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PHARM 213 Infectious Diseases > 9. Antimicrobial Stewardship > Flashcards

9. Antimicrobial Stewardship Flashcards

1
Q

Antimicrobial stewardship

A
  • ISDA: “…coordinated interventions designed to improve & measure the appropriate use of antimicrobials by promoting the selection of the optimal antimicrobial drug regimen, dose, duration of therapy, & route of administration
  • Improve appropriate antimicrobial use & therefore patient outcomes
  • NOT the intention to solely reduce antimicrobial use
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2
Q

Why do we need Antimicrobial Stewardship (AMS)?

A

ALL ANTIMICROBIAL USE DRIVES HARM

  • Patient level harm
  • Population level harm

Direct adverse effects on patients:

  • Allergies, side effects, supra-infections
  • Antimicrobial resistance

Adverse effects on community:

  • “The problem of the commons” aka global cost
  • Antimicrobial resistance
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3
Q

Discovery of Antimicrobial Resistance (AMR)

A
  • Penicillin (1943) – 3 years
  • Tetracycline (1950) – 1 year
  • Erythromycin (1953) – 15 years
  • Methicillin (1960) – 2 years
  • Gentamycin (1967) – 12 years
  • Vancomycin (1972) – 16 years
  • Imipenem (1985) – 13 years
  • Ceftazidime – 2 years
  • Levofloxacin (1996) – 0 years
  • Linezolid (2000) – 1 year
  • Daptomycin (2003) – 2 years
  • Ceftaroline (2010) – 1 year
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4
Q

Antimicrobial use = AMR

A
  • Antimicrobial use is proportional to antimicrobial resistance
  • NZ is a high user of antibiotics, and the rates are slightly decreasing
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5
Q

Individual AMR

A
  • After taking a macrolide for CAP, a patients likelihood that their next infection is related to a resistant organism is increased significantly (10x in the week after & 2x 6 months after)
  • For UTIs being treated with amoxicillin or trimethoprim, 30 % increase in resistant infections are seen a year after taking a single course of antibiotics
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6
Q

Patient outcomes

A
  • Although there are many different types of antibiotics that can be used, if they’re colonised with more resistant bacteria, they will have poorer outcomes
  • Increased cost and length of hospital stay, increased mortality & delay in appropriate therapy
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7
Q

Economic costs by 2050:

A
  • 1.1 – 3.8% reduction in total global GDP
  • +$0.3 trillion increase p/a on health
  • ~100 trillion in total
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8
Q

Drivers of antimicrobial use

A 
Prescribers:
\+ Clinical need
\+ Anxiety/concerns
- Patient expectations
- Economic – esp. agriculture
- Lack of alternatives – e.g. phage therapy, monoclonal antibodies
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9
Q

Improving antimicrobial use

A
  1. MOH: New Zealand Antimicrobial Resistance Action Plan

2. WHO: Global Action Plan on Antimicrobial Resistance

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10
Q

Governance

A
  • Ensure executive awareness & responsibility
  • Regular review of quality indicators of AMR
  • Regular improvement in antimicrobial use
  • Appropriate resourcing
  • Primary Care: DHBs, PHOs, Aged care etc
  • Secondary care: DHBs, Directories
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11
Q

Population interventions

A
  • Surveillance of antimicrobial use
  • Formulary, restriction & control
  • Review & feedback to prescribers
  • Education
  • Development of antimicrobial guidelines
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12
Q
  1. Surveillance of antimicrobial use
A
  • In 2017, almost 1/3rd (32.7%) of the 21,034 prescriptions that were assessable did not comply with guidelines
  • In addition, ¼ of the 24,987 prescriptions that were accessible were classified as inappropriate
  • …but when you cannot measure it, when you cannot express it in numbers, your knowledge is of a meagre & satisfactory kind…
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13
Q
  1. Formulary, restriction & control
A
  • Simple, effective, evidence-based intervention
  • Set a list of approved medicines:
    + WHO: Access, Watch, Reserve (“AWaRe”)
    + PHARMAC: HML
  • Introduce controls to access
  • Funding, physical removal, expert approval
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14
Q
  1. Review & feedback
A

HARD, effective, evidence-based intervention

Audit & feedback to prescribers:

  • Quality improvement cycle
  • Adherence to guidelines
  • Documentation of indication & review

Feedback/reporting to target audience:

