2016 Updates to the Hospital Acquired- and Ventilator Associated-Pneumonia Guidelines

Janessa M. Smith, PharmD, BCPSClinical Pharmacy Specialist, Infectious DiseasesThe Johns Hopkins Hospital

Objectives

• List risk factors for development of pneumonia with multidrug resistant organisms

• Describe the role of an antibiogram in the empiric treatment of hospital acquired pneumonia (HAP) and ventilator associated pneumonia (VAP)

• Identify the role of pharmacokinetic and pharmacodynamic parameters in dose optimization

• Discuss the role of biomarkers in diagnosing and treating HAP and VAP

Epidemiology

• Pneumonia is the most common healthcare-associated infection (HAI)

• HAP and VAP account for 22% of HAI annually• Up to 50% of patients with HAP develop serious

complications – Respiratory failure, pleural effusions, septic shock, renal failure

and empyema• All-cause mortality from VAP ranges from 20-50% and

attributable mortality has been estimated at 13%Magill SSl. N Engl Med. 2014;370:2542; Sopena N. Chest. 2005;127:213; Melson WG. Lancet Infect Dis. 2013;13:665; Muscedere JG. Clin Infec Dis. 2010;51 (supp 1):S120; Kollef MH. Infec Control Hosp Epidemiol. 2012;33:250.

Impact on the Healthcare System

• VAP prolongs length of ventilation (7.6 to 11.5 days) and hospital stay (11.5 to 13.1 days)

• VAP estimated to result in excess health care costs of $40,000 per patient

• Limited data on the impact of HAP

Magill SS, et al. N Engl Med. 2014;370:2542; Sopena N, et al., Chest. 2005;127:213; Melson WG, et al. Lancet Infect Dis. 2013;13:665; Muscedere JG, et al. Clin Infec Dis. 2010;51 (supp 1):S120; Kollef MH, et al. Infec Control Hosp Epidemiol.2012;33:250.

Definitions

• Pneumonia – Presence of a new lung infiltrate plus clinical evidence of an

infectious cause (fever, purulent sputum, leukocytosis and decline in oxygenation)

• VAP– Pneumonia that develops >48 hours after endotracheal

intubation• HAP

– Pneumonia that develops >48 hours after hospital admission

Am J Respir Crit Care Med. 2005;171:388-416.

Major Changes in the 2016 Update

• Recommend less invasive microbiologic methods for diagnosis

• Redefine risk factors for multidrug resistant organisms (MDRO)

• Emphasis on antibiograms to guide empiric therapy• Emphasis on optimizing antimicrobial dosing based on

pharmacokinetic (PK) and pharmacodynamic (PD) parameters

• Suggest duration of therapy of 7 days for all HAP/VAP treatment

Kalil AC. Clin Infect Dis. 2016;63:1-51.

Microbiologic Methods to Diagnosis

Recommendation• Non-invasive sampling with

semiquantitative cultures preferred– Expectorated or induced sputum cultures– Endonasotracheal cultures

• If invasive sampling methods used, should be quantitative and should be used to stop therapy if below diagnostic threshold:– Bronchoalveolar lavage: <104 CFU/mL – Protected brush specimen: <103 CFU/mL

Rationale• No evidence that invasive sampling

impact clinical outcomes, including changes in antibiotics

• Non-invasive sampling can be done more rapidly and with fewer complications and resources

Kalil AC. Clin Infect Dis. 2016;63:1-51.

Selecting Empiric Therapy

• Antibiotics should be started early and should target potential pathogens

• Potential pathogens determined by surveillance data and patient-specific risk factors

Adequate early

antibioticsSuperfluous

coverage

Kalil AC. Clin Infect Dis. 2016;63:1-51.

Removal of HCAP Definition

2005 Guidelines • HCAP: Healthcare-associated

pneumonia– Any patient who was hospitalized in an

acute care hospital for > 48 hours within prior 90 days

– Residing in a nursing home or long-term care facility

– Received recent IV antibiotics, chemotherapy, or wound care in the prior 30 days

– Attended a hospital or hemodialysis clinic• Role: to identify patients at risk for

MDRO

2016 Guidelines• Removed from guidelines • Rationale: new evidence

suggesting that many patients identified as HCAP did not have MDRO isolated as a cause of VAP or HAP

Am J Respir Crit Care Med. 2005;171:388-416.; Kalil AC. Clin Infect Dis. 2016;63:1-51.

