Humans ; Inflammation ; etiology ; Sepsis ; complications ; Signal Transduction

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 ; Sepsis ; etiology ; prevention & control

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

Pylephlebitis usually occurs secondary to infection in the region drained by the portal venous system. A most common antesecent focus of infection is diverticulitis and the most common blood isolate is E. coli (54%), followed by Proteus mirabilis (23%). Overall mortality is 32% and most of the patients who had died had severe sepsis prior to the initiation of antibiotic therapy. We describe a case of pylephlebitis which had appendicitis and consequent septic thrombosis of the portal vein and its branches, with dissemination of infection to the liver. The patient had recovered due to timely antibiotic treatment alone and resulted in complete resolution. Early diagnosis and treatment are basic to a favorable clinical course.
Adult ; Appendicitis/complications* ; Case Report ; Human ; Liver Abscess/etiology ; Male ; Portal Vein* ; Sepsis/etiology ; Thrombophlebitis/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

Since the definition of sepsis was proposed in Chest by American College of Chest Physicians and Society of Critical Care Medicine in 1992, researches on burn sepsis have focused on the regulation of immune-inflammation response resulting in minimizing tissue injury resulted from excessive inflammatory response. Treatment of sepsis should focus on effect of early circulation oxygenation support in preventing and treating multiple organ dysfunction. The hypothesis of producing a hibernation-like state which might prevent multiple organ dysfunction in patients with sepsis provides us a new therapeutic strategy in protecting organs in the early stage of sepsis in future.
Burns ; complications ; therapy ; Humans ; Sepsis ; diagnosis ; etiology ; therapy

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

Child ; Chromobacterium ; Female ; Humans ; Sepsis ; drug therapy ; etiology ; microbiology ; mortality