Causes And Effect Of Sepsis And Inflammation

Risk factors for infection can be anything that suppresses the ability of the host to resist the infectious pathogen, including the following: drugs, such as steroids and chemotherapy; disorders that affect the innate and adaptive immune responses, such as cancer, leukopenia, and HIV/AIDS; and a breakdown of the first line of defense, such a trauma, broken skin, or surgical wounds. Patients are at risk for developing sepsis and septic shock if they are very old or very young and have and inability to fight off the infection. Some other risk factors for the

According to information published by the Mayo Clinic, sepsis has three stages: sepsis, severe sepsis and septic shock. The mortality rate for septic shock is nearly 50 per cent, and an episode of severe sepsis increases the risk of future infections. Severe sepsis causes blood flow to the vital organs, such as the brain, heart and kidneys, to become impaired. Sepsis can also cause blood clots to form in organs and extremities such as arms, legs, fingers and toes, which can lead to organ failure and tissue death (gangrene).

As sepsis progresses, tissues become less perfused and acidotic, compensation begins to fail, and the patient begins to show organ dysfunction. The cardiovascular system also begins to fail, the blood pressure does not respond to fluid resuscitation and vasoactive agents, and signs of end-organ damage are evident (e.g., renal failure, pulmonary failure, hepatic failure). As sepsis progresses to septic shock, the blood pressure drops, and the skin becomes cool, pale, and mottled. Temperature may be normal or below normal. Heart and respiratory rates remain rapid. Urine production ceases, and multiple organ dysfunction progressing to death occurs. Adventitious lung sounds occur throughout the lung fields, not just in the upper fields of the lungs.

This leads us to the next step in the pathophysiology of Sepsis. Stage 2 of sepsis, which is when SIRS plus the confirmation of an infection has been made. At this stage, the patient’s body has been continuously fighting something in their body and it is starting to have an effect on the patient. Signs and symptoms of sepsis are often nonspecific and include the following: Fever, chills, or rigors, Confusion, Anxiety, Difficulty breathing, Fatigue, malaise, Nausea and vomiting. It is important to identify any potential source of infection. Localizing signs and symptoms referable to organ systems may provide useful clues to the etiology of sepsis and are as follows: Head and neck infections: Severe headache, neck stiffness, altered mental

The unresolved infection has landed the patient on septic shock. Sepsis is the body’s response to inflammation of a particular or unknown infection. The presence of hypotension despite adequate fluid infusion and inadequate tissue perfusion is the result of septic shock. The treatment of shock is centered on the restoration of blood pressure to normal, the presence of adequate tissue perfusion, making sure organs return to functioning well, and avoiding further complications (Lewis, Dirksen, Heitkemper, Bucher, & Harding,

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

The fundamental principle of the phenomenon known as sepsis is an amplified immune response to a pathogen. It is important to note that the insult originates from the excessive host response to, rather than the pathogenicity of, the infective agent1. The upregulation of pro-inflammatory (TNF-α, IL-1α/β, IL-6, IL-12, IFN-γ, and MIF) and anti-inflammatory (IL-10, TGF-β, and IL-4) mediators have been found in various sepsis states2. The exact function, value, and limits of this peculiar, and extravagant, immune response is not fully understood3. Historically, sepsis and processes within the sepsis spectrum have been difficult to truly identify and diagnose1. In 2012, the Surviving Sepsis Campaign identified three major categories of the phenomenon: sepsis, severe sepsis, and septic

Sepsis is the body’s response to infection. The onset of sepsis is often undetected until the condition has become critical. Sepsis progresses into severe sepsis, septic shock, and eventually death; typically from organ failure. The condition affects over 500,000 individuals annually, has a mortality rate of over 25%, and presents a risk to patients in every inpatient setting regardless of acuity level (Whelchel et al., 2011). My first experience with sepsis was enlightening because it affected a patient under my care. I was surprised at the insidious onset of the symptoms, the rapid decline in the patient’s condition, and the missed opportunities that the healthcare team had to implement the recommended care bundle protocols.