  • To prescriber (RMO, SMO, GP)
  • To prescribers’ team
  • To management group
  • To governance
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15
Q

Education to users

A
  • Undergraduate
  • Continuing professional development
  • Easy to provide but limited benefit
  • Service specific messaging
  • In combination with audit & feedback
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16
Q

Education to END users

A

Continual education is important to change culture:

  • Children through to adults
  • Understand disease processes
  • Understand benefits & risks

Consistent managing:

  • Stop direct to consumer advertising
  • Encourage vaccination
  • Taking antimicrobials correctly – “as directed”
17
Q

Patient level interventions

A
  • Use of guidelines
  • Reporting lab results
  • Optimising therapy
  • Preventing infection pharmaceutically
  • Improving medical records
  • Assessing antibiotic allergies
18
Q
  1. Antimicrobial guidelines
A
  • Adherence reduces mortality & length of stay
  • Best guess or empiric therapy for disease states or specific organisms
  • Written by expert groups
  • Used to treat a patient based on population data
  • International guidelines useful for e.g. PKPD & durations

Local guidelines preferable:

  • Difference in causative organisms (rare)
  • Difference in susceptibility (common)

How local is local?

  • International – Australia, South Africa, USA, UK?
  • National > Regional > Hospital > Unit
  • NZ > Auckland > ACH > BMTU
19
Q

Examples of guidelines

A

International:

  • WHO TB
  • European Society of Cardiology IE
  • BSAC (UK) or TG (Australia)

Local:

  • National BPAC community guidelines
  • Health pathways (GP guidelines)
  • Hospital guidelines (ADHB Script; Southern Regional)
20
Q

Key components in guideline development

A
  • Causative pathogens in disease – e.g. E. coli in cystitis, S. pneumoniae in CAP
  • Local susceptibility of pathogens – Antibiograms
  • Dosing regimen for optimal PKPD – e.g. cefuroxime 750 mg IV q8h for S. pneumoniae or 750 mg IV q6h for K. pneumoniae
  • When to start & stop
  • Patient factors
    + Allergies
    + PK variations e.g. Vd, CL, F (Obesity, renal impairment, functioning gut)
    + Immunosuppression
21
Q

ADME

A
  • Absorption – route of administration & bioavailability (vancomycin)
  • Distribution – solubility & protein binding (rifampicin)
  • Metabolism – activation of pro-drugs (colistin)
  • Elimination – hepatic or urine (UTI)
22
Q

Site of infection - “penetration”

A
  • Pharmacokinetics
  • Penetration may be governed by distribution OR elimination
  • Does the antimicrobial get to the site of infection in sufficient concentrations?
  • Usually studies in ‘normal’ tissue e.g. abdominal or skin
  • Difficult/sanctuary sites e.g. CSF, eyes, prostate
23
Q

When to start?

A
  • Dependent on infection being treated
  • Critically unwell patients (sepsis/septic shock)
    + Timeline of effectiveness antibiotics critical 7% increase in mortality/hour
  • Less severe presentations/less urgency
24
Q

When to stop?

A
  • Determining a stop date or duration of therapy
  • Population studies
  • Patient response “complete the course”
  • Biomarkers e.g. temperature, CRP, PCT
25
Q

Guideline non-adherence

A
  • Prescribing to adhere to guidelines
  • Developed by specialists to provide best evidence

Why wouldn’t you?

  • Availability & ease of use
  • Perceived correctness of content
  • Need for variation based on patient features
  • Clinical judgement trumping guideline
  • Time pressure
  • Past experience/teaching is basis of practice

Changing people’s opinions are not easy to do

26
Q

Reporting microbiology results

A
  • Selected microbiology reporting
  • Nudge theory
  • Allows narrowing of spectrum
  • Results to be considered in patient view
  • Clinical condition & site of infection
  • Relationship to timing of antimicrobials
    + Antibiotics or sample first?
  • Effect of PKPD
27
Q

Optimising the route - IVOS

A
  • Changing patients from IV to oral
  • Reduced length of stay, healthcare costs, secondary infections, line associated complications, nursing time
  • Increased patient satisfaction

Criteria to change oral OR to continue IV

  • Absorption of drug – patient & bioavailability
  • Site of infection e.g. endocarditis
  • Type of host e.g. neutropenic
  • Does this all optimise PKPD?

