Page 104 Complete Your CE Test Online - Click Here 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, an elevated PCT level from a bacterial infection can be a very useful diagnostic tool to help confirm diagnosis. There are limitations in the use of PCT as a biomarker for sepsis. A high PCT level can also be seen in other conditions, such as SIRS from a noninfectious source, localized bacterial infection, autoimmune disease, pancreatitis, severe trauma, and burns (Chakraborty, 2015). Another downside to using PCT level as a prognostic indicator of sepsis is that it is not sensitive to viral, fungal, or parasitic causes of sepsis. It is still a useful tool, however, and the Surviving Sepsis Campaign (SSC) recommends the use of PCT level when deciding to discontinue the use of antibiotic therapy (Rhodes et al., 2017). A PCT value of less than 0.5 ng/ml in a patient with SIRS without the evidence of infection and negative cultures can be a useful tool to support the decision to discontinue antibiotics (Rojas-Mereno & Hariharan, 2016). C-reactive protein In the acute phase of sepsis, c-reactive protein (CRP) is elevated (LaRosa, 2010). CRP binds to components of bacteria, fungi, and parasites in the presence of calcium, and these complexes trigger the complement system (Povoa, 2002). Gram-positive and gram-negative bacteria and fungal infections cause a significant rise in the level of CRP (Povoa, 2002). CRP levels can be lower in some acute viral infections but higher in others (Povoa, 2002). CRP levels can indicate infection. High CRP levels are also seen in such conditions as burns, trauma, tissue necrosis, advanced cancer, and other inflammatory diseases (Povoa, 2002). Diagnostic criteria for sepsis Nurses should be alert to the following diagnostic criteria for sepsis in their patients and report identified symptoms to the patient’s physician or nurse practitioner (Dellinger et al., 2013). General variables ● ● Fever > 38.3˚C (100.9˚F). ● ● Core temperature < 36˚C (96.8 ˚F). ● ● Heart rate > 90 bpm or 2 standard deviations (SD) above normal value for age. ● ● Tachypnea. ● ● Altered mental status. ● ● Edema or positive fluid balance > 20 ml/kg over 24 hours. ● ● Hyperglycemia > 140 mg/dL in a nondiabetic patient. Inflammatory variables ● ● Leukocytosis (blood cell count > 12 000). ● ● Leukopenia (white blood cell < 4000). ● ● Normal white blood cell count with > 10% immature forms. ● ● Plasma c-reactive protein > 2 SD above normal value. ● ● Procalcitonin level > 2 SD above normal value. Hemodynamic variables Hypotension < 90 mmHg, MAP, 70 mmHg, or a systolic blood pressure drop > 40 mmHg in adults or less than 2 SD below normal for age. Organ dysfunction variables ● ● Arterial hypoxemia (PaO2/FiO2 < 300). ● ● Acute oliguria (< 0.5 mL/kg/hr for at least 2 hours despite fluid resuscitation). ● ● Creatinine increase ( > 0.5 mg/dL or 44.2 mmol/L). ● ● Coagulation abnormalities (PTT > 60 seconds, INR > 1.5). ● ● Ileus (absent bowel sounds). ● ● Thrombocytopenia (platelet count < 100 000). ● ● Hyperbilirubinemia (plasma bilirubin > 4 mg/dL or 70 mmol/L). Tissue performance variables ● ● Hyperlactatemia ( > 1 mmol/L). ● ● Decreased capillary refill or mottling. Nursing consideration: The first step in sepsis screening is to look for signs and symptoms of infection or worsening infection. Nurses are often the first to evaluate a patient’s vital signs, symptoms, and laboratory results and should suspect sepsis in a patient with known or suspected infection who may present with abnormal clinical findings. Early identification of sepsis can save a patient’s life. Self-evaluation: Question 3 Betty, who has diabetes and degenerative joint disease, is recovering from hip surgery and is now 10 days postop. She recently noticed that she feels increasingly sluggish, and her swelling, which was subsiding, is now getting worse along with an increase in pain, redness, and purulent drainage at the incision site. She calls the nurse at the surgeon’s office to express her concerns and is told to come in immediately for evaluation. Upon evaluation, the nurse finds her vital signs and blood glucose levels to be the following: ● ● Temperature: 36.1˚C (97˚F). ● ● Heart rate: 84 bpm. ● ● Blood pressure: 138/70. ● ● Respiratory rate: 26 rpm with a pulse oximetry reading of 91% without oxygen supplementation. ● ● Blood glucose level: 148 mg/dL. What abnormal findings should alert the nurse that the patient may be developing sepsis? a. Elevated blood glucose level of 148 mg/dL. b. Elevated blood pressure. c. Low body temperature. d. Respiratory rate of 26 rpm with a low oxygen saturation level. Endocrine dysfunction in septic shock The endocrine system consists of glands throughout the body that produce hormones and regulate body processes. During septic shock, the endocrine system is disrupted; this disruption can contribute to the deleterious effects of shock. For example, the renin-aldosterone hormones that regulate sodium and electrolyte balance are disrupted, and renin levels increase while aldosterone levels decrease contributing to salt loss and hypovolemia (Annane, Bellissant, & Cavaillon, 2005). In later stages of shock, vasopressin (also known as antidiuretic hormone) synthesis and release are impaired. Vasopressin causes constriction of blood vessels and raises blood pressure. But in septic shock, the impaired synthesis and impaired release of vasopressin contribute to low blood pressure (Annane et al., 2005). Cytokine- induced insulin resistance contributes to hyperglycemia in the patient with sepsis and septic shock (Gheorghiţă,, Barbu, Gheorghiu, & Căruntu, 2015). Key points ● ● Septic shock is clinically present when a patient requires vasopressors to maintain a mean arterial pressure of 65 mm/Hg and a serum lactate level of greater than 2 mmo/L in the absence of hypovolemia. ● ● Endocrine dysfunction – including increased renin levels, decreased aldosterone levels, impaired synthesis and release of vasopressin, and cytokine-induced insulin resistance – contribute to septic shock.