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CONTINUING PROFESSIONAL DEVELOPMENT
Page 56
Sepsis multiple choice
questionnaire
Page 59
Deborah Muldoon-Smith’s
practice profile on
isolation precautions
Page 60
Guidelines on how to
write a practice profile
Developments in the management
of patients with sepsis
NS504 Steen C (2009) Developments in the management of patients with sepsis. Nursing Standard.
23, 48, 48-55. Date of acceptance: October 7 2008.
Describe the pathophysiology of the
inflammatory process.
Summary
Sepsis is associated with a high incidence of mortality and
morbidity, however with appropriate strategies for monitoring and
early targeted intervention mortality rates decline. This article
examines the basic pathophysiology of the inflammatory response
to tissue injury and the effects this has on circulation. A partnership
of the Society of Critical Care Medicine, the European Society of
Intensive Care Medicine and the International Sepsis Forum
has developed the surviving sepsis strategy, which includes the
sepsis six treatment pathway and early goal-directed therapy
incorporating the six-hour care bundle.
Author
Colin Steen is lecturer in critical care, School of Nursing, Midwifery
and Social Work, University of Manchester, Manchester.
Email: [email protected]
Keywords
Infection; Inflammation; Organ dysfunction; Sepsis
These keywords are based on the subject headings from the British
Nursing Index. This article has been subject to double-blind review.
For author and research article guidelines visit the Nursing Standard
home page at nursingstandard.rcnpublishing.co.uk. For related
articles visit our online archive and search using the keywords.
Aims and intended learning outcomes
This article aims to provide the reader with an
increased understanding of the causes, signs and
symptoms of sepsis and strategies such as the
Surviving Sepsis Campaign, which aims to reduce
the incidence of the condition. After reading this
article you should be able to:
Identify the differences between sepsis, severe
sepsis and septic shock.
48 august 5 :: vol 23 no 48 :: 2009
Explain the epidemiology of sepsis.
Describe the sepsis six treatment pathway in
the management of a patient with severe sepsis.
Reflect on how the sepsis six treatment
pathway could be implemented in clinical
practice.
Introduction
Sepsis is a condition characterised by a systemic
inflammatory response syndrome (SIRS) and the
presence of infection. Chinese Emperor Sheng
Nung, circa 2737 BC, presented one of the earliest
descriptions of inflammation and described the
herbal medicines available to treat it. Today,
inflammation, sepsis and SIRS are increasing in
incidence around the world (Angus et al 2001).
Colloquially known as ‘blood poisoning’, sepsis
is associated with a high mortality rate, however
appropriate treatment and management of the
condition can reduce mortality rates (Angus and
Wax 2001, Alberti et al 2002, Martin et al 2003).
Angus et al (2001) identified an increase in the
incidence of sepsis over time, which is expected to
continue to rise as a result of an increasing ageing
population, underactive immune systems arising
from chemotherapy, organ transplantation,
complex co-morbidities such as heart disease and
diabetes, human immunodeficiency virus and
drug-resistant invading organisms.
In England, Wales and Northern Ireland the
incidence of patients admitted to intensive care
units with severe sepsis has increased by more than
1.5% per year since reliable data started to be
collected in 1996 (Harrison et al 2006). The rise in
incidence has led to an increase in hospital-related
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deaths from severe sepsis, from 23 deaths per
100,000 of the population in 1996 to 30 deaths
per 100,000 of the population in 2003 (Harrison
et al 2006). More people die from sepsis than from
lung, bowel or breast cancer (Dellinger et al 2008),
costing Europe approximately £6 billion per year
(Bone et al 1992, Angus et al 2001). Precise
mortality figures are difficult to determine with
absolute accuracy as the primary disease is
predominately documented as the cause of death
and not the subsequent sepsis.
The Surviving Sepsis Campaign (Dellinger et al
2008) aims to build awareness of sepsis, improve
diagnosis, increase the use of appropriate
treatment, educate healthcare professionals,
improve post-intensive care unit care, develop
guidelines for care and facilitate data collection
for the purposes of audit and feedback.
