Transcript Sepsis What’s Bugging Your Patient? A Tutorial for Nurses Alverno College MSN Program Advanced Anatomy and Physiology Project Linda M.

Sepsis
What’s Bugging Your Patient?
A Tutorial for Nurses
Alverno College MSN Program
Advanced Anatomy and Physiology Project
Linda M. Bay, RN, BSN, CCRN
[email protected]
Click on the
Bug to Begin Tutorial
Directions for Using the Tutorial
• When you see a
you are on a menu page. Clicking on
it moves you to another section of the tutorial.
• Use the navigation arrows at the bottom of a page to move
between pages of the tutorial:
Clicking on the
Clicking on the
arrow sends you to the opening page.
arrow sends you to the last page.
Clicking on the
Clicking on the
arrow moves you to the next page.
arrow moves you to the previous page.
• Review Question pages have True and False answers that
will register your response when you click on them
At the end of this tutorial the learner
will be able to:
Define sepsis and related terms
Discuss the incidence of sepsis
Discuss the causes and pathophysiology of
sepsis
Identify signs and symptoms of sepsis
Discuss how other disease processes can
affect outcomes in patients with sepsis
Discuss nursing interventions and the latest
evidence based practice for the treatment of
sepsis
What is Sepsis?
Sepsis is a serious
medical condition caused
by the body’s response to
an infection.
Before we can more
fully define sepsis we
need to discuss related
terms.
Related Terms
Infection – A microbial phenomenon
characterized by an inflammatory response to
the presence of microorganisms
Bacteremia – The presence of viable bacteria
in the blood
Source: Core Curriculum for Critical Care Nursing, 2006
Related Terms
Systemic inflammatory response syndrome (SIRS)
A systemic or whole body response to an infection
manifested by two (2) or more of the following
conditions:
• Temperature above 100.4°F or below 96.8°F
• Heart rate above 90 beats per minute
• Respiratory rate above 20 per minute or
PaCO2 below 32 mm Hg
• White blood cell count above 12,000uL-1 or
below 4,000uL-1
Critical Care Medicine, 2003
Definition of Sepsis
Sepsis can now be more accurately defined as a
systemic inflammatory response syndrome (SIRS)
resulting from infection
Infection + SIRS = Sepsis
Source: www.sepsis.com
More Related Terms
Septic shock – A sepsis induced state of severe
hypotension despite aggressive fluid therapy.
Multiple Organ Dysfunction Syndrome (MODS) – A
progressive dysfunction in two or more organs of the
body after the onset of sepsis where intervention is
needed to sustain life.
Source: Core Curriculum for Critical Care Nursing, 2006
The Incidence of Sepsis in the
United States
•
The incidence of sepsis has increased 91.3 percent over the last ten years.
•
This year, severe sepsis will likely take 215,000 lives.
•
Sepsis is the leading cause of death in the non-coronary ICU.
•
Severe sepsis takes more lives than breast, colon/rectal, pancreatic, and
prostate cancer combined.
•
One of every three patients who develop severe sepsis
will die within a month.
Source: Society of Critical Care Medicine , 2004
Causes of Sepsis
• Bacterial infections are the
most common cause of
sepsis, but sepsis can also
be caused by fungal,
parasitic, or viral
infections.
• The infection can originate
from anywhere in the
body.
Source: www.clevelandclinic.org
Pathophysiology of Sepsis
• Sepsis can lead to widespread inflammation
and blood clotting.
• Inflammation may result in redness, heat,
swelling, pain, and organ failure.
• Blood clotting during sepsis causes reduced
blood flow to limbs and vital organs, and
can lead to organ failure or tissue damage.
Source: Critical Care Nurse Supplement, 2004
Pathophysiology of Sepsis
• In simple terms sepsis can
be viewed as an imbalance
of inflammation,
coagulation, and
fibrinolysis.
• In normal patients
homeostasis is maintained
when these are balanced.
Pathophysiology of Sepsis
During a normal response to bacteria in the blood
the immune system releases inflammatory
mediators to promote recovery of the tissue.
These mediators are known as:
•
•
•
•
•
Tumor Necrosis Factor (TNF)
Interleukins (IL)
Cytokines
Prostaglandins
Platelet Activating Factor
Source: New England Journal of Medicine, 2003
Pathophysiology of Sepsis
• The release of the inflammatory mediators starts
the Coagulation Cascade leading to the
development of a clot.
• To maintain this clot, inhibitors are released
to suppress fibrinolysis or breakdown. This is
necessary to have time for the body to destroy the
bacteria before the clot is gone.
