Sepsis An Overview Health And Social Care Essay

Sepsis is an infection of the bloodstream. The infection tends to spread quickly and often is difficult to recognize. One of our roles as a nurse is that of patient advocate, and as such we are closest to the patient, placing us in a key position to identify any subtle changes at their earliest onset and prevent the spread of severe infection. Knowledge of the signs and symptoms of SIRS, sepsis, and septic shock is key to early recognition. Early recognition allows for appropriate treatment to begin sooner, decreasing the likelihood of septic shock and life-threatening organ failure. Once sepsis is diagnosed, early and aggressive treatment can begin, which greatly reduces mortality rates associated with sepsis.

sepâ€¢sis (Ëˆsep-sÉ™s) n. Sometimes called blood poisoning, sepsis is the body’s often deadly response to infection or injury (Merriam-Webster, 2011)

Sepsis is a potentially life-threatening condition caused by the immune system’s reaction to an

infection; it is the leading cause of death in intensive care units (Mayo Clinic Staff, Mayo Clinic

2010). It is defined by the presence of 2 or more SIRS (systemic inflammatory response

syndrome) criteria in the setting of a documented or presumed infection (Rivers, McIntyre,

Morro, Rivers, 2005 pg 1054). Chemicals that are released into the blood to fight infection

trigger widespread inflammation which explains why injury can occur to body tissues far from

the original infection. The body may develop the inflammatory response to microbes in the

blood, urine, lungs, skin and other tissues. Manifestations of the systemic inflammatory

response syndrome (SIRS) include abnormalities in temperature, heart, respiratory rates and

leukocyte counts. This is a severe sepsis that arises from a noninfectious cause. The condition

may manifest into severe sepsis or septic shock.

Severe sepsis is characterized by organ dysfunction, while septic shock results when blood

pressure decreases and the patient becomes extremely hypotensive, even with the administration

of fluid resuscitation (Lewis, Heitkemper, Dirksen, O’Brien and Bucher (2007), pg 1778). The

initial presentation of severe sepsis and septic shock is usually nonspecific. Patients admitted

with relatively benign infection can progress in a few hours to a more devastating form of the

disease. The transition usually occurs during the first 24 hours of hospitalization (Lewis, et al

2007, pg 1779). Severe sepsis is associated with acute organ dysfunction as inflammation may

result in organ damage (Mayo Clinic Staff, Mayo Clinic 2010). As severe sepsis progresses,

it begins to affect organ function and eventually can lead to septic shock; a sometimes fatal drop

in blood pressure.

People who are most at risk of developing sepsis include the very young and the very old,

individuals with compromised immune systems, very sick people in the hospital and those who

have invasive devices, such as urinary catheters or breathing tubes (Mayo Clinic Staff, Mayo

Clinic, 2010). Black people are more likely than are white people to get sepsis and black men

face the highest risk (Mayo Clinic Staff, Mayo Clinic 2010).

Severe sepsis is diagnosed if at least one of the following signs and symptoms, which indicate

organ dysfunction, are noted; areas of mottled skin, significantly decreased urine output, abrupt

change in mental status, decrease in platelet count, difficulty breathing and abnormal heart

function (Lewis et al, 2007 pg 1779). To be diagnosed with septic shock, a patient must have the

signs and symptoms of severe sepsis plus extremely low blood pressure (Mayo Clinic Staff,

Mayo Clinic 2010).

Sepsis is usually treated in the ICU with antibiotic therapy and intravenous fluids. These

patients require preventative measures for deep vein thrombosis, stress ulcer and pressure ulcers.

Hunter (2006) explains that the reason why sepsis is rarely given attention and popularized for

public information and attention is because it is not a disease in itself, but a reaction of the body

to a lowered immunological response.

Sepsis is the leading cause of death in non-coronary intensive care units (ICUs) and the 10th

leading cause of death in the United States overall (Slade, Tamber and Vincent, 2010, pg 2). The

incidence of severe sepsis in the United States is between 650,000 and 750,000 cases. Over 10

million cases of sepsis have been reported in the United States based on a 22-year period study

of discharge data from 750 million hospitalizations Annually, approximately 750,000 people

develop sepsis and more than 200,000 cases are fatal (Slade, et al 2010, pg 1). More than 70% of

these patients have underlying co-morbidities and more than 60% of these cases occur in those

aged 65 years and older (Slade, et al 2010, pg 1). When patients with human immunodeficiency

virus are excluded, the incidence of sepsis in men and women is similar. A greater number of

sepsis cases are caused by infection with gram-positive organisms than gram-negative

organisms, and fungal infections now account for 6% of cases (Slade, et al 2010, pg 1). After

adjusting for population size, the annualized incidence of sepsis is increasing by 8%. The

incidence of severe sepsis is increasing greatest in older adults and the nonwhite population. The

rise in the number of cases is believed to be caused by the increased use of invasive procedures

and immunosuppressive drugs, chemotherapy, transplantation, and prosthetic implants and

devices, as well as the increasing problem of antimicrobial resistance (Slade, et al 2010, pg 1).

