Nosocomial_pneumonia_Dr_Suruchi

Views:
 
Category: Entertainment
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

Tracking NI has become difficult:

Tracking NI has become difficult Shorter inpatient stays (average postoperative stay, now approximately 5 days, is usually shorter than the 5- to 7-day incubation period for S. aureus surgical wound infections) Surveillance systems are optional to hospitals with infection-control programs

Prevention of Ventilator Associated Pneumonia (VAP) :

Prevention of Ventilator Associated Pneumonia (VAP) AACN VAP Practice Alert

Lecture Content:

Lecture Content Epidemiology of VAP Prevention strategies HOB elevation Ventilator equipment changes Continuous removal of subglottic secretions Handwashing AACN VAP Practice Alert

Epidemiology of Ventilator Associated Pneumonia (VAP):

Epidemiology of Ventilator Associated Pneumonia (VAP) AACN VAP Practice Alert

Nosocomial Pneumonias:

Nosocomial Pneumonias Account for 15% of all hospital associated infections Account for 27% of all MICU acquired infections Primary risk factor is mechanical ventilation (risk 6 to 21 times the rate for nonventilated patients) CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 Cook et al, Ann Intern Med 1998;129:433 AACN VAP Practice Alert

Critical Care Interventions Increase Susceptibility to Nosocomial Pneumonias:

Critical Care Interventions Increase Susceptibility to Nosocomial Pneumonias Tracheal Colonization Altered Host Defenses Increased Nosocomial Pneumonias Intubation AACN VAP Practice Alert

VAP Etiology:

VAP Etiology Most are bacterial pathogens, with Gram negative bacilli common: Pseudomonas aeruginosa Proteus spp Acinetobacter spp Staphlococcus aureus Early VAP associated with non-multi-antibiotic-resistant organisms Late VAP associated with antibiotic-resistant organism AACN VAP Practice Alert

Significance of Nosocomial Pneumonias:

Significance of Nosocomial Pneumonias Mortality ranges from 20 to 41%, depending on infecting organism, antecedent antimicrobial therapy, and underlying disease(s) Leading cause of mortality from nosocomial infections in hospitals CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 Heyland et al, Am J Respir Crit Care Med 1999;159:1249 Bercault et al, Crit Care Med 2001;29:2303 AACN VAP Practice Alert

Significance of Nosocomial Pneumonias:

Significance of Nosocomial Pneumonias Increases ventilatory support requirements and ICU stay by 4.3 days Increases hospital LOS by 4 to 9 days Increases cost - Heyland et al, Am J Respir Crit Care Med 1999;159:1249 Craven D. Chest 2000;117:186-187S Rello et al, Chest 2002;122:2115 AACN VAP Practice Alert

VAP Prevention:

VAP Prevention AACN VAP Practice Alert

Continuous Removal of Subglottic Secretions:

Continuous Removal of Subglottic Secretions Use an ET tube with continuous suction through a dorsal lumen above the cuff to prevent drainage accumulation CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 Kollef et al, Chest 1999;116;1339 AACN VAP Practice Alert

PowerPoint Presentation:

HOB Elevation HOB at 30-45 o CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 Drakulovic et al, Lancet 1999;354:1851

Frequency of Equipment Changes:

Frequency of Equipment Changes Ventilator Tubing Inner Cannulas of Trachs Ambu Bags No Routine Changes Not Enough Data Between Patients CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 AACN VAP Practice Alert

Handwashing:

Handwashing What role does handwashing play in nosocomial pneumonias? Albert, NEJM 1981; Preston, AJM 1981; Tablan, 1994 AACN VAP Practice Alert

PowerPoint Presentation:

VAP Prevention All recommendations are level IA CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 AACN Practice Alert for VAP, 2004 Wash hands before and after suctioning, touching ventilator equipment, and/or coming into contact with respiratory secretions. AACN VAP Practice Alert

PowerPoint Presentation:

Use a continuous subglottic suction ET tube for intubations expected to be > 24 hours Keep the HOB elevated to at least 30 degrees unless medically contraindicated VAP Prevention All recommendations are level II CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 AACN Practice Alert for VAP, 2004 AACN VAP Practice Alert