Source: Critical Care Nurse Supplement, 2004
Clotting Cascade
To review the Clotting Cascade or learn more about
Coagulation follow the link below:
Disorders of Coagulation and Haemostasis
http://www.surgical-tutor.org.uk/default-home.htm?core/preop2/clotting.htm~right
Used with permission: Stephen Parker BSc MS DipMedEd, 2006
Pathophysiology of Sepsis
Once the bacteria or
antigen is isolated, the
pro-inflammatory
mediators attract
neutrophils or WBCs
which attack the antigen
and try to engulf it.
Graphics: Delores Zittel, 2006
Pathophysiology of Sepsis
To prevent the response from damaging
normal tissue, anti-inflammatory mediators
are released including transforming growth
factors and interleukins (IL-4). This balance
of inflammatory and anti-inflammatory
mediators restricts the inflammation response
to the local site of infection.
Source: Critical Care Nurse Supplement, 2004
Pathophysiology of Sepsis
When the body is unable to maintain the
appropriate balance, the immune response is
no longer local but becomes systemic.
Inflammation and altered clotting quickly
spread through the body.
Source: Critical Care Nurse Supplement, 2004
Pathophysiology of Sepsis
The person with the
infection which was
once localized could
become critically ill if
this process is not
corrected.
Let’s Stop for a Review
Answer True or False to the following questions
Click on the correct answer.
1. True or False - Sepsis is the leading cause of
death in the ICU setting.
2. True or False - Sepsis can lead to widespread
inflammation and blood clotting.
3. True or False - Sepsis can be viewed as a
dysfunction of coagulation, inflammation and
fibrinolysis.
That’s right! Hurray!
Return to Review Questions
Oops! Wrong answer!
Sepsis is the leading cause of death in
ICU settings.
Return to Review Questions
You are correct!!! Way to go!!!
Return to Review Questions
Sorry that is wrong.
Sepsis can lead to widespread
inflammation and blood clotting.
Return to Review Questions
Yeah! Right Again!
Return to Review Questions
Sorry that is incorrect.
Sepsis can be viewed as a dysfunction of
coagulation, inflammation and fibrinolysis.
Return to Review Questions
Let’s Look a Little Deeper
There are 3 integrated responses to sepsis
Activation of Inflammation

Activation of Coagulation

Impairment of Fibrinolysis
Activation of Inflammation
Inflammation is the body’s response to infection.
When this occurs white blood cells (WBCs) generate
and release cytokines or mediators of inflammation.
Inflammatory mediators include: Tumor necrosis
factor-a, Interleukin-1(IL-1), Interleukin-6 (IL-6)
and Platelet activating factor.
Source: Critical Care Nurse, 2003
Activation of Inflammation
Although these cytokines (TNF, IL-1,IL-6) play a
critical role to fight off infection the body tries to
reestablish balance by releasing anti-inflammatory
cytokines as well.
Anti-inflammatory cytokines include interleukin -4
(IL-4) and interleukin-10 (IL-10)
Source: Critical Care Nurse, 2003
Activation of Inflammation
There is basically a tug of
war going on between the
pro-inflammatory and antiinflammatory components of
the body.
Pro-inflammatory (IL-1,IL-6,TNF)
In sepsis, continued release
of pro-inflammatory
cytokines overwhelms the
anti-inflammatory cytokines.
Source: Critical Care Nurse, 2003
Anti-inflammatory
(IL-4, IL-10)
Activation of Coagulation
Inflammation and coagulation are closely
linked. The cytokines from inflammation
stimulate coagulation pathways. This results
in the forming of the enzyme thrombin.
This produces clotting in the body.
Source: Critical Care Nurse, 2003
Activation of Coagulation
The enhanced clotting
continues making tiny
clots or “microthrombi”
in the vascular system
which impairs blood
flow and organ
perfusion.
Source: Critical Care Nurse, 2003
Activation of Fibrinolysis
Fibrinolysis, or the breakdown of clots, is the body’s response
to the increased clotting and inflammation.
In sepsis this breakdown is inhibited or slowed because of
mediators. These mediators are called:
• Plasminogen Activator Inhibitor-1 (PAI-1)
• Thrombin Activatable Fibrinolysis Inhibitor (TAFI)
Source: Critical Care Nurse, 2003
Activation of Fibrinolysis
The increase levels of these two inhibitors,
Plasminogen Activator Inhibitor-1(PAI-1) and
Thrombin Activatable Fibrinolysis Inhibitor
(TAFI), suppress fibrinolysis even more
creating a state of “coagulopathy”.