Promoting early detection and intervention with
goal-directed therapy and adopting the sepsis six
strategy in the management of severe sepsis can
help to reduce the mortality rates associated with
the condition (Dellinger et al 2008).
BOX 1
Stages of sepsis
Sepsis = Signs and symptoms of infection (SSI)
+ infection.
Severe sepsis = SSI + infection + signs of tissue
hypoperfusion/organ dysfunction.
Septic shock = SSI + infection + organ dysfunction
+ circulatory failure.
(Bone et al 1992)
FIGURE 1
Cascade of sepsis-induced failure
Source of injury
Infection – tissue damage provoking an
inflammatory response
Severe sepsis
Defining sepsis
Sepsis is a global term that is often misused.
Patients who develop signs of circulatory collapse
that are not attributable to another cause are
often thought to be experiencing sepsis. Sepsis is
an acute and severe disease associated with high
mortality. The European Society of Intensive Care
Medicine launched the Barcelona Declaration,
which calls for an increase in the awareness of
sepsis and the effects it has on individuals and
society. The aim of the campaign was to reduce
the sepsis mortality rate by 25% within five years
(Bone et al 1992, Silva et al 2006).
Sepsis is a term that is given to a systemic
inflammatory response that arises from an
infective process, which may be caused by
bacterial, viral or fungal invasion that provokes
an inflammatory response (Box 1). Alternatively,
an inflammatory response can arise from a
non-infective process commonly known as
systemic inflammatory response syndrome (SIRS).
Examples of this may be severe trauma, surgery,
complications related to adrenal insufficiency,
myocardial infarction, burns or acute pancreatitis.
The inflammation arises as a result of either tissue
ischaemia or tissue damage. It is important to be
aware that the causative agents can arise from
non-infective causes as well as infection.
As an alternative to SIRS, the term signs and
symptoms of infection (SSI) is being promoted by
the Surviving Sepsis Campaign (Dellinger et al
2008). While the majority of patients present
with an infective cause of sepsis there is a danger
in using SSI to describe the condition in that
attention may be distracted from non-infective
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Septic shock
Organ dysfunction
Multiple organ failure
Death
Levy et al (2005)
causes. The term SIRS will be used in this article
to indicate a non-infective cause.
Severe sepsis Severe sepsis occurs when there is
induced organ dysfunction. This arises from
hypoperfusion resulting in tissue hypoxia.
Septic shock The consequence of unresolved severe
sepsis is multiple organ failure and death from
septic shock (Figure 1). Septic shock is defined as
sepsis-induced hypoperfusion that persists despite
adequate fluid resuscitation. Where there is early,
targeted intervention the development of severe
sepsis and septic shock is averted and organ
dysfunction and death does not occur.
Epidemiology
The incidence of sepsis has increased over time and
is predicted to increase further (Angus and Wax
2001). There are many reasons for this. Patients
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with sepsis who experience subsequent
deterioration are often high risk because of
co-morbidities, increased age, compromised
immune systems or recent invasive medical
procedures. However, it is difficult to gain absolute
figures on the incidence of sepsis because of the
different contributing factors and the constantly
changing evolution of disease pathology. A panEuropean study showed that more than one third
of adult patients in intensive care units developed
sepsis; 25% of these individuals had sepsis on
admission to the intensive care unit having
developed it on the wards (Vincent et al 2006). In
the UK, the incidence of deaths related to sepsis has
increased from 23 to 30 cases per 100,000 of the
population between 1996 and 2003 (Harrison et al
2006). These patients account for 46% of all
intensive care unit bed days and 33% of all hospital
bed days (Intensive Care National Audit and
Research Centre 2003).
Time out 1
Identify five symptoms of
inflammation and describe
how each symptom may arise.
