Presentation on theme: "Sepsis Mechanism of Disease Quick Overview Last Updated on 2/25/2014."— Presentation transcript:
Sepsis Mechanism of Disease Quick Overview Last Updated on 2/25/2014
So why are we here ? Building awareness of Sepsis Improving your ability to recognize sepsis early Increasing the use of Early Goal Directed Therapy Educating healthcare professionals Developing guidelines of care Using the Code Sepsis Rapid Response System
Building Awareness of Sepsis Dr. Emanuel Rivers Formally conceptualized severe sepsis and/or septic shock in 2001 with a landmark paper Developed an Algorithm for the management of Sepsis EGDT Early Goal Directed Therapy Recommendations have been replicated in many publications since 2001 European Society of Intensive Care Medicine and the Society of Critical Care Medicine
Did you know? The word “Sepsis” was derived from the Ancient Greek for ROTTEN FLESH AND PUTREFACTION
Did you know? Sepsis is growing healthcare challenge 1.It is the #1 cause of death in non-coronary ICU 2.11 th leading cause of death overall 3.28-day mortality: 30- 50% 4.>750,000 US cases annually 5.Long term complications and treatment may qualify the patient for transfer to an Acute Long Term Care Hospital
Did you know? Sepsis is growing healthcare challenge 6. Incidence is growing faster than overall population 7.Sepsis is the most expensive reason for hospitalization ($17.0 billion cost of treatment in the US) 8.Sepsis is a major cause of mortality throughout the world killing about 1,400 per day
RISK Factors for Developing Sepsis Age (Newborn or over 35 years old) Being pregnant Having chronic disorders such as Diabetes or Cirrhosis, Lupus, Cancer, Poly-Substance Abuse Having a weakened immune system (HIV, taking immune modulating drugs, chemotherapy, etc.) Having medical devices inserted into the body (catheters, tubes, etc).
What is Sepsis? Sepsis is defined as a suspected or documented infection in the presence of two or more Systemic Inflammatory Response Syndrome Identifiers (SIRS). Similar to acute MI, Stoke and Poly-trauma, rapid treatment (within the first few hours) influences the outcome. Similar to acute MI, Stoke and Poly-trauma, rapid treatment (within the first few hours) influences the outcome.
Defining SIRS The causes of SIRS are broadly classified as: Infectious or Noninfectious
The Symptoms Associated with SIRS: Hypothermia (temp 100 ◦ ) Tachycardia (HR >100bpm) Tachypnea (resp>20/min) or Hypocapnia (arterial CO 2 20/min) or Hypocapnia (arterial CO 2 <32mmHg) Leukopenia or Leukocytosis AMS
Noninfectious causes of SIRS include Trauma Burns Pancreatitis Ischemia Hemorrhage Complications of surgery Adrenal Insufficiency Pulmonary Embolism Complicated Aortic AneurysmAortic Aneurysm Cardiac Tamponade Anaphylaxis Drug Overdose
People Admitted To The Hospital With Serious Diseases Are At The Highest Risk For Sepsis Because Of: 1.Underlying diseases such as diabetes, cancer, etc. 2.Presence of drug resistant bacteria in the hospital 3.The fact that they often require an Invasive Lines 4.Being Immuno – compromised / Auto-Immune Disease 5.Surgery / Invasive procedure 6.Mechanical ventilation 7.Having wounds or injuries from burns, a car crash or a bullet
There are 3 Levels of Sepsis Sepsis: 2 SIRS identifiers with a confirmed source of infection Severe Sepsis: Sepsis plus Organ Dysfunction (24 to 72 hrs) Septic Shock: Is Severe Sepsis with persistent hypotension and hypo-perfusion, which can lead to cell death, end- organ damage, multi-system organ failure and death.
What is Severe Sepsis? Inflammation + Infection + Organ Dysfunction The progression: SIRS: Manifested by two or more of the following: Temp > 100.4 or 100.4 or < 96.9 HR > 90 bpm HR > 90 bpm RR > 20 cpm RR > 20 cpm WBC > 12,000 or 10% WBC > 12,000 or 10% AMS AMS
The Symptoms of Septic Shock: Hypotension BP< 90 despite fluid bolus of 20 ml/kg. Map <65 High lactic acid levels > 4mmoL Hypothermia (temp 100 ◦ ) Tachycardia (HR >100bpm) Tachypnea (resp>20/min) or hypocapnia (arterial CO 2 20/min) or hypocapnia (arterial CO 2 <32mmhg) Resp. Rate >20 bpm
Diagnosing Sepsis Routine screening of potentially infected patients (12 hrs) Sudden development of high or low temperature Rapid heart or breathing rate Low blood pressure Positive blood or suspected cultures Laboratory Data Use of the sepsis bundles may lead to reduced mortality and improvement in sepsis care.