No Data to Support These Strategies:

No Data to Support These Strategies Use of small bore versus large bore gastric tubes Continuous versus bolus feeding Gastric versus small intestine tubes Closed versus open suctioning methods Kinetic beds CDC Guideline for Prevention of Healthcare Associated Pneumonias 2003 AACN VAP Practice Alert

Potential consequences of inappropriate antibiotic therapy:

Potential consequences of i nappropriate antibiotic therapy Inappropriate empiric antibiotic therapy can lead to increases in: mortality morbidity length of hospital stay cost burden resistance selection

Inappropriate antibiotic therapy:

Inappropriate antibiotic therapy Inappropriate antibiotic therapy can be defined as one or more of the following: ineffective empiric treatment of bacterial infection at the time of its identification the wrong choice, dose or duration of therapy use of an antibiotic to which the pathogen is resistant

Evidence of improved clinical outcomes with appropriate empiric antibiotic therapy:

Evidence of improved clinical outcomes with appropriate empiric antibiotic therapy A number of studies have demonstrated the benefits of early use of appropriate empiric antibiotic therapy for patients with nosocomial infections Several key clinical studies are reviewed in the following slides

Inappropriate antibiotic therapy is a risk factor for mortality among patients in the intensive care unit (ICU):

Inappropriate antibiotic therapy is a risk factor for mortality among patients in the intensive care unit (ICU) Infection-related mortality rates were assessed in a prospective cohort, single-centre study of 2000 patients admitted to medical/surgical ICUs 655 patients had a clinically recognised infection: 442 (67.5%) had a community-acquired infection 286 (43.7%) developed a nosocomial infection 73 (11.1%) had both community-acquired and nosocomial infections 169 (25.8%) patients received inappropriate initial antimicrobial treatment Kollef et al. Chest 1999;115:462–474

Inappropriate antibiotic therapy is a risk factor for mortality among patients in the ICU:

Inappropriate antibiotic therapy is a risk factor for mortality among patients in the ICU Kollef et al. Chest 1999;115:462–474 Hospital mortality (%) 0 20 50 60 Appropriate therapy Inappropriate therapy 40 30 10 All causes Infectious disease-related p<0.001 p<0.001 Mortality type

Appropriate antibiotic therapy reduces mortality and complications in patients with nosocomial pneumonia:

Appropriate antibiotic therapy reduces mortality and complications in patients with nosocomial pneumonia The frequency of and reasons for changing empiric antibiotics during the treatment of hospital-acquired pneumonia were assessed in a prospective multicentre study across 30 Spanish hospitals Of the 16 872 patients initially enrolled, 530 developed 565 episodes of pneumonia after ICU admission Empiric antibiotics (administered in 490 [86.7%] of episodes) were modified in 214 (43.7%) cases because of: isolation of micro-organism not covered by treatment (62.1%) lack of clinical response (36.0%) development of resistance (6.6%) Alvarez-Lerma et al. Intensive Care Med 1996;22:387–394

Appropriate antibiotic therapy reduces mortality and complications in patients with nosocomial pneumonia:

Alvarez-Lerma et al. Intensive Care Med 1996;22:387–394 Appropriate antibiotic therapy reduces mortality and complications in patients with nosocomial pneumonia Appropriate therapy (n=284) Attributable mortality No. complications/patient Shock Gastrointestinal bleeding Respiratory failure Multiple organ failure Extrapulmonary infection Inappropriate therapy (n=146) p - value 16.2% 1.73 ± 1.82 17.1% 10.7% 24.9% 12.5% 13.2% 24.7% 2.25 ± 1.98 28.8% 21.2% 32.2% 21.2% 17.1% 0.04 <0.001 <0.005 0.003 NS NS NS

Appropriate early antibiotic therapy reduces mortality rates in patients with suspected ventilator-associated pneumonia (VAP) (Study 1):

