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Superbugs and Sepsis

Superbugs and Sepsis. Overview: MRSA in your Ambulance! Sepsis: Definitions and Pathophysiology Role of the EMS Provider in Early Goal Directed Therapy for Severe Sepsis and Septic Shock Prehospital Testing of Lactate. Faculty . Michael Schmitz, DO, MS

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Superbugs and Sepsis

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  1. Superbugs and Sepsis Overview: MRSA in your Ambulance! Sepsis: Definitions and Pathophysiology Role of the EMS Provider in Early Goal Directed Therapy for Severe Sepsis and Septic Shock Prehospital Testing of Lactate

  2. Faculty Michael Schmitz, DO, MS Department of Emergency Medicine Southern Maine Medical Center Andrew Turcotte, RN, BS, NREMT-P/CCEMT-P Kennebunk Fire Rescue

  3. Thank you • Cynthia Pernice, MPA, Maine Health • Jennifer Granata, RN SMMC • Christopher Pare, EMT-P • Matthew Sholl, MD, MPH, FACEP

  4. MRSA in Your Ambulance!

  5. Objectives • Describe the basic characteristics of the bacteria, Staphylococcus aureus • Discuss the history of drug-resistant Staphylococcus aureus in the hospital and the community • Discuss the types of infections associated with MRSA • Present current research describing the prevalence of MRSA in the prehospital environment • Describe best Infection Control practices

  6. What is MRSA? Methicillin Resistant Staphylococcus Aureus

  7. Definition • Bacteria commonly carried on the skin or in the nose of healthy people • MRSA may be present without causing infection • 25% to 30% of the population is “colonized” • “Staph” bacteria are one of the most common causes of skin infections in the U.S.

  8. History - MRSA • First described in 1961 in the United Kingdom • First recognized in the 1970’s causing epidemics in healthcare settings. These strains are referred to as (HCA-MRSA) • Generally resistant to most antibiotics: all beta-lactams, usually macrolides, clindamycin, quinolones, and tetracyclines • Risk factors for HCA-MRSA: – prolonged hospitalization – care in an intensive care unit – prolonged antimicrobial therapy – surgical procedures – close proximity to an infected/colonized patient • Usually considered an infection of chronically ill, hospitalized patients

  9. Community-Acquired Methicillin-ResistantStaphylococcus aureus (CA-MRSA) • A new strain of MRSA presenting from the community in persons without traditional risk factors for MRSA • First known CA infection reported in 1980 • Differing from HCA-MRSA in terms of – Epidemiology – Antibiotic sensitivity patterns – Virulence – Presentation – Treatment • Thought to have evolved separately in the community based on genetic differences

  10. CA-MRSA- Prevalence • Infection rates are increasing A recent meta-analysis found CA-MRSA to account for 30%- 37% of all hospitalized MRSA patients • In Los Angeles, a study demonstrated that CA-MRSA was the most common cause of community-acquired skin/soft tissue infections presenting to emergency rooms • A Houston study demonstrated that CA-MRSA accounted for 56% in 2000-2001, 57% in 2002 and 78% in 2003 of community-associated Staph aureus infections in hospitalized pediatric patients • A Rhode Island study has demonstrated that up to 40% of children with MRSA have community acquired strains

  11. MRSA-associated Diseases • Skin/soft tissue 1,266 (77%) • Wound (Traumatic) 157 (10%) • Urinary Tract Infection 64 (4%) • Sinusitis 61 (4%) • Bacteremia 43 (3%) • Pneumonia 31 (2%) • Fridkin et al NEJM 2005;352:1436-44

  12. CA-MRSA Risk Factors • CA-MRSA appears to spread by close contact • In one study 26% of CA hand infections were MRSA-positive • Factors conducive to spread of the bacteria include: – Close skin to skin contact – Cuts or abrasions – Shared contaminated items or surfaces – Poor hygiene – Crowded living conditions

  13. CA-MRSA: Signs/Symptoms • CA-MRSA most often causes severe skin and soft tissue infections. • Skin and soft tissue infections often present as cellulitis, boils, or furuncles often in the thighs and buttocks. • Patients may think they have been bitten by a spider. • Children may present with a severe necrotizing pneumonia. • More serious infections like blood stream infections, septic arthritis, osteomyelitis, septic arthritis, and endocarditis are possible

  14. EMS and MRSA • A 2007 study tested five specific areas in a fleet of 21 ambulances for MRSA contamination • Steering wheel, left patient handrail, stretcher cushion, work area to the patient’s right, yankauer suction tip • Thirteen samples isolated from 10 of the 21 ambulances tested were positive (47.6%). • 7/13 samples from the work area to the right of the patient tested positive -Prehospital Emergency Care 2007;11:241-244

  15. EMS and MRSA • A 2009 study examined the prevalence of MRSA on the stethoscopes of EMS providers • Stethoscopes, like doctor’s ties, are known fomites for MRSA • Of 50 stethoscopes that were swabbed, 16 (32%) were colonized with MRSA • LTTE in subsequent issue challenges this paper’s lab protocol Prehospital Emergency Care 2009;13:71-74

  16. PREVALENCE OF METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS IN AMBULANCES IN SOUTHERN MAINE Robert Brown, OMS-IV, Julianne Minnon, OMS-IV, Stephanie Schneider, OMS-IV, James Vaughn, PhD • Study published in 2010 • Lead author UNE MS-IV • Obtained samples from specified areas in 51 ambulances in southern Maine • 25 (49%) had at least one area that was positive for MRSA • No statistical difference between fire-based vs. non-fire based services or based on call-volume • Statistically different lower rate of contamination among services providing paid, 24-hour coverage vs. those that did not

