Improving Patient Outcomes in Sepsis

1
Improving Patient Outcomes in Sepsis

• Miriam Hospital
• Heidi Paradis RN

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IntroductionSBAR

• Situation
• Despite advances in health care, outcomes for
  sepsis patients remain poor. These patients
  desperately need our help.
• Severe sepsis leading cause of death in the
  non-coronary ICU
• 1/3 of the 750,000 cases/yr are fatal
• 18 million cases of sepsis/yr worldwide
• Kills 1400 people worldwide every day
• of cases in US growing

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IntroductionSBAR

• Situation cont
• Mortality for severe sepsis 30-50, septic shock
  it is even higher 50-60
• This has only slightly improved in last 20 yrs
• Significant cost burden 16.7 billion in US (2000)
• In a 2002 survey many physicians reported sepsis
  as difficult to diagnose and treat

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Introduction

• Background
• 2001 Rivers et al published a study that
  demonstrated 16 reduction in mortality using a
  protocol called Early Goal Directed Therapy.
• Involves rapid diagnosis and treatment
• The Society of Critical Care Medicine, the
  European Society of Intensive Care Medicine, the
  International Sepsis Forum collaborated to
  develop the Surviving Sepsis Campaign

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Surviving Sepsis CampaignA 3 Phase Plan

• Phase I Initiative was introduced at
  international Critical Care Medicine Conference
• An action plan was developed to reduce mortality
• Phase II A Group of experts developed and
  published guidelines for sepsis management
• Phase III Translate the guidelines into clinical
  practice
• A partnership was developed with IHI (Institute
  for Healthcare Improvement) to develop bundles
  and a database to measure outcomes

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IntroductionSBAR

• Assessment
• Despite attempts to implement the bundles and
  follow the guidelines, mortality remains over 60
  at Miriam
• We are not consistently meeting our indicators
  and complying with the guidelines
• An order set exists in POM for sepsis
• Getting a central line in the patient and
  transfer to ICU has been delaying treatment

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IntroductionSBAR

• Recommendation
• We need to rapidly identify sepsis patients and
  initiate treatment as outlined in the guidelines
  to improve our outcomes
• A collaborative effort is needed
• ED and Critical Care need to work together to
  start treatment early and streamline transfer to
  ICU
• A protocol should be individualized to the Miriam
• Education so everyone is working toward same
  goals
• Tools for implementing the protocol placed in
  doorbooks
• Nurse driven to increase autonomy in implementing
  
• Data collection through ICU Collaborative with
  evaluation and feedback for improvement

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Comic relief

• If we can identify sepsis earlier
• We can improve outcomes

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Defining Sepsis

• What is Sepsis? It is a profound systemic
  inflammatory response to an infection.
• An infection triggers the inflammatory response
  to the presence of microorganisms in normally
  sterile host tissue

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SIRS

• Systemic Inflammatory Response Syndrome is a
  systemic inflammatory response resulting from
  activation of the immune system in response to
  any physiologic insult (regardless of the cause).
  The insult could be related to pancreatitis,
  ischemia, trauma or tissue injury, or burns Two
  or more of the following must be present
• Temp gt38 or lt36 degrees Celsius
• Heart rate gt90
• Resp rategt20 or PaCO2 lt32mmhg
• WBC gt12,000 or lt4,000 or gt10 immature forms

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Defining Sepsis

• Sepsis is SIRS plus a confirmed or suspected
  infection (bacterial, viral, fungal or
  parasitic). It can be a complication following
  burns, trauma, surgery, or illness. Widespread
  inflammation, coagulation and suppression of
  fibrinolysis occurs.

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Defining Sepsis

• Is the history suggestive of new infection?
• Pneumonia
• UTI
• Acute abdomen infection
• Meningitis
• Skin/soft tissue infection
• Bone joint infection
• Wound infection
• Catheter related Blood stream infection
• Endocarditis
• Implantable device infection

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Severe Sepsis

• Severe sepsis is sepsis associated with the
  dysfunction of one or more organs. Hypotension
  and hypoperfusion with lactic acidosis occurs.
  Low blood pressure, high lactate levels and signs
  of organ dysfunction are seen.
• Arterial hypoxemia (PaO2/FIO2 lt300)
• Spo2 lt90 on Room air or supplemental O2
• Acute oliguria (UOlt.5ml/kg/hr)
• Acutely altered mental status
• Creatinine gt2.0
• Bilirubin gt2.0
• Thrombocytopenia plt lt100,000
• Lactate gt 4 mmol/L
• SBP lt90 MAPlt65 These are the classic
  indicators to trigger EGDT
• Coagulopathy INRgt1.5 PTTgt60
• The patient may also exhibit chills, tachypnea,
  tachycardia, poor capillary refill and petechiae

