Cath Lab Digest

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Patient risk factors of which most nurses are well aware include age, the presence of comorbidities, and a history of trauma or surgery. Treatment factors include nutritional management, effectiveness of infection control measures, and management of tissue perfusion. Each type of risk factor may carry substantial implications for the development of complications and organ system failure. Skin, the largest organ in the body, is not immune to these risks; it, too, can develop complications, become dysfunctional, and ultimately fail.

  The increasing use of technology in providing life support to critically ill patients has contributed to prolonged survival in this patient population. Thus, it is not uncommon for patients to die from conditions unrelated to their initial injury or condition.² Multi-organ failure was first described in 1973 by Tilney³ as the postoperative failure of uninvolved organs after significant blood loss and shock. Over the years, this syndrome has been referred to as multi-system organ failure, multiple organ failure, and most recently multi-organ dysfunction syndrome (MODS).⁴ MODS is defined as “the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without an intervention.”⁵

  In contrast to organ failure due to other causes, failure of organs in MODS often is not due to direct insult to the failing organ; there is a period of time, ranging from days to weeks, from the initiating event to failure of the distant organ. The sequence of distant organ failure is typically respiratory failure followed by hepatic failure, intestinal failure, and finally renal failure. Heart and hematopoetic failure may occur later. This sequence may be influenced by pre-existing conditions.⁶ A systemic inflammatory response syndrome usually precedes MODS. The most common condition leading to MODS is sepsis; however, not all patients with MODS have evidence of infection. Other risk factors are severity of illness, severe trauma, major operations, age >65 years, persistent lack of oxygen availability after circulatory shock, and pre-existing end-stage liver failure.⁷

  Several hypotheses have been posed concerning the cause of MODS, and overlap exists in some theories of causality. The endotoxin macrophage hypothesis proposes endotoxin as a primary mediator due to the formation and release of cytokines. In the gut hypothesis, bacteria or endotoxin derived from the intestine initiate the septic state. The vulnerability of the intestines to ischemia promotes bacterial translocation. This helps explain why a specific source of septicemia is not identified for many septic patients with MODS.⁸ The two event hypothesis assumes that an event such as hypotension readies the immune system, so a second insult such as infection at a vulnerable time will result in systemic inflammation that leads to MODS. Finally, the tissue hypoxia microvascular hypothesis states that microvascular changes result in an inadequate oxygen supply and cause tissue hypoxia that may lead to organ dysfunction and cellular death.⁷

  Identifying patients susceptible to failure of more than one organ system is key to preventing additional organ system failure, including MODS. In a case presentation and literature review, Walsh⁹ noted various risk factors for the development of MODS, including advanced age, presence of chronic diseases, tissue hypoperfusion, immunosuppression, multiple blood transfusions, infections, burns, and sepsis.

  Skin failure. The skin helps maintain homeostasis within the body and protects against external assaults. The skin measures approximately 3,000 square inches and “receives one third of the body’s circulating blood volume”¹⁰ via the capillaries.