Definition of MDRO

• Microorganisms that are resistant to one or more classes of antimicrobial agents– E.g., MRSA, VRE, certain Gram-negative bacilli

www.cdc.gov

MDRO Definition in Clinical Studies

Reference Pneumonia Type Definition

Gross (2014) HCAP/CAP MRSA, Pseudomonas aeruginosa, extended-spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae, carbapenem-intermediate or -resistant Enterobacteriaceae (CIRE), Acinetobacter spp., and Stenotrophomonasmaltophilia

Chamlers (2014) HCAP/CAP MRSA, Gram-negative Enterobacteriaceae, and P. aeruginosa

Valles (2014) HCAP MRSA, P. aeruginosa, S. maltophilia, A. baumannii, Klebsiella spp., and S. marcescens

Depuydt (2008) VAP MRSA, ESBL, Acinetobacter spp., Pseudomonas spp., Stenotrophomonasspp. resistant to at least one of the following: ceftazidime, piperacillin, imipenem

Giantsou (2005), Trouillet (1998), Martin-Loeches (2013)

VAP P. aeruginosa, MRSA, A. baumannii, S. maltophilia

Chamlers JD, et al. Clin Infec Dis. 2014;58:330.; Gross AE. Antimicrob Agents Chemother. 2014;58:5262.; Valles J.Intensive Care Med. 2014;40:572.; Depuydt P. Intensive Care Med.2008;34:675.; Giantsou E. Intensive Care Med. 2005;31:1488.; Trouillet JL. Am J Respir Crit Care Med. 1998; 157:531.Martin-Loeches I. Intensive Care Med.2013;39:672.

Trends in Antibiotic Use with HCAP

Jones BE. Clin Infect Dis. 2015;61:1403-10.

• 128 VA Hospitals evaluated trends in antibiotic prescribing and antibiotic resistance for pneumonia 2006-2010

• 95,511 hospitalizations were included

2006 2010 P-valueAntibiotic UseVancomycin 16% 31% <0.001Piperacillin-tazobactam 16% 27% <0.001Ceftriaxone 39% 33% <0.001Azithromycin 39.5% 36% <0.001MDRO Pathogens IsolatedMRSA 2.5% 2% <0.001P. aeruginosa 1.9% 2% 0.14Acinetobacter spp. 0.2% 0.2% 0.17

Sensitivity and Specificity of HCAP for Identifying MDRO

• HCAP more often associated with P. aeruginosa, S. aureus, Enterobacteriaceae but overall poor predictor of MDRO

• Meta-analysis of 24 studies comparing incidence of MDRO HCAP vs CAP found low sensitivity and specificity of HCAP definition

Chamlers JD, et al. Clin Infec Dis. 2014;58:330.

Sensitivity SpecificityAll MDRO 53.7% 71.2%MRSA 69% 65.7%Enterobacteriaceae 42.9% 66.1%Pseudomonas aeruginosa 52.2% 67.7%

Isolation of MDRO by HCAP Definition

• Retrospective review characterized the etiology of pneumonia and risk factors for MDRO CAP or HCAP

• Only 19% had an identifiable etiology

• Viral pneumonia was the most common cause, followed by S. pneumoniae

• Overall MDRO prevalence was 3.8%

• MDRO independent predictors: – Antibiotics in the last 90 days– Duration of hospitalization in prior 90

and 180 days – P. aeruginosa colonization/infection

in the previous 12 months

Gross AE. Antimicrob Agents Chemother. 2014;58:5262.

HCAP(n = 258)

CAP (n = 263)

Any MDRO 5.9% 1.9%MRSA 3.1% 1.1%P. aeruginosa 2.7% 0.8%

Risk Factors for Any MDRO Pneumonia

MDRO-VAP vs non-MDRO-VAP• Use of intravenous antibiotics in the

past 90 days• >5 days of hospitalization prior to

VAP• Acute respiratory distress

syndrome before VAP• Renal replacement therapy prior to

VAP • Septic shock at the time of VAP

MDRO-HAP vs non-MDRO-HAP• Use of intravenous antibiotics in the

past 90 days

Risk factors for MRSA HAP/VAP

• More common in late-onset (>4 days of hospitalization) than early-onset

• Major risk factor for MRSA HAP/VAP is prior intravenous antibiotic exposure within 90 days– Unclear which antibiotics put patients are higher risk as

studies did not evaluate this• The role of MRSA nasal surveillance is unclear

Case-Control Studies for MRSA HAP/VAP

Reference Pneumonia Type Risk Factors OR (95% CI)Wooten (2013)