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Septic Shock

• Is acute circulatory failure unexplained by other
  causes
• Patient has persistent arterial hypotension
  SBPlt90 MAP lt60 despite adequate volume
  resuscitation
• Patients dont always look sick until this point

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Be on the lookout for disaster
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MODS

• Multiple organ dysfunction syndrome is the
  presence of altered organ function in an acutely
  ill patient such that homeostasis cannot be
  maintained without intervention.
• Patients that progress to this state are
  critically ill and have extremely poor prognosis

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SIRS a progression

• Infection?sepsis?severe sepsis?septic shock?
  MODS?death
• Mortality is 50-60 in septic shock
• Early intervention is key
• We need to Identify patients quickly and initiate
  treatment Bundles
• Bundles are a group of interventions based on
  scientific evidence

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Understanding Sepsis

• Gram neg organisms cause most of adult cases
• E. Coli, Klebsiella, Enterobacter and
  Psuedomonias
• Gram positive organisms such as staphylococcus,
  streptococcus, pneumococcus and enterococcus
  cause others (these are associated with invasive
  devices)
• Viruses, Protozoa, parasites, fungi (Candida) and
  anaerobic organisms like Clostridium can also
  cause sepsis
• Most common sites of origin are
• Skin and wounds, GI, Respiratory, Urinary tract

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Understanding SepsisWhat happens

• Regardless of what caused it, the inflammatory
  response is the same and is designed to help the
  body fight infection and repair itself.
• SIRS is local inflammatory response that gets out
  of control.
• An avalanche of chemical mediators is set off
  that leads to tissue/organ damage
• Endotoxins from bacteria signal release of
  cytokines and other mediators that circulate
  throughout the body and cause a number of
  responses

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Understanding Sepsis

• Systemic vasodilation which causes hypotension
  and decreased afterload (svr)
• Increased capillary permeability (leaky) which
  causes edema and decreased preload (cvp)
• Platelet aggregation, fibrin deposits and
  activation of clotting cascade cause
  microcirulatory coagulation further tissue
  hypoxia and other chemicals prevent the breakdown
  of these clots
• Multiple organ disfunction results due to
  hypoperfusion caused by the hypotension,
  hypovolemia and thrombus formation.
• Hypermetabolic state where the body breaks down
  fat and muscle for energy
• As tissue damage progresses, more organs begin to
  fail ultimately leading to death
• ? The good news is we can stop this train in its
  tracks by intervening early

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Treating Sepsis

• Goal is to identify patients with Severe Sepsis
  And Septic Shock early
• Initiate treatment using the Early Goal-Directed
  Therapy Protocol and following the Surviving
  Sepsis Guidelines

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Identifying PatientsWho is at risk?

• Very young and very old
• Those who have a compromised immune system e.g..
  Patients on steroids, chemo, pneumonia
• Have wounds or injuries (burns/ trauma)
• Have alcohol or drug addiction
• Any one with intravenous catheters, wound
  drainage, urinary catheters etc.
• Those with malnutrition (TPN)
• Pts with no spleen
• Recent surgery
• Diabetics

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IdentifyingRisk for Sepsis

• Patients who are admitted to the hospital with
  serious diseases are at the highest riskof
  developing sepsis because of
• Their underlying disease
• Their previous use of antibiotics
• The presence of drug-resistant bacteria in the
  hospital
• The fact that they often require invasive tubes
  or lines. Especially if intubated/mechanically
  ventilated gt48hours

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Patient Assesment

• A complete nursing assessment can help identify
  patients at risk for developing sepsis and should
  include medical surgical history, chronic or
  acute illness, wounds, and medication history.