Septic shock is the stage of sepsis when multiple organ failure is evident and uncontrolled bleeding of the body occurs. Septic shock results from the complication of an infection where toxins initiate a full body inflammatory response. Viral, fungal, and bacterial infections can all lead to septic shock, but the most common causes of sepsis are gram- negative bacteria and gram-positive bacteria. Sepsis causes severe hypovolemic shock and hypodynamic cardiac function to affect the body, platelets and clotting factors are consumed and thus the body cannot clot blood. Capillary leak occurs and cardiac contractility is poor from cellular ischemia (Ignatavicius & Workman, 2011). For a person to be diagnosed with septic shock, they must have symptoms

LBP is an acute-phase reactant that forms a complex with LPS. The LPS-LBP complex binds to CD14 and to the Toll-like receptor 4/MD2-complex resulting in transcription of cytokines and other pro-inflammatory mediators [5, 6]. In human serum, LBP is constitutively present at a concentration of 5 to 10 μg/ml [17]. During sepsis, LBP levels increase to median peak levels of 30-40 μg/ml within 24 h [7, 8, 17 These properties made LBP promising for the diagnosis of sepsis. Indeed, a good discrimination between SIRS and sepsis was reported].

Sepsis is a life-threatening response to an infection and is the leading cause of death for hospitalized patients. It is estimated that 1.6 million hospitalized patients are treated for sepsis annually, with the approximate health care cost of $16.7 billion dollars. The mortality rate for sepsis is estimated to be as high as fifty percent. However, research evidence shows that early detection of sepsis can improve survival rates by twenty percent (Winterbottom, 2012, p. 247). In 2010, the Surviving Sepsis Campaign created evidence-based guidelines to improve outcomes for patients with early sepsis, and to create awareness and education for health care professionals regarding the impact of early detection (Levy et al., 2010). Recommendations for the early detection of sepsis include specific monitoring of lab work and vital signs, goal-directed therapy such as fluid replacement, and the early administration of the appropriate board-spectrum antibiotic’s.

Sepsis can develop into septic shock which is the point where the patient’s blood pressure drops to a dangerous level due to the presence of bacteria in the body.

Sepsis and Septic Shock have been my personal topic after the life of young Kamil Williams and a 31-year-old Texas man who both contacted a bacterial infection later turn into sepsis. Although I have not formally studied it during my school or university years, I still find the human body, how it can break down and react to certain ailments interesting. The next question would be why does this happen? Well when there is infection or insult upon the body’s immune system normal reacts and causing an inflammatory response. This normally a good thing and it promotes healing and the resolution of the insult, however in Septic Shock the inflammatory response comes explosive and uncontrollable. According to Allison Hotujec, the author of “Severe Sepsis and Septic Shock Protocols,” Sepsis has been called a “malignant intravascular inflammation.” The term malignant is because it is uncontrolled unregulated and self-perpetuating, in the usual immune response here is release of both pro-inflammatory and anti-inflammatory mediators, these balance to promote tissue

To code this one must assign the appropriate code for the underlying infection. Also if it is not clear whether an "acute organ dysfunction is related to the sepsis, question the provider".

There is an immediate surge of cytokines within few hours of the administration of sepsis inducing agents in experimental models of sepsis in animals. An increased level of circulating cytokines such as TNF-α, IL-6, IL-12 and migration inhibitory factor (MIF) of macrophage in sepsis is documented as scientific knowledge Central nervous system (CNS) inflammation and increased level of cytokines in CNS are directly correlated with the increase in seizure susceptibility. Role of increased levels of cytokines secondary to the cause other than central nervous system, in seizure susceptibility is not yet fully elucidated. Research in this arena may point out at novel potential targets for therapeutic intervention of antiepileptic drugs6. The present study was designed to evaluate the seizure susceptibility experimental model of sepsis induced by lipopolysaccharides (LPS).