Page 132 nursing.elitecme.com Complete Your CE Test Online - Click Here Multiple organ dysfunction syndrome Multiple organ dysfunction syndrome (MODS) is present when there is more than one failing organ in the body. MODS is progressive organ dysfunction in which the patient cannot maintain homeostasis without medical intervention. It may be caused by an infectious etiology as in sepsis or septic shock, or it may be of noninfectious etiology as in the case of SIRS from pancreatitis (Neviere, 2017). Multiple organ dysfunction syndrome can be primary or secondary in nature. Primary MODS is organ dysfunction related to the injury directly, and secondary MODS results from the host’s response to an injury elsewhere. MODS is the cause of death from sepsis (Cohen, 2012). As sepsis progresses and is left unchecked, different organs begin to fail. The number of organs that fail correlates to the risk of mortality. If four or five organs fail, the mortality risk is 90% regardless of treatment (Cohen, 2002). Key points ● ● Sepsis can cause endothelial injury in the lungs that leads to pulmonary edema and poor oxygenation and, eventually, acute respiratory distress syndrome. ● ● Sepsis can lead to ileus in the gastrointestinal tract and can cause translocation of bacteria and leaking of endotoxin into the blood. ● ● Sepsis can lead to kidney failure requiring hemodialysis. ● ● Sepsis can cause liver failure allowing more endotoxins and bacteria into systemic circulation. ● ● Mental status changes can be seen in the patient with sepsis as evidenced by confusion, restlessness, or agitation. ● ● Sepsis can cause metabolic changes, such as hyperlactatemia and hyperglycemia. ● ● Sepsis can progress to multiple organ dysfunction syndrome in which organs begin to fail, ultimately leading to death. SEPTIC SHOCK Shock is a result of circulatory failure that is life-threatening (Gaieski & Mikkelsen, 2016). It is a state of cellular and tissue hypoxia caused by reduced oxygen delivery or increased oxygen consumption or inadequate oxygen utilization that can be attributed to various causes, including the following (Gaieski & Mikkelsen, 2016): ● ● Cardiogenic: Occurs after myocardial infarction. ● ● Neurogenic: Occurs after severe brain or spinal cord injury. ● ● Anaphylactic: Related to a severe allergic reaction. ● ● Endocrine: Occurs as a result of severe endocrine dysfunction. ● ● Hypovolemic shock: Occurs as a result of low intravascular volume and can be hemorrhagic or nonhemorrhagic. ● ● Drug-induced shock. ● ● Septic shock that occurs in the presence of sepsis. Septic shock is defined as sepsis with the presence of circulatory, cellular, and metabolic dysfunction associated with a higher risk of mortality than sepsis alone (Singer et al., 2016). Clinically, septic shock is present when the patient has a vasopressor requirement to maintain a mean arterial pressure of 65 mmHg or greater and serum lactate level greater than 2 mmol/L (> 18 mg/dL) in the absence of hypovolemia (Singer et al., 2016). Patients who are hypotensive despite vasopressors and volume resuscitation and have a high lactate level are considered to be in septic shock and have a 40% chance of dying (Singer et al., 2016). RECOGNIZING SEPSIS Early recognition of sepsis is critical. It can be recognized by a comprehensive evaluation of the patient. The clinician should be aware of general variables—such as vital signs, blood glucose levels, and mental status—and should obtain specific laboratory results that may indicate worsening infection or sepsis with organ involvement. Abnormalities in laboratory values associated with the coagulation cascade—such as prolonged PTT/PT, elevated D-dimer, protein C deficiency, and antithrombin deficiency—can be seen even before organ failure (LaRosa, 2010). High platelet counts can be found in the early onset of sepsis. Low platelet counts are found later in patients with disseminated intravascular coagulation (LaRosa, 2010). Creatinine levels, AST/ALT, alkaline phosphatase, and bilirubin levels that are high may indicate organ failure (LaRosa, 2010). Lactate, procalcitonin, and c-reactive protein levels are also routinely monitored in patients with suspected or confirmed sepsis. Lactate Lactate is an indicator of lack of oxygen in cells, or cellular hypoxia. When there is lack of oxygen to the cells, the body goes into anaerobic metabolism to create small amounts of energy (Blomkalns, 2006). Lactate is produced as a result of anaerobic metabolism. Lactic acidosis can occur as a result of many different causes (Blomkalns, 2006): ● ● Septic shock. ● ● Increased oxygen demands from strenuous exercise. ● ● Anemia. ● ● Blood loss. ● ● Seizures. ● ● Shivering. ● ● Hypothermia. ● ● Volume depletion. ● ● Trauma. ● ● SIRS. ● ● Diabetes. ● ● HIV. ● ● Certain medications. ● ● A parental nutrition regime. Some fluctuations in lactate levels are normal, and in the healthy person, the body clears the lactate in a timely fashion. In patients who are septic, higher lactate levels have been associated with an increase in mortality (Shapiro et al., 2004). Lactate levels are useful in diagnosing sepsis, as higher levels indicate tissue hypoxia associated with sepsis. Procalcitonin Procalcitonin (PCT) is the precursor of calcitonin produced by cells in the thyroid gland and is cleaved into calcitonin; it is undetectable in a healthy person. In bacterial sepsis, procalcitonin is unable to cleave into calcitonin and is released into the bloodstream. Elevated procalcitonin is used to differentiate infectious SIRS from noninfectious SIRS (LaRosa, 2010). Procalcitonin has been researched as a potential biomarker for the diagnosis of sepsis. PCT levels rise in the presence of a bacterial cause of sepsis. A higher level of PCT has been associated with increased morbidity and mortality (Liu, Su, Han, Yan, & Xie, 2015). One of the benefits of obtaining a PCT level is that PCT levels rise quickly in the blood in the presence of a bacterial infection. If sepsis is suspected,