Despite advances in critical care management, sepsis has a mortality rate of 30 to 50 percent and

is among the primary causes of death in intensive care units ((Brunn and Platt, 2006, 12: 10-6).

It is believed that the increasing incidence of severe sepsis is due to the growing population

among the elderly as a result of increasing longevity among people with chronic diseases and the

high prevalence of sepsis developing among patients with acquired immune deficiency syndrome

(Slade, et al 2010, pg 1).

During an infection, the body’s defense system is activated to fight the attacking pathogens.

These invading pathogens, especially bacteria, possess receptive lipopolysaccharide (LPS)

coverings or release exotoxins and endotoxins that activate the T-cells and macrophages and

trigger the Toll-like receptors (TLR’s) to respond by releasing antibodies, eicosanoids and

cytokines such as tumor necrosis factor (TNF) and interleukins. The antigens may also result in

the production of lysozymes and proteases, cationic proteins and lactoferrin that can recognize

and kill invading pathogens. Different microbes also induce various profiles of TNF and

interleukin to be released. These molecules results in a heightened inflammatory response of the

body and vascular dilation. The TLR’s also affect a different cascade that involves coagulation

pathways, which results in preventing the bleeding to occur at the area of infection. With too

much molecular responses and signals, the recognition of the molecules sometimes fails and

attacks even the body’s endothelial cells. These compounded immune and inflammatory actions

result in the development of the symptoms of sepsis (Hunter, 2006 pg 668; Van Amersfoort,

2001 pg 400). Brunn and Platt (2006) believes that events leading to breakdown of the tissue

such as injuries or infection, that naturally results in the activation of the immune system, is a

major event that causes sepsis. During host infection, the release of tumor necrosis factor and

interlekin-1 signals the dilation of the arteries and inflammation. These released cytokines also

activate the coagulation pathway to prevent fibrinolysis but an increase in the concentration of

these molecules may result in abnormalities in the host’s defense system (Gropper, 2004 pg 568).

The common belief that sepsis is caused by endotoxins released by pathogens has fully been

established but genomic advancements is shedding light on current insights that sepsis can also

occur without endotoxin triggers, that is even without microbial infections (Gropper, 2004 pg

568).

Diagnosing sepsis can be difficult because its signs and symptoms can be caused by other

disorders. Doctors often order a battery of tests to try to pinpoint the underlying infection. Blood

tests and additional laboratory tests on fluids such as urine and cerebrospinal fluid to check for

bacteria and infections and wound secretions, if an open wound appears infected. In addition,

imaging tests to visualize problems such as x-ray, computerized tomography (ct), ultrasound and

magnetic resonance imaging (mri) to locate the source of an infection are also ordered. Early,

aggressive recognition boosts a patient’s chances of surviving sepsis.

Sepsis should be treated as a medical emergency. In other words, sepsis should be treated as

quickly and efficiently as possible as soon as it has been identified. This means rapid

administration of antibiotics and fluids. A 2006 study showed that the risk of death from sepsis

increases by 7.6% with every hour that passes before treatment begins. (Mayo Clinic Staff, Mayo

Clinic 2010). Early, aggressive treatment boosts the chances of surviving sepsis. People with

severe sepsis require close monitoring and treatment in a hospital intensive care unit. Lifesaving

measures may be needed to stabilize breathing and heart function. (Mayo Clinic Staff, Mayo

Clinic 2010). People with sepsis usually need to be in an intensive care unit (ICU). As soon as

sepsis is suspected, broad spectrum intravenous antibiotic therapy is begun. The number of

antibiotics may be decreased when blood tests reveal which particular bacteria are causing the

infection. The source of the infection should be discovered, if possible. This could mean more

testing. Infected intravenous lines or surgical drains should be removed, and any abscesses

should be surgically drained. Oxygen, intravenous fluids, and medications that increase blood

pressure may be needed. Dialysis may be necessary if there is kidney failure, and a breathing

machine (mechanical ventilation) if there is respiratory failure (Mayo Clinic Staff, Mayo Clinic,

2010).

While severe sepsis requires treatment in a critical care area, its recognition is often made

outside of the Intensive Care Unit (ICU). With nurses being at the side of a patient from

admission to discharge, this places them in an ideal position to be first to recognize sepsis.

Thorough assessments are crucial and being able to recognize even the most minimal changes in

a patient could be the difference between life and death.

Once severe sepsis is confirmed, key aspects of nursing care are related to providing

comprehensive treatment. Pain relief and sedation are important in promoting patients’ comfort.

