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.
sep•sis (ˈsep-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
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,
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
hospitalized patients (Mayo Clinic Staff, Mayo Clinic, 2010. Good hand hygiene can be
achieved by using either a waterless, alcohol-based product or antibacterial soap and water with
adequate rinsing. Using universal precautions, adhering to infection control practices, and
instituting measures to prevent nosocomial infections can also help prevent sepsis (Lewis, et al
2007, pg 248). Nursing measures such as oral care, proper positioning, turning, and care of
invasive catheters are important in decreasing the risk for infection in critically ill patients
(Fourrier, Cau-Pottier, Boutigny, Roussel-Delvallez, Jourdain, Chopin, 2005 pg 1730). Newly
released guidelines on the prevention of catheter-related infections stress the use of surveillance,
cutaneous antisepsis during care of catheter sites, and catheter-site dressing regimens to
minimize the risk of infection (Fourrier, 2005 pg. 1731). Other aspects of nursing care such as
sending specimens for culture because of suspicious drainage or elevations in temperature,
monitoring the characteristics of wounds and drainage material, and using astute clinical
assessment to recognize patients at risk for sepsis can contribute to the early detection and
treatment of infection to minimize the risk for sepsis.
Critical care nurses are the healthcare providers most closely involved in the daily care of
critically ill patients and so have the opportunity to identify patients at risk for and to look for
signs and symptoms of severe sepsis (Kleinpell, Goyette, 2003 pg 120). In addition, critical care
nurses are also the ones who continually monitor patients with severe sepsis to assess the effects
of treatment and to detect adverse reactions to various therapeutic interventions. Use of an
intensivist-led multidisciplinary team is designated as the best-practice model for the intensive
care unit, and the value of team-led care has been shown (Kleinpell, et al 2003, pg 121). As key
members of intensivist-led multidisciplinary teams, critical care nurses play an important role in
the detection, monitoring, and treatment of sepsis and can affect outcomes in patients with severe
sepsis (Kleinpell, et al 2003, pg 121).
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).
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.  

Pathophysiology of sepsis | Case Study

Thomas, a 70-year-old man, admitted to hospital with a five-day history of coughing with yellow-green sputum, pyrexia, rigors, poor appetite, mild chest pain and increasing difficulty of breathing.
The initial observations are:
Neurological: Altered neurological status, GCS 11/15. Agitated and confused.
Cardiovascular: Sinus tachycardia, HR 135bpm. Hypotension, 90/45 mmHg.
Respiratory: Tachypnoeic, RR 35bpm. Decreased saturation while receiving 6L O2 through Hudson mask.
Metabolic: Febrile, 39 degree
Renal: Oliguric with 20ml/hr urine output. Indwelling catheter (IDC) was inserted.
The blood test revealed that the patient was suffering from hypernatremia, hyperkalaemia, hyperglycaemia, elevated urea, poor creatinine, increased WCC and low platelet count. The ABG indicated that Thomas was experiencing combined respiratory and metabolic acidosis. Thomas was finally diagnosed as sepsis complicated by the right middle lobe streptococcus pneumonia. He required intubation and invasive ventilation support.
In this case study, the pathophysiology of sepsis will be discussed and the mechanism of synchronised intermittent mandatory ventilation (SIMV) volume control ventilation mode will be explained.
Sepsis is defined as the dysregulated inflammatory response caused by severe infection (Neviere 2015). It has the interchangeable definition as Systemic inflammatory response syndrome (SIRS) while the SIRS is resulted by a suspected or confirmed infectious source (Neviere 2015). The concept of SIRS was first introduced by the American College of Chest Physicians (ACCP) and Society of Critical Care Medicine (SCCM) in 1992 (Kaplan 2014). It is characterised by two or more following symptoms. They are fever of high than 38 degree or hypothermia; tachycardia; tachypnoea or partial pressure of arterial carbon dioxide (PaCO2) less than 32 mmHg; deranged white cell count of more than 12,000/µL or less than 4,000/µL (O’brien et al. 2007). Associated with Thomas’s symptoms, it is clear to see that he was definitely experiencing sepsis. It is because that he was febrile up to 39 degree, tachycardic with heart rate of 135 bpm, and had increased respiratory rate of 35bpm as well as the elevated leucocytes count of 14,000 per microliter. The clinical signs are related to the inflammation process which is activated by the body immune system. Due to the severe infection, a large number of proinflammatory mediators are released which in turn result in the serial inflammatory reaction and extensive tissue damage (Neivere 2015). It is reported that SIRS can lead to high mortality rate because of high occurrence of SIRS induced multiple organ dysfunction syndrome (MODS) (Singh et al. 2009). In the following paragraphs, the pathophysiology of sepsis/SIRS will be more comprehensively examined.
The pathophysiology of SIRS is complex. There are a few elements that need to be emphasised. They are acute stress response, inflammatory process and cytokine storm.
Firstly, stress response is the acute phrase reaction when the body tries to defence against the threatening triggers. Those triggers are also known as ‘stress’. Stress can be caused by daily life events, environmental factors or physical illness (Better Health Channel 2012). In Thomas’s case, the stress response is initiated by infection.
Under the influence of stress, the body steady state is disrupted. To maintain the homeostasis, the stress response is activated to reverse the body balance and redistribute the oxygen and energy to maintain the function of vital organs (Kyrou et al. 2012). Hypothalamus plays a vital role in processing the distress signals (Seaward 2015). Once it senses the stress, it triggers the activation of sympathetic nervous system. The sympathetic nervous system then stimulates the adrenal gland to produce epinephrine. It is also known as adrenaline. The adrenaline can lead to increased heart rate and myocardial contractility; dilated pupils and bronchi; peripheral vasoconstriction; accelerated respiratory rate; decreased digestive activity and increased production of glucose from liver (Seaward 2015).