MRSA vs MSSApneumonia (all)

Recent antibiotics (w/in 90 days)Tobacco useIllicit drug useLiver disease

7.01 (3.54-13.01)2.66 (1.38-5.14)3.52 (2.21-5.59)3.50 (1.51-8.11)

Moreira (2008)

MRSA vs MSSA VAP Previous antibiotic therapyAge >60 yearsUse of corticosteroids

5.93 (1.30-30.74)5.33 (1.48-20.04)5.79 (1.53-23.18)

Bouza(2012)

MRSA vs non-MRSA VAP

Antibiotic exposurePleural effusionAPACHE II score

2.38 (1.35-4.19)2.74 (1.23-6.12)1.10 (1.04-1.16)

Wooten DA. Resp Med. 2013;107:1266-70.; Moreira MR. Braz J Infect Dis. 2008;12:499-503.; Bouza E. J Hosp Infect. 2012;80:150-5.

MRSA Active Surveillance

• Screening of asymptomatic patients to identify carriers• Swab of nares, oropharynx and/or perineum• Identification of carriers for intervention to prevent

spread of MRSA (e.g., contact precautions)• Standard culture or PCR methods

Role of Surveillance in Empiric MRSA Treatment

• Concurrent or recent positive MRSA screen increases the likelihood of respiratory infection with MRSA

• Better negative predictive value (98%) vs positive predictive value (30%)– May have a better role in deciding which patients do NOT need

MRSA-active therapy – About 30% of respiratory infections due to MRSA are in patients

with positive MRSA surveillance studies• Recent surveillance (<7 days) is more relevant as patients

can acquire MRSA while hospitalized

Robicsek A. J Clin Microbiol. 2008;46:588-92. Davis KA. Clin Infect Dis. 2004;39:776-82. Sarikonda KV. Crit Care Med. 2010;38:1991-5.

Risk factors for MDR P. aeruginosaHAP/VAP

• Mechanical ventilation• COPD• Cystic fibrosis or bronchiectasis• Prior antibiotic use

– Specifically carbapenems, broad spectrum cephalosporins and fluoroquinolones

Montero M. Eur J Clin Microbiol Infect Dis. 2010;29:335-9.; Parker CM. J Crit Care. 2008;23:18-26.

Antibiogram

• Summary of antimicrobial susceptibilities of bacterial isolates within an institution over a defined period of time

• Used to track resistance rate over time and to inform clinicians about empiric antibiotic selection

• IDSA Guidelines on Implementing an Antimicrobial Stewardship Program recommend using a stratified antibiogram over a non-stratified antibiogram– Stratified by location (e.g., ICU vs non-ICU) or patient age

Barlam TF. Clin Infect Dis. 2016;62:e51-77.

Example Antibiogram

Empiric Treatment of VAP

• Initial therapy for VAP should be based on local antibiogram, ideally ICU-specific

• In absence of local antibiogram data, clinicians should refer to large national and international surveys of organisms and resistance patterns

• Surveillance studies indicate the most common organisms:– S. aureus (20-30%)– P. aeruginosa (10-20%)– Other enteric Gram-negative organisms (20-40%)– A. baumanii (5-10%)

Sievert DM. Infect Control Hosp Epidemiol. 2013;34:1-14.

Sievert DM. Infect Control Hosp Epidemiol. 2013;34:1-14.

Empiric Treatment of VAP – S. aureus

• For empiric coverage, use an agent with activity against Gram-negative bacilli and MSSA – Cefepime, piperacillin-tazobactam, levofloxacin, imipenem or meropenem

• Therapeutic regimen should include an agent targeted at MRSA if:– Patient has been exposed to intravenous antibiotics within the prior 90 days– Patient being treated in a unit with >10-20% of S. aureus isolates are MRSA

or if the prevalence of MRSA is unknown– Weak recommendation with low-quality evidence

• Empiric therapy targeted at MRSA should include Vancomycin or Linezolid

Targeted Therapy – S. aureus

MRSA MSSA

VancomycinLinezolid

OxacillinNafcillin

Cefazolin

MRSA Agents – Vancomycin vs Linezolid

Author Patient population ResultsStevens et al. (2002) Suspected MRSA infection

(MRSA pneumonia, n = 64)Clinical cure, MRSA pneumonia (NS):Linezolid 52.2%Vancomycin 53.8%

