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Sepsis power point presentation
1. Sepsis
How sick is your patient?
ESSEX COUNTY FIRE CHIEFS
ASSOCIATION
SEPSIS SPECIAL PROJECT WAIVER
2. Objectives
Understand the causes and risk factors of sepsis.
Be able to indentify a septic patient.
Understand and follow the components of the
Special Project Waiver
3. Why is this important?
Mortality*
More than 750,000 severe sepsis cases are reported
annually in the U.S. and, of those, 215,000 patients
die.
4. Why is this important?
Sepsis
According to the most recent CDC statistics: Sepsis is the 11th leading
cause of death in the United States.
6. SIRS
Systemic Inflammatory Response Syndrome-It’s the
first step in the path to sepsis
Causes:
Trauma
Severe Burns
Pancreatitis
Ischemia
Infection (Can Lead to Sepsis)
7. SIRS – Signs & Symptoms
Two or More
White Blood Cell (Leukocyte) Count
> 12,000 or < 4,000
Respiratory Rate:
> 20 breaths.min or mechanically ventilated
Heart Rate:
> 90 beats/min
Temperature:
> 38 C (100.4 F) or < 36 C (96.8 F)
8. Sepsis is Defined as:
Sepsis is SIRS with documented or suspected
infection.
Bacterial
Viral
Fungal
Protozoa
9. Sepsis
Common Causes
Pneumonia
Urinary Tract Infection
Abdominal Surgery
Cellulitis
IV Drug Users
Ear Infections
10. Sepsis – High Risk Factors
Higher Risk
Extremes of Age
Multiple Co-morbidities
Recent Hospitalization
2 million Hospital Acquired Infections per year.
11. Sepsis – High Risk Factors
Cough Present
Indwelling Foley/IV
Wounds/Injuries
Para/Quadriplegic
Bedridden
Recent Antibiotic Use
12. Sepsis – High Risk Factors
Immune Compromise
Diabetic
Cancer
HIV
Systemic Steroids
Anti-rejection Medications
Powerful Anti-inflammatory Medications
14. Pathophysiology
Immune and inflammatory response causes
vasodilation, and so reduces venous return and
cardiac output.
The immune response is where bacteria invade
phagocytes, causing damage or even death to the
cell. This leads to the release of histamine and
proteolytic enzymes leading to vasodilatation
Also can cause poor tissue perfusion and tissue
death (necrosis).
All of this increases cellular metabolism which causes the
cells to switch to anerobic metabolism.
15. MODS
Multiple Organ Dysfunction Syndrome (MODS)
Presence of altered organ dysfunction in the septic patient.
Last stop before death.
16. How can we help????
Early recognition and treatment are the key to better
patient outcomes. Good thorough assessment
including measure of lactate
Identifying these patients and notifying hospital staff
early, has shown to decrease mortality 30%.
The main goal of our assessment of the patient is to
identify the septic patient to facilitate transition to
goal directed therapy at the hospital.
17. What is Lactate???
It is a measure of tissue perfusion, it can tell you how
well cells are being oxygenated regardless of blood
pressure.
When cells do not receive enough oxygen, they
convert to anaerobic metabolism
The byproduct of anaerobic metabolism are lactate
and hydrogen ions.
Unit of Measurement is mmol/l (millimoles per liter)
18. EMS Lactate Levels
Pre-Hospital Lactate Meters
Developed for Endurance Athletes
Works just like a Glucometer
19. EMS Treatment
Early Recognition Key
History
Physical exam
Look for Infection
Strict Aseptic Practices
Patient already compromised
20. EMS Treatment
Fluid Resuscitation
Large Bore IVs
30 ml/kg bolus if no signs or history of CHF*
Or CRF.
20 ml/kg if signs or hx of CHF or CRF*
*This is specific to this special project
24. EMS Treatment
Place supine with feet elevated.
NOT Trendelenberg
May Impede Breathing
Rapid Transport
Our hand off report must include the results of
assessment and suspicion of sepsis as well as our
Lactate Measure.
25. ER Treatment
Early Goal Directed Therapy (EGDT)
Goal Oriented Manipulation of:
Cardiac Preload
Cardiac Afterload
Contractility
Balanced between oxygen delivery and oxygen
demand
26. EGDT - Goals
Resuscitation Bundle (< 6 hours):
Serum Lactate Levels
Blood Cultures Prior to Antibiotics
Antibiotic therapy within 1 hour of diagnosis
Each hour of delay during the first 6 hours of hypotension was
associated with a 7.6% increase in mortality
28. EGDT - Treatment
Mean Arterial Pressure (MAP)
Maintain at 65-70 mm Hg
Vasoactive Agents
Norepinephrine
Dopamine
29. EGDT - Results
Severe Sepsis or Septic Shock after 72 hours
EGDT Standard Therapy
Mortality 30.5% 46.5%
ScvO2 70.4% 65.3%
Lactate 3.0 mmol/L 4.4 mmol/L
Rivers, E, Et Al. Early Goal directed Therapy in the treatment of Severe Sepsis and Septic Shock. N Engl J Med 2001; 19:1368-1377.