  17. PREVALENCE OF METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS IN AMBULANCES IN SOUTHERN MAINE

  18. PREVALENCE OF METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS IN AMBULANCES IN SOUTHERN MAINE

  19. PREVALENCE OF METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS IN AMBULANCES IN SOUTHERN MAINE

  20. Why is EMS at risk? • Fast turn-around times • Difficult to clean thoroughly following a call • Working quickly in a confined space • Patient’s isolation status may not be shared at time of transfer or be “buried” in the chart

  21. Prevention • CDC’s “Five C’s” • Crowding • Skin to skin contact • Compromised Skin • Contaminated Items and Surfaces • Lack of Cleanliness

  22. Prevention • Keep hands clean by washing thoroughly with soap and water or using an alcohol-based hand sanitizer • Keep cuts and scrapes clean and covered with a bandage until healed • Avoid contact with other people’s wounds or bandages • Avoid sharing personal items such as towels or razors • If skin is dry, use a moisturizer to prevent cracking

  23. Handwashing • Without question, the most effective way to prevent transmission • Alcohol based hand sanitizers are effective against MRSA, must be at least 60% alcohol (CDC)

  24. Handwashing

  25. Handwashing

  26. Handwashing

  27. Celebrity Endorsement?

  28. Objectives: • Discuss the prevalence of sepsis in the United States • Define systemic inflammatory response syndrome, sepsis and septic shock • Briefly discuss the pathophysiology of this complex problem • Discuss the presentation of the septic patient • Why is this important?

  29. Sepsis is…. • COMMON • LETHAL • EXPENSIVE

  30. Sepsis By the Numbers • More than 750,000 cases of severe sepsis in the US each year • Mortality about 20% (recent decline) • Economic cost of $17 billion each year • Incidence is projected to increase by 1.5% yearly • Although prognosis has improved, because of increased incidence, actual deaths per year will increase

  31. What is Sepsis?

  32. Severe Sepsis Septic Shock SIRS Sepsis The Sepsis Continuum • A clinical response arising from a nonspecific insult, with 2 of the following: • T >38oC or <36oC • HR >90 beats/min • RR >20/min • WBC >12,000/mm3or <4,000/mm3 or >10% bands SIRS with a presumed or confirmed infectious process Sepsis with organ failure Refractory hypotension SIRS = systemic inflammatory response syndrome Chest 1992;101:1644.

  33. SEPSIS DEFINED: • “An inciting infectious event and host-pathogen interaction leading to hemodynamic consequences cause by the relationship among proinflammatory, antiinflammatory and apopotic mediators” • Rackow EC, Astiz ME. JAMA 1991; 266:548-554

  34. Sepsis: Pathogenesis • Systemic proinflammatory reaction causes endothelial damage, microvascular dysfunction, and impaired tissue oxygenation. • Excessive antiinflammatory response triggers anergy and host immunosuppression. • In addition, pro- and anti-inflammatory processes may interfere with each other, creating a state of destructive immunologic dissonance Am J Physiol 1980; 239:F135.

  35. SEPSIS: PRESENTATION • Pathogenesis starts before ICU admit • Patient vital signs alone may fail to detect global tissue hypoxia • Early presentation may be subtle (do not rely on fever alone) • Early recognition is the key to successful treatment

  36. ROLE OF LACTATE • Lactate is a marker of anaerobic metabolism • Indicates global tissue hypoxia, critical step is recognition and aggressive treatment • High lactate is associated w/ increased morbidity/mortality

  37. Chest 2006;130;159-1595

  38. SEPSIS • Sepsis can be thought of as “a process of malignant intravascular inflammation” • End result: a potentially lethal and complex type of distributive shock • Troubling thought: “No autopsy studies have revealed why patients with sepsis die.” NEJM 2003;348:2 138-150

  39. SO WHAT CAN BE DONE TO INTERVENE ?

  40. EARLY GOAL-DIRECTED THERAPY FOR SEVERE SEPSIS AND SEPTIC SHOCK

  41. Objectives: • Define Early Goal-Directed Therapy (EGDT) for Severe Sepsis and Septic Shock • Review the literature evaluating EGDT • Discuss the impact of EGDT for treating sepsis • Discuss the importance of fluid resuscitation in this patient population • Discuss how to apply EGDT in the pre-hospital environment

  42. Purpose: “to evaluate the efficacy of early goal-directed therapy before admission to the intensive care unit”. NEJM 2001;345:1368

  43. Early Goal Directed Therapy “The administration of IV fluids, pressors and transfusion based upon targets for central venous pressure, blood pressure, urine output, mixed venous oxygen saturation and hematocrit to reduce mortality in patients with severe sepsis and septic shock”

  44. History • Physicians at Henry Ford Hospital had previously established lactate measurement as a screening test for severe sepsis (Chest 1996;110:145S) • Prevalence study estimated baseline mortality of 51% for patients with severe sepsis and septic shock at their facility (Acad Emerg Med 1997;4:402-403) • Basis for “standard treatment” arm of protocol

  45. NEJM 2001;345:1368-77

  46. Early Goal-Directed Therapy CVP: central venous pressure MAP: mean arterial pressure ScvO2: central venous oxygen saturation NEJM 2001;345:1368-77.

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