Meeting the needs of patients’ families is also an essential component of care. Research on the

needs of patients’ families during critical illness supports provision of information as an

important aspect of family care (Gropper et al, 2004 pg. 569). Teaching patients and their

families is also essential to ensure that they understand various treatments and interventions

provided in severe sepsis.

Ultimately, prevention of sepsis may be the single most important measure for control

(Mayo Clinic Staff, Mayo Clinic, 2010). Hand washing remains the most effective way to

reduce the incidence of infection, especially the transmission of nosocomial infections in

5 Priority Nursing Diagnosis

Diagnosis #1: Deficient fluid volume related to vasodilatation of peripheral vessels leaking of capillaries.

Intervention #1: Watch for early signs of hypovolemia, including restlessness, weakness, muscle cramps, headaches, inability to concentrate and postural hypotension. .

Rationale #1: Late signs include oliguria, abdominal or chest pain, cyanosis, cold clammy skin, and confusion (Kasper et al, 2005).

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Intervention #2: Monitor for the existence of factors causing deficient fluid volume (e.g., vomiting, diarrhea, difficulty maintaining oral intake, fever, uncontrolled type 2 diabetes, diuretic therapy).

Rationale #2: Early identification of risk factors and early intervention can decrease the occurrence and severity of complications from deficient fluid volume. The gastrointestinal system is a common site of abnormal fluid loss (Metheny, 2000).

Intervention #3: Monitor daily weight for sudden decreases, especially in the presence of decreasing urine output or active fluid loss. Weigh the client on the same scale with the same type of clothing at same time of day, preferably before breakfast.

Rationale #3: Body weight changes reflect changes in body fluid volume (Kasper et al, 2005). Weight loss of 2.2 pounds is equal to fluid loss of 1 liter (Linton & Maebius, 2003).

Diagnosis #2: Imbalanced nutrition less than body requirements related to anorexia generalized weakness.

Intervention #1: Monitor for signs of malnutrition, including brittle hair that is easily plucked, bruise, dry skin, pale skin and conjunctiva, muscle wasting, smooth red tongue, cheilosis, “flaky paint rash” over lower extremities and disorientation (Kasper, 2005).

Rationale #1: Untreated malnutrition can result in death (Kasper, 2005).

Intervention #2: Recognize that severe protein calorie malnutrition can result in septicemia from impairment of the immune system or organ failure including heart failure, liver failure, respiratory dysfunction, especially in the critically ill client.

Rationale #2: Untreated malnutrition can result in death (Kasper, 2005)

Intervention #3: Note laboratory test results as available: serum albumin, prealbumin, serum total protein, serum ferritin, transferring, hemoglobin, hematocrit, and electrolytes.

Rationale #3: A serum albumin level of less than 3.5 g/100 milliliters is considered and indicator of risk of poor nutritional status (DiMaria-Ghalli & Amella, 2005). Prealbumin level was reliable in evaluating the existence of malnutrition (Devoto et al, 2006).

Diagnosis #3: Ineffective tissue perfusion related to decreased systemic vascular resistance.

Intervention #1: If the client has a period of syncope or other signs of a possible transient ischemic attack, assist the client to a resting position, perform a neurological assessment and report to the physician.

Rationale #1: Syncope may be caused by dysrhythmias, hypotension caused by decreased tone or volume, cerebrovascular disease, or anxiety. Unexplained recurrent syncope, especially if associated with structural heart disease, is associated with a high risk of death (Kasper et al, 2005).

Intervention#2: If the client experiences dizziness because of postural hypotension when getting up, teach methods to decrease dizziness, such as remaining seated for several minutes before standing, flexing feet upward several time while seated, rising slowly, sitting down immediately if feeling dizzy and trying to have someone present when standing.

Rationale #2: Postural hypotension can be detected in up to 30% of elderly clients. These methods can help prevent falls (Tinetti, 2003).

Intervention #3: If symptoms of a new cerebrovascular accident occur (e.g., slurred speech, change in vision, hemiparesis, hemiplegia, or dysphasia), notify a physician immediately.

Rationale #3: New onset of these neurological symptoms can signify a stroke. If the stroke is caused by a thrombus and the client receives thrombolytic treatment within 3 hours, effects can often be reversed and function improved, although there is an increased risk of intracranial hemorrhage (Wardlaw, et al, 2003)

Diagnosis #4: Ineffective thermoregulation related to infectious process, septic shock.

Intervention #1: Monitor temperature every 1 to 4 hours or use continuous temperature monitoring as appropriate.