30. EGDT - Results
EGDT save lives
Meeting all EGDT goals in less than 6 hours
decreases mortality
Studies support even better results with earlier
intervention
31. EMS Sepsis Special Project
Goal
Identify Septic Shock Patients
Start Fluid Resuscitation
Start Pressors (if needed)
Transfer to closest appropriate facility
Consider emergent Transport
32. EMS Sepsis Notification Criteria
Initiate sepsis special project waiver for patients
18 years and older
NOT Pregnant
TWO or more of the below SIRS Criteria (Systemic
Inflammatory Response Syndrome)
Temperature >38 C (100.4 F) or <36 C (96.8 F)
Pulse >90
Respiratory rate > 20
AND
33. EMS Sepsis Notification Criteria
Suspected or Documented Infection
AND
One of the following:
Hypoperfusion evidenced by SBP < 90
Lactate ≥ 4
34. Treatment Flowchart
S e p s i s
A g e ≥ 1 8
If no , f o llo w ST P
Suspected or D o c u m e n t e d
I n f e c t i o n
If no , f o llo w ST P
A t l e a s t 2 o f t h e F o l l o w i n g
• H R ≥ 9 0 /min
• RR ≥ 2 0 /min
• T emp < 9 6 .8 f o r > 1 0 0 .4 f
If no , f o llo w ST P
A N D a n y o f t h e F o l l o w i n g
• SBP < 9 0 mmH g
• MAP < 6 5
• L a c tate ≥ 4 mmo l/L
If patient satisfies all criteria, administer NS 30cc/kg over 1st hour unless history of
or signs and symptoms of CHF/CRF in which case administer 20cc/kg NS
in first hour and oxygen. Alert hospital to septic shock identification.
35. Case #1 – EMS Findings
56 y/o Female
Responsive to painful stimuli
Witnessed Seizure
HR: 135
Temp: 103.5 F
BP: No Radial Pulse
Glucose: High
36. Case #1 – EMS Findings
History:
Flu-like Symptoms
Weakness X 2 Days
Diabetes
Headaches
37. Case #1 – EMS Findings
Allergy:
Codeine
Medications:
Oral hypoglycemic (prescribed to husband) occasionally.
38. ER Findings
Pulse: 134
BP: 75/39
Resp: 8
Temp: 39.8 C (103.6 F)
Lactate 7.7
Glucose: >1,600
39. ER Findings
WBC: 6.4
Jumped to >20 in 24 hours
Infection Sites:
Urinary tract Infection
Bacteria in blood
Fungus is Blood
40. ER Treatment
Intubated
Central Line Placement (CVP)
Dopamine
Normal Saline
6 liters!!!!
41. ER Treatment
Antibiotics
Insulin
Admitted to ICU
Diagnosis: Sepsis, DKA and
Bleeding Gastric Ulcer
50. Hospital Treatment
Intubation
Central line
Normal Saline
First 72 hours – 22 Liters!!!
Total – 51 Liters!!!!
Antibiotics
51. Cryptic Sepsis
Patients with severe sepsis accompanied by lactic
acidosis may display global tissue hypoxia in the
absence of hypotension.
Early identification and goal-directed therapy of this
subgroup leads to a reduction in morbidity and
mortality.
Donnino, M, Et. Al. Cryptic Septic Shock: A Sub-analysis of Early, Goal-Directed Therapy. Chest 2003; 124 (4): 90
Henry Ford Hospital, Detroit, MI
54. Notify your EMS director each time you use the
Lactate Meter.
All cases will be reviewed by the EMS director as well
as the affiliate medical director.
Editor's Notes
The financial toll is also devastating. Total hospital costs associated with the care of severely septic patients is $16.7 billion annually. The excess length of stay per post-operative sepsis case is nearly 11 days, and the cost of treating an ICU patient with sepsis is six times greater than that of treating a patient without sepsis.
Representing the number-one cause of preventable mortality in hospitals, sepsis leaves a staggering and unnecessary human toll in its wake. Saving lives and reducing unnecessary costs are the driving forces behind several federal initiatives aimed at eliminating sepsis and events that lead to it. For example, the Medicaid 1115 Waiver, a federal pay-for-performance initiative that reimburses hospitals for higher-quality care, is currently being beta-tested in California&apos;s public hospitals.
SIRS was first described by Dr. William R. Nelson, of the University of Toronto, in a presentation to the Nordic Micro Circulation meeting in Geilo, Norway in February 1983. There was intent to encourage a definition which dealt with the multiple (rather than a single) etiologies associated with organ dysfunction and failure following a hypotensive shock episode. The active pathways leading to such pathophysiology may include fibrin deposition, platelet aggregation, coagulopathies and leukocyte liposomal release. The implication of such a definition suggests that recognition of the activation of one such pathway is often indicative of that additional pathophysiologic processes are also active and that these pathways are synergistically destructive. The clinical condition may lead to renal failure, respiratory distress syndrome, central nervous system dysfunction and possible gastrointestinal bleeding.
Criteria for SIRS were established in 1992 as part of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference.
