Pulmonary injury in burned patients

1. With improvements in treatment of burn shock and wound sepsis, inhalation injury has emerged as the number one cause of fatality in the burn patient; it accounts for 20 to 84 per cent of burn mortality. 2. Only steam is capable of inflicting direct thermal damage; most injury is caused by incomplete products of combustion, the most important being aldehydes. 3. More accurate diagnostic techniques, including fiberoptic bronchoscopy and 133Xe scanning, have been added to the traditional clinical signs of inhalation injury, such as facial burns, singed nasal vibrissae, and closed space injury, and have led to a new estimation of a 30 per cent incidence among patients with major burns. 4. Patients with inhalation injury typically pass through three stages, those of acute pulmonary insufficiency, pulmonary edema, and bronchopneumonia. 5. The major early pathophysiologic changes seen in the lungs of burned patients related to edema. With inhalation injury this is probably mediated by the products of activated neutrophils. Later changes are the result of the reduction of surfactant and thus lung compliance. 6. Treatment consists of intubation at the first hint of respiratory distress; the issue of tracheostomy versus endotracheal intubation has not been scientifically resolved, but most centers employ prolonged nasotracheal intubation. Prophylactic antibiotics or steroids are not of benefit. Further care is only supportive and includes CPAP, PEEP, vigorous pulmonary toilet, humidification of inspired air, and antibiotics for documented infection. 7. Further advances await the development of pharmacologic methods of affecting the lung's response to injury, which includes altered capillary permeability and decreased immune function.     

Smoke inhalation and airway management at a regional burn unit: 1974-1983. Part I: Diagnosis and consequences of smoke inhalation

Victims of smoke inhalation with and without burns and burn patients with respiratory insufficiency for reasons other than smoke at a regional burn unit are profiled in terms of age, burn size, length of stay, and mortality. The diagnostic characteristics of patients with an inhalation injury (N = 108) are listed; 7% of all patients (N = 52) have known smoke exposure with equivocal evidence for injury to the airway or pulmonary parenchyma. The degree of respiratory (visceral) failure experienced by patients with inhalation injury is not uniformly severe. Many of the clues to this diagnosis are indirect and not always related to the severity of pulmonary injury. Timing and degree of visceral failure control the severity of the injury, which increases progressively from that in patients with a burn only (parietal injury) through those with a visceral injury only (smoke without burn), those with both smoke and burn, to those with a burn and uniformly severe respiratory failure on the basis of sepsis.     

对48例烧伤死亡病例的分析与建议

目的从死亡病例的总结中汲取经验教训，探讨更有效的护理措施，提高护理质量。方法收集我院48例烧伤死亡病例的资料，对其病死率、烧伤面积、深度、致伤原因、院前救治情况、人院时间、合并伤、复合伤、死亡原因进行统计学分析。结果48例烧伤死亡病例中，死于多器官功能障碍综合征20例、创面脓毒症18例、吸人性损伤窒息2例、休克2例、药物性肝损害2例，复合伤2例、翻身床翻身窒息1例、麻醉后未清醒窒息1例。结论积极做好休克期及吸人性损伤病人的护理、重视新护士的训练和培养、加强消毒隔离、注意药物副作用的观察，对预防烧伤并发症、提高救治成功率具有重要意义。     

