Cindy Johnson, MS, RN, CAPA Clinical Simulation Educator-NGHS

Susan A. Irick MS, RN, ACNP-C Disease Manager Sepsis & Pneumonia-NGHS

¡  Identify  knowledge  about  the  impact  of  sepsis  in  healthcare  

¡  Review  basic  pathophysiology  involved  in  sepsis  

¡  Identify  the  importance  of  early  recognition  and  rapid  interventions  for  improved  patient  outcomes  

¡  Identify  nursing’s  role  in  the  process  ¡  Review  Surviving  Sepsis  Campaign’s  updated  guidelines  

SEPSIS

In  2009,  Sepsis:  

¡  Caused  1.7  million  hospitalizations  in  U.S.  

¡  Caused  258,000  deaths  in  2009  

¡  Sepsis  care  costs  $15  -­‐  $17  billion  dollars  per  year  in  the  U.S.  

¡  Sepsis  has  a  higher  annual  death  rate  than  heart  attacks,  stroke,  or  cancer  

¡  In-­‐hospital  incidence  of  sepsis  has  increased  9%  yearly  since  2000.  

Non-healthcare providers commonly refer to sepsis as blood poisoning or blood infection. Although blood poisoning is a

common term for sepsis, it isn’t an accurate description of the disease and the two terms should not be used interchangeably. Sepsis is not an infection in of itself. Sepsis is the body's often

deadly response to infection or injury

2011 Sepsis Alliance/Harris Poll demonstrated that less than ½ of Americans have ever even heard the word “SEPSIS”

Sepsis is a Medical Emergency that is caused by an overwhelming immune response of the body to infection.

The body’s normal defense mechanism is amplified, setting off a

cascade of events that can lead to widespread inflammation, leaky vessels, and microvascular coagulation

This causes impaired blood flow to the organs thus causing damage by

depriving them of nutrients and oxygen, which leads to organ failure.

Symptoms are not caused by the germ (microorganism) itself, but by the body’s response to fight the germ !!!

§  Triggered  by  invasion  of  bacteria  in  the  tissue  §  Complex  process  ▪  Localizes/controls  bacterial  invasion  ▪  Activates  phagocytic  cells  ▪  Generates  cytokines            (nonspecific  mediators  of  inflammation)  ▪  Neutrophils  are  activated  to  perform  phagocytosis  and  release  of  mediators  

 

§  Results  in  tissue  repair  and  healing    

Neviere,  R.  (2013).  Pathophysiology  of  sepsis.    UpToDate.    

¡  Generalized  immune  response  leads  to  widespread  cellular  injury  

¡  Cellular  injury  results  in  organ  dysfunction  ¡  Circulatory  dysfunction  results  in  diffuse  vasodilation,  redistribution  of  intravascular  fluid  

¡  Decreased  microcirculation  and  microvascular  clotting  

¡  Coagulation  abnormalities  Neviere,  R.  (2013).  Pathophysiology  of  sepsis.    UpToDate.    

Sepsis  is  defined  by  the  following  stages:    ¡  SIRS  :      defined  by  2  or  more  of  the  following  criteria    

¡  SEPSIS  :    SIRS  plus  present  or  suspected  infection  

¡  SEVERE  SEPSIS  :    Sepsis  plus  one  other  criteria    

¡  SEPTIC  SHOCK    :    Severe  Sepsis  that  fails  to  respond  to  fluid  resuscitation  –(30ml/kg)    

¡ SIRS  -­‐    10%  ¡ Sepsis  -­‐  20%  ¡ Severe  Sepsis  20  –  40%  ¡ Septic  Shock    40  –  60%      

Kleinpell  R,  Aitken  L,  Schorr  CA.  (2013).Implications  of  the  new  international  sepsis  guidelines  for  nursing  care.  Am  J  Crit  Care,  22(3):212-­‐22.  

Systemic  Inflammatory  Response  Syndrome  (defined  by  TWO  or  more  of  the  following)  

   ¡ Heart  rate  >  90  beats  per  minute  ¡ Temperature  <  96.8ºF  (36º  C)  or    

>  1oo.4º  F  (38º  C)  ¡ Respiratory  rate  >  20  breaths  per  minute  or  PaCO2  <  32mmHg  

¡ White  blood  cell  count  >  12,000/mm3    or      <  4000  mm  

¡ OR  normal  WBC  with    >  10%    bands  

¡ SIRS  criteria  met:  § plus  present  or  suspected  infection    §  Other  symptoms  include:  ▪  Altered  mental  status  ▪  Hyperglycemia  (>140mg/dl  with  no  hx  diabetes)  ▪  Mottled  skin,  delayed  capillary  refill  ▪  Tachypnea  ▪  Lactate  >  1  

 

The  key  to  this  stage  is  the  presence  of  infection.    Studies  show  the  actual  source  of  infection  is  not  known  in  49%  of  

sepsis  cases.  

