Page 34 nursing.elitecme.com Complete Your CE Test Online - Click Here Self-evaluation: Question 2 Which of the following statements best fits what is known in the pathophysiology of the development of sepsis? a. Sepsis develops as a result of a hyperresponse of proinflammatory mediators to infection. b. Sepsis is a localized response that occurs in response to a large release of cytokines. c. Sepsis is a dysregulated response of both proinflammatory mediators (cytokines) and anti-inflammatory mediators. d. Sepsis is normally caused by an infection but can be attributed to noninfectious etiologies as well. EFFECTS OF SEPSIS ON THE BODY All of the organs of the body are susceptible to damage from sepsis. Sepsis causes cellular injury that may be caused by tissue ischemia (lack of oxygen to tissues), cytopathic injury (injury to cells by proinflammatory mediators), and altered apoptosis (programmed cell death) (Neviere, 2017). Apoptosis is the mechanism in which the body gets rid of dysfunctional cells; it is a normal and necessary function of the body. Proinflammatory cells may delay apoptosis in activated immune cells, such as neutrophils and macrophages, and may speed up apoptosis in other cells, such as gut endothelium, leading to disruption of normal functions and contributing to the injury found in sepsis (Al- Khafaji, 2016). The dysregulation of cytokine release leads to endothelial dysfunction. Endothelial dysfunction causes increased capillary permeability and vasodilation, which ultimately leads to hypotension, hemoconcentration (concentration of red blood cells and other cellular products in blood), and edema (Shulte, Berhagen, & Bucala, 2013). Vasodilation and subsequent hypotension and hypoperfusion occur in the patient with sepsis causing poor oxygen delivery and damage to organs in the body. Eventually, in the case of septic shock, activated neutrophils release nitric oxide, which is a strong vasodilator that leads to hypotension seen in septic shock (LaRosa, 2010). Coagulation dysfunction and disseminated intravascular coagulation Interleukin-1 (IL-1) and tumor necrosis factor (TNFa) are proinflammatory cytokines that are released in response to inflammation. IL-1 and TNFa trigger tissue factor that is the first step in the pathway of coagulation. Tissue factor leads to the production of an inflammatory substance known as thrombin that causes fibrin clots to form. Small blood clots may develop during sepsis and impair circulation, especially in the microvascular system, which includes the capillaries. When the blood clots form in the small vessels, oxygenation to organs is reduced leading to organ dysfunction. In patients with sepsis, fibrinolysis (the breakdown of fibrin and clots) is impaired leading to further disruption of a normalized response. Disseminated intravascular coagulation (DIC) occurs in approximately 35% of patients with sepsis (Sepsis Alliance, n.d,). DIC is a condition where small clots form in the microvascular system, leaving the body depleted of clotting factors that in turn can lead to bleeding out in other areas (Sepsis Alliance, n.d.). Symptoms of disseminated intravascular coagulation (Sepsis Alliance, n.d.) ● ● Skin mottling or bruising. ● ● Blood clots. ● ● Drop in blood pressure. ● ● Bleeding from multiple sites. Treatment of DIC related to sepsis includes treatment of the underlying cause of infection and administration of anticoagulants and blood products as necessary (Sepsis Alliance, n.d.). In some cases, amputation of an infected limb may be necessary if circulation impairment has led to tissue death. About 50% of those with DIC die (Sepsis Alliance, n.d.). Lungs The lungs are highly susceptible to damage when a patient is septic. The endothelial injury that occurs during sepsis leads to increased capillary permeability and vasodilation within the lung tissue that causes interstitial and alveolar pulmonary edema. Neutrophils become entrapped in the microcirculation of the lungs causing further injury. The patient is unable to oxygenate properly, and hypoxemia ensues. (Neviere, 2017). This effect can lead to acute respiratory distress syndrome (ARDS). ARDS is acute onset hypoxemia that can be caused by sepsis, trauma, aspiration, and toxins (O’Sullivan & Kerrigan, 2015). Sepsis is the cause of ARDS in 25% to 40% of all acute respiratory distress cases. The risk of ARDS increases with the severity of sepsis and in the case of septic shock (De Haro, Martin-Loeches, Torrents, & Artigas, 2013). The best way to prevent the development of ARDS in patients with sepsis is early identification of symptoms and appropriate antibiotic therapy (De Haro et al., 2013). Kidneys Kidney failure can occur during sepsis, requiring the patient to receive dialysis. It is unknown exactly how the kidneys fail in the cascade of sepsis. Hypoperfusion may contribute to the development of kidney failure as well as dysfunction of the microvascular circulation. Acute tubular necrosis (the death of tubular epithelial cells that make up the renal tubules of the kidney) can occur from hypoxemia and hypoperfusion. It may also occur from systemic hypovolemia, direct renal vasoconstriction, release of cytokines, or activation of neutrophils by endotoxin (Neviere, 2017). Clinical signs of kidney failure include oliguria and increased creatinine levels. Gastrointestinal tract Sepsis causes circulatory abnormalities that may affect the normal barrier function of the gut, leading to translocation of bacteria and endotoxin into the systemic circulation, contributing to sepsis (Neviere, 2017). Clinical symptoms of gastrointestinal involvement include absent bowel sounds indicating paralytic ileus, seen in patients with septic shock. Paralytic ileus is thought to be caused by excess production of nitrous oxide (Al-Khafaji, 2016). Liver The liver plays an important part in helping to clear the body of infectious agents. During sepsis, the liver can be damaged through hemodynamic changes or through direct or indirect insult to hepatocytes (Nesseler, Launey, Aninat, Morel, Malledant, & Seguin, 2012). Liver dysfunction can prevent the clearing of endotoxin and bacterial products eventually allowing spillover of these products into systemic circulation (Neviere, 2017). Clinical evidence of liver failure is seen in elevated bilirubin levels. Central nervous system (CNS) Confusion and changes in mental status may be evidence of central nervous system involvement, possibly as a result of hypoperfusion to the brain. Clinical symptoms of CNS involvement can be seen as mental status changes, such as confusion, restlessness, or agitation. The Glasgow Coma Scale is the tool used to measure mental status in patients. Any decrease in the Glasgow Coma rating may be an early indication of impending sepsis (German Sepsis Society, n.d.).