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Identifying Sepsis

• What do these patients look like?
• Fatigued, anorexic
• Fever (or hyothermic)
• Edema
• Tachycardic
• Tachypnea and or dyspnea
• Altered mental status (especially gt65)
• Hypotensive
• Skin may be flushed, warm and dry or cool and
  mottled

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Identifying Sepsis

• Look for
• Low spo2, abnormal blood gases
• CO2 may decrease as an early attempt to
  compensate for lactic acidosis
• Low urine output, creatinine over 2
• Abnormal WBC
• Hyperglycemia (serum glucose elevates as part of
  the stress response)
• Abnormal coagulation studies
• High bilirubin
• Key signs are sbp lt90 lactategt4
• Cultures can help identify infection and source

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Treatment Bundles

• Resusitation Bundle (starts in ER)
• The goal is to perform all of the tasks 100 of
  the time within the first 6 hours of identifying
  a patient with severe sepsis (sepsis plus organ
  dysfunction infection, 2 signs of SIRS and any
  sign of organ dysfunction but especially low BP
  or high lactate)
• Plan ICU transfer ASAP but start and continue
  bundle no matter where the patient is
• The object is to achieve optimal hemodynamic
  stability by meeting these goals
• Central venous pressure (CVP) 8-12 mm Hg
• Mean arterial pressure (MAP) gt65 mm Hg
• Urine output gt 0.5 ml/kg/hr
• Central venous oxygen saturation gt70 or Mixed
  venous oxygen saturation gt 65

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Resuscitation BundleTasks in the first 6 hours

• Measure serum lactate
• Obtain Blood cultures prior to antibiotic
  administration
• Administer broad spectrum antibiotic within 3 hrs
  if in ED (1 hr if inpatient)
• In event of hypotension and/or lactate gt4
• Deliver initial fluid bolus of 20cc/kg
  crystalloid or equivalent
• Vasopressors for hypotension not responsive to
  initial fluid to maintain MAP gt 65
• For persistent hypotension despite fluid
  resuscitation (septic shock) and/or lactate
  gt4mmol/L
• a. Achieve CVP gt8
• b. Achieve ScVO2 gt 70 or SVO2 gt 65

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Management Bundle

• The maintenance bundle can be considered
  immediately but may be completed within 24 hours.
• Whether or not to continue would be evaluated
  daily during patient care rounds.

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Management BundleFirst 24 hours

• 1. Consider low dose steroids for septic shock
  according to a standard policy
• Or document why it is not appropriate
• 2. Consider human activated protein C (XIGRIS)
  according to a standard policy
• Or document why it is not appropriate
• 3. Maintain glucose control gt70 but lt150
• 4. Maintain median Inspiratory plateau pressures
  lt30 for mechanically ventilated patients
  

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Treating SepsisFollowing the Guidelines

• If lactate gt 4 or patient is hypotensive (sbp
  lt90)
• Patient is given a fluid bolus of at least
  20cc/kg
• Initiate protocol and call ICU fellow
• Expedite transfer to ICU
• Labs (CBC, Chem 7, abg, Ca, MG,Phos, LFTs, TS,
  coag profile), ekg
• Blood cultures, sputum, urine as indicated
• Prior to antibiotics (but dont delay
  antibiotics)
• Cxr r/o pneumonia
• Broad spectrum antibiotic within 3 hours of
  identification of severe sepsis (1 hr if
  inpatient)

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Treating Sepsis

• Rapid placement of a central venous line is
  priority
• IJ or SC
• To measure CVP and ScVO2
• Fluid challenges are given to
• CVP 8-12 (15-18 if mech vent)
• SBP gt90 or MAP gt65
• UO gt 0.5ml/kg/hr
• Levophed is started if hypotension is
  unresponsive to fluid
• For ScVo2 lt70
• If Hgb lt7 consider transfusing blood to goal of
  Hgb 7-9g/dl
• Dobutamine is started if ScVo2 still lt70
• O2 therapy or intubation/ventilation if needed

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Treating Sepsis

• Transfer to ICU ASAP
• Central line is priority if not already in
• Arterial line may be needed to monitor blood
  pressure
• Continue sepsis protocol
• Fluid for cvp lt8 MAP lt65
• Vasopressor if not fluid responsive
• Inotrope and transfusion for scvo2 lt70 and Hg lt7
• Monitor cvp, ScVo2, lactate every 30 min
• Until goals met

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Treating Sepsis

• Continuing Treatment
• Airway Ventilator management
• HOB is at 30 degrees mouth care to prevent VAP
• Stress ulcer prevention
• DVT prophylaxis
• Plateau pressures lt 30 (consult with Respiratory)
• Weaning assessed daily
• Consideration of hydrocortisone 50mg IV Q 6 hrs
  for 7 days
• Strict glucose control gt70 lt150 with protocol or
  sliding scale (median glucose of 100)
• Consider Xigris (Activated protein C)