The inflammatory response
Inflammation can be described as redness, heat,
swelling, pain and loss of function (Jenkins et al
2007). The body is under constant attack from
invading organisms and has mechanisms for
combating this invasion. Examples of natural
barriers to infection are the skin, eyes, nasal
passages, lungs and gastrointestinal tract. Unless
the skin is damaged invading organisms are unable
to gain access. The lungs have the mucociliary
escalator that removes debris and bacteria, the eyes
have tears containing the enzyme lysosome, which
engulfs bacteria and viruses, the nose has nasal
hairs, which filter debris and bacteria, and the
stomach has acid, which destroys invading
organisms (Smith et al 2004). These host defence
mechanisms are constantly working. However,
these defence mechanisms can be breached at any
time provoking an inflammatory response
(Jenkins et al 2007).
BOX 2
Development of sepsis
Mechanism of injury
(Infection
of tissue)
+
Body’s response = Disease
(Inflammation)
(Sepsis/systemic
inflammatory response
syndrome/signs and
symptoms of infection)
50 august 5 :: vol 23 no 48 :: 2009
An inflammatory response is desirable and
normal. It enables survival from infection and
protects against further injury. For example, a
winter dose of influenza results in the body
creating an inflammatory response that mobilises
the immune system to combat the invading
organism and creates an adverse environment for
the invading organism. Over time the invading
organism is overcome and the body’s
environment returns to normal and the individual
regains health. A simple equation can summarise
how sepsis affects the individual (Box 2).
Wherever there is a mechanism of injury the body
will respond appropriately to ensure survival of
the individual, however this response can also
develop into a disease process.
The body’s response to the mechanism
of injury is complex. When there is either an
invasion of foreign material such as bacteria
or damage to tissue such as ischaemia or muscle
damage an immune response is provoked
(Jenkins et al 2007). Initially the immune
response is triggered by a humoral activity where
the circulating antibodies react to the invading
organism. These antibodies stick to the bacteria
marking them for destruction. Cell-mediated
immunity occurs, involving the activation of
macrophages, especially neutrophils, to destroy
the marked bacteria (Jenkins et al 2007).
The first stage of the inflammatory
response promotes blood flow to the site of
injury through vasodilation. This creates the
first classic sign of inflammation, redness
(erythema). The increased blood flow also
results in the area feeling hot, the second
symptom of inflammation. As part of the
inflammatory process the micro-capillaries
allow fluid to leak out of the circulation into
the interstitial space. This fluid delivers white
blood cells and proteins to the site of injury
which attack the invading organism and
promote growth and repair (Jenkins et al 2007).
This results in the third classic symptom of
inflammation, swelling. Swelling stretches the
tissues creating pain – the final symptom of
inflammation. Pain encourages the individual
to rest the affected area limiting further damage.
In the normal inflammatory response, the
damage that occurs to the endothelium of the
microcirculation enables fluid to leak out and
activates the clotting cascade. The endothelial
damage promotes clot formation in the
microcirculation at the site of injury preventing
debris from macrophage action and the invading
organisms entering the systemic circulation.
At the appropriate time the clot is dissolved and
blood flow is restored. Cessation of blood flow
combined with excessive inflammatory-induced
swelling results in a marked reduction in blood
supply to the area (Jenkins et al 2007).
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The inflammatory process is self-contained by
feedback mechanisms that increase then limit
inflammation, promote the leakage of fluid into
the interstitial space from the capillary bed and
promote coagulation followed by anticoagulation.
These inherent checks and balances permit the
body to remain in homeostasis (Jenkins et al 2007).
Homeostasis occurs continuously in the body
mostly without the individual realising it and
certainly without the individual feeling severely ill.
When an individual starts to display symptoms of
illness and physiological deterioration, the
inflammatory process is no longer localised to the
site of injury and is having a systemic effect. At this
point a person can be described as having sepsis or
SIRS (Levy et al 2003).
Time out 2
What are the early presenting
symptoms of sepsis or SIRS?
Review the strategies that you
might implement to detect these
symptoms early in the disease process.
List the criteria for diagnosing sepsis.
