Sepsis induced by invasive infection is a challenging problem and the major cause of death after severe burn. With the increasing understanding of sepsis, diagnostic criteria of sepsis were proposed and revised consecutively so that they could be consistent with the clinical practice. Being different from other trauma and critical diseases, diagnostic criteria of sepsis after severe burn were also proposed, and they need further clinical verification. It is believed that comprehensive measures for the treatment of severe sepsis after burn should be advocated. These measures include rapid and effective resuscitation of burn shock, early escharotomy and closure of burn wound, metabolic support, immunoregulation and anti-inflammation, reinforcement of organ support, etc. Although a number of advances have been achieved in the past decades, the mechanism of sepsis need further elucidation, diagnostic criteria of sepsis need further revision, and novel therapeutic measures for burn sepsis should be developed.
Burns ; complications ; Humans ; Sepsis ; diagnosis ; etiology ; therapy

Pediatric burn patients account for more than 1/3 of the inpatients in the same period, and its incidence surpasses that of burn patients in other age groups. However, it brings about much difficulty to treat pediatric burn patients complicated by sepsis, which brings a significantly higher mortality than that of the adult. Moreover, the physiological characteristics, development of organs, drug metabolism, and body response to burn injury in children are obviously different from those of the adult. Therefore, it is clinically important to understand the clinical characteristics of sepsis in pediatric burn patients in order to improve the diagnosis and treatment of this ailment.
Burns ; complications ; Child ; Humans ; Sepsis ; diagnosis ; etiology

Burns ; complications ; Humans ; Hypoxia ; Ischemia ; Shock ; etiology

Burns ; complications ; Humans ; Sepsis ; etiology ; prevention & control

Ammonia is commonly used in industry and agriculture. It is also one of the most frequently accidentally spilled chemicals. Exposure to ammonia can cause severe cutaneous burn or freezing injury, ocular injury, and inhalation injury, among them inhalation injury is the most lethal one. Although the diagnosis and treatment of ammonia burns have been improved, the long-term prognosis is not satisfactory. In this article, we reviewed the literature concerning ammonia burns, in order to summarize the clinical features and treatment of such injury.
Ammonia ; adverse effects ; Burns, Chemical ; etiology ; physiopathology ; therapy ; Burns, Inhalation ; Humans ; Inhalation Exposure ; adverse effects ; Prognosis

Multiple organ dysfunction (or failure) syndrome (MODS or MOFS) remains a hurdle for us to overcome before further improvement in the survival rate can be achieved in the patients with extensive deep burns. It is, however, generally recognized that MODS is the final result of the liberation and interplay of multiple inflammatory mediators or cytokines, and there is a two hit phenomenon in its pathogenesis. In extensive burns, the first hit is usually the burn injury itself and the ensuing hypovolemic shock, followed by septic response. The large amount of devitalized tissues, along with the development of invasive infection, constitutes frequently the second hit. Since as yet nearly all therapeutic strategies directed specifically toward neutralizing inflammatory mediators or cytokines to control sepsis have failed in clinical trials, and the treatment of established organ failure is usually not successful, it is deemed rational to focus our attention instead on the prevention of this dreadful syndrome in the clinical practice. It is our belief that the strategies of treatment should be: blunt the first hit and prevent the second hit and supplemented with visceral support and nutritional support.
Burns ; complications ; Cytokines ; adverse effects ; Endotoxemia ; etiology ; Humans ; Hypovolemia ; etiology ; Multiple Organ Failure ; etiology ; prevention & control ; Sepsis ; etiology ; Shock ; etiology

A series of studies demonstrated that myocardial damage and cardiac dysfunction occur immediately after severe burn even before the intervention of significant reduction in blood volume as a result of increased capillary permeability. Because the heart is the power organ of the circulation, such myocardial damage and cardiac dysfunction lead not only to cardiac deficiency, it is also a precipitating factor of burn shock and ischemic/hypoxic injury. Therefore, we nominate this phenomenon as "shock heart". New measures including "volume replacement" plus "dynamic support" proposed according to this new recognition is of important clinical significance for burn shock resuscitation and prevention and treatment of ischemic/hypoxic injury, as well as reducing organ complications resulting from insufficient or excessive fluid resuscitation during early postburn stage.
Burns ; complications ; Humans ; Hypoxia ; etiology ; Myocardial Reperfusion Injury ; etiology ; Shock ; etiology