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In addition, stress can also activate another pathway of stress response. That is the hypothalamic-pituitary-adrenal (HPA) axis (Seaward 2015). It means the stress triggers the release of corticotrophin-releasing factor (CRF) from anterior hypothalamus. The CRF then promotes the pituitary gland to produce adrenocorticoid trophic hormone (ACTH). The ACTH stimulates the production of cortisol and aldosterone through the adrenal cortex. Those corticosteroids can result in increased metabolism, sodium and water retention (Seaward 2015).
Therefore, it is obvious that Thomas was under the effect of stress. He was tachycardic, tachypnoeic and slightly hyperglycaemic due to the effect of sympathetic nervous response. He was oliguric because of the acute kidney injury secondary to the vasoconstriction. His hypernatremia status can be contributed by the impact of aldosterone. He had poor oral intake can be cause by the suppressed digestion function.
Secondly, the inflammatory cascade plays an essential role in the pathophysiology of systemic inflammatory response syndrome. Sagy et al. (2013) summarised the inflammation mediator related mechanisms in the systemic inflammatory response. It is indicated that the excessive release of pro-inflammatory mediators result in the inflammation, inhibit the function of compensatory anti-inflammatory response, and compromise the immune system eventually (Sagy et al. 2013).
Cytokines are the essential components of immune system. Bone et al. (1992) explained that the local cytokines are activated immediately after an insult in order to repair the wound and initiate the innate immune system. Because of the release of local cytokines, a small amount of cytokines go into the circulation. This promotes the production of growth factor and adhesion of macrophages and platelets to help with the recovery of the local damage. However, when the infection is severe and the homeostasis is unable to be restored, cytokine storm occurs.
More specifically, cytokine storm is formed from a complex progression. Cytokines are made up by macrophages, monocytes, mast cells, platelets and endothelial cells, which are the initial immune defensive components (Plevkova 2011). The multitude of cytokines can soon induce the cytokine tissue necrosis factor-alpha (TNF-a) and interleukin-1 (IL-1). Those two elements result in the removal of nuclear factor-KB (NF-KB) inhibitor. This in turn prompts the production of more proinflammatory mediators, such as IL-6, IL8 and interferon gamma (Plevkova 2011). In other words, cytokines stimulate the production of immune cells, which in turn induce more cytokines in the circulation.
The cytokines have a great impact on the body, including direct or indirect contribution of mortality in SIRS. TNFa is discovered causing fever, abnormal haemodynamic values, low white cell count, increased liver enzymes and clotting problems (Jaffer et al. 2010). IL-1 is reported having connection with fever, haemodynamic abnormality, loss of appetite, general weakness, headache and neutrophilia (Jaffer et al. 2010). IL-6 is found having strong relationship with fever and impaired lung function as well as acting a determinant of severity of SIRS and mortality rate (Jaffer et al. 2010). The massive accumulation of cytokines can cause widespreading vasodilatory effect. It is because the cytokines stimulate the release of vasodilators such as nitric oxide (Sprague and Khalil 2009). Additionally, cytokines promotes adhesion of the immune cells and the endothelial cells, which in turn leads to leaky endothelium and loss of fluid from intercellular space to extracellular space (Sprague and Khalil 2009). Moreover, the cytokines cascade can also lead to the clotting disorder. It is because of the high concentration of fibrinogen in the inflammation process (Esmon 2005). The fibrinogen is converted from thrombin, which is generated by tissue factor. Tissue factor is a substance that is expressed by the surface of white cell. It can also be induced by TNFa and endotoxin from the infection (Esmon 2005). The fibrinogen can be transferred into fibrin which in turn forms clots. As the excessive amount of fibrin in the inflammation status, it can result in extensive clotting disorder.
To sum it up, it can be concluded that Thomas’s fever is highly likely related to the release of TNFa, IL-1 and IL-6. IL-1 could be one of the contributors of his poor appetite and elevated white cell count. IL-6 could worsen Thomas’s existing affected lung function. Thomas had increased white cell count can be contributed by the immune response and IL-1. The hypotension is related to the vasodilation effect. Due to the hypotensive, the kidney perfusion dropped and then led to the acute kidney failure and poor urine output. The acute kidney injury may affect the elimination of potassium so that Thomas was found having high potassium level. The low platelet count could be related to the massive production of cytokines and damaged endothelium.
In the next section, the synchronised intermittent mandatory ventilation volume control will be explained as Thomas’s mechanical ventilation management.
The synchronised intermittent mandatory ventilation (SIMV) is commonly used in ICU. With the volume control mode, the patient is given the ventilation support with a set tidal volume during the mandatory breaths (Deden 2010). To provide the effective ventilation support, there are a few specific values that need to be set up for the SIMV volume controlled mode. They are tidal volume and respiratory rate. The tidal volume refers to the amount of oxygen delivered by the ventilator or the amount of oxygen the patient breathes voluntarily. The respiratory rate is set up for mandatory breaths. In the SIMV volume controlled mode, the ventilation is trigger by the ventilator or patient self. It means the actual respiratory rate can be upon the preset rate (Goldsworthy and Graham 2014). There is a window of time for the ventilator to sense the patient’s inspiratory effort. This trigger window helps avoid the ventilator deliver the oxygen when the patient exhales (Deden 2010). If the patient is able to trigger the ventilation within the time frame, the patient-triggered mandatory breath is induced. After reaching the demand tidal volume, the inspiratory phrase ends and expiratory starts. Between each mandatory breaths, the patient is able to initial own spontaneous breath, the breathing volume and length depend on the patient’s respiratory effort (Pierce 2007). If the patient is heavily sedated and unable to initiate the spontaneous breath within the trigger window, the machine-triggered mandatory breath will be activated to provide constant ventilation support according to the set respiratory rate and tidal volume (Deden 2010). Once the ventilator delivers the demand tidal volume, the inspiratory cycle ends and expiratory phrase starts until the next scheduled inspiratory cycle. If the patient’s attempt of breathing is not strong enough to trigger the patient-triggered mandatory breath, the assisted synchronised breath will be provided to achieve the desired the tidal volume. Like the other mode, the inspiratory cycle ends once the set tidal volume is delivered (Deden 2010).
It is believed that Thomas would be beneficial from the SIMV volume controlled mode. It is because that SIMV mode could help him reduce the work of breathing, especially when he was in the high energy-consuming septic status. In addition, due to the SIMV mode, the ventilator allows him to have extra breath to blow off the accumulative carbon dioxide. This can improve his acidosis. Moreover, because of the systemic inflammatory response syndrome and severe pneumonia, his lungs could be stiff and fragile secondary to the inflammation effect and accumulation of cytokines. The volume controlled ventilation acts as a protective strategy to avoid the ventilator related complications, such as volutrauma. It is recommended not to set the tidal volume more than 8-10ml/kg (Deden 2010).
In conclusion, sepsis is a systemic inflammatory response syndrome resulted by the infection. The stress response, inflammation reaction and cytokines play essential roles in the progression of SIRS. As SIRS can cause high mortality rate, it is vital to control the infection and manage the widespreading inflammation as well as providing appropriate support to treat the symptoms. In Thomas’s case, the volume controlled synchronised intermittent mandatory ventilation would be the better option of managing his severe pneumonia and respiratory distress.
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Ying Hu 76898

Causes and Treatments of Sepsis

Sepsis is a major cause of morbidity and mortality in hospitals today. It has been defined as ‘the body’s response to an infection when organisms invade the body’ (Baudouin 2008). It’s an infection which is caused by micro organisms or bacteria’s that invade the body. Sepsis can lead to acute organ dysfunction followed by multi-organ failure and death. In the early stages of sepsis the immune response can be characterised as a systemic inflammatory response syndrome (SIRS) (Chamberlain 2008). This is the body’s response to a variety of severe clinical insults. It is characterised by the presence of two or more of the following features: Temperature >38°C or 90/min, Respiratory rate > 20/min or PaCO2 12 x 109/l altered mental status, blood glucose>7.7mmol/l in absence of diabetes (LTHTR Sepsis Care Pathway 2009).Sepsis is defined as SIRS in response to infection (I, Mackenzie 2001).