Similar to other acute illnesses one of the first
symptoms of sepsis is an increase in respiratory
rate. This arises from subtle changes in acid-base
balance, which excite the medulla oblongata to
stimulate respiration. The acid-base changes occur
as a result of cellular hypoxia from a reduction
in oxygen supply to cells, resulting from tissue
hypoperfusion. This results in anaerobic cellular
respiration, the consequence of which is the
production of lactate causing a reduction in pH,
known as acidosis (Morton and Fontaine 2009).
Septic shock is sometimes referred to as
distributive shock, which describes accurately
the effects of the disease process on the movement
of fluid around the different compartments of
the body (Morton and Fontaine 2009). The early
symptoms of systemic vasodilation can be observed
– the patient appears red and flushed with a full
and bounding pulse and a rapid capillary refill.
This systemic response results in an increase in
peripheral circulation and the permeability of the
micro-vasculature creating a major loss of volume
from the core circulation. The consequence of this is
the derangement of organ functioning (Jenkins et al
2007). The effects on organ dysfunction are easily
detected. For example, early signs may include an
increase in respiratory rate, an increase in heart rate
and an altered mental state. A reduction in urine
output will occur, but the evidence for this may be
delayed if the patient is not catheterised. An initial
rise in diastolic pressure followed by a drop in blood
pressure and alterations in temperature are late
symptoms of a lack of oxygen supply to the tissues
(Morton and Fontaine 2009).
NURSING STANDARD
The body titrates cardiac output to the
metabolic demands, but aims to maintain
a cardiac output of 4-8 litres per minute
(Morton and Fontaine 2009). During the early
phases of sepsis and because of systemic
vasodilation, the venous return and stroke
volume (the amount of blood ejected by the
ventricle during contraction) fall, resulting in
a reduced cardiac output. To compensate the
body will immediately raise the heart rate and
increase levels of adrenaline to improve cardiac
output and increase vascular tone (Jenkins et al
2007). In response to reduced blood flow, the
renin-angiotensin-aldosterone system is
activated, increasing vascular tone and
conserving fluid by reducing urine output.
As the disease process develops the combined
effect of loss of venous return and loss of
circulating volume results in significant reduction
in cardiac output and blood flow. This in turn
results in an inadequate oxygen supply to the
tissues, cellular hypoxia and organ dysfunction.
The patient may start to display symptoms of
deterioration many hours before sepsis becomes
detrimental to the individual’s health. The
consequences of missing these early symptoms
are that when the patient becomes acutely ill he or
she will have had compromised oxygen supply to
the tissues and organ dysfunction for many hours,
which will lead to organ failure and severe sepsis.
The criteria for diagnosing severe sepsis are
presented in Table 1.
Time out 3
Describe the differences
between sepsis, severe sepsis
and septic shock.
Septic shock is the term given to the profound
effects that the systemic inflammatory response
has on oxygen delivery to the tissues. It needs to be
treated urgently before irreparable organ damage
TABLE 1
Criteria for diagnosing severe sepsis
General variables
Change
Change in body temperature
>38.3°C or <36°C
Heart rate
>90 beats per minute
Tachypnoea
>20 breaths per minute
Mental state
Altered mental state
Significant oedema or positive
fluid balance
20ml/kg over 24 hours
Hyperglycaemia (in the absence
of a diagnosis of diabetes)
Plasma glucose >7.7mmol/l
(Dellinger et al 2008)
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Fluid resuscitation.
Measurement and monitoring of urine output.
occurs. It refers to shock that is unresponsive to
intravascular volume replacement. Septic shock
can lead to refractory shock where blood pressure
does not respond to vasoactive drugs and this will
rapidly lead to death (Annane et al 2005).
Treatment
Prevention is important in managing and reducing
the incidence of sepsis. Asepsis, preventing
contamination of vulnerable patients, is an
important strategy and there are various national
strategies (Department of Health (DH) 2003)
in place to reduce the incidence of cross-infection
in the healthcare system. Removal of invasive
intravenous and urinary catheters that are
no longer needed is an important element.
Implementing simple procedures such as
employing a non-touch technique will help to
reduce the complications that can result in sepsis,
and the nurse is at the centre of these strategies.