Severe  Sepsis  :      ¡  Sepsis  plus  one  other  criteria  –  organ  dysfunction  

§  Acute  oliguria  for  two  hours  (<0.5  ml/kg  per  hour)    despite  fluid  resuscitation  

§  Organ  dysfunction  (serum  lactate  >  4)  §  Hypo-­‐perfusion  (MAP  <  65  mmHg,  acute  oliguria,  increase  in  creatinine)  

§  Platelets  count  <  100,000    §  Hypotension  SBP  <  90mm/hg  or    >  40mm  drop  below  baseline  BP  

 

¡ Septic  Shock  is  severe  sepsis  that  fails  to  respond  to  fluid  resuscitation  –(30ml/kg)    §  Acute  Lung  Injury  with  PaO2/FiO2  ratio<250  in  absence  of  pneumonia  or  <200  in  presence  of  pneumonia  

§  New  elevation  bilirubin  >2.0,  Creatinine  >  2.0  §  New  Platelet  Count  <100,000  §  Unexplained  PT  (INR)>  1.5              

Bone RC, et al. Chest 1992;101:1644-55.

►  Sepsis ●  Known or suspected

infection, plus ●  ≥2 SIRS criteria

►  Severe Sepsis ●  Sepsis plus ●  ≥1 organ dysfunction

►  Septic Shock ●  Sepsis with hypotension

despite fluid resuscitation, plus perfusion abnormalities

Sepsis Definitions - Summary

Macrophage Ingesting Staphyloccocus Bacteria

www.cellsalive.com

Active Phagocytosis www.cellsalive.com  

Pathogenic  insult  resulting  in  infection  

Microthrombi formation Endothelial damage ↑ Capillary permeability and

edema formation

Enhanced expression of adhesion molecules

Massive cytokine production

Effector molecule release

Inflammatory/Immune System Response

Specific genetic signaling

Neutrophil and Monocyte activation

Endothelial cell activation Platelet dysfunction

Apoptosis Imbalance between inflammation and

antiinflamation

↓ Fibrinolysis

↑ Coagulation

Quadrad of dysfunction in sepsis

Reduced tissue/cellular perfusion

Oxygen & substrate debt

Organ dysfunction

Insult phase

Molecular activation

phase System

dysfunction phase

Organ dysfunction

phase

¡  ↑  formation  of  microthrombi    

¡  ↓  clot  breakdown  (impaired  fibrinolysis)  

¡   Results  in:  §  Widespread  coagulopathy  

§  Microvascular  thrombosis  

§  Multiple  organ  dysfunction  

Ahrens,  T.  (2013).  Sepsis  update:  Early  identification  and  management.  AACN  Webinar  Series  

¡  Role  of  endothelium  §  Lines  blood  vessels  §  Reacts  to  mediators  §  Results  in  dysfunction  

¡  Increase  in  vascular  permeability  §  Physical  disruption  allows  capillary  leak  into  interstitial  space  and  results  in  peripheral  hypoxia  

§  Vasodilation  –  hypotension  

 

Ahrens,  T.  (2013).  Sepsis  update:  Early  identification  and  management.  AACN  Webinar  Series  

Stimulation of Mediator Release via WBC

   

Journal  of  Critical  Illness,  1991  

Interruption  of  Endothelium  Integrity  

   

Journal  of  Critical  Illness,  1991  

Progression of Endothelial Dysfunction

Journal  of  Critical  Illness,  1991  

1.   Assess  for  adequacy/patency  of  airway  –  high  flow  oxygen  

2.   Antibiotics  –  within  the  first  hour  along  with  rapid  source  identification  and  control.  Do  not  delay  initiation  of  antibiotics.    

3.   IV  Fluid  therapy  –  Maintain  BP  and  hemodynamic  parameters.  Initial  fluid  resuscitation  should  be  with  crystalloid  IVF(NS,  LR,  etc)  at  30mL/kg.    

4.   Vasopressors  –  ONLY  if  fluids  not  effective.  Target  MAP  >65  mmHg.  

 Norepinephrine,    Epinephrine,  Vasopressin  

1.   Labs  –  Blood  Cultures  x  2    PRIOR  to  antibiotics  within  1  hour  of      sepsis  diagnosis,  Lactate  level,  CBC  w/diff  

For  every  hour  delay  in  antibiotic  administration,  the  patient’s  risk  of  dying  increases  by  7.6%.  