Source: Critical Care Nurse, 2003
The Inflammatory, Coagulation, and
Fibrolytic Response to Infection
Graphics: Delores Zittel, 2006
Making Matters Worse
The Role of Endothelium in Sepsis
Graphic: Delores Zittel, 2006
The endothelium is a layer of cells lining the inside
of blood vessels. It sits between flowing blood and
the extracellular space.
Source: www.MedicineNet.Com
Making Matters Worse
The Role of Endothelium in Sepsis
Normal endothelium has anticoagulant abilities and plays a role in the
body’s homeostasis abilities including:
• Vasomotor tone
• Movement of cells and nutrients
• Maintaining blood fluidity
When activated, endothelium also plays a role in the inflammatory,
coagulation, and fibrinolytic components of sepsis.
Source: Critical Care Nurse, 2003
Making Matters Worse
The Role of Endothelium in Sepsis
• In sepsis the endothelium becomes damaged
which makes the “inflammatory process” worse
by releasing more cytokines (TNF-a and IL-1)
causing neutrophils to stick to its’ lining.
• The “activation” of the capillary endothelium
leads to increased permeability causing fluid to
“leak” out of the capillaries and into the
extracellular spaces.
Source: http://www.xigris.com/Learning_Modules/course_01/module_02/index.htm
Damaged Endothelium
Graphics: Delores Zittel, 2006
Putting it all Together
The imbalance
of Inflammation,
Coagulation, and
Fibrinolysis and the
effects on endothelium
can lead to organ failure
even death if left
undetected or untreated.
Putting it all Together
Let’s Stop for a Review
Answer True or False to the following questions
Click on the correct answer.
1. True or False – Inflammation is caused by
the release of cytokines Tumor Necrosis
Factor-a, Interleukin-1(IL-1), Interleukin6 (IL-6) and Platelet activating factor.
2. True or False – Endothelium plays a key
role in the progression of sepsis.
You are right!
Return to Review Questions
I am sorry that is wrong.
Inflammation is caused by the release of
cytokines Tumor Necrosis Factor-a,
Interleukin-1(IL-1), Interleukin-6 (IL-6) and
Platelet activating factor.
Return to Review Questions
You are right!
Return to Review Questions
No. I am sorry that is wrong. Endothelium
plays a key role in the progression of sepsis.
Return to Review Questions
Sepsis – What Does it Look Like?
Signs and symptoms of
sepsis can vary. Patients
with sepsis can
progressively become
worse. For this reason
early detection or
identification of sepsis
and treatment of
infections is important.
Signs and Symptoms of Sepsis
•
•
•
•
•
•
•
•
•
Heart rate >90bpm
Increased respiratory rate
Decreased blood pressure
High/Low WBC count
Fever or low body temperature
Altered mental status
Shaking
Chills
Nausea
Source: Core Curriculum for Critical Care
Nursing, 2006
Sepsis can progress to severe sepsis
and multi-organ dysfunction
syndrome.
Source: http://www.xigris.com/recognition/continuum.jsp?reqNavId=2.7
Copyright © 1994-2006 Eli Lilly and Company. All rights reserved.
Sepsis – What Does it Look Like?
Let’s look at some Case Studies to help you
understand the progression.
Case Study 1
Mrs. C. Hicken is an 80 year old
woman admitted to the medical unit.
She states that she has a sore throat,
persistent cough, and chest pain
when she takes deep breaths. She
tells you she has felt this way for
several days prior to coming to the
hospital.
Vital Signs are as follows:
Temperature - 101.2 °F
Pulse -110 beats per minute
Respirations – 40 breaths per minute
Blood Pressure – 110/60mmHg
Review of Case Study 1
What clinical symptoms related to sepsis
does she show?
