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

Burns ; complications ; Humans ; Shock ; etiology ; prevention & control ; Universal Precautions

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

Burns ; complications ; Humans ; Multiple Organ Failure ; etiology ; prevention & control

Burns ; complications ; metabolism ; Humans ; Inflammation ; etiology ; metabolism ; prevention & control

The prevention and treatment of complications are very important aspects in burn treatment. We should pay attention to the fundamental research, clinical prevention and treatment of complications. We have had good grasp of the subjects by fundamental research such as MODS. We must keep complications in mind when signs, symptoms, monitoring index and laboratory reports are inconsistent to the usual course of the injury, and we must guard against the occurrence of complications in the whole course of burn treatment. Consideration must be given to the treatment of both complications and the primary disease in order to slow down deterioration of patient, and guarantee the curative effect. There are still many unknown areas of burn complications for us to explore and discover.
Burns ; complications ; Multiple Organ Failure ; etiology ; prevention & control

Most of the major advances in the prevention and treatment of burn sepsis and MODS have been made within the last 20 years. Improvements have been made in gaining a better understanding of the pathophysiology of burn sepsis and MODS, in revising the definition of sepsis and MODS, and in prevention and treatment of burn shock. Additionally, improvements have been made in fluid resuscitation in patients with burn shock and in early gastrointestinal feeding to prevent translocation of endotoxins from the gut. Other achievements have been made in using recombinant human growth hormone combined with intensive insulin therapy to control hyperglycemia, and potassium chloride to prevent hypokalemia in order to accelerate protein synthesis. Additional advances include early closure and coverage of the burn wound, rational use of antibiotics, immunological modulation to combat immunological dissonance. Also, advances have been made by using early anticoagulation treatment to prevent coagulopathy. In prevention and treatment of burn sepsis and MODS, comprehensive support for all organs during the course of treatment is emphasized. Although the advances in burn treatment have been extremely encouraging over the last 50 years, burn sepsis and MODS remain the most common cause of mortality in the critical ill. To cope with extreme environmental conditions, such as armed conflict and natural disasters, research is needed to optimize the oral resuscitation regime, and more efficacious treatment strategies that are based on an indepth understanding of the pathogenesis of sepsis.
Burns ; complications ; metabolism ; Humans ; Multiple Organ Failure ; etiology ; prevention & control ; Sepsis ; etiology ; prevention & control

Ischemia/hypoxia is one of the key clinical issues following severe burns, and ischemic/hypoxic damage of tissues and organs is still hard to be prevented or minimized by various fluid resuscitation regimens. To those who suffered severe burns, even though fluid replacement therapy is delivered promptly, ischemic/hypoxic damage of organs is still inevitable. Previously, blood flow in vital organs such as heart was considered not to be reduced because of blood redistribution under the circumstance of stress. The postburn cardiac dysfunction has been mainly attributed to the reduced blood flow returned to the heart due to decreased blood volume caused by increased capillary permeability. Therefore, postburn cardiac dysfunction has been considered to be the result of burn shock. During the past two decades, we have performed serial studies on severe burns, and found that ischemic/hypoxic myocardial damage and functional impairment of myocardium due to activation of renin angiotensin system existing in the heart itself occur immediately after severe burns even before significant reduction in blood volume secondary to an increase of capillary permeability. Such prompt myocardial damage leads to cardiac deficiency, and it is also a precipitating factor for burn shock and ischemic/hypoxic injury of systemic tissues and organs. Therefore, we called it "shock heart" in our reports. The cellular and molecular mechanisms leading to myocardial damage were systematically investigated. Strategies for prevention of early postburn myocardial damage and dysfunction, and a new effective burn shock resuscitation regimen "volume replacement" plus "dynamic support" (cardiac support and myocardial protection) have been proposed based on our previous studies.
Burns ; complications ; metabolism ; Humans ; Hypoxia ; etiology ; prevention & control ; Myocardial Reperfusion Injury ; etiology ; prevention & control ; Myocardium ; metabolism

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