Sepsis

The number of documented cases has been rising every year. “This may be due to the aging population, the increased longevity of people with chronic disease, the spread of antibiotic-resistant organisms, an upsurge in invasive procedures and broader use of immunosuppressive and chemotherapeutic agents” (National Institute of General Medical Sciences, 2014). The mortality rate for sepsis ranges from about thirty percent for patients with sepsis to fifty percent in patients who develop septic shock. Mortality rate varies as to how many organs have been affected. Twenty percent mortality for one organ failure, forty percent for two organs failing, sixty-five to seventy percent for three failed organs, and seventy-five to eighty-five percent when four or more organs have failed. The cost related to sepsis is about seventeen billion dollars per year (about twenty-two thousand dollars per patient), which is six times greater than the cost of patients without sepsis.

Under the Core measures, Sepsis is one of the problem-focused trigger for systemic infection and if untreated which can lead to death. In United States, it is the 11th leading cause of death and consumes the large amount of costs about $20.3 billion in 2011 (Jones et al.,2016). According to Centers for Disease Control and Prevention (CDC), more than 1.5 million people diagnosed with sepsis, and at least 250,000 patients die from that yearly (CDC, 2017). The evidence-based research revealed with results of certain pre existing conditions, pathophysiological studies, preventive measures and sepsis bundle for treating and preventing sepsis to save the life of the patients.

The early sepsis protocol has a huge impact on Emergency Department (ED) patients that are suspected of sepsis. The studies have shown that early recognition has a significant effect on the patient’s outcome. My paper will only analyze data collected in the critical care settings and focus mainly on the importance of early recognition of the signs and symptoms of sepsis to meet the three hour window treatment as recommended by the Surviving Sepsis Campaign (SSC).

A methodical search was undertaken of the databases – PubMed, CINAHL and ScienceDirect to ascertain the most appropriate evidence. Search terms used were “Sepsis Prevention”, “Sepsis Management” “Sepsis Early Recognition” and “Sepsis Detection” and merged using Boolean Logic (Glasper and Rees,

The word “sepsis” is derived from the ancient Greek word for rotten flesh and putrefaction. Since then, a wide variety of definitions have been applied to sepsis, including sepsis syndrome, severe sepsis, bacteremia, septicemia and septic shock In 1991, the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) developed a new set of terms and definitions to define sepsis in a more “precise manner” [1, 2]. These definitions take into account the findings that sepsis may result from a multitude of infectious agents and microbial mediators and may not be associated with detectable bloodstream infection. The term “systemic inflammatory response syndrome” (SIRS) was coined to describe the com- mon systemic response to a wide variety of insults. When SIRS was the result of a suspected or confirmed infectious process, it is termed “sepsis”.

Thirty to 50 percent of the 400,000 to 500,000 cases of sepsis in the United States each year are fatal, emphasizing the seriousness of this public health concern [2]. Recent research into possible alternative treatment options indicates that patients being treated with statin therapy are less likely to develop sepsis from a serious infection, die from sepsis or develop serious complications due to sepsis; however, the mechanism of action is unknown and therefore is the focus of this study [2, 6, 10-12]. Possible mechanisms of action include a direct interaction of the statin with the sepsis-causing organism, an interaction between the statin and the host immune system or a combination of the two [9, 14, 16-17]. Additionally, recent studies indicate that statins may have a direct antimicrobial effect and has suggested that statins may diminish the replication and infectivity of some pathogens responsible for sepsis [11, 14, 16-17]. Thus, we hypothesized that statins could benefit septic patients by

Sepsis and the lasting physiological effects of survivors are major concerns for the Center for Medicare/Medicaid Services (CMS),