Immunosuppression of the burned patient

The burn patient is highly susceptible to infection due to the loss of the skin as a barrier to microorganisms. Immune defenses are activated in response to the burn injury; however, some of these defenses are altered. Neutrophil chemotaxis is compromised by decreased perfusion caused by hypovolemia and the formation of microthrombi. Chemotaxis and phagocytosis are dependent on complement components that are reduced in a large burn wound. Neutrophil intracellular killing power is reduced as oxygen delivery to the wound is decreased. Humoral immunity is altered with the drop in IgG levels. Cell-mediated immunity is depressed and T cell lymphocyte counts are deceased. Suppressor T cells are generated. Specific sources of infection for the burn patient include the patient's own bacterial flora; hospital personnel; respiratory equipment; and catheters, both urinary and intravascular. The best control for burn wound infection is the closure of the wound by early excision and grafting. When lack of donor sites prohibits this surgical therapy, control centers on the environment and wound care techniques. The selection of wound topical antibiotics on the basis of visual inspection and surface culturing assists in the prevention of burn wound sepsis. When wound sepsis does occur, systemic antibiotics are instituted. Although burn wound sepsis is an obvious cause of death for the burn patient, it is not the primary cause. Increasing sophistication in fluid resuscitation and in intensive care therapy has resulted in patients living beyond the initial insult and the following few days. Burn patient mortality is now associated with a syndrome presenting clinically as sepsis but without any identifiable septic source.(ABSTRACT TRUNCATED AT 250 WORDS)     

Attenuating burn wound inflammation improves pulmonary function and survival in a burn-pneumonia model

OBJECTIVE: We previously showed that topical inhibition of inflammatory signaling in burn wounds reduced systemic inflammatory response and burn-induced pulmonary inflammation. We hypothesized that this topical intervention would attenuate burn-induced lung injury, improve pulmonary function, protect lungs from bacterial invasion, and reduce mortality. DESIGN: Controlled, in vivo, laboratory study. SETTING: University laboratory. SUBJECTS: Female mice, 8-10 wks old. INTERVENTIONS: Animals received 30% total body surface area burn followed by topical application of a specific inhibitor of p38 mitogen-activated protein kinase, a key inflammatory signaling pathway, or vehicle to the wound. Twenty-four hours after injury, pulmonary collagen deposition and pulmonary function were assessed. One day postburn, some of the animals received intratracheal instillation of Klebsiella pneumoniae and were subsequently monitored for 7 days. MEASUREMENTS AND MAIN RESULTS: Topical inhibition of p38 mitogen-activated protein kinase significantly decreased pulmonary collagen deposition and prevented a decline in pulmonary function at 1 day after burn injury. Compared with sham controls, animals with burn injury had a significantly higher mortality in response to intratracheal bacterial challenge. Application of p38 mitogen-activated protein kinase inhibitor to the burn wound attenuated pulmonary neutrophil infiltration and reduced the mortality rate to a level experienced by sham controls. CONCLUSIONS: Inflammatory source control in burn wounds with topical p38 mitogen-activated protein kinase inhibition attenuates acute lung injury, avoids pulmonary dysfunction, protects lungs from bacterial challenge, and improves survival.     

Altering metabolism

A significant proportion of the mortality and morbidity of severe burns is attributable to the ensuing hypermetabolic response. This response can last for as long as 1 year after injury and is associated with impaired wound healing, increased infection risks, erosion of lean body mass, hampered rehabilitation, and delayed reintegration of burn survivors into society. Pharmacologic and nonpharmacologic strategies may be used to reverse the catabolic effect of thermal injury. Nonpharmacologic strategies include early excision and wound closure of burn wound, aggressive treatment of sepsis, elevation of the environmental temperature to thermal neutrality (31.5 +/- 0.7 degrees C), high carbohydrate, high protein continuous enteral feeding, and early institution of resistive exercise programs. Pharmacologic modulators of the postburn hypermetabolic response may be achieved through the administration of recombinant human growth hormone, low-dose insulin infusion, use of the synthetic testosterone analog, oxandrolone, and beta blockade with propranolol. This review article discusses these modulators of postburn metabolism.     