Click here
to review clinical signs and symptoms
Is this considered Systemic Inflammatory
Response Syndrome? (SIRS)
Click here
to review clinical signs and symptoms
Review Signs and Symptoms of Sepsis
Mrs. C. Hicken is exhibiting the
following signs and symptoms:
•
•
•
•
•
Vital Signs are as follows:
Temperature - 101.2 °F
Pulse -110 beats per minute
Respirations – 40 breaths per minute
Blood Pressure – 110/60mmHg
The clinical signs and symptoms of
Sepsis are:
•
•
•
•
•
•
•
•
•
Heart rate >90
Increased respiratory rate
Decreased blood pressure
High/Low WBC count
Fever or low body temperature
Altered mental status
Shaking
Chills
Nausea
Source: Core Curriculum for Critical Care
Nursing, 2006
Return to the Case Study
Review Signs and Symptoms of SIRS
Mrs. C. Hicken is exhibiting the
following signs and symptoms:
•
•
•
•
•
Vital Signs are as follows:
Temperature - 101.2 °F
Pulse -110 beats per minute
Respirations – 40 breaths per minute
Blood Pressure – 110/60mmHg
The clinical signs and symptoms of
SIRS are the manifestation of two
(2) or more of the following
conditions:
• Temperature above 100.4°F or
below 96.8°F
• Heart rate above 90 beats per minute
• Respiratory rate above 20 per
minute or PaCO2 below 32 mm Hg
• White blood cell count above
12,000uL-1 or below 4,000uL-1
Source: Critical Care Medicine, 2003
Return to the Case Study
Review of Case Study 1
Mrs. C. Hicken is showing three (3)
of the conditions that make up SIRS
or Systemic Inflammatory Response
Syndrome.
Fever above 100.4°F or below 96.8°F
Heart rate above 90 beats per minute
Respiratory rate above 20 per minute
or PaCO2 below 32 mm Hg
White blood cell count above
12,000uL-1 or below 4,000uL-1
Case Study 2
Mr. M. Oose is a 47 year old male admitted
with an infected elbow. On his second day in
the hospital you find him in his room confused
and agitated.
Vital signs are as follows:
Temperature – 96.2 °F
Pulse -140 beats per minute
Respirations – 40 breaths per minute
Blood Pressure – 90/40 mmHg
Labs include a WBC count of 3,000uL-1
Further assessment of him includes:
• Urine output of 100cc for the last 8
hours
• Pulse oximetry of 88% on room air
• Pallor
Review of Case Study 2
What clinical signs and symptoms related
to sepsis does he show?
Click here
to review clinical signs and symptoms
Is he showing signs and symptoms of multiple
organ dysfunction syndrome (MODS)?
Click here
to review clinical signs and symptoms
Review Signs and Symptoms of Sepsis
The clinical signs and symptoms of
Sepsis are:
Mr. M. Oose is exhibiting the
following signs and symptoms:
•
•
•
•
•
Temperature – 96.2 °F
Pulse -140 beats per minute
Respirations – 40 breaths per minute
Blood Pressure – 90/40 mmHg
Labs include a WBC count of
3,000uL-1
•
•
•
•
•
•
•
•
•
Heart rate >90
Increased respiratory rate
Decreased blood pressure
High/Low WBC count
Fever or low body temperature
Altered mental status
Shaking
Chills
Nausea
Source: Core Curriculum for Critical Care
Nursing, 2006
Return to the Case Study
Review Signs and Symptoms of MODS
Upon further assessment Mr. M.
Oose is exhibiting the following
signs and symptoms:
• Urine output of 100cc for the last 8
hours
• Pulse oximetry of 88% on room air
• Pallor
Multiple Organ Dysfunction
(MODS) is a progressive
dysfunction in two or more organs
of the body after the onset of sepsis
where intervention is needed to
sustain life
Return to the Case Study
Review of Case Study 2
Mr. M. Oose is displaying four (4) of the
signs and symptoms of clinical sepsis.
They are:
Temperature – 96.2 °F – Low temperature
Pulse -140 beats per minute – Heart rate
over 90 beats per minute
Respirations – 40 breaths per minute –
Increased respiratory rate
Labs include a WBC count of 3,000uL-1
- Low WBC count
Review of Case Study 2
Further assessment of him includes:
•Urine output of 100cc for the last 8
hours
•Confusion
•Pulse oximetry of 88 on room air
•Pallor
Low urine output indicates possible
altered blood flow to the kidneys.
Confusion, a low pulse oximeter and
pallor indicate poor perfusion to the
tissues.
Mr. M. Oose is demonstrating multiple
organ involvement or MODS.
Case Study 3
Mr. G. Erbil is an 80 year old male
who entered the emergency room with
abdominal pain. His wife says he has
had the “flu” for days and now he is
“very sick”.
Vital signs are:
Temperature 95.7 °F
Heart rate 145 beats per minute
Respiratory rate 45 breaths per minute
Blood pressure 70/30mmHg
Further assessment of him shows a
WBC count of 2,000uL-1
Review of Case Study 3
What clinical signs and symptoms related to
sepsis does he show?
Click here
to review clinical signs and symptoms
After the review of Case Study 3 you will see
there are other factors that affect how people
respond to sepsis.