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The surviving Sepsis campaign was launched in October (2002) aiming to increase awareness of sepsis, severe sepsis and septic shock among healthcare staff and the general public, develop evidence based guidelines for the management of severe sepsis and ensure that guidelines are put to practice globally. In the Nice Clinical guideline 50- acutely ill patients in Hospital they made key recommendations to ensure early identification of the acutely ill patient and prevent deterioration of condition thus reduce patient mortality, morbidity and length of stay, to reduce ICU admissions and re admission.
Initial management of a critically ill patient includes:

Immediate assessment of the airway, breathing and circulation
Baseline observations HR, RR, BP, O2 sats, capillary refill, EWS and AVPU to assess level of consciousness
A brief history
A limited examination of the relevant systems of the body.
A secondary assessment after stabilisation of the patient including a more thorough history, detailed examination by system and appropriate investigations. The golden hour an early window of opportunity immediate resuscitation with oxygen and fluids prevents secondary injury to organs as a result of hypoxemia and hypovalaemia helping to reduce mortality and morbidity. The timing of clinical intervention is essential to the survival of septic patients (Chamberlain 2008).

Respiratory failure is common and may develop at any stage so repeated assessments are necessary. A depressed conscious level is the most common cause of airway obstruction (I, Mackenzie 2001). A clear airway does not indicate effective breathing. Failure of gas exchange may be caused by lung problems (pneumonia, lung collapse, pulmonary oedema), failure of the mechanics of ventilation. Respiratory failure is suggested by signs of respiratory distress including dyspnoea, increased respiratory rate, use of accessory muscles, cyanosis, confusion, tachycardia, sweating. The diagnosis is made clinically but may be confirmed by pulse oximetry and arterial blood gases. Patients with a depressed conscious level may not react normally to hypoxia and signs of respiratory failure may be difficult to detect. Patients with inadequate ventilation, gas exchange or both require ventilatory support. This usually necessitates intubation and mechanical ventilation although in some patient’s gas exchange and oxygenation can be improved by the application of continuous positive airway pressure (CPAP) by face mask or non-invasive ventilation. As per LTHTR sepsis care pathway (2009) high flow oxygen to be given to maintain a target of >94% using a non rebreath mask. Oxygen to be reduced when patient stable. In critically ill patients, high concentration oxygen should be administered immediately and this should be recorded afterwards in the patient’s health record (BTS guideline for emergency oxygen use in adult patients 2008).
Tachycardia and hypotension are almost universal findings in the septic patient and result from a number of cardiovascular problems. In early sepsis, and in patients who have been partially or fully fluid resuscitated, the low blood pressure and high heart rate are associated with a high cardiac output and a low peripheral vascular resistance with warm peripheries and bounding pulses. In contrast, patients who have not been significantly resuscitated or have presented late in the course of their illness have a low cardiac output and high systemic vascular resistance. These patients are peripherally cold, sweaty, with weak, thready pulses and they need urgent resuscitation. However resuscitation aims to restore circulating volume, cardiac output and reversal of hypotension (I, Mackenzie 2001).
Initially infuse i/v crystalloid or colloid rapidly guided by the clinical response. The optimal resuscitation fluid however, remains the subject of debate. Fluid resuscitation of severe sepsis may consist of natural or artificial colloids or crystalloids. Fluid challenge should be administered and repeated based on response (increase in blood pressure and urine output) and tolerance (V, Jean-louis 2004). Administering large volumes of fluid to patients with known cardiac disease or myocardial dysfunction related to their acute illness is a problem. Ronco, C et al (2004) argued that it is the quantity of fluid given rather than the type of fluid explaining that more crystalloid is needed to achieve the same effect as colloid but colloids are more expensive and carry their own risks. Adequacy of fluid infusion can be facilitated by repeated fluid challenges in which a pre defined amount of fluid e.g. 250 or 500mls is in fused over a set time. Sherman et al (2007) states that aggressive volume resuscitation and administering broad spectrum antibiotics should be given early to all septic patients using 2-4litres of normal saline. All patients should be monitored closely to see the response to resuscitation (urine output mental status, BP). If the patients blood pressure is 40mmgh lower than the patients normal BP fluid challenges nacl 0.9% 500ml given over 5-10mins (ALERT 2003). LTHTR Sepsis Care Pathway 2009 states if patient hypotensive give up to 3 boluses of 500ml (0.9% Saline) to maintain MAP>65/systolic 100mmgh. Urinary catheter hourly urine measurements.
Perform investigations to confirm or clarify problems that are clinically evident, or to look for complications that are likely. Bloods including FBC, coagulation screen, U&E, Liver function, Amylase, cardiac enzymes, Glucose, lactate and ABG’s. Other tests may include a blood glucose, ECG and chest x-ray. You may consider sending samples for microbiology to confirm the presence of infection, i.e. blood cultures should be taken, sputum if suspecting chest infection and mid-stream urine (MSU) or catheter specimen of urine f suspecting urine infection. Blood cultures are only to be taken when there is clinical need to do so and not as routine (DOH 2007). Indepth search for the source of sepsis with rapid institution of appropriate antibiotic therapy. Delayed or initially ineffective antibiotic therapy has been shown to be associated with worse prognosis and if it is important that all likely microbial culprits are covered by the empiric antibiotic which can be altered when culture results are available (Ronco, C et al 2004).
Monitoring is not dependent on expensive equipment, but it requires the continuous presence of trained nursing staff. Clear documentation aids the assessment of subtle changes in the patient’s clinical state. Patients with severe SIRS / sepsis should have observations recorded hourly. Record body temperature, pulse, blood pressure, urine output, CVP, respiratory rate and SpO2 (if available). Accurate fluid balance is essential. An accurate Early Warning Score is essential as per LTHTR trust protocol along with every set of observations taken. EWS used widely throughout the trust it acts as an assessment of recognising deterioration in patients an identifies at risk patients. It requires the charting of observations such as systolic BP, HR, RR on a regular basis each is given a score from 0-3 and then added together to give an EWS. This is then used to trigger further assessment of the patient by senior nursing or medical staff and referral to critical care outreach who support nurses at ward level to tackle early detection and treatment to prevent intensive care admissions. Early detection and recognition of a patient that is deteriorating is vital (DOH 2007).
The initial antibiotic prescription is a ‘best guess’, and will depend on the clinical picture of the patient, local patterns of antibiotic resistance and the local availability of antibiotics. It should be broad enough to cover the most likely pathogens, but not so broad as to encourage antibiotic resistance. The advice of a local microbiologist or infectious diseases specialist is valuable. Surviving Sepsis Campaign (2008) states the choice of antibiotics should be guided by the susceptibility of likely pathogens in the community and the hospital, as well as any specific knowledge about the patient, including drug intolerance, underlying disease, the clinical syndrome.  The regimen should cover all likely pathogens since there is little margin for error in critically ill patients. There is ample evidence that failure to initiate appropriate therapy promptly (i.e., therapy that is active against the causative pathogen) has adverse consequences on outcome. Although restricting the use of antibiotics, and particularly broad-spectrum antibiotics, is important for limiting super infection and for decreasing the development of antibiotic resistant pathogens, patients with severe sepsis or septic shock warrant broad-spectrum therapy until the causative organism and its antibiotic susceptibilities are defined. Shermon et al (2007) states that early use has been clearly demonstrated to reduce the mortality in sepsis an if no known source of infection is present then give broad spectrum antibiotic therapy to cover aerobic and anaerobic infections. LTHTR Sepsis Care Pathway (2009) states antibiotics to be given in first hour and all antibiotics to be reviewed after 48hours.
Medical staff have been implicated in the spread of infectious agents between patients. All staff must wash their hands before and after attending to a patient. Equipment should not be shared between patients if possible, but where this is necessary the equipment should be thoroughly cleaned between patients. Staff should protect themselves and their clothes from becoming contaminated with biological material by wearing disposable aprons and gloves. Visitors should be discouraged from moving between patients. Wounds, including drain sites and intravenous cannulae sites, should be inspected, cleaned and dressed at regular intervals. Intravenous cannulae and central lines should be removed as soon as practical. Ensure correct documentation is filled in i.e. Vascular access device tool, wound charts and care plans as per trust protocol.
In conclusion sepsis remains a major cause of morbidity and mortality in hospitals today. Many authors have looked at best practice in the early recognition and treatment of sepsis. It is vital that nurses and clinicians recognise and treat critically ill patients for the best outcome to reduce the risk of deterioration and potential cardiac arrests. NPSA (2007) Recognising and responding appropriately to early signs of deterioration in hospitalised patients. Within LTHTR trust and other trusts there are many policies in ensuring this with the early recognition policy, early warning scores to help assist the staff on recognising the deteriorating patient and sepsis care pathway to assist with the treatment of the deteriorating patient. With the use of these policy’s and the help of critical care outreach teams within the trust early recognition and treatment within the golden hour reduces the morbidity and mortality thus educing admissions into the intensive care unit. It appears that there remains much discussion into which fluid works best during fluid resuscitation. Trust protocols should be followed. Recognition of ‘at risk’ patients can only be achieved by appropriate and timely assessment and monitoring. Nice made key recommendations in patients at risk policy, assessment and monitoring, response, critical care and staff competencies the LTHTR policy ‘Procedure for the timely recognition and response for patients at risk of deterioration’ encompasses these key recommendations. There is no predictive scoring system which gives accurate predictions of outcome for individual patients. Survival from an episode of severe sepsis is dependent the patient’s age, previous health and the time delay before the onset of medical intervention, as well as the appropriateness and quality of medical care. Few countries have limitless resources, and so difficult decisions face all intensive care doctors when deciding between the potential benefits for one critically ill patient and need for provision of healthcare to several less critically ill patients (I, Mackenzie 2001).
Word Count 2008