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Treating Sepsis

• Other Considerations
• Nutrition is important due to the hyper-metabolic
  state
• Skin care and assessment to prevent breakdown
• Sedation, analgesia, paralytics, must be used
  cautiously to optimize ventilation yet prevent
  prolonged intubation
• RAAS / Pain scales are used to measure patients
  progress
• Strict I/O Use foley catheters only if truly
  necessary

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Highlights from the Guidelines

• Supplemental oxygen
• Sepsis causes an imbalance between tissue oxygen
  supply and demand. Adequate tissue oxygenation is
  essential to the treatment of a patient with
  sepsis. Continuous pulse oximetry is performed.
  Supplemental oxygen is utilized to maintain the
  oxygen saturation 94.

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Diagnostic tests

• Cultures of blood, urine, sputum and any wounds
  should be performed as soon as possible. Two or
  more blood cultures are recommended. These
  cultures are critical to identifying the source
  of infection and the causative organisms and
  using the appropriate antibiotic.
• serum lactate is typically elevated in patients
  with severe sepsis or septic shock and may be
  secondary to anaerobic metabolism that ocurrs
  with hypoperfusion. It is possible to have normal
  vital signs, yet still have tissue hypoxia. So
  this is a key tool in identifiying patients
  early.
• CBC can show changes is WBC(increased, decreased
  or immature cells)
• Arterial blood gas may reveal metabolic acidosis
  or respiratory difficulties.
• Chest x-ray is ordered to rule out pneumonia or
  other respiratory difficulties.
• EKG may be needed to identify cardiac
  abnormalities.

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Antibiotic therapy

• Intravenous antibiotic therapy should be started
  within the first hour of recognition of severe
  sepsis, after appropriate cultures have been
  obtained. Broad-spectrum agents are ordered
  initially. This treatment should be reevaluated
  after culture results are available.

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Fluid therapy

• Two large bore peripheral catheters should be
  inserted initially and a central venous catheter
  should be placed ASAP.
• Fluid resuscitation (the number one priority) is
  accomplished with either crystalloids or
  colloids. Neither has been proven to be better
  than the other.
• The target is to maintain a CVP between 8-12
  mmHg, with a higher CVP recommended for a
  mechanically ventilated patient. (due to positive
  pressure ventilation)

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Vasopressor therapy

• Once fluid resusitation has been accomplished, if
  adequate blood pressure and organ perfusion has
  not been restored, vasopressor therapy should be
  started.
• Norepinephrine is the initial vasopressor of
  choice. An arterial catheter should be placed as
  soon as possible for monitoring of arterial
  pressures and blood gases.
• Vasopressin may be added in patients with
  refractory shock despite adequate fluid
  resuscitation and high dose vasopressor agents.

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Inotropic Therapy

• In patients with low cardiac output despite
  adequate fluid resuscitation, dobutamine may be
  used to increase cardiac output. If the blood
  pressure is low, it is used in combination with a
  vasopressor. ScVo2 of gt70 is the goal. Blood
  transfusion should be considered if Hg is less
  than 7 to optimized the oxygen carrying capacity
  of the blood.

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Steroids

• IV corticosteroids (hydrocortisone 200-300
  mg/day for 7 days in 3 or 4 divided doses or by
  continuous infusion) are recommended in patients
  in septic shock who, despite adequate fluid
  replacement, require vasopressor therapy to
  maintain an adequate blood pressure. Once
  vasopressor therapy is no longer required,
  steroid therapy can be weaned. Documentation is
  necessary that treatment was considered but not
  used for whatever reason.

43
Recombinant Human Activated protein C (rhAPC)

• Activated protein C is a naturally occurring
  protein made by the body and is both an
  anticoagulant and anti-inflammatory. It promotes
  fibrinolysis and inhibits thrombosis as well as
  reducing inflammation by blocking the release of
  cytokines.
• But the bodys ability to convert protein C to
  activated protein C in severe sepsis is impaired
  in sepsis. Some studies have shown that patients
  treated with activated protein C were more likely
  to survive. It is recommended only in those
  patients at high risk of death due to severe
  sepsis that has resulted in multiple organ
  failure, septic shock, or sepsis-induced adult
  respiratory distress syndrome (ARDS). It may
  potentially increase the risk of bleeding and is
  expensive.
• Documentation that this drug was considered and
  the reason why it was used or not must be
  provided.