Review Signs and Symptoms of Sepsis
The clinical signs and symptoms of
Sepsis are:
Mr. G. Erbil is exhibiting the
following signs and symptoms:
• Temperature 95.7 °F
• Heart rate 145 beats per minute
• Respiratory rate 45 breaths per
minute Blood pressure 70/30mmHg
• A WBC count of 2,000uL-1
•
•
•
•
•
•
•
•
•
Heart rate >90
Increased respiratory rate
Decreased blood pressure
High/Low WBC count
Fever or low body temperature
Altered mental status
Shaking
Chills
Nausea
Source: Core Curriculum for Critical Care
Nursing, 2006
Return to the Case Study
Review of Case Study 3
He is showing signs of severe sepsis.
Temperature 95.7°F –
Low temperature
Heart rate 145 beats per minute –
Heart rate over 90
Respiratory rate 45 breaths per minute –
Increased Respiratory rate
Blood pressure 70/30mmHg –
Decreased BP
Further assessment of him shows a WBC
count of 2,000uL-1 –
Low WBC count
Other Factors Affect Outcomes in
Patients with Sepsis
Genetics and Sepsis - Is there a
relationship?
All stressed out?
Sepsis and the stress response.
Metabolism and Sepsis
Lipid Metabolism and Sepsis
Are some patients at risk for
sepsis?
Genetics and Sepsis – Is There A
Relationship?
When the natural
immune system is
altered genetically it
interrupts the body’s
way of protecting
itself from infection.
Source: Chest, 2003
Genetics and Sepsis – Is There A
Relationship?
Research is showing that
there is a genetic component
to an individual’s response to
infection. In other words,
some people may be
genetically predisposed to
sepsis.
Source: Chest, 2003
Genetics and Sepsis – Is There A
Relationship?
In addition, scientific studies
suggest a strong genetic
influence on the outcomes of
sepsis and indicate that
genetics can play a major
part in overall mortality rates
for sepsis.
Source: Chest, 2003
Genetics and Sepsis – Is There A
Relationship?
The body’s normal defense
includes inflammatory and
anti-flammatory proteins or
Cytokines which make
attempts at keeping
infections away.
These cytokines include:
•Tumor Necrosis Factors
• Interleukins
Source: Chest, 2003
Genetics and Sepsis – Is There A
Relationship?
• Genetic alterations in
Tumor Necrosis Factors
(TNF) are associated with
adverse outcomes in a
variety of infectious
diseases.
• TNF- a is associated
with macrophages
• TNF- b is associated
with lymphocytes
Source: Chest, 2003
Genetics and Sepsis – Is There A
Relationship?
• Other genetic alterations
linked with sepsis include
those associated with
Interleukin Cytokines (IL):
• IL-1 and IL-6 are
associated with the proinflammatory response
• IL-10 is associated with the
anti-inflammatory
response
Source: Chest, 2003
Genetics and Sepsis – Is There A
Relationship? YES!
One’s innate immunity can play a key
role in the prevention of sepsis. Genetic
or DNA alterations in cytokines can
affect mortality rates of infection.
Genetic testing has also been used to
take the guesswork out of predicting
how a person will respond to
medications. In the future, this could
affect how we treat patients with sepsis.
Source: Chest, 2003; AJN, 2004
Pharmacogenetics
Pharmacogenetics is the
study of DNA or gene
differences associated
with an individuals
responses to drugs.
AJN, 2004
Pharmacogenetics
Most research in
pharmacogenetics has focused
on DNA that produces proteins
involved with drug
metabolism.
A mutation in a gene that
controls enzymes that
metabolizes drugs can affect
how people react to antibiotics
used in the treatment of sepsis.
AJN, 2004
Pharmacogenetics
In the future, treatments
for sepsis could involve
genetic testing to identify
how someone will
metabolize a drug and
whether the drug will be
effective in treating the
infection.
AJN, 2004
All Stressed Out?
Sepsis and the “Stress Response”
The metabolic response to stress is
initiated by stimulation of the central
nervous system.
This is called the “Stress Response”.
Some factors that trigger the “Stress
Response” include:
•
Hypoglycemia
•
Alterations in intravascular
volume
•
Acidosis
•
Hypoxia
•
Pain
Source: Critical Care Clinics, 2000
All Stressed Out?
Sepsis and the “Stress Response”
This response is controlled by
Corticotropin Releasing Hormone (CRH)
and the chemicals Epinephrine and
Norepinephrine.
CRH promotes release of pituitary
Adreno-Corticotropic Hormone or ACTH.
The result is release of Glucocortioids
(hormones that affect metabolism).