Triage Tool for Sepsis Recognition

“Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.  Sepsis and septic shock are major healthcare problems, affecting millions of people around the world each year.  Early identification and appropriate management in the initial hours after sepsis develops improves outcomes,” (Rhodes, et al., 2017). According to the National Institute of Health Statistics, more than a million Americans develop severe sepsis every year.  Between 28 and 50 percent of these people die.  This high mortality rate creates a clinical problem and generates interest in improving the care of septic patients.

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The systemic inflammatory response syndrome (SIRS) criteria served
as the original definition of sepsis. 
SIRS definition contains two or more of the following: temperature
greater than 38 degrees Celsius or less than 36 degrees Celsius, heart rate
greater than 90 beats per minute, respiratory rate greater than 20 breaths per
minutes or PaCO2 less than 32mmHg, and white blood cell count greater than
12,000/mm3 or less than 4,000/mm3 or greater than 10%
immature bands.  Another tool to identify
organ dysfunction is the quick Sequential Organ Failure Assessment (qSOFA). Two
points is a positive qSOFA, with increasing points patient outcomes are
associated with higher mortality rates (Bhattacharjee, Edelson, & Churpek,
2017). Quick Sequential Organ Failure Assessment (qSOFA) criteria contains:
respiratory rate greater than or equal to 22 breaths per minutes, altered
mentation, and systolic blood pressure less than 100mmHg. These two, SIRS and
qSOFA, are sepsis recognition tools.
Emergency departments play a vital role in identifying,
treating, and managing septic patients. 
The problem with SIRS criteria as a screening tool for sepsis is
patients presenting to an emergency department do not have these laboratory
tests, white blood cell and PaCO2, drawn hours prior to arrival.  This is one component that cannot be
incorporated into a triage screening tool but updated throughout the stay in an
emergency department.  Unless two other
vital signs are abnormal there is potential to fail at recognizing a septic
patient initially presenting to an emergency department.  Similarly, the qSOFA criteria has shown high
specificity to sepsis and poorer outcomes (Bhattacharjee, Edelson, &
Churpek, 2017).
Sepsis recognition is not enough to decrease risk of
mortality in septic patients. Kumar, et al. (2006) discovered an association
between effective antimicrobial administration within the first hour of
documented hypotension increased survival in adults with septic shock. The 2016
International Sepsis Guidelines strongly recommends administration of IV
antimicrobials initiation within one hour of sepsis recognition. The best way
to improve patient outcomes for septic patients is to identify those with
sepsis. The second way is to manage the septic patient, which includes
initiation of antibiotics. To assess this clinical problem, the PICO question
formulated is, in adult septic
patients, how does a sepsis triage screening tool based on qSOFA, compared to
the current 2+SIRS criteria, affect door to antibiotic time?
An electronic literature search was conducted using the
CINAHL database. The search included 4 keywords: sepsis, antibiotic
administration, SIRS, and qSOFA. All searches conducted were restricted to
adults, 2010-2017-time frame, and articles in English. My first search resulted
in 3,527 articles. A focus on articles that used SIRS or qSOFA for
identification took priority. These terms, SIRS and qSOFA, were searched title
specific.  This resulted in a final 289
articles. A secondary electronic literature search with the keyword of ‘nursing
intervention and sepsis’ showed a few hundred articles. The research question
was assessed using four journal articles that were peer reviewed. The
independent variables were qSOFA and SIRS.
Summary of Evidence
Tromp, Hulscher, Bleeker-Rovers et al. (2010) researched the effects of a nurse driven implementation of a sepsis protocol care bundle. A prospective before and after intervention study at an emergency department of a university hospital in the Netherlands was conducted using three different five month increments. Period 1, July 1, 2006 – November 6, 2006, occurred before introducing the new care bundle based sepsis protocol. Period 2, November 6, 2006 – June 25, 2007, occurred after the sepsis protocol was put into place and before training. Period 3, June 25, 2007 – October 1, 2007, was after training and performance feedback. The sepsis care bundle consisted of seven elements. Six elements were required, the seventh was not required unless the patient was hypotensive or had an elevated serum lactate. The bundle included: measuring serum lactate concentration within six hours, obtaining two blood cultures before starting antibiotics, taking a chest radiograph, taking a urine sample for urinalysis and culture, starting antibiotics within three hours, hospitalize or discharge the patient within three hours, and volume resuscitation for serum lactate >4.0mmol/L or hypotension. The researchers used 2+ SIRS criteria to identify septic patients entering the emergency department. The sample size included 825 people, 16 years of age or older (Tromp, Hulscher, Bleeker-Rovers et al., 2010).
The findings showed that implementing a nurse-driven
sepsis care bundle provided an increase in early recognition of sepsis in
patients presenting to the emergency department. Additionally, when staff received
education and training on this intervention, compliance to the bundle improved
early recognition and treatment of patients with sepsis. Compliance to the
complete sepsis care bundle increased from 3.5% to 12.4%. This study measured antibiotics
started within three hours after staff training. Antibiotic administration
increased from which increased from 38% to 56%. These results are statistically
and clinically significant. Evidence exists that delay in care for septic
patients leads to worse outcomes (Bhattacharjee, Edelson, & Churpek, 2017).
This intervention study provides level IV (Melnyk & Fineout-Overhold, 2015)
evidence for an increased compliance to implementing a sepsis care bundle after
training. Some limitations to the study include that is was an uncontrolled study
at a single center and only one year in length. Having a broader understanding
of this disease across multiple countries and over extended periods of time
would improve the validity of the results. Strengths of this study include the
large sample size, nurse driven implementation, and SIRS criteria for sepsis
screening. Another strength is that this study, like other studies, reveal
education improves sepsis recognition and sepsis care. From this study, it can
be determined that the training and implementation of a sepsis care bundle
increases sepsis recognition and improves adherence to the bundle, improving
patient outcomes.
Yousefi, Nahidian, and Sabouhi (2012) conducted a study
to review the effects of an educational program about sepsis care of intensive
care unit (ICU) nurses.  This study was a
quasi-experimental interventional study with two groups over three time
periods: before, immediately after, and three weeks after.  Nurses with a bachelor’s degree or higher
level of education and one year ICU experience were included in the study.
Infection control committee or members that participated in a similar study
were excluded.  The sample size included thirty-two
nurses randomly enrolled into each of the test and control groups.  The data collection tool was a four-part
questionnaire to measure knowledge, attitude, and practice of ICU nurses.  The results obtained earn Level III evidence
