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8/2/2019 Nosocomial Pneumonia Sid
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Nosocomial Pneumonia
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DefinitionNosocomial pneumonia:
Occurring at least 48 hours after admissionand not incubating at the time of hospitalization
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IntroductionNosocomial pneumonia is the 2nd most common hospital-acquired infections after UTI.
Accounting for 31 % of all nosocomial infections
Nosocomial pneumonia is the leading cause of death from hospital-acquired infections.
The incidence of nosocomial pneumonia ishighest in ICU.
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IntroductionThe incidence of nosocomial pneumonia inventilated patients was 10-fold higher than
non-ventilated patients
The reported crude mortality for HAP is 30%to greater than 70%.
--- Medical Clinics of North America Therapy of Nosocomial pneumonia 2001 vol.85 1583-94
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Pathogenesis
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PathogenesisFor pneumonia to occur, at least one of thefollowing three conditions must occur:
1. Significant impairment of host defenses
2. Introduction of a sufficient-size inoculum to overwhelmthe host's lower respiratory tract defenses
3. The introduction of highly virulent organisms into the
lower respiratory tractMost common is microaspiration of oropharyngeal secretions colonized withpathogenic bacteria.
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Pathogenesis
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
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ClassificationEarly-onset nosocomial pneumonia:
Occurs during the first 4 days
Usually is due to S. pneumoniae, MSSA, H. Influenza,or anaerobes.
Late-onset nosocomial pneumonia:
More than 4 days
More commonly by G(-) organisms, esp. P. aeruginosa,
Acinetobacter, Enterobacteriaceae (klebsiella,
Enterobacter, Serratia) or MRSA.
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Causative AgentEnteric G(-) bacilli are isolated mostfrequently particularly in patients with late-
onset disease and in patients with seriousunderlying disease often already on broad-spectrum antibiotics.
Prior use of broad-spectrum antibiotics andan immunocompromised state make resistantgram-negative organisms more likely.
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Causative AgentP. aeruginosa and Acinetobacter arecommon causes of late-onset pneumonia,particularly in the ventilated patients.
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Causative Agent Anaerobes are common in patientspredisposed to aspiration
VAP with anaerobes occurred more often withoropharyngeal intubation than nasopharyngealintubation.
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Causative AgentLegionella pneumophilia occurs sporadically butmay be endemic in hospitals with contaminated watersystems. The incidence is underestimated because the
test to identify Legionella are not performed routinely.
Because the incubation period of Legionella infection is2 to 10 days. cases that occur more than 10 days afteradmission are considered to be nosocomial, and cases
that develop between 4 and 10 days are considered aspossible nosocomial.
Patients who are immunocompromised, critically ill, oron steroids are at highest risk for infection.
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Ventilator-associated
Pneumonia (VAP)
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Ventilator-associated
Pneumonia (VAP)Definition:
Nosocomial pneumonia has developed in patient who
are receiving mechanical ventilation
Classification:
Early-onset: within 48-72 hours after tracheal
intubation, which complicates the
intubation process
Late-onset: after 72 hours
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PathogenesisRequire 2 important processes:
1. Bacterial colonization of the aerodigestive tract
2. Aspiration of contaminated secretion into the
Lower airway
Prevents mechanical clearance by cough andthe mucociliary escalator.
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Prevention for VAPThe oral regimen (topical gentamicin, Colistin,
Vancomycin cream q6h for 3 weeks) treating
oropharyngeal colonization could prevent VAP.
--- Prevention of VAP by oral decontamination
American journal of respiratory critical care medicine2001 164:382-8
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Preventions for VAPNon-pharmacologic strategies
Effective hand washing and use of protective gowns
and gloves Semirecumbent positioning
Avoidance of large gastric volume
Oral (non-nasal) intubation
Continuous subglottic suctioning Humidification with heat and moisture exchanger
Posture change
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
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Preventions for VAPPharmacologic strategies
Stress-ulcer prophylaxis
Combination antibiotic therapy
Prophylactic antibiotic therapy
Chlorhexidine oral rinse
Prophylactic treatment of neutropenic p’t
Vaccines
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
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Treatment
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TreatmentInitially be treated with a broad-spectrumantibiotic regimen aimed at covering all
likely bacterial pathogen
This regimen should subsequently benarrowed, according to the result of
culture
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TreatmentThe pathogen may be influenced bycoexisting illnesses, prior treatment, and
length of hospitalization.