Tests used to identify Sepsis Blood tests to measure lactic acid levels Lactate Levels > 4 Cultures and blood cultures to help determine the type and site of infection prior to antibiotic administration CBC with Diff Elevated Neutrophil Count Bands > 10% Pulse oximetry to measure oxygen levels Temperature SCVO2 Levels
We Check and Check and Check Lactatic Acid Levels ? 1.3 5.6 1.3 3.6 >4 is a good Indicator of Sepsis
Goals for Treatment of Severe Sepsis and Septic Shock (EGDT) Early identification IV access Treat infection with empiric antibiotics in a timely manner Source control Resuscitation with IV fluids and pressors if necessary(hemodynamic bundle) Emergency supportive care for acute organ dysfunction Infection prevention
Treating Sepsis and Septic Shock with Fluids Ineffective arterial circulation in patients with severe sepsis and septic shock is due to vasodilatation associated with infection Crystalloid fluid, such as normal saline can be administered at 30ml/kg over 30 minutes using a pressure bag.
Sepsis – Be A Member of the “Golden Hour” Club “Sepsis Bundle.” Lactate Levels Blood Cultures Blood Cultures Antibiotic Use And Fluid Resuscitation Items that need to be completed within 6 hours: Items that need to be completed within 6 hours: Vaso-pressors for BP not responding to fluid, Measurement of CVP and SCVO2, MAP, Measurement of CVP and SCVO2, MAP, Re-measure lactate if originally elevated. Re-measure lactate if originally elevated.
Empiric Antibiotic Selection When the potential infection source or pathogen is not obvious, BROAD SPECTRUM COVERAGE may be an appropriate empiric choice. If Pseudomonas is NOT suspected: Vancomycin + Meropenem or Pip/Taz If Pseudomonas are suspected: Vancomycin + 2 of the following »Meropenem »Levofloxacin »Pip/Taz »Aztreonam
Nurses Role in Sepsis Severe Sepsis Screening begins on admission !!! Recognize early signs and symptoms of sepsis Re-assess patients at least every 12 hours Utilize the SEPSIS SCREENING TOOL (Meditech) SPEAK UP Call a Code Sepsis
My Patient has a Positive Sepsis Screen – Now what do I do? Notify your charge nurse / Sepsis Champion to review the screen If positive call Code Sepsis Notify the ER Physician / Hospitalist / Intensivest / PCP Implement Sepsis Bundle Move patient up to the next level of care Add Problem to Plan of Care Document Implementation of Sepsis Bundle
Increasing the use of appropriate treatment Code Sepsis 1.Obtain a Lactated Level 2.Draw Blood Cultures 3.Give a broad spectrum Antibiotic 4.Normal Saline Bolus at a rate of 30cc / Kg / 30 minutes 5.Prepare for possible transfer to a Higher level of care: ICU
Increasing the use of Appropriate Treatment (EGDT) Severe Sepsis without Shock Check lactate q4hrs till less than 2 mmol / L Check SCVO2 Optimal value is 70% Tight Glucose Control Watch for signs of Clinical Deterioration Severe Sepsis with Shock Initiate ICU Admission Airway Management Arterial Line Flow-Trac for Hourly Hemodynamic Monitoring CVP Placement (Pre-Sep Catheter) CVP Monitoring Foley Catheter Tight Glucose Control Start of Vasopressors
Why Monitor ScVO2 Tissue hypoxia is often occult, reaching an advanced and lethal stage before its presence is known and resuscitation is attempted. Lactic Acid and ScVO 2 measurements allow us to monitor occult tissue hypoxia. Vital signs are inadequate for detecting global tissue hypoxia and not adequate as a resuscitation end point. Patients with normal blood pressure can still have global tissue hypoxia. Up to 50% of patients resuscitated from shock may have continued global tissue hypoxia (Elevated lactate and decreased ScVO 2 ) despite normalized vital signs and central venous pressure.