(Melnyk & Fineout-Overholt, 2015).
The findings revealed there was no significant
difference between the control (c) and test (t) groups in terms of age, sex,
education, experience, and employment status. Mean scores of knowledge (t=62.5,
c=63.7), attitude (t=73, c=72.8), and practice (t=81.8, c=82.2) of ICU nurses
in the test and control groups had no significant difference before the
intervention. In the test group, attitude (t=79.7, c=73.3) and practice
(t=90.5, c=82.2) increased immediately after and attitude (t=83.3, c=73.2) continued
to trend up at the three weeks later mark. Education was found to be effective and
have a positive impact on attitude, knowledge, and practice on sepsis care of
ICU nurses, like other studies. The
study did have some limitations which included the ability of the nurses to
utilize books, media, and articles on the subject which could influence the
study.  This study is limited due
to the small sample size.  A larger
sample size in various departments and facilities would strengthen the evidence
and improve clinical significance. One important thing to consider with this
article is that the nurses observed were bachelor’s degree nurses.  Associate degree nurses are the majority of
the nursing workforce.  This could be a
weakness for the article in that they fail to capture the majority education of
nurses. The strength of this study
provides evidence supporting training statistically improved levels of attitude,
knowledge, and practice of ICU nurses in sepsis care.  Findings of this article are like
other studies.
Tarrant, O’Donnell, Martin, Bion, Hunter, & Rooney
(2016), conducted a qualitative design-grounded theory study using focused
ethnography to gain an understanding of the barriers to implementing the sepsis
six bundle components within an hour of recognition of sepsis.  Data collection occurred through various ways
including: over three hundred hours of observations, 43 staff members
interviewed, and shadowing multiple units and staff members across six pilot
hospitals in Scotland from March 2013 – May 2014. The results of this study
provide Level VI evidence (Melnyk, & Fineout-Overholt, 2015). 
The main findings include that the Sepsis Six clinical bundle is not
six simple tasks but a series of complex processes. Gaining a better
understanding of the problems of interruptions and operational failures that
get in the way of task completion is ideal to improve compliance for Sepsis Six
within one hour. The researchers suggest focusing on individual behavior change
to improve compliance to Sepsis Six with a combination of reducing barriers and
challenges in the everyday workflow that are responsible for the delays in
Sepsis Six. The research hypothesizes that there would be greater compliance to
Sepsis Six within one hour window if the everyday barriers and challenges were
reduced. This study is limited to one country, Scotland.  Additionally, the length of study could have
missed problems and barriers associated with night shift.  Night shift tends to run with fewer resources
and less access to providers. Night shift is also associated with less
experience providers. These barriers need to be assessed to gain a better
understanding of delays in compliance to sepsis six bundle.  The strengths of this study lie in the
qualitative perspective to gain a better understanding of barriers to
implementing sepsis six bundle. The study highlights that a focus on education
and knowledge of sepsis is not enough, and emphasize the importance to reducing
barriers to promote ultimate compliance. 
Gunn, Haigh, and
Thomson (2016) conducted a retrospective study, over a six-month period, on
patients presenting to the ED who had a sepsis six form completed.  The emergency department currently uses SIRS
criteria to identify septic patients. 
The purpose of the study was to determine if qSOFA would reliably
identify septic patients within the emergency department population.  The sample size was two hundred patients with
sepsis diagnosis.  One hundred and ninety-five
were positive for SIRS.  Twenty-nine were
positive for qSOFA. SIRS and qSOFA were compared to determine specificity and
sensitivity to identifying septic patients. This article is rated Level IV
evidence (Melnyk & Fineout-Overhold, 2015). 
had a higher sensitivity at 97%, and a 2.4% specificity. qSOFA showed a 90%
specificity and a 48% sensitivity.  SIRS
was reliable in identifying sepsis and qSOFA was reliable with detecting those
required higher levels of care and mortality. These finding show clinical and
statistical significance.  The
researchers conclude that SIRS criteria serves as a useful triage tool in
identifying septic patients.  The
researchers further conclude that once positive SIRS criteria is established
qSOFA should be conducted to assess severity and critical care need. Limitations
of this study include the sample size, location, and length of time where the
study took place.   Increasing the sample size over a longer period of time to gain a
broader population would increase the strength of this article.  This study would be strengthened if an
observation of a larger sample size took place, over a longer period, and over
multiple facilities.  The strength of
this study is the results that provide evidence for SIRS criteria as the better
septic recognition tool.  The results
indicate SIRS is best at identifying sepsis. 
These results are statistically and clinically important.  If qSOFA was used
instead of SIRS, many people would not have been included in a sepsis workup
and could potentially have worse outcomes due to delay in recognition and
sepsis care.  From this article, keeping
SIRS criteria is vital for sepsis recognition. 
However, including a qSOFA could benefit those critically ill in
identifying those at higher risk for worse outcomes. 
et. al (2017) published a retrospective cohort analysis study on the prognostic
accuracy of the SOFA score, SIRS criteria, and a qSOFA within the first 24
hours of admission in discriminating in-hospital mortality among patients with
suspected infection admitted to the ICUs. This study began in 2000 and
continued to 2015. The sample size included 184,875 adults with
infection-related primary admission diagnosis. The study took place in 182 ICUs
in Australia and New Zealand. This study was rate a Level IV using Melnyk & Fineout-Overhold, (2015) evidence appraisal guidelines.
results of this study showed SOFA had significantly greater discrimination for
in-hospital mortality than SIRS criteria or qSOFA.  A SOFA of 2 or more points showed a 90.1%
accuracy in mortality or ICU length of stay of three days or more.  The SIRS score of 2 or more points had a
86.7% accuracy, while a qSOFA score of 2 or more points revealed 54.4%
accuracy.  The overall results favored a
SOFA score over qSOFA and SIRS, showing greater accuracy for in-hospital
mortality.  The
strengths of this study include the duration, sample size, and location. Having
this much diversity in the study decreases variables or outliers altering
results. Additionally, the information gathered utilized a quality-surveillance
data collection process reducing bias. One limitation the researchers address
is the inability to apply this study to emergency department patients. This
study used patients in the ICU. The statistical significance and clinical
significance could be applied to an ICU setting, but for the clinical problem
stated earlier this would not hold clinical significance in an emergency
department setting.  Like the previous
study, the use of SOFA in conjunction with SIRS criteria would be beneficial in
determining those with greater critical care needs for proper placement and to
identify those at higher mortality risk. 