Burn infection occurs when pathogenic bacteria colonized on the burn wound surface, and they then invaded the viable tissue causing sepsis or sepsis with blood stream invasion. This infection pattern is particular to burn injury. Both in a model of pseudomonas burn wound sepsis and a clinical study of early eschar excision for bacteria quantification indicate that the bacteria not only are located on the burn wound surface but also invaded the deeper tissues. Finally, the bacteria penetrate into the neighboring viable tissue and even blood vessels. Therefore, we can say that burn infection is from local wound infection to invasive infection, and finally sepsis is developed ,and it is termed as burn wound sepsis. The cutoff count of subeschar tissue bacteria is 10(5)/g. However, the burn wound sepsis may not occur when the number of subeschar tissue bacteria reaches 10(5)/g. The criteria for the diagnosis of burn wound sepsis are mainly listed as below: (1) The number of bacteria in the subeschar reaches > or =10(5)/g. (2) Bacteria can be detected in the biopsy specimen. (3) Sepsis associated symptoms and signs. However, the sepsis associated symptoms and signs must be obvious in patients to make the clinical diagnosis of burn wound sepsis. If the sepsis associated symptoms and signs do not appear, we should not make the diagnosis of burn wound sepsis eyen with the number of bacteria in the subeschar tissue reaching 10(5)/g or bacteria can be found in the biopsy specimen. Sepsis has been defined as the body % response to bacteria and their products. The occurrence of sepsis depends primarily on immune function and stress response intensity, and it is closely related to wound infection degree such as bacteria density and invasion depth in the burn wound, or plasma endotoxin level to certain extent.
Bacterial Infections ; etiology ; Burns ; microbiology ; Humans ; Sepsis ; etiology ; Wound Infection ; etiology

For five decades it has been recognized that severe burn injury may precipitate in marked alterations in immune function, resulting in life-threatening systemic infections, sepsis, multiple organ failure, and even death. Extensive and deep burns exert widespread and profound impacts on various cells and molecules of the immune system. The general characteristics of abnormal immune responses following major burns are hyperinflammatory response and hypoimmune response of innate and adaptive immunity. These are recognized as postburn immune dysfunction (PID). The stress reaction, massive necrotic tissue, shock, infection, malnutrition and various therapeutic procedures after burns alter the microenvironment of the immune cells and molecules in which they reside, and consequently result in the changes in immune cells and their secretions in quantity and/or activity, and also aberrant signal transduction in different immune cells. These events constitute the cellular and molecular bases in the pathogenesis of PID. The main clinical consequences of PID include tissue damages and increased susceptibility to opportunistic pathogens caused by refractory inflammation and suppressed adaptive immunity. In order to decrease the morbidity of these lethal complications, efforts to improve the immune dysfunction after burn injury have been made not only at the integral level of etiological factors, but also at the cellular and molecular levels of its mechanisms. In this review, all these above-mentioned aspects of PID are comprehensively discussed.
Burns ; immunology ; Humans ; Immune System Diseases ; etiology ; prevention & control

Sepsis and septic shock as a result of an invasive infection are challenging problems in extensively burned patients, and frequently end in multiple organ dysfunction syndrome (MODS). It is of great significance to further elucidate the pathogenetic mechanisms, and to seek novel intervention strategies to prevent and treat sepsis/MODS secondary to severe burns. A more complete understanding of the pathogenetic mechanisms of postburn sepsis would certainly elicit a number of potential therapeutic strategies for it. It is our belief that comprehensive clinical measures for management of severe sepsis should include rapid, adequate fluid resuscitation for burn shock, early feeding, effective control of infection, early escharectomy, and reinforcement of organ support. Once burn wound sepsis occurs, prompt removal of infected necrotic tissue is the key procedure to ensure a successful result. Further study is necessary to determine the precise mechanisms of these protective effects and the clinical advantages for postburn sepsis using evidence-based methodology system.
Burns ; complications ; Humans ; Sepsis ; epidemiology ; etiology ; prevention & control