Kohno et al. (2007) Suspected MRSA infection (MRSA pneumonia, n = 54)

Clinical cure, MRSA pneumonia (NS):Linezolid 60%Vancomycin 47.4%

Wunderink et al (2008) VAP, MRSA (n = 146)

Clinical response (NS):Linezolid 66.7%Vancomycin 52.9%

Wunderink et al (2012) HAP or HCAP, MRSA (n = 448)

Clinical success (p = 0.042):Linezolid 57.6%Vancomycin 46.6%

Stevens DL. Clin Infect Dis.2002;34:1481-90.; Kohno S. J Antimicrob Chemother. 2007;60:1361-9. Wunderink RG. Chest. 2008;134:1200-7.; Wunderink RG. Clin Infect Dis. 2012;54:621-9.

NS, Not statistically significant

Empiric Treatment of VAP –Pseudomonas spp.

• Two agents targeted at Pseudomonas spp. should be used in the following situations: – Patients with prior intravenous antibiotic exposure in the past 90 days– Units where >10% of isolates are resistant to an agent being considered for

monotherapy or resistance rates are unknown– Patients with structural lung disease (e.g., bronchiectasis or cystic fibrosis)– Weak recommendation with low-quality evidence

• Combination therapy increases the likelihood that at least one of the agents used will be active against the pathogen. Monotherapy should be used once an organism has been isolated and susceptibilities are known.

Empiric Treatment of VAP –Pseudomonas spp.

• Avoid aminoglycosides and Colistin if alternative agents are available– Given poor lung penetration, toxicities, and poorer clinical

response– Patients randomized to aminoglycoside-containing

regimens had similar mortality rates but lower clinical response rates compared to aminoglycoside-free regimens

Empiric Treatment of HAP

• Bacterial etiologies of HAP– Non-glucose fermenting Gram-negative bacilli: 19%,

• Pseudomonas spp. 13% and Acinetobacter spp. 4%– Enteric Gram-negative organisms: 16%– S. aureus: 16%

• MRSA 10%, MSSA 6%

Kalil AC. Clin Infect Dis. 2016;63:1-51.

Empiric Treatment of HAP – S. aureus

• For empiric coverage, use an agent with activity against Gram-negative bacilli and MSSA – Cefepime, piperacillin-tazobactam, levofloxacin, imipenem or meropenem)

• Therapeutic regimen should include an agent targeted at MRSA if:– Patient has been exposed to intravenous antibiotics within the prior 90 days– Patient being treated in a unit with >20% of S. aureus isolates are MRSA or

if the prevalence of MRSA is unknown– Patients with high risk of mortality (e.g., patients requiring ventilatory

support or with septic shock)– Weak recommendation with low-quality evidence

• Empiric therapy targeted at MRSA should include Vancomycin or Linezolid

Empiric Treatment of HAP –Pseudomonas spp.

• Two agents targeted at Pseudomonas spp. should be used in the following situations: – Patients with prior intravenous antibiotic exposure in the past 90 days– Patients with high risk of mortality (e.g., patients requiring ventilatory

support or with septic shock)– Patients with structural lung disease (e.g., bronchiectasis or cystic fibrosis)– Weak recommendation with low-quality evidence

• Combination therapy increases the likelihood that at least one of the agents used will be active against the pathogen. Monotherapy should be used once an organism has been isolated and susceptibilities are known.

PK/PD Dose Optimization

• Antibiotic dosing should be determined using PK/PD data, rather than manufacturer’s prescribing information

• Clinical studies have found that PK/PD-optimized dosing results in:– Reduced mortality (12% vs 24%, RR 0.49)– Reduced ICU length of stay (mean difference -2.48)– Improved clinical cure rate (81% vs 64%, RR 1.40)

Pharmacokinetics(drug concentrations)

Antimicrobial Therapy PK/PD

What does the BODY do to the drug?

AbsorptionDistributionMetabolismElimination

Pharmacodynamics(antimicrobial effects)

What does the drug do to the BUG?

Bacteriostatic/BactericidalPost-antibiotic effectMinimum inhibitory concentration

PK-PD

Drug concentrations

andeffect

Owens RC, et al. Am J Health-Syst Pharm 2009;66:S23-30.