Discussion and Conclusions
Sepsis is a terrible disease with poor outcomes.  Understanding the best recognition tool and management are key to surviving sepsis.  The overall articles bring collective information on improving sepsis recognition and decreasing door-to-antibiotic time.  The studies described range from Level III to Level VI according to Melnyk and Fineout-Overholt’s (2015) level of evidence guide.  Having meta-analysis, randomized control trials, or even well-designed controlled trials without randomization would increase the validity of the results.  As previously stated, education is found effective in increasing knowledge and recognition on sepsis care.  Implementing an educational program on sepsis recognition and care is clinically significant to improve sepsis outcomes. Education should be incorporated into a sepsis care bundle to improve compliance and sepsis recognition. Additionally, if qSOFA or SOFA were used after SIRS criteria to determine critical care status this would increase results and provide knowledge on patient outcomes.
The overall evidence in the studies is not enough to
make changes in clinical practice.  There
is not enough collective strength of evidence to make a change in clinical
practice. However, the articles did support SIRS criteria for greatest
sensitivity to sepsis recognition with qSOFA showing higher sensitivity to
mortality. The sources of evidence support the continuing use of SIRS criteria
for a sepsis triage screening tool. Recognizing sepsis and reducing barriers
are key to improving antibiotic administration. The results of the study showed
the importance of education and reducing barriers to improving sepsis
recognition and management. According to the evidence, SIRS criteria is
providing better recognition for sepsis. The evidence leads to septic patients benefiting
from an additional screening tool, the qSOFA, if they have 2+ SIRS criteria to
rule out higher mortality and critical care needs. Further evidence is needed
on qSOFA replacing SIRS for sepsis identification prior to implementing in the
clinical setting. It appears most evidence conducted is from retrospective
studies. Randomized control trials or meta-analysis would strengthen this claim
for SIRS over qSOFA in emergency department triage screening tool for sepsis
Bhattacharjee, P.,
Edelson, D. P., & Churpek, M. M. (2017). Identifying Patients With Sepsis
on the Hospital Wards. Chest, 151(4), 898-907.
Gunn N, Haigh C, Thomson J.
(2016) Triage of Sepsis Patients: SIRS or qSOFA – Which is best?
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Roberts, D., Wood, K. E., Light, B., Parrillo, J. E., Sharma, S., . . . Cheang,
M. (2006). Duration of hypotension before initiation of effective
antimicrobial therapy is the critical determinant of survival in human septic shock. Critical
Care Medicine, 34(6), 1589-1596. doi:10.1097/01.ccm.0000217961.75225.e9
Rhodes, A., Evans,
L. E., Alhazzani, W., Levy, M. M., Antonelli, M., Ferrer, R., . . . Dellinger, R. P. (2017). Surviving Sepsis Campaign. Critical Care
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the Intensive Care Unit. Jama, 317(3), 290.
Tarrant, C.,
O’Donnell, B., Martin, G., Bion, J., Hunter, A., & Rooney, K. D. (2016). A
complex endeavour: an ethnographic study of the implementation of the Sepsis
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History, Causes and Interventions of Puerperal Sepsis

The purpose of the report is to understand what puerperal sepsis is and to raise awareness of the condition to expectant mothers, women that have miscarried, families and physicians. To understand the risks that is linked with the condition and to be able to spot signs and symptoms, as well as how to prevent further cases through aseptic techniques and principles and hand hygiene.

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The information that will be included is background information on the condition: what is it, how it came about, what treatment was used and what caused it. The report will include information on what are the symptoms, what causes it, who is at risk, how it can be diagnosed, how to treat it, what are the complications and how to prevent further cases from occurring.
The report will focus on national statistics for the UK. This will include statistics to show how the prevalence of puerperal sepsis within the UK has decreased from 1900’s to today through medical advances and research. The research used will be secondary: books, journals, and internet. Primary research will not be used as the report is based on facts and information that is already available through reports and medical advice.
Puerperal sepsis is a term giving to an infection that affect expectant mothers and those who have recently delivered. Infections within pregnancy can be severe as the genital tract has an increased surface area. (Knight, M. 2015). (Awori, N. et al. 1999). The infection can affect the cavity and walls of the uterus, which can lead to pelvic abscesses. The pus can spread high into the pelvis or into the lower abdomen. Infection tends to spreads after long labour or severe bleeding due to haemorrhaging which can cause peritonitis, septicaemia or death. (Awori, N. et al. 1999).
Puerperal Sepsis formerly known as childbed fever or puerperal fever was a mystery; it killed those at the cruellest of moments. It was understood that wherever physicians went the disease became more prevalent, especially within hospitals. During the 1700’s it was believed women were delivered from the peril of childbirth, not deliver a child into the world. Physicians believed sepsis occurred when there was a failure to urinate, it then became known as ‘milk metastasis’ as the internal organs of those that had died looked like they were covered in milk, it was later identified as pus. (Burch, D. 2009).
It was believed that puerperal fever was caused by various environmental factors: sewage, poor ventilation, cold, mists, vague ‘putrid tendencies,’ not bacterium and infection control. During the late 1700’s, Alexander Gordon leading obstetrician studied childbed fever and came to the conclusion that the disease was spread by physicians, it was related to skin infections and the only treatment was bloodletting. Bloodletting was widely accepted as a cure, however physicians understood more needed to be done to stop the spread of sepsis. (Burch, D. 2009).
Puerperal sepsis is caused by bacterium being introduced into the genital tract and women that are in labour or giving birth are more susceptible due to large genital tract surface area. The genital and urinary tracts have warm, moist environments that bacteria need to multiple. The bacterium can enter the body through pelvic exams, trauma during labour or prolonged labour. During pelvic exams the bacterium is introduced into the genital tract by unclean hands during examinations or through the use of non-sterile instruments. (Nall, R. 2014). Bacteria that are known to cause a puerperal sepsis include:

