Sepsis [a word] derived from the Greek verb sepo (meaning “I rot”), has been recognized for millennia and refers to the disseminated inflammatory response elicited by microbial infections. Despite its ancient etymology, sepsis remains a current challenge: it is increasing in frequency, expensive to treat, and lethal, with an associated rate of death as high as 70%.
Lee & Slutsky, 2010
Nancy Murphy, a 46-year-old female, who is in a confused state with a 3-day fever and a wet cough producing yellow bloody sputum, is taken to the emergency department by a friend. In the ED a chest x-ray reveals right lower lobe pneumonia. Vital signs are:
BP 122/68; T 100.1 F; R-22; P-88
The diagnosis is acute pneumococcal pneumonia. Though she is prescribed an antibiotic, because the ER is extremely busy it is overlooked.
After three hours of waiting for a bed she is admitted to the medical/surgical unit. It is two hours more before her antibiotic infusion is given and still no blood culture has been taken. Her responsiveness worsens and her vital signs continue to decline.
A rapid response team is called when her vital signs are:
BP 100/60; T 102.1 F; R-26; P-102; and an Sa02 of 86%
She is moved to ICU, when it is determined she has developed respiratory hypoxia and sepsis.
What is the possible cause for her sepsis and sudden decline? Is the delay in antibiotic administration a causative factor? Why should a blood culture be ordered before the initial antibiotic dose? Would you as the nurse know what to do to identify the cause and prevent further deterioration? What are the different stages of sepsis? What orders would you anticipate to treat sepsis? What can be done for Nancy while she is on your watch and care?
Sepsis is a life-threatening condition caused by an over-reactive immune response to an infection and is a major cause of death globally. Normally, when bacteria or other microbes enter the human body, the immune system efficiently destroys the invaders. In sepsis the immune system goes into overdrive, and the chemicals it releases into the blood to combat the infection trigger widespread inflammation that can ravage the entire body (Recknagel et al., 2012).
Most often, the infection is bacterial, but infections of fungi, viruses, and protozoa can also trigger sepsis. The infection can be bloodborne or limited to one small area—but once a septic reaction is triggered, the resulting damage is widespread, extensive, and life threatening.
People who are elderly, immunocompromised, or neutropenic (have an abnormally low levels of white blood cells) are the most likely to develop a septic response to an infection. Because of our aging population and because medical care is increasing the longevity of immunocompromised patients, the cases of sepsis are increasing in the United States. Because there is difficulty identifying causes of death due to sepsis on death certificates the Centers for Disease Control and Prevention (CDC) estimate between 300 and 1000 deaths/100,000 are due to sepsis in the United States (Gaieski, 2013). It is significant that each year from 2004 to 2009 the incidence and prevalence of sepsis increased approximately 13% each year and a mortality rate of 35% to 50% was seen (Surviving Sepsis Campaign, 2011).
In a classic systemic infection, such as a strep throat, the body’s immune response is self-limiting: the immune forces are called into action, the battle is fought, and the army retires. Sepsis begins like a typical infection and often it presents with the signs of a classic systemic infection—fever, tachycardia, tachypnea, and an elevated white blood cell count. However, in sepsis the natural checks and balances fail. Instead of tapering off and disappearing, the inflammatory forces spread beyond the infected region.
The response begins as pro-inflammatory signal molecules enter the bloodstream in large numbers. As they travel through the vascular system, these molecules cause dilation and leaking of the endothelium that lines the blood vessels, causing damage. The usual orderly movement of oxygen, nutrients, and fluids through the capillary walls is disrupted and organs become hypoxic.
If the sepsis continues, organ hypoxia and damage becomes organ failure, and at this point the condition is called severe sepsis. Severe sepsis increases the likelihood that the patient will die. When the organ system that fails is the circulatory system, the arterial wall muscles can no longer contract sufficiently to maintain adequate blood pressure. Now the patient is in septic shock, and the chance of surviving declines further (Shapiro et al., 2010).
The systemic collapse that occurs in sepsis is called systemic inflammatory response syndrome (SIRS). SIRS can be triggered by a variety of causes, including noninfectious causes such as pancreatitis, trauma, or burns. When it is triggered by an infection, SIRS is called sepsis and, unlike other types of SIRS, sepsis must be treated with antibiotics to remove or control the primary source of the infection.
Did You Know . . .
To optimize a patient’s chance of survival, sepsis must be treated rapidly and efficiently. Every hour of delay in treatment reduces the average patient’s survival by 8%.
- Disseminated intravascular coagulation (DIC).
- Systemic inflammatory response syndrome (SIRS).
- Acute respiratory distress system (ARDS).
- Acute inflammatory syndrome (AIS).
The average patient who has sepsis spends 2 1/2 to 4 weeks in a hospital. Even with experienced care, approximately 1 in 5 septic patients die. The mortality rate is worse for severe sepsis and for septic shock. Appropriate antibiotics are necessary to treat sepsis successfully, but even the correct antibiotics will not stave off the high mortality rates of sepsis if they are given too late (Daniels, 2011). More public attention was seen after sepsis claimed the life of celebrities Mohammad Ali and Patti Duke.