Epinephrine and Norepinephrine speed up
the heart and creates “fight or flight” in
the body.
Source: Critical Care Clinics, 2000
All Stressed Out?
Sepsis and the “Stress Response”
During stress or illness such as sepsis
chemicals are released and levels of CRH
and ACTH are elevated.
This affects the body’s metabolism
including stimulation of triglyceride
production, catabolism of muscle, and
prevention of fat breakdown.
It affects the kidneys by releasing
hormones that make them hold on to
fluid.
It increases the work of the heart by
increasing the rate and force of
contraction, and increases lung activity.
Sources: Critical Care Clinics, 2000
Core Curriculum for Critical Care Nursing, 2006
All Stressed Out?
Sepsis and the “Stress Response”
Patients who present with signs
and symptoms of sepsis are going
through this “stress” process.
Although mechanisms are unclear,
theories suggest it may be
exacerbated or made worse by
inflammatory cytokines. The same
cytokines released in sepsis. (TNF,
IL-1, IL-6)
Source: Critical Care Clinics, 2000
Metabolism and Sepsis
Persons with sepsis have
increased demands on
the body.
They need more energy
to sustain homeostasis
because their body’s are
“Stressed”.
Metabolism and Sepsis
When homeostasis is
not balanced as in a
state of sepsis, the
organs and tissues of
the body do not get
the oxygen or energy
they need to meet the
increased demands.
Metabolism and Sepsis
In septic shock the energy in cells is decreased due to
the increased requirements of oxygen involved in the
inflammatory, coagulation, and stress processes. This
causes hypoxia in the tissues.
This lack of oxygen to the cells causes glycolysis or
breakdown of sugars in order for the cells to have
more energy. It also causes the production of lactic
acid or Anaerobic Metabolism.
Source: Critical Care Clinics, 2000
Metabolism and Sepsis
Energy levels in the cells
are usually maintained
during the initial phases
of sepsis but in late
sepsis when demands are
high and stores of energy
are low, effects on the
body cause further
problems.
Metabolism and Sepsis
Metabolism changes in sepsis include:
Hypermetabolism – The body’s oxygen consumption can be up to 25%
above baseline.
Altered protein metabolism – The body uses protein primarily within
skeletal muscles to maintain energy levels.
Altered glucose metabolism – Blood glucose levels increase because of
stress hormones, insulin resistance occurs, and glycogen stores from the
liver are used.
Altered fat metabolism – Lipids stored in fat tissues are broken down and
used for energy.
Source: Core Curriculum for Critical Care Nursing, 2006
Metabolic Effects and Sepsis
The metabolic
demands of sepsis
only add to the
imbalance causing
increased acuity
levels and decreasing
patient survival rates.
Lipid Metabolism and Sepsis – Are
some patients at risk for sepsis?
Sepsis is associated with a significant
increase in lipid metabolism.
Plasma fatty acids are greatly increased
during sepsis and they break down into
triglycerides so hypertriglyceridemia is
commonly seen in severe sepsis.
Sources:
Critical Care Clinics. 16(2):319-36, vii, 2000 Apr.
Society of Critical Care Medicine, www.sccm.org,
2005
Graphic
from:http://en.wikipedia.org/wiki/Image:Lipid_bil
ayer_and_micelle.png
Lipid Metabolism and Sepsis – Are
some patients at risk for sepsis?
High-density lipoproteins (HDLs or good
cholesterol) are decreased during sepsis and
studies have shown that the magnitude of
this decrease correlates with the severity of
sepsis.
This adds to the theory that HDLs can be
protective against the inflammatory injury
that can occur to organs during sepsis.
Sources:
Critical Care Clinics. 16(2):319-36, vii, 2000 Apr. &
Society of Critical Care Medicine, www.sccm.org, 2005
Graphic from:
http://en.wikipedia.org/wiki/Image:Lipid_bilayer_and_mic
elle.png
Review
Answer True or False to the following questions
Click on the correct answer.
1.
2.
3.
True or False. Studies have shown that genetics may
play a role in how people respond to infection or
sepsis.
True or False. Metabolism in patients with sepsis is
altered, which can make the patients condition
worse.
True or False. Patients with sepsis are also having a
“stress response”, releasing chemicals that increase
heart rate and decrease urine output.
You are correct!
Return to Review Questions
Sorry, that is incorrect.
Studies are showing
that genetics plays a
role in the severity of
infections and in
sepsis.
Return to Review Questions
That’s Right! Way to go!
Return to Review Questions
Incorrect.
Metabolism is altered in sepsis
which makes matters worse for
patients.