¡  Pneumonia  ¡  Intra-­‐abdominal  infection  ¡  Acute  pyelonephritis  ¡  Skin/soft  tissue  infection  ¡  Possible  necrotizing  fasciitis  ¡  Neutropenic  fever  ¡  Unknown  source  

¡  Treatment  should  not  be  delayed  ¡  Importance  of  protocols  to  implement  

¡  Essential  elements  §  Definitive  antibiotics  §  Supportive  treatment  with  oxygenation,  ventilation  

§  Circulatory  support  with  fluid  &  inotropic  administration  

§  Maintain  glucose  level  <180  mg/dL  

 

¡  Knowledge  of  the  pathophysiology,  signs  &  symptoms,  and  treatment  of  severe  sepsis  is  critical    §  Early  detection  is  key  to  reducing  mortality  

§  Recognition  of  SIRS  criteria    §  Recognition  of  clinical  evidence  of  sepsis  

§  Prompt  institution  of  treatment  measures  

 Kleinpell, Graves & Ackerman. AACN Clinical Issues 2006;17;4:1-9  

Surviving Sepsis Campaign: Phase III

► A  global,  multi-­‐center,  2-­‐year  trial  ● Multiple  hospital  networks  ●  166  sites  ●  15,022  patients  

► Primary  outcome  ● The  impact  of  a  model  for  changing  bedside  management  of  sepsis  

► Secondary  outcome  ● Mortality  

Surviving Sepsis Campaign

► Primary outcome of SSC: Use multi-faceted intervention – Facilitate knowledge transfer and

change clinical practice •  20% increase in compliance over 24 months

► Secondary outcome – Change in clinical practice would be

associated with decreased mortality •  7.0% ARR, 19% RRR •  5.4% ARR after severity adjustment

¡  To  be  completed  within  3  hours  §  Measure  lactate  level  §  Obtain  blood  cultures  prior  to  antibiotic  administration  §  Administer  broad  spectrum  antibiotics  §  Administer  30ml/kg  crystalloid  for  hypotension  or  lactate  ≥  4  mmol/L  

¡  To  be  completed  within  6  hours  §  Apply  vasopressors  (for  hypotension  that  does  not  respond  to  initial  fluid  

resuscitation)  to  maintain  a  MAP  ≥  65  mmHg  §  In  the  event  of  persistent  arterial  hypotension  despite  volume  resuscitation  

(septic  shock)  or  initial  lactate  ≥  4:  ▪  Measure  central  venous  pressure  (CVP)**  ▪  Measure  central  venous  oxygen  saturation  (Scvo2)**  ▪  Remeasure  lactate  if  initial  lactate  was  elevated.  

¡  American  Association  of  Critical  Care  Nurses  

¡  Society  of  Critical  Care  Medicine  (Survivingsepsis.org)  

¡  Sepsis  Alliance  (sepsisalliance.org)  

¡  World  Sepsis  Day  (world-­‐sepsis-­‐day.org)  

¡  American  College  of  Emergency  Physicians  (www.acep.org/sepsis/)  

¡  I.D.S.A.  –  Infectious  Disease  Society  of  America  (www.idsociety.org)  

¡  Delinger,  RP,  Levy,  MM,  et.al.  (2013).  Surviving  Sepsis  Campaign  :    International  guidelines  for  management  of  severe  

sepsis  and  septic    shock.  Critical  Care  Medicine  Journal,  41,  2.  

¡  Picard,  K.,  O’Donoghue,  S.,  Young-­‐Kershaw,  D.,  &  Russell,  K.  (2006).  Development  and  Implementation  of  a  

Multidisciplinary  Sepsis  Protocol.  Critical  Care  Nurse,  26,  43-­‐54.  

¡  Levinson,  A.,  Casserly,  B.,  Levy,  M.  (2011).  Reducing  mortality  in  severe  sepsis  and  septic  shock.  Seminars  in  Respiratory  

and  Critical  Care  Medicine,  32:2.  

¡  Casserly,  B.,  Baram,  M.,  et.al.  (2011).  Implementing  a  collaborative  protocol  in  a  sepsis  intervention  program  :  lessons  

learned.  Lung  ,189:  11-­‐19.  

¡  Giardis,  M.,  Rinaldi,  L.,  Donno,  L.  et.al.  (2009).  Effects  on  management  and  outcome  of  severe  sepsis  and  septic  shock  

patients  admitted  to  the  intensive  care  unit  after  implementation  of  a  sepsis  program  :  a  pilot  study.    Critical  Care  ,13:R143.  

¡  Ahrens,  T.  (2013).  Sepsis  update:  Early  identification  and  management.  AACN  Webinar  Series.    

¡  Kleinpell  R,  Aitken  L,  Schorr  CA.  (2013).  Implications  of  the  new  international  sepsis  guidelines  for  nursing  care.  Am  J  Crit  

Care,22(3):212-­‐22.  

THANK    YOU  !!!