Mortality related to gender, age, sepsis, and ethnicity in severely burned children

Several studies have noted gender differences in adult mortality related to thermal injury, however, little is published on gender-related outcomes of burn patients 17 years of age or less. The aim of this study was to evaluate the relationships between mortality, gender, prepubertal and during puberty, ethnic origin, and age, with or without identified sepsis in severely burned children. Seven hundred forty-seven children admitted to our burn hospital from March 1985 to January 2005 with burns greater than 40% total body surface area were studied. Mortality associated with identified sepsis, gender, age, and ethnic origin were outcomes of interest. Two hundred sixty (35%) of the patients studied were girls and 487 (65%) were boys. No significant difference could be shown between girls and boys for the number of operations, time from burn to hospital admission, or the presence of identifiable inhalation injury. Nearly 60% of the male nonsurvivors and 48% of the female nonsurvivors in this study had identifiable sepsis at postmortem. The mortality rate was higher in infants and toddlers, age 0 to 2.9 years, compared with children and adolescents, age 3 to 17 years; however, there was no significant difference in rate of mortality between genders, prepuberty versus puberty, those with septic episodes, or ethnic origin. Burn mortality among infants and toddlers, children, and adolescents with greater than 40% total body surface area burns with or without identified sepsis could not be shown to be gender or ethnic origin dependent.     

Admission chest CT complements fiberoptic bronchoscopy in prediction of adverse outcomes in thermally injured patients

In burned patients, inhalation injury can result in progressive pulmonary dysfunction, infection, and death. Although bronchoscopy is the standard for diagnosis, it only assesses the proximal airway and does not provide a comprehensive analysis of pulmonary insult. Chest radiographs have not been proven helpful in diagnosis of inhalation injury. Our hypothesis is that a CT scan alone or in conjunction with bronchoscopy can be used as a prognostic tool for critically ill burn patients, especially those with inhalation injury. The authors performed a retrospective study of all patients admitted to the U.S. Army Institute of Surgical Research Burn Center between 2002 and 2008 with chest CT within 24 hours of admission. They divided subjects into two groups, those with evidence of inhalation injury on bronchoscopy and those without. They used a radiologist's score to assess the degree of damage to the pulmonary parenchyma. The primary endpoint was a composite of pneumonia, acute lung injury/acute respiratory distress syndrome, and death. The inhalation injury group consisted of 25 patients and the noninhalation injury group of 19 patients. Groups were not different in age, TBSA burned, and percentage full-thickness burn. By multiple logistic regression, detection of inhalation injury on bronchoscopy was associated with an 8.3-fold increase in the composite endpoint. The combination of inhalation injury on bronchoscopy and a high radiologist's score was associated with a 12.7-fold increase in the incidence of the composite endpoint. Admission CT assists in predicting future lung dysfunction in burn patients.     

Is tracheostomy warranted in the burn patient? Indications and complications

Considerable controversy exists as to whether a tracheostomy (TT) is ever indicated in burn patients. Eighty-eight tracheostomies were performed over a 48-month period. An inhalation injury was present in 59.6% of the patients, and 96% had preceding endotracheal intubation (ET). The mean duration of ET was 14 days. Seven percent, 17% and 58% of the TTs were performed within the 1st, 8th, and 14th postburn day, respectively. The indications for TT were: emergency airway access, 7%; complications secondary to ET, 8%; pulmonary sepsis, 75%; pulmonary failure, 10%. The mean duration of TT was 33 days (range: 1-209). Major complications associated with TT included: tracheomalacia, tracheostenosis, tracheoinnominate artery and tracheoesophageal fistulae, and posttracheostomy dysphagia. The decision to perform a TT or to continue with ET should not be predicated on an arbitrary number of days, but must be individualized and based on the clinical condition of the patient. The complications associated with a TT are related to previous ET and to the underlying pulmonary pathology necessitating ventilatory support.     

Smoke inhalation and airway management at a regional burn unit: 1974 to 1983. II. Airway management

According to criteria established to define patients with smoke inhalation, the airway management of all victims of smoke and burns (1974 to 1984; n = 805) was reviewed. Fourteen percent of all patients were intubated (n = 117); patients intubated on the day of injury (n = 41) were more likely to extubate themselves or have technical problems with the endotracheal tube. Twelve percent of patients with smoke inhalation without burns required endotracheal intubation versus 62% of those with burns. An endotracheal tube was required for a median of 5 days. Tracheotomies were performed in 48 patients: 40% of those intubated and 6% of all patients. The mean postburn day for tracheotomy was day 15. There was no difference in the mortality rate for patients with an endotracheal tube only and those who had a tracheotomy as well: 42% and 37%, respectively. The prolonged length of stay for patients with a tracheotomy relates to the severity of the burn. Tracheotomy was not the cause of death in any patient. The strategy of grafting the neck before tracheotomy was used successfully in eight patients.     