Return to Review Questions
That’s Right! Way to go!
Return to Review Questions
Sorry that is wrong.
Septic patients are having a stress
response to infection.
Return to Review Questions
Summary
What’s Bugging Your Patient?
Mortality or deaths related to
severe sepsis remain
unacceptably high, 30-50%.
There are approximately
750,000 new sepsis cases per
year with almost 1/3 of those
patients dying.
Source: Institute for Healthcare Improvement
Summary
What’s Bugging Your Patient?
Understanding of the
pathophysiology
of sepsis will increase
your appreciation of
the interventions
designed to decrease
mortality rates of
sepsis.
Latest Treatments for Sepsis and the
Role of Nursing
Early identification of the signs
and symptoms of sepsis is
crucial to patient outcomes.
Once SIRS or sepsis has been
identified, interventions that
are evidenced based should
implemented.
Nursing Interventions
•
•
•
•
•
•
•
•
Administer antimicrobial agents on time
Monitor antibiotic levels
Monitor for reactions to antibiotics (allergy, resistance)
Monitor and adhere to unit specific infection control protocols
recommended by the Centers for Disease Control or CDC
Provide at least twice a day teeth brushing with oral cleansing every
two hours, and if patients are on a ventilator, suction above the
endotracheal tube
Assist with treatments that limit infection, i.e. debridements, drainage
Stabilize fractures to limit tissue damage
Maintain strong rapport with family, providing frequent updates and
education.
Source: Core Curriculum for Critical Care Nurses, AACN, 2006
Nursing Interventions
•
•
•
•
•
•
•
•
•
•
•
Monitor hemodynamic parameters for change
Monitor urine output
Be prepared to administer fluid resuscitation
Be prepared to administer vasoactive medications
Be prepared to assist with central line insertions
Monitor for signs of visceral or intestinal perfusion
Avoid putting patient in Trendelenburg or head down position for lengths of
time
Maximize oxygen use and demand
• Control body temperature
• Limit patient activity
Continual assessments for decreasing physical status
Provide enteral feedings as ordered
Assist in maintaining therapeutic glucose levels
Source: Core Curriculum for Critical Care Nurses, AACN, 2006
Nursing Interventions
Involvement in the interdisciplinary team effort to reduce the
incidence and mortality rates of sepsis which includes
implementation of a “Sepsis Bundles”.
A “bundle” is a group of interventions when used together
result in better outcomes. (IHI.org)
Source: Critical Care Medicine, 2004, Institute for Healthcare Improvement
Sepsis Bundles
Sepsis Resuscitation Bundle
•
Monitor serum lactate levels
•
Blood cultures prior to antibiotic
administration
•
Broad spectrum antibiotic
administration within 3 hours for ED
admission and one hour non ED
admission
•
Fluids for hypotension and elevate
lactate levels
•
Central line placement if persistent
hypotension
Source: Institute for Healthcare Improvement
Sepsis Bundles
Sepsis Management Bundle
•
Low dose steroid administration for
septic shock
•
Recombinant Activated Protein C if
available
•
Maintain glucose <150mg/dl
•
Maintain airway pressures <30cm for
patients on ventilators
Source:
Institute for Healthcare Improvement
Conclusion
Sepsis is the leading cause of death
in intensive care units with over
2000 new cases occurring daily in
the United States.
Source: Core Curriculum for Critical Care Nursing, 2006
Research is ongoing regarding
pathophysiology as well as
treatments. But understanding
relationships of the body’s
responses to infection helps to
understand why treatment as well
as prevention is crucial to saving
lives.
References
•
•
•
•
•
•
•
Alspach, J. G. (2006). Core Curriculum for Critical Care Nursing (6th ed.). St. Louis,
Missouri: Saunders Elsevier.
Ahrens, T., & Tuggle, D. (2004, October). Surving severe sepsis: Early recognition and
treatment. Critical Care Nurse , Supplement, pp.1-15.
Cleveland Clinic (2005, July 8). Sepsis. Retrieved March 1, 2006, from
http://www.clevelandclinic.org/health/health-info/docs/3800/3887.asp?index=12361
Dellinger, R. P., Carlet, J. M., Masur, H., Gerlach, H., Calandra, T., & Cohen, J. et al.
(2004). Surviving sepsis campaign guidelines for management of severe sepsis and
septic shock. Critical Care Medicine, 32(3), pp. 858-873.