Clostridium tetani
Clostridium welchii
Escherichia coli (E.coli)

(Nall, R. 2014).
Other causes of puerperal sepsis are mastitis, pyelonephritis, ruptured membranes, respiratory complication, first birth, poor socioeconomic status, caesarean delivery and superficial or deep-vein thrombosis. (Baring, N. 2013).
Symptoms for puerperal sepsis normally appear between 24 hours to 10 days after infection begins. If one or more symptoms are present, action should be taken and treat as appropriate. Women should be monitored closely for any of the following symptoms:

Fever – higher that 38⁰C or 100.4⁰F
Shivering and chills
Uterus does not return to normal size
Pain and discomfort in lower abdomen
Tenderness and pain in the uterus
Discharge from the vagina – foul-smelling and containing pus
Pale and discoloured skin
Short of breath
Fatigued, difficult to rouse
Altered mental state
Flu like symptoms

(Nall, R. 2014) (Sepsis Alliance 2015).
Who is at Risk?
Any woman that is pregnant, has miscarried, aborted or delivered are at risk of sepsis but certain factors increase that risk. Women that are more susceptible are those that have liver disease, lupus a condition of the immune system, diabetes, congestive heart failure, are obese, first pregnancy, women that are under 25 or women that are over 40. Women over 40 are at risk of sepsis from infections due to placenta praevia and placenta abruption. Women that are underwent invasive procedures to become pregnant or invasive tests during pregnancy are more prone to infections that can lead to sepsis. (Sepsis Alliance 2015)
Abnormal changes in the patient temperature, heart and breathing rate can indicate infection. The vagina and uterus will be checked for swelling and tenderness by abdominal and internal exams. Broad-spectrum antibiotics will be prescribed if sepsis is suspected to prevent the infection from spreading, long term damage to the body and death. Further tests will be carried out to determine the type of infection, where it is located and if bodily functions have been affected. These tests can include:

Blood and urine test
Wound swabs
Blood pressure checks
Ultrasound scan, X-rays or computerised tomography (CT) scan
Organ function tests – liver, kidney, heart
Lumbar puncture
Stool samples

(NHS Choices. 2014) (Nall, R. 2014)
If sepsis is suspected broad-spectrum antibiotics will be given orally or intravenously to prevent infection spreading. When results from further testing have been received then a focused antibiotic is used to kill the bacterium. Anti-fever medication and cold compresses may be used to keep the fever under control. Oxygen may be given as levels in the blood can become low due to the body demand for oxygen. Intravenous fluids may be given to prevent dehydration and kidney failure, normally given within the first 48 hours after hospital admission. Sepsis can cause the blood pressure to drop; medication called vasopressors will be given to increase blood pressure allowing the patient condition to improve. Infection sites need to be keep clean and dry; pus to be drained away allowing infected tissue to repair and to prevent bacteria from entering. (Nall, R. 2014) (NHS Choices. 2014)
Sepsis can lead to serious complications and the damage can be irreversible. Complications for the women include:

Septic shock
Pulmonary embolism
Disseminated intravascular coagulation
Compromise fertility