The frequency of ICU-acquired P. Aeruginosacarriage or colonization/infection was 23.4%
at 7 days and 57.8% at 14 days.
---- Current opinion in infectious disease 2002, 15:387-94, copyright LWW
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TreatmentThe mortality can be reduced with earlyappropriate empiric therapy.(Form 30 % with
appropriate therapy to more than 90 % with inappropriate therapy)
Inappropriate initial antibiotic therapy wasassociated with:1. Higher crude hospital mortality (60.7 vs. 47.3%)
2. Longer ICU stay in survivors (20 vs. 12 days)
3. Longer duration of mechanical ventilator
---- Current opinion in infectious disease 2002, 15:387-94, copyright LWW
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TreatmentGuideline was published in 1996 by Americanthoracic society and separated patients into
three groups, each with a set of probablepathogens.
Group 1: mild to moderate HAP with no risk factor
Group 2: mild to moderate HAP with risk factor
Group 3a: severe HAP, early-onset with no risk factor
Group 3b: severe HAP, late-onset or with risk factor
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Group 1. & 3a.
(Or 4th cephalosporin, Cefepime)
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Group 2.
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Group 3b.
prolonged ICU course
structural lung disease
previous antibiotic use
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TreatmentFor mild-to-moderate HAP, monotherapy hasbeen shown to be effective.
For severe HAP in which infection withresistant organisms is likely, combinationtherapy probably should be instituted until
culture result are available.
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TreatmentPatients for S. aureus infection, agents againstthis organism are necessary, including
Vancomycin if MRSA is suspected.
Linezolid is comparable with Vancomycin.
The advantage of Linezolid is less possiblenephrotoxicity
---- current opinion in infectious disease 2002, 15:387-94, copyright LWW
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TreatmentCombination of antipseudomonal drugs iscontroversial:
1. Traditional:antipseudomonal beta-lactam with an Aminoglycoside.
Synergy but potential nephrotoxicity.
2. Another approach:
antipseudomonal beta-lactam with a Fluoroquinolone. No benefit of synergy but reduce concern of nephrotoxicity,and quinolone gets into the lungs at higher concentrations.
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TreatmentResults:
1. Some pathogens, such as H. influenzae, cure
rate is high, and 7 to 10 days is adequate.
2. Highly resistant G(-) organisms (Acinetobacter or
pseudomonas) require prolonged combination
therapy for 21 days.
3. MRSA , requiring prolonged therapy.
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Response of Therapy
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Response of TherapyBecause of the delays in clinical response of treatment,it is thought that unless there is significant clinicaldeterioration or new microbiologic information,
therapy should not be changed for at least thefirst 48 to 72 hours
Measured by quantitating the bacterial load in thelower respiratory tract at the initiation of therapy and
several days later.
Bacterial concentrations decreased or no growth -- clinical improvement
Elevated -- experienced clinical failure
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Response to Therapy
If no clinical response is noted or deterioration occurs,we need to consider:
1. Infectious causes:
Resistant pathogen
Superinfection
Unusual pathogens
Lung abscess
Extrapulmonary infection
2. Noninfectious events:
Heart: CHF
Lung: fibroproliferative ARDS, pulmonary emboli, Atelectasis…
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ReferenceThe prevention of ventilator-associated pneumonia
NEJM vol.340 Feb 25, 1999
Therapy of nosocomial pneumonia
Medical clinics of north America 2001 vol.85 1583-94
Prevention of VAP by oral decontamination
American journal of respiratory critical care medicine 2001 164:382-8
Current opinion in infectious disease Copyright LWW 2002, 15:387-94