Early mobilisation reduces the risk of hypostatic
pneumonia and improves circulation. Where
mobilisation is not possible, optimising
respiratory function with incentive spirometery
and physiotherapy will help. Maintaining
adequate hydration and nutrition are effective
strategies that can limit the risk of sepsis from
hospital-acquired infection. Where prevention
fails, early intervention is imperative in preventing
further deterioration (Rivers et al 2001, Levy et al
2005). Early warning scoring systems also known
as modified early warning systems (MEWS) or
track and trigger systems are now widely used in
hospitals. However, they are not currently in use in
the community setting or in nursing homes, where
they may also be helpful. MEWS have a positive
effect on clinical outcome (Subbe et al 2001, 2003)
in a variety of patient groups by identifying those
at risk of clinical deterioration (Goldhill and
McNarry 2004).
It is recommended that the sepsis six
treatment pathway is implemented within the
first six hours of identifying the septic patient
(Dellinger et al 2008). Delays in implementing
fluid resuscitation will result in further patient
decline, hastening tissue hypoperfusion and
resulting in enduring organ failure.
The sepsis six treatment pathway
The sepsis six treatment pathway comprises the
following elements, each of which is discussed in
turn (Surviving Sepsis Campaign 2007):
Oxygen therapy.
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Blood cultures.
Antibiotic therapy.
Lactate, haemoglobin and routine blood
monitoring.
A care bundle is designed to ensure that all the
tasks are carried out at a specific time and place. It
is a collection of interventions, each one of which
is based on identified best knowledge or practice
as recommended and supported by the DH (NHS
Modernisation Agency 2004).
Once the symptoms of deterioration or
organ dysfunction have been detected the
following steps need to be implemented as soon as
possible and within six hours for the remainder of
the care bundle. Where compliance with the care
bundle has been good there has been a reduction
in patient mortality (Gao et al 2005).
Step 1: oxygen therapy Missing from the six-hour
care bundle are recommendations for oxygen
therapy in the management of severe sepsis,
however this is included in the sepsis six guidelines
(Robson and Daniel 2008). All acutely ill
patients should receive high-dose oxygen via
a non-rebreathing mask to normalise oxygen
saturation of haemoglobin during the acute phase
of illness, aiming for an oxygen saturation within
normal limits (McQuillan et al 1998). Following
this, the focus of sepsis management is on
restoration of the failing circulation.
Step 2: fluid resuscitation and central venous
pressure monitoring
Early goal-directed therapy On identifying
a deteriorating patient, Rivers et al (2001)
recommended the implementation of an early
goal-directed therapy strategy in the management
of sepsis. The first element of this is fluid
resuscitation. Patients should receive fluid
resuscitation as soon as hypoperfusion is identified
and treatment should not be delayed. Rivers et al
(2001) recommended administration of fluid
resuscitation to achieve a central venous pressure
(CVP) of 8-12cmH2O. In ventilated patients, to
reflect the changes in intrathoracic pressure
resulting from positive pressure ventilation, a
higher CVP target of 12-15cmH2O is
recommended (Bendjelid and Romand 2003).
Fluid resuscitation Fluid resuscitation should
follow the fluid challenge principle where fluid
is continued so long as there are improvements
in blood pressure, heart rate and urine output
(Vincent and Gerlach 2004). Dellinger et al
(2008) recommended administering one litre
of crystalloid or 300-500ml of colloid over
30 minutes, with a more rapid rate and increased
volumes if there are significant signs of
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hypoperfusion. Where there are no indications of
improvement in blood pressure or where there is
evidence of cardiac insufficiency or a documented
history of heart failure then the volume of fluid
should be reduced or administered more
cautiously (Dellinger et al 2008).
The Rivers et al (2001) study recommends the
use of CVP monitoring, however this is rarely
available on general wards. The Comprehensive
Critical Care document (DH 2000) recommends
‘critical care without walls’ and advocates that
the resources required for the treatment and
management of acutely ill patients should be
made available on occasions where patients
require aggressive treatment and close
monitoring in the short term. With the advent
of critical care outreach, understanding and
application of such procedures should be
enhanced and achievable.