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Blood product administration

• The recommendation is to transfuse packed red
  blood cells when the hemoglobin decreases to lt 7
  g/dl. This optimizes the oxygen carrying capacity
  of the patients blood.
• Platelets may be needed for those patients with a
  platelet count lt5000 mm3.

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Glucose control

• Hyperglycemia and insulin resistance occur in
  severe sepsis. Tight glucose control with insulin
  is used to maintain blood glucose lt 150 mg/dl.
  Insulin protocol should be followed.

46
Maintain inspiratory plateau pressure lt 30 cm
H2O) for mechanically ventilated patients

• Patients with sepsis are at increased risk for
  developing acute respiratory failure. Most
  patients with severe sepsis and septic shock will
  require mechanical ventilation. Nearly 50 of
  patients with severe sepsis will develop acute
  lung injury (ALI (acute respiratory distress
  syndrome). High tidal volumes along with high
  plateau pressures should be avoided. The goal is
  to maintain a tidal volume of 6mL/kg lean body
  weight in addition to end-inspiratory plateau
  pressure lt 30 cm H2O. Collaborate with
  Respiratory therapy to achieve this goal.
• Deep vein thrombosis prophylaxis and stress ulcer
  prophylaxis are best practices and should be
  included for all ventilated patients

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Conclusion

• Because the mortality rate and the economic costs
  from sepsis are so high, it is important to
  recognize the signs and symptoms of sepsis, SIRS,
  severe sepsis, and septic shock early.
• Every patient suspected of having sepsis should
  have a serum lactate level drawn to identify
  those patients with severe sepsis. Early
  aggressive treatment and adherence to the
  Surviving Sepsis Campaign guidelines can decrease
  morbidity and mortality.
• Miriam is collaborating on a program in
  conjunction with Quality Partners of RI and the
  ICU collaborative to follow the Surviving Sepsis
  Campaign guidelines to improve outcomes for
  patients admitted with sepsis.
• Your knowledge of this evidence based practice is
  essential.

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Your patients need you

• Goal is to improve survival
• Be a life saver

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References

• Alspach, JoAnne Grif, editor Core Curriculum for
  Critical Care Nursing, ed 6, St. Louis, Missouri,
  2006
• Dellinger, R.Phillip et al Surviving Sepsis
  Campaign International Guidelines for Management
  of Severe Sepsis and Septic Shock2008 Critical
  Care Medicine 2008 Vol.36, No.1
• International Sepsis Forum (www.sepsisforum.org)
• Institute for Healthcare Improvement
  (www.ihi.org)
• Jones, Alan E. Shapiro, Nathan Roshon, Michael.
  Implementing Early Goal Directed Therapy in the
  Emergency Setting the Challenges and Experiences
  of Translating Research Innovations into Clinical
  Reality in Academic and Community settings 2007
  by the Society for Academic Emergency Medicine
  doi.1197/j.aem.2007.04.014
• Rivers E, Nguyen B, Havstad S, et al. Early
  goal-directed therapy in the treatment of severe
  sepsis and septic shock. N Engl J Med 2001
  34513681377
• Rowey, L. Sepsis Self Learning Packet Landmark
  Medical Center, 2008
• Society of Critical Care Medicine (www.sccm.org)
• Townsend, Sean Dellinger, R.Phillip Levy,
  Mitchell Ramsey, Graham editors. Surviving
  Sepsis.2006

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Feedback

• We want to hear from you
• What is working/ what isnt
• What would help
• What are barriers
• You need to hear from us
• How are we improving
• What could be better

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Next Steps

• Please look at materials in the patient door
  books.
• There is a sepsis protocol binder with helpful
  information on the units
• Badge cards with the bundles printed on them are
  in here for you to have
• Review the articles in this module
• Check out the weblinks provided
• Become familiar with the continuous ScVO2 monitor
  (contact Heidi if you need inservice)
• Please print complete the post test and case
  study questions and return to educator
• Please contact Heidi Paradis with any questions
  or feedback
• Watch for posted data from ICU collaborative on
  how we are doing
• THANK YOU for your time and interest in improving
  outcomes for our sepsis patients