High frequency percussive ventilation in pediatric patients with inhalation injury.

The objective of this study was to present data that showed high frequency percussive ventilation (HFPV) was superior to traditional mechanical ventilation for the treatment of children with inhalation injuries. Inhalation injuries continue to be the number one cause of death of patients with thermal injuries in the United States. Therapy for this condition has consisted of conservative pulmonary toilet and mechanical ventilation. Despite improvements in the management of burn injury, patients with inhalation injury develop pneumonia and pneumothorax, leading to adult respiratory distress syndrome. Unfortunately, inhalation injury that is complicated by pneumonia has been shown to increase mortality by 60% in these patients. Cioffi has shown that prophylactic use of HFPV in adult patients with inhalation injury has been a successful method of reducing the incidence of pneumonia and mortality. The effects of HFPV on the incidence of pneumonia, peak inspiratory pressures, and arterial partial pressure of oxygen/fraction of inspired concentration of oxygen (P/F) ratios were retrospectively studied in 13 children with inhalation injuries and compared with historic controls treated with conventional mechanical ventilation. All patients were treated with our standard inhalation injury protocol and extubated when they met standard extubation criteria. Patients ranged in age from 6 to 9 years, and most had burns covering greater than 50% of their total body surface areas. No deaths occurred in either group, but the patients who were treated with HFPV had no cases of pneumonia (P < .05), better P/F ratios (P < .05), lower peak inspiratory pressures, and less work of breathing (P < .05) as compared with our control group. On the basis of our clinical experience and data, the use of HFPV seems to be an effective treatment for the reduction of pulmonary morbidity in pediatric patients with inhalation injuries.     

Effects of ethanol on pulmonary inflammation in postburn intratracheal infection

Infectious complications are a major cause of mortality in trauma patients. Burn patients with prior ethanol exposure have a worse prognosis than those who sustain injury but had not been drinking. We examined pulmonary infection and lung pathology in mice given ethanol (1.2 g/kg) 30 minutes before being subjected to 13 to 15% total body surface area scald burn followed by intratracheal inoculation with Pseudomonas aeruginosa (1-2 x 10(3) colony-forming units [CFUs]). Survival was monitored for up to 48 hours. Sham control groups had 100% survival after intratracheal infection regardless of ethanol exposure. Infected burned animals had 55% survival; however, survival of infected mice exposed to ethanol and burn injury was significantly lower (27%, P < .0001). When pulmonary infection was evaluated, the lungs of sham groups were negative for bacterial colonies. In addition, at 24 hours there were no significant differences in lung CFUs from infected burned animals regardless of ethanol exposure (3.0 x 10(4)). However, pulmonary bacterial content significantly decreased (1.2 x 10, P < .02) at 48 hours in mice given burn injury alone, where CFUs from the lungs of mice exposed to ethanol prior to burn did not decline (5.4 x 10(5)). At the same time point, lungs from animals given ethanol and burn injury had about a 2-fold (P < .02) increase in leukocyte infiltration and vascular congestion, as well as decreased pulmonary oxygen saturation (82.8%, P < .02), when compared with other treatment groups. In summary, ethanol exposure in postburn intratracheal infection results in the inability to clear pulmonary infection marked by a prolonged pulmonary leukocyte accumulation and a decrease in pulmonary function.     