Eli Lilly & Company (2003). Xigris E-Learning Program: The pathophysiology of
severe sepsis. Retrieved April 16, 2006, from
www.xigris.com/Learing_Modules/course_01/module_02/index.htm
Eli Lilly and Company (2006). Sepsis overview: Clinical manifestation. Retrieved April
10, 2001, from www.sepsis.com/overview/clinical.jsp?regNavId=1.4
Holmes, C. L., Russell, J. A., & Walley, K. R. (2003, September). Genetic
polymorphisms in sepsis and septic shock: role in prognosis and potential for therapy.
Chest, 124(3), 1103-115. Retrieved March 1, 2006, from
http://www.chestjournal.org/cgi/content/full/124/3/1103
References
•
•
•
•
•
•
•
Hotchkiss, R. S., & Karl, I. E. (2003, January 9). The pathophysiology and treatment of
sepsis. New England Journal of Medicine, 348(2), pp.138-150.
Institute for Healthcare Improvement (2006). Critical Care: Reducing sepsis mortality.
Retrieved March 9, 2006, from http://www.ihi.org/IHI/Topics/CriticalCare/
Institute for Healthcare Improvement (2006). Severe sepsis bundles. Retrieved March 9,
2006, from
http://www.ihi.org/IHI/Topics/CriticalCare/Sepsis/SepsisSubtopicHomepage.htm
International Sepsis Forum. Understanding sepsis: Questions and answers. Retrieved
April 1, 2006, from http://www.survivingsepsis.org/index.html
Kleinpell, R. (2003, June 2003). Advances in treating patients with severe sepsis: Role
of Drotrecogin Alfa (Activated). Critical Care Nurse, 23(3), pp. 16-29.
Levy, M. M., Fink, M. P., Marshall, J. C., Abraham, E., Angus, D., & Cook, D. et al.
(2003). 2001 SCCM/ESICM/ACCP/ATS/SIS International Definitions Conference.
Critical Care Medicine, 31(4), pp. 1250-1256.
Medterms.Com (2006). Definition of Endothelium. Retrieved April 16, 2006, from
www.medterms.com/script/main/art.asp?articlekey=3248
References
• Mizock, B. (2000, April). Metabolic derangements in sepsis and septic
shock. Critical Care Clinics, 16(2), pp. 319-336.
• Parker, S. (2006, April 17). Disorders of coagulation and haemostasis.
Retrieved April 17, 2006, from www.surgicaltutor.org.uk/default.htm?core/preop2/clotting.htm-right
• Prows, C. A., & Prows, D. R. (2004). Medication selection by
genotype. American Journal of Nursing, 104(5), pp. 60-70.
• Society of Critical Care Medicine (2005, August 29). Low HDL levels
indicates poor prognosis for sepsis. Retrieved February 20, 2006, from
http://www.sccm.org/press_room/press_releases/August292005.asp
• Society of Critical Care Medicine (2006). Press room: Sepsis statistics.
Retrieved April 15, 2006, from
http://www.sccm.org/press_room/sepsis_statistics.asp
References
• Wikipedia contributors (2006). Coagulation. Wikipedia, The Free
Encyclopedia. Retrieved 05:03, April 17, 2006 from
http://en.wikipedia.org/w/index.php?(Kleinpell,
2003)title=Coagulation&oldid=48558801.
• Wikipedia contributors (2006). Lipid. Wikipedia, The Free
Encyclopedia. Retrieved 16:36, April 18, 2006 from
http://en.wikipedia.org/w/index.php?title=Lipid&oldid=48380254.
• Wikipedia contributors (2006). Multiple organ dysfunction syndrome.
Wikipedia, The Free Encyclopedia. Retrieved 14:57, April 17, 2006
from
http://en.wikipedia.org/w/index.php?title=Multiple_organ_dysfunction_
syndrome&oldid=46050908.
• Wikipedia contributors (2006). Septic shock. Wikipedia, The Free
Encyclopedia. Retrieved 15:00, April 17, 2006 from
http://en.wikipedia.org/w/index.php?title=Septic_shock&oldid=486350
56
Special thanks to the people who helped me
get through the development of this tutorial.
Keith - my wonderful husband and personal
computer geek
My mom Delores - the artist
Toni Balistieri, RN, MSN,CCNS- mentor
and friend
The great nurses I work with and tutorial
testers – Judi Luedke #1, Allie bear, Mary
Kay, Bonnie P., Angelina, Dennis, Debbie
and Don
Ms. Brunn for giving me time off from work
Pat Bowne – for keeping me on task
Nathan – my favorite grandson who let me
do homework instead of play baseball on
those really nice days!
My children for putting up with me in my not
so good moods.
And Sammie – thanks for babysitting
The End
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