Appropriate early antibiotic therapy reduces mortality rates in patients with suspected ventilator-associated pneumonia (VAP) (Study 1) A prospective observation and bronchoscopy study of patients with VAP assessed the impact of bronchoalveolar lavage (BAL) data on the selection of antibiotics and clinical outcomes in a medical/surgical ICU 132 mechanically ventilated patients (hospitalised >72 hours) with clinically confirmed VAP underwent BAL within 24 hours of diagnosis 107 patients received antibiotics prior to bronchoscopy 25 patients received antibiotics immediately after bronchoscopy Mortality rates were assessed in relation to the adequacy and time of initiation of antibiotic therapy Luna et al. Chest 1997;111:676–685

Appropriate early antibiotic therapy reduces mortality rates in patients with suspected VAP (Study 1):

Luna et al. Chest 1997;111:676–685 Appropriate early antibiotic therapy reduces mortality rates in patients with suspected VAP (Study 1) Mortality (%) Pre-BAL Post-BAL Post-culture result 0 60 100 20 40 80 p<0.001 Appropriate antibiotic No antibiotic Inappropriate antibiotic

Appropriate early antibiotic therapy reduces mortality rates and length of hospital stay in patients with bloodstream infection (Study 1):

Appropriate early antibiotic therapy reduces mortality rates and length of hospital stay in patients with bloodstream infection (Study 1) An observational prospective cohort study of patients with bloodstream infection examined whether appropriate antibiotic therapy improved survival rate Of the 3413 evaluable patients, 2158 (63%) received early appropriate antibiotics defined as starting within 2 days of the first positive blood culture, and if the causative pathogen was susceptible in vitro to the administered drug Mortality rates and median duration of hospital stay for surviving patients were determined Leibovici et al. J Intern Med 1998;244:379–386

Appropriate early antibiotic therapy reduces mortality rates and length of hospital stay in patients with bloodstream infection (Study 1):

Appropriate early antibiotic therapy reduces mortality rates and length of hospital stay in patients with bloodstream infection (Study 1) Leibovici et al. J Intern Med 1998;244:379–386 Appropriate therapy (n=2158) Mortality rate Median duration of hospital stay Inappropriate therapy (n=1255) p - value 20.2% 9 days (range 0–117) 34.4% 11 days (range 0–209) 0.0001 0.0001

Summary:

Summary Clinical evidence suggests that early use of appropriate empiric antibiotic therapy improves patient outcomes in terms of: reduced mortality reduced morbidity reduced duration of hospital stay

Resistance to antibacterial agents:

Resistance to antibacterial agents Antibiotic resistance either arises as a result of innate consequences or is acquired from other sources Bacteria acquire resistance by: mutation: spontaneous single or multiple changes in bacterial DNA addition of new DNA: usually via plasmids, which can transfer genes from one bacterium to another transposons: short, specialised sequences of DNA that can insert into plasmids or bacterial chromosomes

Mechanisms of antibacterial resistance (1):

Mechanisms of antibacterial resistance (1) Structurally modified antibiotic target site, resulting in: reduced antibiotic binding formation of a new metabolic pathway preventing metabolism of the antibiotic

Structurally modified antibiotic target site:

Structurally modified antibiotic target site Interior of organism Cell wall Target site Binding Antibiotic Antibiotics normally bind to specific binding proteins on the bacterial cell surface

Structurally modified antibiotic target site:

Structurally modified antibiotic target site Interior of organism Cell wall Modified target site Antibiotic Changed site: blocked binding Antibiotics are no longer able to bind to modified binding proteins on the bacterial cell surface

Mechanisms of antibacterial resistance (2):

Mechanisms of antibacterial resistance (2) Altered uptake of antibiotics, resulting in: decreased permeability increased efflux

Altered uptake of antibiotics: decreased permeability:

Altered uptake of antibiotics: decreased permeability Interior of organism Cell wall Porin channel into organism Antibiotic Antibiotics normally enter bacterial cells via porin channels in the cell wall

Altered uptake of antibiotics: decreased permeability:

Altered uptake of antibiotics: decreased permeability Interior of organism Cell wall New porin channel into organism Antibiotic New porin channels in the bacterial cell wall do not allow antibiotics to enter the cells