Rationale #1: Normal adult temperature is usually identified as 98.6 degrees F (37 degrees C) but in actuality the normal temperature fluctuates throughout the day. In the early morning it may be as low as 96.4 degrees F (35.8 degrees C) and in the late afternoon or evening as high as 99.1 degrees F (37.3 degrees C). (Bickely & Szilagyj, 2007). Disease injury and pharmacological agents may impair regulation of body temperature (Kasper et al, 2005).

Intervention #2: Measure the temperature orally or rectally. Avoid using the axillary or tympanic site.

Rationale #2: Oral temperature measurement provides a more accurate temperature than tympanic measurement (Fisk & Arcona, 2001; Giuliano et al, 2000). Axillary temperatures are often inaccurate. The oral temperature is usually accurate even in an intubated clients (Fallis, 2000). The SolaTherm and DataTherm devices correlated strongly with core body temperatures obtained from a pulmonary artery catheter (Smith, 2004). A study performed in Turkey found that axillary and tympanic temperatures were less accurate than oral temperatures (Devrim, 2007).

Intervention #3: Take vital signs every 1 to 4 hours, noting changes associated with hypothermia; first, increased blood pressure, pulse and respirations; then decreased values as hypothermia progresses.

Rationale #3: Mild hypothermia activates the sympathetic nervous system, which can increase the levels of vital signs; as hypothermia progresses, the heart becomes suppress, with decreased cardiac output and lowering of vital sign readings (Ruffolo, 2002; Kaper et al, 2005).

Diagnosis #5: Risk for impaired skin integrity related to desquamation caused by disseminated intravascular coagulation.

Intervention #1: Monitor skin condition at least once a day for color or texture changes, dermatological conditions, or lesions. Determine whether the client is experiencing loss of sensation or pain.

Rationale #1: Systemic inspection can identify impending problems early (Ayello & Braden, 2002; Krasner, Rodeheaver & Sibbald, 2001).

Intervention #2: Identify clients at risk for impaired skin integrity as a result of immobility, chronological age, malnutrition, incontinence, compromised perfusion, immunocompromised status or chronic medical conditions such as diabetes mellitus, spinal cord injury or renal failure.

Rationale #2: These client populations are known to be at high risk for impaired skin integrity (Maklebust & Sieggreen, 2001: Stotts & Wipke-Tevis, 2001). Targeting variables (such as age and Braden Scale Risk Category) can focus assessment on particular risk factors (e.g., pressure) and help guide the plan of prevention and care (Young et al, 2002).

Intervention #3: Monitor the client’s skin care practices, noting type of soap or other cleansing agents used, temperature of water and frequency of skin cleansing.

Rationale #3: Individualize plan according to the client’s skin condition, needs, and preference (Baranoski, 2000).

As a nursing student with a strong interest in working with trauma patients, I am intrigued by

the fact that as to why some trauma patients are more susceptible to contracting sepsis than

others. Therefore my suggestion for future research would be to determine if there is an

underlying factor that we, as healthcare professionals are overlooking. Apparently, I am not

alone in my thinking and in performing additional reading on sepsis I was pleasantly surprised to

learn that an investigation into this matter is underway. Hinley (2010), a staff writer for Medical

News Today, reports how an emergency room nurse’s curiosity about why some trauma patients

develop sepsis while others don’t has led to an expanded career as a researcher studying the

same, burning question.

Dr. Beth NeSmith, assistant professor of physiological and technological nursing in the

Medical College of Georgia School of Nursing received a three-year, $281,000 National

Institutes of Health grant in September, 2010 to examine risk factors for sepsis and organ failure

following trauma. Based on her own research, Dr. NeSmith concluded that trauma kills more

than 13 million Americans annually and sepsis is the leading cause of in-hospital trauma deaths,

yet little data existed to explain differences in population vulnerability to these deadly outcomes.

NeSmith believes lifetime chronic stress may be the culprit and a simple test on hair may identify

those at risk. Her theory is that a person who grows up with chronic stress, such as socio-

economic stress or abuse, will have a different response to trauma in terms of their inflammation

profile,” NeSmith said. “Inflammation is a normal body response to trauma, but if it gets out of

hand it’s dangerous. The only care for it is supportive until – if – the body gets better.” (Hinley,

P., Medical News Today, 2010)

As the trauma clinical nurse specialist at MCG Health System from 1997-2003, NeSmith was

intrigued by the limited treatment options available for sepsis. Her grant will allow her to test the

theory that people with existing chronic stress respond differently physiologically to trauma than

non-stressed individuals. NeSmith spends three days a week in the lab working with basic

science research techniques.

Nurses play a critical role in improving outcomes for patients with sepsis. To save the lives of

those with sepsis, all nurses, no matter where they work, must develop their skills for

recognizing sepsis early and initiating appropriate therapy. With nurses dedicated to

understanding and stopping this deadly disorder, the goal of reducing mortality will be realized.

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