Blood transfusion Rivers et al (2001) transfused
patients to maintain a haematocrit ≥30%, and
the Surviving Sepsis Campaign recommend
administering blood products to a target
haemoglobin of 7.0-9.0g/dl (Dellinger et al
2008). This may seem lower than the normal
haemoglobin level, but consideration needs to be
given to balancing the oxygen-carrying capacity
of the blood and blood viscosity. The higher the
haemoglobin level the higher the viscosity.
Blood pressure monitoring Early goal-directed
therapy recommends aiming for a mean arterial
pressure of ≥65mmHg (Rivers et al 2001).
Measuring and recording this value is assisted
by automated non-invasive blood pressure
monitoring equipment, where is it calculated
automatically and displayed.
Venous oxygen saturation It has been
recommended that central venous oxygen
saturation should be measured as an indication
of tissue oxygen delivery and consumption.
It should be maintained at ≥70% (Rivers et al
2001). Venous oxygen saturation is the same
as arterial oxygen saturation, only the blood
originates from the central venous system.
Venous saturation can only be monitored by
sampling blood gases from a central venous
catheter, thus strengthening the argument for
inserting these catheters as soon as possible.
Inotrope and vasoactive support The use of an
inotrope to support cardiac output has been
recommended (Rivers et al 2001). Rivers et al
(2001) used dobutamine at a maximum dose
of 20μg/kg/min. However, this should only be
used following fluid resuscitation to target levels
and in patients where cardiac insufficiency is
demonstrated by a low cardiac output. All
inotropes and vasoactive drugs have the capacity
to cause harm to patients and should be used with
specialist advice and knowledge. However, where
there is evidence of targeted fluid administration
NURSING STANDARD
with persistent hypotension a vasopressor such
as noradrenaline should be used (LeDoux et al
2000, Hollenberg et al 2004). A vasopressor
is a drug that causes a rise in blood pressure by
causing constriction of the blood vessels. An
alternative vasopressor, dopamine, may be used
to support blood pressure, but controversy exists
regarding the use of low-dose dopamine to
support renal perfusion and is not currently
recommended (Bellomo et al 2000).
Step 3: urine output Although there is a
delayed response to fluid resuscitation,
Rivers et al (2001) recommended that urine
output should be monitored closely. This
should be maintained at ≥0.5ml/kg/hour.
The insertion of a urinary catheter with an
appropriate measuring bag is required to
accurately measure urine output in patients.
Steps 4 and 5: blood cultures and antibiotic
therapy During insertion of new (<48 hours)
intravenous catheters, such as central venous
catheters and peripheral catheters for rapid fluid
resuscitation, blood cultures should be taken. In
addition, the recommendation is to take blood
cultures from all existing central catheters that
have been in situ for more than 48 hours (Dellinger
et al 2008). Other potential sites of infection,
for example, sputum, urine and wounds, should
also be cultured. Cultures should be taken before
the administration of antibiotics to prevent
sterilisation of blood cultures, which can occur a
few hours after the first antibiotic dose. Following
sampling and culturing, broad-spectrum
antibiotics should be administered (Dellinger et al
2008). This should be achieved within one hour of
recognition of severe sepsis or septic shock. Each
hour of delay results in a significant increase in
mortality (Kumar et al 2006).
Step 6: lactate measurement An elevated
lactate measurement is an important indicator
of the need to start treating the patient with sepsis
(Rivers et al 2001). In sepsis, lactate rises when
the supply of oxygen to the cells cannot meet
the demand for normal aerobic respiration.
However, the absolute measurement can lack
accuracy owing to variations in blood flow to
tissues during poor tissue perfusion. Treatment
for septic shock should commence at a lactate
level of ≥4mmol/l (Rivers et al 2001, Dellinger
et al 2008). Other laboratory investigations
should be performed as indicated, including
routine urine and electrolytes, haemoglobin
and liver function tests.
Time out 4
List the components of the
six-hour care bundle and reflect
on how you might implement
these in practice.