大鼠深Ⅱ度烫伤后创面自噬及凋亡的表达规律

目的 观察大鼠深Ⅱ度烫伤后72 h内创面自噬及凋亡的表达规律,探讨其与深Ⅱ度创面早期加深之间的关系.方法 Wistar大鼠背部10％ TBSA深Ⅱ度烫伤,观察烫伤后1h、6h、12 h、24 h、48 h、72 h创面组织自噬标志蛋白LC3、Beclin-1的表达及变化规律;TUNEL法检测创面凋亡水平的变化规律;HE染色及Masson染色显示创面组织形态和创面深度的变化.结果 烫伤后创面组织LC3、Beclin-1蛋白水平持续下降,至伤后24h达到最低,此后稍有升高,但仍远低于正常水平;伤后创面组织TUNEL阳性细胞持续增多,至伤后48 h达到最高,此后稍有下降,但仍远高于正常水平;创面组织真皮深层自噬被激活;烫伤后创面深度随着时间的推移进行性加深.结论 大鼠深Ⅱ度烫伤后早期创面组织自噬减少,凋亡增加,可能是参与创面加深的因素;真皮深层自噬的激活,可能是一种保护机制.     

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.     

Early pulmonary immune hyporesponsiveness is associated with mortality after burn and smoke inhalation injury

This prospective study aims to address mortality in the context of the early pulmonary immune response to burn and inhalation injury. The authors collected bronchoalveolar lavage fluid from 60 burn patients within 14 hours of their injury when smoke inhalation was suspected. Clinical and laboratory parameters and immune mediator profiles were compared with patient outcomes. Patients who succumbed to their injuries were older (P = .005), had a larger % TBSA burn (P < .001), and required greater 24-hour resuscitative fluids (P = .002). Nonsurvivors had lower bronchoalveolar lavage fluid concentrations of numerous immunomodulators, including C5a, interleukin (IL)-1β, IL-1RA, IL-8, IL-10, and IL-13 (P < .05 for all). Comparing only those with the highest Baux scores to account for the effects of age and % TBSA burn on mortality, nonsurvivors also had reduced levels of IL-2, IL-4, granulocyte colony-stimulating factor, interferon-γ, macrophage inflammatory protein-1β, and tumor necrosis factor-α (P < .05 for all). The apparent pulmonary immune hyporesponsiveness in those who died was confirmed by in vitro culture, which revealed that pulmonary leukocytes from nonsurvivors had a blunted production of numerous immune mediators. This study demonstrates that the early pulmonary immune response to burn and smoke inhalation may be attenuated in patients who succumb to their injuries.     

Blood transfusions are associated with increased risk for development of sepsis in severely burned pediatric patients

OBJECTIVE: To determine the risk of developing sepsis following transfusion of blood products in severely burned pediatric patients. DESIGN: Retrospective, cohort study. SETTING: Shriners Hospital for Children and University Hospital. PATIENTS: Severely burned pediatric patients with >30% total body surface area (TBSA) burn. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Two hundred seventy-seven pediatric burn patients over a period of 7 yrs (1997-2004) were included in the study, with 25 patients being septic at admission and therefore excluded. Patients were stratified according to TBSA burn and presence or absence of inhalation injury. The amounts of packed red blood cells (RBCs) and fresh frozen plasma (FFP) were recorded during hospital stay before the development of sepsis. Blood product administration was normalized for the number of surgeries and divided into two groups: high (RBCs>20/FFP>5) or low (RBCs<20/FFP<5) amount of blood products. Sepsis was diagnosed based on the criteria set by the Society of Critical Care Medicine in conjunction with positive blood culture or presence of organisms in the organs at autopsy. By stratifying the groups into low and high blood transfusion, we found that patients with >60% TBSA burn with inhalation injury have an 8% risk of developing sepsis in the low RBC group, which increases to 58% in the high RBC group (p<.05). Similar results were found for RBCs per operation, FFP, and FFP per operation (p<.05). There were no differences in age and gender between groups. CONCLUSIONS: Pediatric burn suffering from a 60% TBSA burn with concomitant inhalation injury are more likely to develop sepsis if they are given high amounts of blood products, indicating an immunocompromised state following blood transfusion.     