Altered uptake of antibiotics: increased efflux:

Altered uptake of antibiotics: increased efflux Interior of organism Cell wall Porin channel through cell wall Antibiotic Entering Entering Antibiotics enter bacterial cells via porin channels in the cell wall

Altered uptake of antibiotics: increased efflux:

Altered uptake of antibiotics: increased efflux Interior of organism Cell wall Porin channel through cell wall Antibiotic Entering Exiting Active pump Once antibiotics enter bacterial cells, they are immediately excluded from the cells via active pumps

Mechanisms of antibacterial resistance (3):

Mechanisms of antibacterial resistance (3) Antibiotic inactivation bacteria acquire genes encoding enzymes that inactivate antibiotics Examples include:  -lactamases aminoglycoside-modifying enzymes chloramphenicol acetyl transferase

Antibiotic inactivation:

Antibiotic inactivation Interior of organism Cell wall Antibiotic Target site Binding Enzyme Inactivating enzymes target antibiotics

Antibiotic inactivation:

Antibiotic inactivation Interior of organism Cell wall Antibiotic Target site Binding Enzyme Enzyme binding Enzymes bind to antibiotic molecules

Antibiotic inactivation:

Antibiotic inactivation Interior of organism Cell wall Antibiotic Target site Enzyme Antibiotic destroyed Antibiotic altered, binding prevented Enzymes destroy antibiotics or prevent binding to target sites

Many pathogens possess multiple mechanisms of antibacterial resistance:

Many pathogens possess multiple mechanisms of antibacterial resistance + – Quinolones – ++ Trimethoprim – ++ Sulphonamide ++ Macrolide + – Chloramphenicol + – Tetracycline ++ + – Aminoglycoside + Glycopeptide ++ + +  -lactam Modified target Altered uptake Drug inactivation

Focus on -lactam antibiotic resistance mechanisms :

Focus on -lactam antibiotic resistance mechanisms Three mechanisms of -lactam antibiotic resistance are recognised: reduced permeability inactivation with -lactamase enzymes altered penicillin-binding proteins (PBPs)

Multiple antibiotic resistance mechanisms: the -lactams:

Multiple antibiotic resistance mechanisms: the -lactams

-lactam antibiotic resistance:

-lactam antibiotic resistance AmpC and extended-spectrum -lactamase (ESBL) production are the most important mechanisms of -lactam resistance in nosocomial infections The antimicrobial and clinical features of these resistance mechanisms are highlighted in the following slides

-lactam resistance: AmpC -lactamase production:

-lactam resistance: AmpC -lactamase production Worldwide problem: incidence increased from 17−23% between 1991 and 2001 in UK Very common in Gram-negative bacilli AmpC gene is usually sited on chromosomes, but can be present on plasmids Enzyme production is either constitutive (occurring all the time) or inducible (only occurring in the presence of the antibiotic) Pfaller et al. Int J Antimicrob Agents 2002;19:383–388 Sader et al. Braz J Infect Dis 1999;3:97–110; Livermore et al. Int J Antimicrob Agents 2003;22:14−27

-lactam resistance: ESBL production:

-lactam resistance: ESBL production An increasing global problem Found in a small, expanding group of Gram-negative bacilli, most commonly the Enterobacteriaceae spp. Usually associated with large plasmids Enzymes are commonly mutants of TEM- and SHV-type  -lactamases Jones et al. Int J Antimicrob Agents 2002;20:426–431 Sader et al. Diagn Microbiol Infect Dis 2002;44:273–280

Antimicrobial features of ESBLs:

Antimicrobial features of ESBLs Inhibited by  -lactamase inhibitors Usually confer resistance to: first-, second- and third-generation cephalosporins (eg ceftazidime) monobactams (eg aztreonam) carboxypenicillins (eg carbenicillin) Varied susceptibility to piperacillin/tazobactam Typically susceptible to carbapenems and cephamycins Often clinically and/or microbiologically non-susceptible to fourth-generation cephalosporins

Clinical features of ESBLs:

Clinical features of ESBLs Even if sensitive to fourth-generation cephalosporins in vitro , treatment failures occur in clinical practice Create clinical difficulties due to cross-resistance with other antibiotic classes (eg aminoglycosides) Associated with nosocomial outbreaks of high morbidity and mortality Result in overuse of other broad-spectrum agents

Clinical failure in the presence of ESBLs:

Clinical failure in the presence of ESBLs Recent data show high clinical failure rates among patients treated with cephalosporins for serious infections caused by ESBL-producing pathogens susceptible to cephalosporins in vitro 4/32 patients received cephalosporins to which pathogens showed intermediate susceptibility and all failed treatment 15/28 remaining patients with cephalosporin-susceptible pathogens failed treatment and 4 died 11 patients required a change in antibiotic therapy Paterson et al. J Clin Microbiol 2001;39:2206–2212

Patients who failed cephalosporin therapy for serious infections due to ESBL-producing organisms:

Patients who failed cephalosporin therapy for serious infections due to ESBL-producing organisms Paterson et al . J Clin Microbiol 2001;39:2206–2212 Clinical failure rate (%) 0 60 100 20  1 40 80 2 4 8 Cephalosporin MIC ( µ g/mL)

Features of methicillin-resistant Staphylococcus aureus (MRSA):

Features of methicillin-resistant Staphylococcus aureus (MRSA) Introduction of methicillin in 1959 was followed rapidly by reports of MRSA isolates Recognised hospital pathogen since the 1960s Major cause of nosocomial infections worldwide contributes to 50% of infectious morbidity in ICUs in Europe surveillance studies suggest prevalence has increased worldwide, reaching 25–50% in 1997 Jones. Chest 2001;119:397S–404S

Serious infections testing positive for MRSA isolates among hospitalised patients (1997 SENTRY data):

Serious infections testing positive for MRSA isolates among hospitalised patients (1997 SENTRY data) Patients (%) 0 30 50 1 0 Pneumonia 20 40 UTI Wound Bloodstream Infection type Jones. Chest 2001;119:397S–404S UTI UTI = urinary tract infection

Features of MRSA: epidemic strains:

Features of MRSA: epidemic strains Problem escalated in the early 1980s with emergence of epidemic strains (EMRSA) first recognised in the UK 17 EMRSAs identified to date Impact on hospitals is variable presence of EMRSA can account for >50% of S. aureus isolates Aucken et al . J Antimicrob Chemother 200 2 ; 50 : 171 – 175

Risk factors for colonisation or infection with MRSA in hospitals :

Risk factors for colonisation or infection with MRSA in hospitals Chamber s . Emerg Infect Dis 2001;7:178–182 Admission to an ICU Surgery Prior antibiotic exposure Exposure to an MRSA-colonised patient

Emergence of MRSA in the community:

Emergence of MRSA in the community MRSA in hospitals leads to an associated rise in incidence in the community Community-acquired MRSA strains may be distinct from those in hospitals In a hospital-based study, >40% of MRSA infections were acquired prior to admission Risk factors for community acquisition included: recent hospitalisation previous antibiotic therapy residence in a long-term care facility intravenous drug use Colonisation and transmission are also seen in individuals (including children) lacking these risk factors Hiramatsu et al. Curr Opin Infect Dis 2002;15:407–413 Layton et al . Infect Control Hosp Epidemiol 1995;16:12–17; Naimi et al. 2003;290:2976−2984

Antimicrobial features of MRSA (1):

Antimicrobial features of MRSA (1) Mechanism involves altered target site new penicillin-binding protein — PBP 2 ' (PBP 2a) encoded by chromosomally located mec A gene Confers resistance to all  -lactams Gene carried on a mobile genetic element — staphylococcal cassette chromosome mec (SCC mec ) Laboratory detection requires care Not all mec A-positive clones are resistant to methicillin Hiramatsu et al . Trends Microbiol 2001;9:486–493 Berger-Bachi & Rohrer. Arch Microbiol 2002;178:165–171

Antimicrobial features of MRSA (2):