Recommended by a pharmacist … or DONE by a pharmacist

28
Q

Optimise concentration

A
  • Measuring a concentration removes estimation of relationship to population-based dosing
  • Aiming for a PKPD target concentration “TDM”
  • Efficacy or toxicity or both
  • Adjust the dose accordingly
  • E.g. Optimising vancomycin concentrations to efficacy AUC 400 improves renal toxicity by reducing AUC > 600-700
29
Q

Optimise prevention

A

Vaccination to prevent infection (& thus antimicrobials)

Use of antimicrobial to prevent infection:

  • Risk due to defect in immune system or response
  • Surgical setting – incision
  • Medical setting – medicines, infection, pathology
30
Q

Optimise prevention - surgical

A

Aim: Prevent surgical site infections (SSI)

  • Likely to have beneficial bacterial contamination or
  • Likely to have catastrophic effects

Similar considerations as starting empiric therapy
- Common pathogens causing SSI & their susceptibilities appropriate dosing & intervals

  • Timing is critical: Optimally within 60 minutes before incision (“knife to skin”) … administration issues?
  • Mostly single dose therapy appropriate, certainly not more than 24 hours
  • If patients on treatment antimicrobials; appropriate prophylaxis still necessary to optimise timing & concentrations
  • Re-dosing when concentration drops; blood loss or surgery > t1/2
31
Q

Optimise prevention - medical

A
  • Aim: To prevent (initial or relapse) bacterial, viral, fungal or protozoal infections
  • Medicines e.g. chemotherapy, corticosteroids
  • Infection e.g. HIV, HSV
  • Pathology e.g. Splenectomy, rheumatic fever
32
Q

Optimise record keeping (?!)

A
  • Documentation of key quality indicators
  • Write down the indication for the antimicrobial
  • Write down a stop or review date
  • Allows review by others e.g. a pharmacist
  • Encourages the prescriber to consider what they are doing
33
Q

Optimise “allergies”

A
  • Common problem is prevalence of “allergy”
  • Differentiate between allergy & ADR
  • Most common antimicrobial allergy recorded is penicillin

Poorer outcomes compared to non-allergic patients:

  • Increased mortality
  • Increased morbidity
  • Increased broad-spectrum use (some inferior)
  • Increased length of stay in hospital
  • Increased healthcare costs
  • Highly over-estimated in literature
  • All antimicrobial allergies should be reviewed at prescribing or admission

De-labelling penicillin allergy:

  • ~65% of patients de-labelled (MMH)
  • ~80% with questions/history alone
  • ~20% with skin testing or oral challenge
  • Update documentation
34
Q

A principled use of antimicrobials

A
  • Make an accurate diagnosis
  • Take microbiology samples (and consider past microbiology)
  • Start empiric guideline-adherent microbiology
  • Adjust therapy accordingly
  • Review patient progress & microbiology
  • Adjust therapy accordingly
35
Q

Making a diagnosis

A
  • Clinician to recognise infection
  • Clinical examination & history
  • Undertake appropriate investigations
  • Interpret laboratory results:
    + Contamination/colonisation/infection
  • Consider likely pathogens & how to treat
36
Q

Starting antimicrobials

A
  • “Start smart then focus”
  • Directed therapy or empiric therapy
  • Directed therapy
    + Known pathogen +/- susceptibility
  • Empiric therapy from guidelines
  • Likely pathogens involved in disease e.g. E. coli predominant in pyelonephritis
  • Local susceptibility patterns of pathogens e.g. Auckland 2018 E. coli 48%(c)/38%(h) S to amoxicillin
  • Appropriate regimen for susceptible organisms e.g. cefuroxime 750 mg IV q8h
  • Appropriate duration of treatment e.g. 10 days for pyelonephritis
  • Difference depending on severity of illness
37
Q

What about a “severe” infection?

A
  • Severity of illness
  • Sepsis or septic shock - Current definition using SOFA score

Disease specific severity scoring systems

  • E.g. CURB-65 for CAP demonstrates increasing mortality
  • E.g. Cellulitis treatment pathway with factors of failure
38
Q

Adjusting therapy

A
  • Initial therapy may need to be narrowed or broadened from results e.g. usually starting broad & de-escalating spectrum once pathogen identified
  • Route of administration could be changed e.g. IVOS
  • Deciding on a duration of therapy; over & under-treatment risks
  • Any change in therapy – start antimicrobial review again (PK/PD)

PHARM 213 Infectious Diseases (13 decks)

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