Microbial contamination in burn patients undergoing urgent intubation as part of their early airway management

Inhalation injuries occur in approximately one third of all major burns and account for a significant number of deaths in burn patients each year. Previous studies have examined ventilator-associated pneumonia in patients with inhalation injury, but no study to date has evaluated the incidence of bacterial contamination of the airways on admission in patients with inhalation injuries. Because pulmonary complications have been found to cause or directly contribute to mortality in as high as 77% of patients, with combined inhalation injury and thermal injury, early detection of community-acquired pneumonia may significantly alter treatment outcomes. The authors conducted a retrospective review of all burn patients with early intubation and inhalation injury admitted between January 1, 2004 and December 31, 2006 who underwent bronchoscopy with bronchoalveolar lavage (BAL) within 24 hours of admission. Seventy-four consecutive patients fulfilled the inclusion criteria. Age, sex, percentage of total body surface area (%TBSA), presence of alcohol, site of intubation, grade of injury, and BAL results were examined. Analysis revealed a patient population that was 67.6% male, with a 42.0 +/- 17.1-year-old mean age, 27.0 +/- 24.7 %TBSA average burn, 1.6 +/- 1.2 inhalation grade, 17.8 +/- 24.4 ventilator days requirement, 27.3 +/- 31.4 days of length of stay, and 21.6% mortality. BAL results were grouped into four categories: 1) No growth, 2) Normal flora, 3) <100,000 colony-forming units (cfu), and 4) >100,000 cfu. By this criteria, 13 patients (17.6%) had no growth, 22 (29.7%) had normal flora, 27 (36.5%) had <100,000 cfu, and 12 (16.2%) had >100,000 cfu on the initial BAL. Therefore, 53% grew pathogenic organisms and 16% had >100,000 cfu on BAL with initial bronchoscopy. The predominant organisms were gram-positive cocci, with Streptococcus viridans found in 15 patients (20%), Staphylococcus aureus in eight (11%), and Streptococcus pneumonia in four (6%). Analysis of the patients with the highest bacterial loads revealed that they were 75% female and had a trend toward an increased ventilator requirement and longer length of stay. Patients with combined thermal and inhalation injury requiring urgent intubation have a high incidence of bacterial bronchial contamination. Inhalation injury creates a damaged tracheobronchial mucosa and early intubation provides a portal for bacterial contamination. Further studies with a larger patient population and randomization to treatment and nontreatment of the BAL culture results may show statistically significant differences in ventilator days, length of stay, and mortality.     

Chest radiographic appearances in severely burned adults. A comparison of early radiographic and extravascular lung thermal volume changes

Chest radiographs (CXRs) have previously been used as a diagnostic tool to detect changes in lung water. In this study CXR changes in severely burned adults, in the absence of an inhalation injury, preceded detectable increases in extravascular lung thermal volume (ELTV) by 3 to 5 days. The hypothesis that early CXR density changes in burned patients have an infectious cause, not related to changes in ELTV, was tested. Blood cultures, CXRs, and ELTV were evaluated during the first 15 days after injury in severely burned adults who had no identified inhalation injury. Chest radiographs were scored daily on a 1 to 5 scale, with 1 = normal, 2 = peribronchial cuffing, 3 = mild interstitial infiltrates, 4 = severe interstitial infiltrates, and 5 = alveolar infiltrates. In all patients, except those who were septic, increases in their CXR density scores correlated well with increases in ELTV. The ELTV/CXR score ratios for septic burn patients on days 1 to 6 postburn was 1.7 +/- 0.2 compared with 4.2 +/- 0.4, (means +/- SEM) for nonseptic (P < .001), whereas the ELTV/CXR score ratios for septic and nonseptic patients, 7 to 15 days postburn, were 3.8 +/- 0.4 and 3.4 +/- 0.5, respectively. We suggest that before any measurable change in ELTV early increases in CXR density scores in burned patients without a concomitant inhalation injury are caused by intraalveolar pneumonitis or hyaline membrane atelectasis and not increased ELTV.