Antimicrobial features of MRSA (2) Cross-resistance common with many other antibiotics Ciprofloxacin resistance is a worldwide problem in MRSA: involves ≥2 resistance mutations usually involves par C and gyr A genes renders organism highly resistant to ciprofloxacin, with cross-resistance to other quinolones Intermediate resistance to glycopeptides first reported in 1997 Hiramatsu et al. J Antimicrob Chemother 1997;40:135–136 Hooper. Lancet Infect Dis 2002;2:530–538

Clinical features of MRSA:

Clinical features of MRSA Common associations include: underlying chronic disease , especially repeated hospital stays prolonged /repeated antibiotics , especially the  -lactams Usually susceptible to at least one other antibiotic Not all MRSAs behave as EMRSAs Methicillin resistance is not a marker of virulence

Clinical features of MRSA: transmission:

Clinical features of MRSA : transmission Occurs primarily from colonised or infected patients via the hands of healthcare workers contact transmission to other patients or staff very common Airborne transmission important in the acquisition of nasal carriage Infection control measures include: screening and isolation of new patients suspected of carrying MRSA or S. aureus with vancomycin resistance implementing infection control programmes establishing adequate antibiotic policy to minimise development of resistance

Management of MRSA:

Management of MRSA Educate on risks and control measures Adhere to strict control measures to prevent transmission, especially through contact Treat patient with appropriate empiric and targeted therapy Consider clearing patient of MRSA carriage

Glycopeptide resistance: focus on vancomycin resistance:

Glycopeptide resistance: focus on vancomycin resistance Vancomycin-resistant enterococci (VRE) Vancomycin-resistant S. aureus (VRSA)

Features of quinolone resistance: Gram-negative organisms:

Features of quinolone resistance: Gram-negative organisms Resistance most common in organisms associated with nosocomial infections Pseudomonas aeruginosa Acinetobacter spp. also increasing among ESBL-producing strains Meropenem Yearly Susceptibility Test Information Collection (MYSTIC) surveillance programme (1997―2000) 13.4% of Gram-negative strains resistant to ciprofloxacin P. aeruginosa and Acinetobacter baumannii are the most prevalent resistant strains increasing prevalence of resistance during surveillance period Masterton. J Antimicrob Chemother 2002;49:218–220 Thomson. J Antimicrob Chemother 1999;43(Suppl. A):31–40

Gram-negative organisms with resistance to ciprofloxacin (1997 SENTRY data):

Gram-negative organisms with resistance to ciprofloxacin (1997 SENTRY data) Organisms (%) 0 30 50 1 0 Stenotrophomonas maltophilia 20 40 Acinetobacter spp. P. aeruginosa Escherichia coli All patients (USA) Lower RTI (USA and Canada) Organism type Jones. Chest 2001;119:397S–404S

Features of quinolone resistance: Gram-positive organisms:

Features of quinolone resistance: Gram-positive organisms MRSA S. aureus occurred in 22.9% of pneumonias in hospitalised patients in USA and Canada (1997 SENTRY data) Enterococcus spp. resistance has developed rapidly, especially among VRE Streptococcus pneumoniae resistance emerging in many countries, including community-acquired resistance Hong Kong (12.1%), Spain (5.3%) and USA (<1%) marked cross-resistance with other frequently used antibiotics Hooper. Lancet Infect Dis 2002;2:530–538

Summary:

Summary Antibiotic resistance in the hospital setting is increasing at an alarming rate and is likely to have an important impact on infection management Steps must be taken now to control the increase in antibiotic resistance Cosgrove et al. Arch Intern Med 2002;162:185–190

Summary:

Summary The Academy for Infection Management supports the concept of using appropriate antibiotics early in nosocomial infections and proposes: selecting the most appropriate antibiotic based on the patient, risk factors, suspected infection and resistance administering antibiotics at the right dose for the appropriate duration changing antibiotic dosage or therapy based on resistance and pathogen information recognising that prior antimicrobial administration is a risk factor for the presence of resistant pathogens knowing the unit’s antimicrobial resistance profile and choosing antibiotics accordingly

authorStream Live Help