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The remainder of this article focuses on the
strategy that should be implemented in the
24 hours following diagnosis of severe sepsis
or septic shock. This relates specifically to
those patients in intensive care and is only
covered briefly.
The 24-hour care bundle
Glucose control It is noted that hyperglycaemia
arising from insulin resistance without a previous
history of diabetes can occur with critical
illness, leading to an increase in mortality. It is
recommended that patients who display raised
levels of blood glucose following severe sepsis or
septic shock should receive intravenous insulin
therapy to reduce levels to <150mg/dl
(8.3mmol/l) (Dellinger et al 2008).
Corticosteroid therapy This should only be
considered if response to fluid resuscitation and
vasoactive support has been poor. The definitive
evidence for the use of corticosteroids has not
been proven, although there is some evidence to
suggest that corticosteroids can reverse the
symptoms of shock (Sprung et al 2008).
Lung protection strategies In patients receiving
intermittent positive pressure ventilation, the
principle of lung protection in sepsis follows
the recommendations of the Acute Respiratory
Distress Syndrome Network trial (Slutsky and
Ranieri 2000). These recommendations include
reduction in tidal volume to 6ml/kg body weight
with permissive hypercapnia (Slutsky and
Ranieri 2000). Maintaining ventilation plateau
pressures <30cmH2O (Slutsky and Ranieri 2000)
with the use of positive end expiratory pressures
helps to prevent lung collapse at end expiration
(Dellinger et al 2008).
Patients who require high levels of ventilation
can be positioned prone. The evidence
regarding the success of prone ventilation is
that it appears to improve oxygenation but not
mortality (Lamm et al 1994, Stocker et al 1997,
Jolliet et al 1998, Gattinoni et al 2001, Guerin
et al 2004). Controversy exists about when in
the disease process to use the prone position,
how long the patient should be left in this
position, when the patient should be turned
back to the supine position and whether the
procedure should be repeated in the event of
deterioration in ventilation.
To prevent aspiration pneumonia in
ventilated patients the head of the bed should
be elevated to 30-45° (van Nieuwenhoven et al
2006). There are also recommendations that
weaning protocols should be in place (Dellinger
54 august 5 :: vol 23 no 48 :: 2009
et al 2008). These include spontaneous
breathing trials, targeted sedation scoring
and restricted use of paralysing agents, early
extubation so long as the patient’s fraction of
inspired oxygen (FiO2) requirements could be
met using a face mask and early tracheostomy
for failed extubation.
Recombinant human activated protein C
Protein C is synthesised by the liver. Once
activated (APC) it is one of the major inhibitors
of the clotting system. The inflammatory
response in severe sepsis is linked to activation
of the clotting cascade. In a large, multicentre,
randomised, controlled trial, recombinant
APC was shown to have anti-inflammatory
properties and improved survival in patients
with sepsis-induced organ dysfunction (Bernard
et al 2001). It is recommended that this treatment
is offered so long as the patient meets the criteria
for administering the drug and that there are no
contraindications.
Other areas for consideration are stress ulcer
and deep vein thrombosis prophylaxis and renal
replacement therapy.
Time out 5
List the components of the
24-hour care bundle. Compare
these recommendations with
current practice in your clinical
area. Consider how you might
implement these evidence-based
recommendations in your practice.
Conclusion
Sepsis is associated with a high incidence of
mortality and morbidity and nurses need to have
an understanding of the causes, signs and
symptoms of the condition to be able to provide
early and appropriate care and treatment.
Strategies such as the Surviving Sepsis Campaign
have helped to raise awareness of the problem and
aim to reduce the death rate associated with sepsis.
The care bundles described offer a systematic
way of identifying the deteriorating patient,
applying simple but effective strategies outside
the high-care area. More intensive treatment
can be offered in high-care areas and again
simple strategies can help to reduce the effects
of sepsis NS
Time out 6
Now that you have completed
the article you might like to
write a practice profile. Guidelines
to help you are on page 60.