The foetus can be affected causing depressed Apgar scores, neonatal septicaemia, pneumonia and death. (Dharmaraj, D. Patriquin, G. 2012)
Willacy (2012) wrote that severe sepsis can cause acute organ dysfunction and has a mortality rate of 20-40%. If septic shock develops the mortality rate rises to around 60%.
Following aseptic techniques and principles is very important. Correct cleaning practice of hospital and home environments need to be followed and use of sterile packs and equipment must be used to prevent contamination; these must only be used once then deposed of. (Johnson, R. Taylor, W. 2011. p. 80). Physicians must exercise the correct hand hygiene techniques (appendixes A) and use antiseptic soap, washes, alcohol-based rubs and sterile gloves. By doing this it reduces the risk of introducing bacterium into a sterile environment. (Johnson, R. Taylor, W. 2011. pp. 73-77). Protective clothing: aprons, shoes covers must be worn to prevent spread of infection and contamination from one situation to another, these to be deposed of after one use. Use of non-touch technique is important by ensuring sterile equipment does not touch with anything unsterile to prevent contamination and potential for infection. The use of an assistant to open packs and equipment can reduced the risk of cross contamination as it prevents touching anything non-sterile with sterile gloved hands. (Johnson, R. Taylor, W. 2011. pp. 80-82).
Analysis of Statistics
During the early 1900’s, just under 1.5% in 1000 births within the UK died from sepsis, greatly decreased on early years. Advances in medicine meant physicians were discovering asepsis was paramount in infection control. The introduction of carbolic spray in operating room, hand washing and rubber gloves were used to minimise contamination. Then in 1920, face masks were introduced into obstetrics to prevent contamination through body fluids. (Chamberlain, G. 2006).
In the last hundred years there has been a significant drop in puerperal sepsis. In 2003-5 0.85% of maternal deaths per 100,000 births were a direct cause of sepsis, which means asepsis was tackling infection. However in 2006-8 there was a rise to 1.13%, through lack of knowledge, not seeking advice when unwell and through infection control. Sepsis is now the leading cause of maternal death within UK above hypertension, thromboembolic disease and haemorrhage, where there has been a reduction in these. It has been noted that over recent years that it has been hard to achieve a reduction in the number of deaths within the UK due to bacterial infections, more needs to be done in order to prevent maternal deaths and these statistics rising further. (Sriskandan, S. 2011).
Puerperal sepsis is now the leading cause of maternal death, which means more medical research need to be undertaken in order to reduce the number of cases. Sepsis through pelvic exams, trauma during labour or prolonged labour needs to be evaluated and assessed on how using aseptic techniques and principles can reduce the risk of cross contamination and introducing bacterium into the genital tracts.
Over the last hundred years puerperal sepsis has declined significantly, however over recent years it has increased from lack of knowledge and infection control. The UK is a developed country and should have infection control and aseptic techniques and principles at the forefront of medical practice.
After miscarriages, during last trimester and during delivery broad-spectrum antibiotic should be given orally or intravenously to expectant mothers to provide the body with a barrier towards infections, this could reduce the number of cases sepsis.
More training and awareness of sepsis and aseptic principles should be provided to physicians, to ensure understanding and they are being diligent in regards to infection control.
Expectant mother and families should receive education through antenatal classes to learn the signs and symptoms of sepsis and what to do if they suspect it. Symptoms can be confused with flu like symptoms and education should be given to seek help and advice off midwives, health visitors and other physicians.
Awori, N. Bayley, A. Beasley, A. Boland, J. Crawford, M. Driessen, F. Foster, A. Graham, W. Hancock, B. Hancock, B. Hankins, G. Harrison, N. Kennedy, I. Kyambi, J. Nundy, S. Sheperd, J. Stewart, J. Warren, G. Wood, M. (1999) ‘Puerperal Sepsis,’ Primary Surgery, 1 [Online]. Available at: (Accessed: 20/04/2015).
Baring, N. (2013) OBSTETRICS – Puerperal Infection. Available at: (Accessed: 23/04/2015).
Burch, D. (2009) When Childbirth Was Natural, and Deadly. Available at: (Accessed: 23/04/2015).
Chamberlain, G. (2006) ‘British maternal mortality in the 19th and early 20th centuries’ Journal of the Royal Society of Medicine. 99(11). 559-563. [Online]. Available at: (Accessed: 20/04/2015).
Dharmaraj, D. Patriquin, G. (2012) Puerperal Infection. Available at: (Accessed: 25/04/2015).
Johnson, R. Taylor, W. (2011) Skills for Midwifery Practice. 3rd edn. London: Churchill Livingstone Elsevier.
Knight, M. (2015) What is a life threatening complication in pregnancy and childbirth? Available at: (Accessed: 12/04/2015).
Nall, R. (2014) Puerperal Infection. Available at: (Accessed: 23/04/2015).
NHS Choices (2014) Sepsis – Diagnosis. Available at: (Accessed: 25/04/2015).
Sepsis Alliance (2015) Sepsis. Available at: (Accessed: 24/04/2015).
Sriskandan, S. (2011) ‘Severe peripartum sepsis’ Royal College of Physicians of Edinburgh, 41 339–46. [Online]. Available at: (Accessed: 26/04/2015)
Willacy, H. (2012) Puerperal Pyrexia. Available at: (Accessed: 25/04/2015).
World Health Organizations (2015) Clean Care is Safer Care. Available at: (Accessed: 26/04/2015).
Awori, N. Bayley, A. Beasley, A. Boland, J. Crawford, M. Driessen, F. Foster, A. Graham, W. Hancock, B. Hancock, B. Hankins, G. Harrison, N. Kennedy, I. Kyambi, J. Nundy, S. Sheperd, J. Stewart, J. Warren, G. Wood, M. (1999) ‘Puerperal Sepsis,’ Primary Surgery, 1 [Online]. Available at: (Accessed: 20/04/2015).
Baring, N. (2013) OBSTETRICS – Puerperal Infection. Available at: (Accessed: 23/04/2015).
Burch, D. (2009) When Childbirth Was Natural, and Deadly. Available at: (Accessed: 23/04/2015).
Chamberlain, G. (2006) ‘British maternal mortality in the 19th and early 20th centuries’ Journal of the Royal Society of Medicine. 99(11). 559-563. [Online]. Available at: (Accessed: 20/04/2015).
Colebrook, L. (1936) ‘The Prevention of Puerperal Sepsis.’ BJOG: An International Journal of Obstetrics & Gynaecology, 43 691–714. [Online]. Available at: (Accessed: 26/04/2015).
Dharmaraj, D. Patriquin, G. (2012) Puerperal Infection. Available at: (Accessed: 25/04/2015).
Encyclopaedia Britannica (2015) Puerperal fever. Available at: (Accessed: 23/04/2015).
Jessica Trust (2015) Childbed fever: the facts. Available at: (Accessed: 24/04/2015)
Johnson, R. Taylor, W. (2011) Skills for Midwifery Practice. 3rd edn. London: Churchill Livingstone Elsevier.
Johnstone, W. (1938) ‘Prevention and Control of Puerperal Sepsis.’ British Medical Journal, 2(4049) 331-335. [Online]. Available at: (Accessed: 26/04/2015).
Khaskheli, M. Baloch, S. Sheeba, A. (2013) ‘Risk factors and complications of puerperal sepsis at a tertiary healthcare centre.’ Pakistan Journal of Medical Science, 29(4) 972-976. [Online]. Available at: (Accessed: 26/04/2015).
Knight, M. (2015) What is a life threatening complication in pregnancy and childbirth? Available at: (Accessed: 12/04/2015).
Macdonald, S. Magill-Cuerden, J. (2011) Mayes’ Midwifery. 14th edn. London: Churchill Livingstone Elsevier. (2012) Definition of Fever, puerperal. Available at: (Accessed: 24/04/2015).
Nall, R. (2014) Puerperal Infection. Available at: (Accessed: 23/04/2015).
NHS Choices. (2015) Peritonitis. Available at: (Accessed: 23/04/2015).
NHS Choices (2014) Sepsis – Diagnosis. Available at: (Accessed: 25/04/2015).
O’Connell, K. (2012) What is septicaemia? Available at: (Accessed: 23/04/2015).
Royal College of Obstetricians & Gynaecologists (2012) Sepsis following Pregnancy, Bacterial. Available at: (Accessed: 26/04/2015).
Sepsis Alliance (2015) Sepsis. Available at: (Accessed: 24/04/2015).
Sriskandan, S. (2011) ‘Severe peripartum sepsis’ Royal College of Physicians of Edinburgh, 41 339–46. [Online]. Available at: (Accessed: 26/04/2015)
Willacy, H. (2012) Puerperal Pyrexia. Available at: (Accessed: 25/04/2015).
World Health Organizations (2015) Clean Care is Safer Care. Available at: (Accessed: 26/04/2015).
World Health Organizations (2015) Managing puerperal sepsis. Available at: (Accessed: 20/04/2015).
Apgar scores – designed to quickly evaluate a newborn’s physical condition.
Asepsis – the absence of sepsis or infection.
Disseminated intravascular coagulation (DIC) – is a serious disorder in which the proteins that control blood clotting becomeover active.
Malaise – is a feeling of general discomfort or uneasiness; normally first indication of infection of other disease.
Mastitis – is the inflammation of breast tissue.
Peritonitis – is the inflammation of the thin layer of tissue that lines the inside of the abdomen called the peritoneum.
Placenta abruption – part of the placenta comes away from the uterus wall),
Placenta praevia – all or part of the placenta covers the cervix.
Pulmonary embolism – is a blockage in the artery that transports blood to the lungs.
Pyelonephritis – inflammation of the substance of the kidney as a result of bacterial infection.
Septicemia – is known as bacteremia or blood poisoning. Septicemia occurs when a bacterial infection enters the bloodstream.
Appendixes A – Hand washing techniques (WHO. 2015)