two study groups in the microvascular permeability of burned tissue. These data suggest that NO produced by iNOS plays an important role in the changes in systemic and pulmonary microvascular permeability in combined smoke inhalation/third-degree burn injury, but does not affect the vascular permeability of third-degree-burned tissue in this type of injury.
Animals↗
Burn mortality. Experience at a regional burn unit. Literature review.
The burn patient population at a regional burn unit in Central New York State, from 1974 through 1980, (N = 507) is described completely in terms of age, total burn size, full thickness burn size, sex, race, etiology of burn, inhalation injury, referral pattern, distance from burn unit, interval to admission, length of hospitalization and causes of death. The interrelationship of these factors is examined to define their contribution to injury severity and identify variables useful in predicting death. Demographic profiles are compared to the population base, and the case-mix of patients is contrasted with that of other burn units. A logistic model to predict death is developed using the variables of full-thickness burn size, age, age 2, and the presence of inhalation injury. The power of statistical methods to predict death is discussed in relation to the 37 patients who died with emphasis on the outliers present in unscreened patient populations. The point is made that any clinically useful index of burn severity must include a factor reflecting the physiologic stress imposed on the individual patient. Clinical issues pertaining to the treatment of nonsurvivors are discussed in relation to the physician's responsibility, euthanasia, and resource consumption. Results of treatment are difficult to evaluate because of the variables of patient selection, injury severity, time, and the absence of a satisfactory measure of morbidity. Effective prevention is the only way to eliminate the deaths of victims who do not survive to enter the health care system and the morbidity that inevitably results from tissue loss. From the standpoint of public health, burn morbidity may have an economic impact far different from that of burn mortality. Supraregional burn units with access limited to seriously but not hopelessly burned individuals are proposed. Supraregional burn units would make the delivery of burn care more efficient and allow the selection of a patient sample homogeneous in terms of severity, thus increasing the reliability of treatment evaluations.
Adolescent↗
HYDROGEN FLUORIDE (HF) INHALATION AND BURNS.
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Burns↗
Acute management of the upper airway in facial burns and smoke inhalation.
Among 740 patients with acute burns who were admitted to our burn center from 1972 through, 1975, thirty-six required upper airway access within the first 24 hours after burn for oral and facial burns or smoke inhalation. Nasotracheal intubation was initially used. Twelve survived; 11 were successfully extubated and one required a tracheostomy. If the patient had not sustained major smoke inhalation, extubation was usually possible without tracheostomy when edema subsided between one and six days after the burn. It is concluded that endotracheal intubation is a satisfactory method of gaining airway control in severe oral and facial burns and in smoke inhalation. The mortality associated with orofacial burns or smoke inhalation is related to the degree of lung damage, patients' s age, and the extent of the burn; it is not related to the method of upper airway control.
Acute Disease↗
[Airway burns and smoke inhalation].
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Burns, Inhalation↗
Acute management of laser-ignited intratracheal explosion.
The laser-ignited airway explosion is a shocking emergency. Techniques available for prevention of an airway fire minimize the risk, but they are not applicable in all circumstances. The severity of the patient's injury depends on the duration and intensity of the burn. Prompt, appropriate management is facilitated if the operating team has previously discussed and "rehearsed" this potential disaster. The distal airway burn produced by an ignited endotracheal tube differs from an inhalation burn in character and severity. The anatomic and respiratory effects occurring subsequent to the laser-induced burn are examined. Emergency care requires immediate elimination of the fire, removal of the tube and any foreign body or debris, and usually a tracheostomy. A program of medical and endoscopic management is suggested.
Bronchoscopy↗
[Inhalation injury in burn patients].
The clinical course of inhalation injury is variable. The routine use of fiberoptic bronchoscopy provides an accurate and safe diagnosis; by this examination it is possible to recognize alterations down to the terminal airway. Biopsies of tracheobronchial mucosa can ensure the diagnosis. By means of fiberoptic examination and blood gases it is possible to realize a differentiation of inhalation injury. According to the analysis of our patients an inhalation injury was found in 20.1%. The mortality rate due to the inhalation injury amounts to 14.4%.
Adult↗
Combined smoke inhalation and scald burn in the rat.
The combination of burn injury with smoke inhalation from fires significantly increases mortality. The mechanism of increased mortality is poorly understood but has been associated with multiple organ dysfunction syndrome, including cardiac dysfunction. Impaired cardiac function correlates with decreased survival in burn patients. We investigated smoke inhalation from burning cotton combined with a 40% body surface area, third-degree burn during the first 4 hours after injury in rats. In the early phase after injury, burn caused a significant rise in lung neutrophil infiltration but no increase in lung water. Smoke led to a rise in lung water but only a mild increase in neutrophil infiltration. Combined smoke and burn did not increase neutrophil accumulation or lung water above that which occurred with either injury alone. Only in combined smoke and burn was there a drop in cardiac output and stroke volume with pulmonary edema and lung neutrophil influx.
Animals↗
[Bronchoscopic methods in complex diagnosis and treatment of burned patients with inhalation injuries].
Chromobronchoscopy was first used in treatment of 37 burned patients with inhalation injuries for better visual manifestation of the injuries of the tracheobronchial tree mucosa. The trachea and bronchi mucosa was irrigated with a viral stain--0.25% aqueous solution of methylene blue. The intensity of staining the mucosa in light blue colour showed the true limits and depth of the injury. Resulting from the clinico-endoscopic examinations supplemented with findings of chromobronchoscopy, cytological and bacteriological analyses, a working classification of inhalation injuries in burned people was developed which allowed the adequate methods of local treatment during fiber bronchoscopy to be worked out taking into account the degree of thermochemical injuries of the respiratory pathways. It resulted in 19.7% lower lethality of burned patients.
Adolescent↗
Endothelin-1 and prostaglandin E2 levels increase in patients with burns.
BACKGROUND: Endothelin-1 (ET-1), a powerful vasoconstrictor, is a 21 amino acid peptide produced by endothelium. It negatively affects pulmonary, cardiac, hepatic, and renal function. It also constricts bronchial and gut smooth muscle. This peptide also stimulates monocytes to produce prostaglandin E2 (PGE2), tumor necrosis factor, interleukin-6 and 8, and substances that stimulate neutrophil superoxide production. Plasma levels of ET-1 also increase in shock, low flow states, ischemia, and sepsis. STUDY DESIGN: Fourteen patients between the ages of seven and 72 years were admitted to the Bridgeport Hospital Burn Unit and resuscitated with a modified Parkland formula. Plasma was drawn on admission, at 12, 24, and 48 hours. Endothelin-1 and PGE2 were measured by radioimmunoassay. RESULTS: Endothelin-1 levels increased ten- to 20-fold in all patients. Prostaglandin E2 levels increased five- to 40-fold in all patients. There was no correlation between plasma ET-1 or PGE2 levels with either size of burn, inhalation injury, patient age, organ dysfunction, or survival in this small study of early burn injury. CONCLUSIONS: The increased plasma ET-1 response in patients with burns may have a role in the genesis of the systemic response to burns. This peptide may also activate monocyte production of PGE2 and other mediators of the systemic inflammatory response syndrome. This study was done to measure ET-1 and PGE2 levels in patients with burns greater than 20 percent of the body surface area on admission, at 12, 24, and 48 hours. The correlations between severity of burn, ET-1 levels, and PGE2 production were also assessed.
Adolescent↗