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References
Alberti C, Brun-Buisson C,
Burchardi H et al (2002)
Epidemiology of sepsis and infection
in ICU patients from an international
multicentre cohort study. Intensive
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Lidicker J, Clermont G, Carcillo J,
Pinsky MR (2001) Epidemiology of
severe sepsis in the United States:
analysis of incidence, outcome, and
associated costs of care. Critical
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Cavaillon JM (2005) Septic shock.
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S, Fox S (2005) The impact of
compliance with 6-hour and
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sepsis: a prospective observational
study. Critical Care. 9, 6,
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et al (2001) Effect of prone
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Page 56
learning zone assessment
Sepsis
TEST YOUR KNOWLEDGE AND WIN A
£50 BOOK TOKEN
HOW TO USE THIS ASSESSMENT
This self-assessment questionnaire (SAQ)
will help you to test your knowledge. Each
week you will find ten multiple-choice
questions that are broadly linked to the
learning zone article. Note: There is only
one correct answer for each question.
Ways to use this assessment
You could test your subject knowledge by
attempting the questions before reading
the article, and then go back over them to
see if you would answer any differently.
You might like to read the article to update
yourself before attempting the questions.
Prize draw
Each week there is a draw for correct entries.
Please send your answers on a postcard to:
Zena Latcham, Nursing Standard,
The Heights, 59-65 Lowlands Road,
Harrow-on-the-Hill, Middlesex HA1 3AW,
or send them by email to:
[email protected]
Ensure you include your name and address
and the SAQ number. This is SAQ no. 504.
Entries must be received by 10am on
Tuesday August 18 2009.
When you have completed your
self-assessment, cut out this page and add it
to your professional portfolio. You can record
the amount of time it has taken. Space has
been provided for comments.
c) Amlodipine
d) Dobutamine
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9. Which of the following is not a
component of the sepsis six
treatment pathway?
a) Oxygen therapy
b) Corticosteroid therapy
c) Blood cultures
d) Monitoring urine output
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10. What is the first classic sign
of inflammation?
a) Erythema
b) Pain
c) Swelling
d) Heat
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This self-assessment questionnaire
was compiled by Tanya Fernandes
The answers to this questionnaire
will be published on August 19
You might like to consider writing a practice
profile, see page 60.
Report back
1. The cost of sepsis per year in
Europe is approximately:
a) £2 billion
b) £4 billion
c) £6 billion
d) £8 billion
2. Sepsis may be caused by:
a) Bacterial invasion
b) Viral invasion
c) Fungal invasion
d) All of the above
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3. Septic shock is also referred to as:
a) Distributive shock
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b) Localised shock
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c) Permanent shock
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d) Temporary shock
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4. Which of the following equations
represents sepsis?
a) Signs and symptoms of infection +
infection
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b) Signs and symptoms of infection +
signs of hypoperfusion
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c) Signs and symptoms of infection +
organ dysfunction
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56 august 5 :: vol 23 no 48 :: 2009
d) Signs and symptoms of infection +
circulatory function
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5. The stomach’s natural barrier to
infection involves:
a) The mucociliary escalator
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b) Acid
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c) Keratinisation
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d) Langerhans’ cells
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6. Early signs of organ dysfunction
may include:
a) Increase in respiratory rate
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b) Increase in heart rate
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c) Altered mental state
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d) All of the above
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7. Modified early warning systems
are also known as:
a) Modified trigger systems
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b) Modified trigger scores
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c) Track and trigger systems
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d) Tracking systems
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8. An example of an inotrope is:
a) Budesonide
b) Risperidone
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This activity has taken me ____ hours to
complete.
Other comments:
Now that I have read this article and
completed this assessment, I think
my knowledge is:
Excellent
Good
Satisfactory
Unsatisfactory
Poor
As a result of this I intend to:
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❑
❑
❑
Answers to immunisation questions
The answers to SAQ no. 502 on
immunisations, which appeared in the
July 22 issue, are:
1. c 2. b 3. d 4. a 5. d
6. c 7. b 8. d 9. a 10. c
NURSING STANDARD