Static vs Cidal

Bacteriostatic• Inhibits growth and replication of

the organism• Require the aid of host defenses to

clear infecting microorganisms• Agents that alter bacterial

physiology such as inhibition of folate synthesis (e.g. sulfonamides)

Bactericidal• Directly cause cell death• Agents that interfere with the

development of the cell wall or membrane (e.g. beta-lactams, vancomycin)

• Agents that inhibit nucleic acid synthesis (e.g. fluoroquinolones) or protein synthesis (e.g. aminoglycosides)

Levison ME, et al. Infect Dis Clin North Am 2009:23:791-815. 35

Minimum inhibitory concentration (MIC)

• The minimal concentration of antibiotic that inhibits bacterial growth

• The MIC usually represents attainable concentrations in serum– Concentrations at the site of infection may be higher (e.g.

urine) or lower (e.g. CSF)– Antimicrobials have variable lung penetration

March 27, 2017 36

Interpreting MIC Values

GREATER THAN 10,000 COLONIES PER ML. ESCHERICHIA COLI--------------------------------------------------------------ANTIBIOTIC MIC (mcg/ml) INTERPRETATIONAmpicillin ----------- <=4 ------------ SusceptibleAmp/Sulbactam --------- 4/2 ----------- SusceptiblePiper/Tazo ------------ 4/4 ----------- SusceptibleCefazolin ------------ <=2 ------------ SusceptibleCefoxitin -------------- 8 ------------ SusceptibleCeftriaxone ---------- <=2 ------------ SusceptibleCefepime ------------- <=1 ------------ SusceptibleAztreonam ------------ <=2 ------------ SusceptibleMeropenem ------------ <=1 ------------ SusceptibleErtapenem ------------ <=0.5 ---------- SusceptibleTrimeth/Sulfa ----- <=0.5/9.5 --------- SusceptibleTetracycline -------------- 4 ------------ IntermediateGentamicin ----------- <=2 ------------ SusceptibleTobramycin ----------- <=2 ------------ SusceptibleAmikacin ------------- <=8 ------------ SusceptibleCiprofloxacin --------- >2 -------------- ResistantNitrofurantoin ------ <=16 ------------ Susceptible

Resistant: growth not inhibited by usually achievable concentrations at normal doses

Intermediate: antibiotic level can usually be obtained in the tissue or blood, but response may be diminished

Susceptible: strain can be treated with antibiotic at recommended doses and schedules. Useful to know when treating an organism in an area that is difficult to penetrate (CSF, osteomyelitis)

PK-PD Principles of Antibiotics

Time-Dependent• fT>MIC:

– The cumulative percentage of a 24 hour period that the drug exceeds the MIC

– E.g., β-lactams

• fAUC/MIC– The ratio of the area under the curve to

the MIC– E.g., vancomycin, fluoroquinolones

Concentration-Dependent• fCmax/MIC

– The ratio of maximal drug concentration to the MIC

– E.g., aminoglycosides

Mandell, Douglas and Bennet’s Principles and Practice of Infectious Diseases. 7th ed.38

PK-PD Measures of Antibiotics

Figure adapted from Amsden G et al. Pharmacokinetics and Pharmacodynamics of Anti-infectives. Mandell, Douglas and Bennett’s Principles and Practice of Infectious Diseases. 7th ed. 301. Print.

39

MIC

fCmax/MIC

fAUC/MIC

fT>MIC

Time

Drug

Con

cent

ratio

n

Beta-lactams

Fluoroquinolones

Aminoglycosides

PK-PD Targets of Beta-Lactams

Drug Class Bacteriostatic%fT > MIC

Bactericidal%fT > MIC

Post-Antibiotic Effect

Penicillins ~30% ~50% 0.1 hours for Gram-negatives1.5-4 hours for Gram-positives

Cephalosporins 35-40% 60-70% None for Gram-negative0.9-5.6 hours for Gram-positives

Carbapenems 20% 40% 0.9 for Gram-negatives 1.5-2.6 hours for Gram-positive

Drusano GL. Clin Inect Dis 2007;45:S89-95. Ambrose P. et al. Clin Infect. Dis 2007;44:79-86. George JM, et al. Pharmacotherapy 2012;32:707-721.

