Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Burn injury results in a rapid loss of intravascular volume as wound edema forms, which reduces the circulating blood volume and generates the need for fluid therapy to combat hypovolemia. Fluid resuscitation of a burn patient is usually carried out with isotonic, sodium- and chloride-containing fluids, such as lactated Ringer's solution. The initial 24 h resuscitation volume is based on the burn size and body weight of the patient. ⋯ Care following resuscitation is focused on topical antimicrobial therapy, burn wound excision, and wound closure by grafting. Nutritional support and the prevention and control of infection are constant themes in burn patient management. A progressive improvement in general care of the acutely injured patient, prevention of shock, effective means of maintaining organ function, prevention and control of burn wound and other infections, and physiologically based metabolic support have significantly increased burn patient survival in recent decades.
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Acute respiratory distress syndrome is a common cause of morbidity and mortality in intensive care units. For the most part, the mortality of this syndrome has arguably not decreased since the syndrome was originally described. ⋯ So encouraging are these reductions that there has been a subtle shift in philosophy of mechanical ventilation toward using lung-protective ventilatory strategies at all times. With broad acceptance of this shift in philosophy, and the use of recently standardized clinical definitions for controlled studies, we optimistically anticipate improved mortality rates for acute respiratory distress syndrome.
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Despite recent advances in antibiotic therapy, aggressive operative intervention and intravenous hyperalimentation, sepsis, and multiple organ failure are still reported to contribute to significant morbidity and mortality in the surgical intensive care unit. In light of this, it is essential to determine the mechanism underlying the pathophysiology of sepsis so that better therapeutic interventions can be designed. Experimental studies indicate that murine polymicrobial sepsis induces a marked suppression in both lymphocytic and macrophage function associated with decreased cellular adenosine triphosphate levels and increased Ca2+. ⋯ We have presented evidence of marked changes in the rate of Ao in immune cells after the onset of sepsis. These data suggest the possibility that mediators released in response to septic insult contribute to the observed changes in immune cell function through the induction of Ao. Inasmuch, understanding the contribution of PCD to the pathophysiology of sepsis, should provide a better basis from which to develop more effective therapy for the septic patient.