Sepsis is a phenomenon in which an infective agent results in a physiological response in excess of the pathogenic insult. Efforts to define and investigate sepsis have been somewhat fruitful in elucidating the nuances of this phenomenon. Yet, gaps exist in identifying and investigating sepsis. Recent efforts have streamlined the definition and identification criteria of sepsis and septic shock. The treatment of sepsis is based on the elements of identification, hemodynamic interventions (fluid and vasopressor resuscitation), and antimicrobial therapy/source control. A two-tiered approach employing the qSOFA (Quick Sepsis-Related Organ Failure Assessment) and SOFA (Sepsis-Related Organ Failure Assessment) tools now provide a succinct criteria for sepsis and septic shock. Various approaches may be taken to assess fluid responsiveness, provide fluid resuscitation, and determine the need for vasopressor support. Early, aggressive antimicrobial therapy is essential to the treatment of sepsis. Obtaining source control and considering early surgical

According to the National Institute of General Medical Sciences severe sepsis strikes about 750,000 people in the United States each year and kills an estimated 28 to 50 percent of those individuals. The most vulnerable populations for sepsis are the elderly and newborns. After completing the whole eleven segments, I learned that anyone with an infection may be at risk for developing sepsis. The whole scenario helped me how to screen for sepsis and how important is to recognize and respond appropriately to early signs of sepsis in hospitalized patients. Once sepsis is diagnosed, early and aggressive treatment can begin which greatly reduces mortality rates associated with sepsis. After completing the whole scenario I learned how to approach

It is becoming an important public health concern because it has a long-term effect on our family, society, community, and economy as well.

The diagnosis of sepsis is obvious in Mr. M. W case. Since sepsis is a syndrome, Mr. M. W’s associated signs and symptoms need a carefully evaluated to avoid misdiagnosis. A disease conditions such as bacteria and cardiogenic shock may have overlapping signs and symptoms. Therefore, these signs and symptoms need to be supported with a source of infection. The clinical findings that justify the diagnosis sepsis will be discussed before identifying and discussing the source of Mr. M. W’s infection.

When dealing with patients, especially in intensive care , it is often difficult to determine the infection 's role in the onset of SIRS , which is common and likely often multifactorial (as a result of trauma, surgery, burns , ischemia / reperfusion , pancreatitis and / or infection ) [6 , 7].

In 1991 the Society of Critical Care Medicine (SCCM) introduced definitions for SIRS. It is intended to define a clinical response to a non-specific insult, either infectious or non-infectious in origin. SIRS is a widespread inflammation that may occur in patients with different disorders such as infection, trauma, shock, inflammation, or ischemia (Sole, Kleain, & Moseley, 2011, p. 259). In short, the inflammatory cascade maintains a balance between pro-inflammation and anti-inflammatory processes (Sole et al., 2011, p.259). Although inflammation is normally a process that is localized, SIRS is associated with the release of mediators. These mediators make the endothelial wall more permeable causing a shift of fluid from the inside of the

The most feared pathophysiological effect of sepsis is the disturbance of the cardiovascular system through vasodilation and fluid loss from the vascular system into the tissue induced by elevated NO• concentrations. The successive drop in blood pressure and reduced supply of tissues leads to systemic circulatory failure and death of the patient. Inhibitor studies have shown that PARP-1 is not only involved in DNA repair, but also in septic shock. Hauschildt and coworkers have shown that the induction of pro-inflammatory cytokines by LPS treatment of macrophages could be prevented by inhibiting PARP (Hauschildt et al., 1997). An anti-inflammatory effect of PARP activity suppression either induced by Parp1 gene knockout or pharmacological inhibition was also reported (Szabó et al., 1997). Also, LPS treatment of rats led to weakened endothelial functions, which could be alleviated by administration of PARP inhibitor 3-aminobenzamide (3AB) (Szabó et al., 1996).

DIC develops as a consequence of systemic activation and consumption of the clotting factors; It does not occur by itself but as a complicating factor from another underlying condition such as sepsis, trauma, head injury, burns, hemorrhage, end stage liver disease, and snake envenomation. Clinically, it can range from mild to severe, and may lead to massive bleeding, the formation of thrombi, and multiorgan dysfunction/failure. Regardless of the triggering event of DIC, once initiated, the pathophysiology of DIC is similar in all conditions. One critical mediator of DIC is the release of a transmembrane glycoprotein called tissue factor (TF) After exposure to inflammatory proteins, TF is thought to activate the coagulation cascade throughout