Post-Antibiotic Effect: time of growth suppression after drug exposure has fallen below MIC

Administration Strategies for Antibiotics

Time (hours)

PK/PD Optimization for Pneumonia

Agent PK/PDParameter

Manufacturer Dosing Optimized Regimen

Levofloxacin AUC/MIC >87 HAP/VAP: 750 mg once daily 750 mg once dailyCiprofloxacin AUC/MIC >125 Nosocomial pneumonia: 400 mg IV Q8H 400 mg Q8HCeftazidime 45-100%

T>MICUncomplicated pneumonia: 1 g Q8H 2 g Q8H over 3 hour

infusionCefepime 100% T>MIC Pneumonia (P. aeruginosa): 2 g Q8H

Pneumonia (not P. aeruginosa): 1-2 g Q8-12H

2 g Q8H over 3 hour infusion

Meropenem 54% T>MIC,Cmin:MIC>5 OR75% T>MIC

Not in labeling 1 g Q8H over 3 hourinfusion

Cefepime

• Probability of varying regimens achieving >50% T>MIC

• With an MIC of 8 mcg/mL– Standard infusion over 30-

minutes• 1 g Q12H: 50%• 2 g Q12H: 75%• 1 g Q8H: 70%• 2 g Q8H: 85%

– Prolonged infusion over 3-hours• 2 g Q8H: 95%

Nicasio AM. Antimicrob Agents Chemother.2009;53:1476-81.

Duration of Therapy

• Both HAP and VAP should be treated for 7 days, rather than a longer duration– Strong recommendation, moderate—quality evidence

• Short courses (7-8 days) are associated with:– Increased 28-day antibiotic-free days (mean 4.02 days)– Reduced recurrent VAP due to MDRO (42.1% vs 62.3%)– No differences in mortality, recurrent pneumonia, treatment

failure, hospital length of stay or duration of mechanical ventilation

De-escalation of Therapy

• De-escalation refers to changing from an empiric broad-spectrum antibiotic to a narrower antibiotic regimen

• Antibiotic therapy should be de-escalated, rather than fixed

Procalcitonin (PCT)

• Produced by parenchymal tissue throughout the body when stimulated by endotoxin and bacterial infection

• PCT should not be used to diagnosis HAP/VAP– When combined with clinical criteria, it has a sensitivity of 67%

and specificity of 83% • PCT combined with clinical criteria can guide

discontinuation of antibiotics– Resulted in shorter duration of antibiotic therapy (9.1 vs 12.1

days; P <.00001) with no effect on clinical outcomes

Kalil AC. Clin Infect Dis. 2016;63:1-51.; Stolz D. Eur Respir J. 2009;34:1364-75.; Bouadma L. Lancet. 2010;375:463-74.

sTREM-1

• Member of immunoglobulin superfamily strongly expressed on neutrophils and monocytes infiltrating tissues invaded by bacteria and fungi

• Measured in BAL fluid, cutoff values have not been validated

• sTREM-1 should not be used to diagnose HAP/VAP – Sensitivity of 84% and specificity of 49% as a diagnostic

tool

Clinical Pulmonary Infection Score (CPIS)

0 Points 1 Point 2 PointsTemperature (C) 36.5-38.4 38.5-38.9 ≤36.4 or ≥39Peripheral WBC 4,000-11,000 <4,000 or >11,000, >50% bands:

add 1 pointTracheal secretions None Non-purulent PurulentChest x-ray No infiltrate Diffuse or patchy infiltrates Localized infiltrateProgression of infiltrate from prior radiographs

None Progression

Culture of ET suction No growth/light growth Heavy growth, same bacteria on Gram stain: add 1 point

Oxygenation (PaO2/FiO2) >240 or ARDS ≤240 and no ARDSIf CPIS ≤6, VAP unlikely. If CPIS remains ≤6 after 3 days, antibiotics can be stopped in most cases

CPIS

• Recommend clinical criteria alone to determine initiation and discontinuation of antibiotics

• CPIS should not be used to diagnose HAP or VAP– Low diagnostic sensitivity (65%) and specificity (64%) for

VAP

Summary

• Empiric antibiotic therapy for HAP and VAP should be based on patient-specific risk factors for MDRO

• Local, stratified antibiograms should be used to guide empiric treatment of HAP and VAP

• Antimicrobial dosing should be optimized based on PK/PD parameters, when feasible

• PCT levels, combined with clinical criteria, may be used to guide discontinuation of antibiotics

2016 Updates to the Hospital Acquired- and Ventilator Associated-Pneumonia Guidelines

Janessa M. Smith, PharmD, BCPSClinical Pharmacy Specialist, Infectious DiseasesThe Johns Hopkins Hospital