Nosocomial pneumonia.ppt

7/27/2019 Nosocomial pneumonia.ppt

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Nosocomial Pneumonia

Presented by Ri


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DefinitionNosocomial pneumonia:

Occurring at least 48 hours after admissionand not incubating at the time ofhospitalization


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IntroductionNosocomial pneumonia is the 2nd mostcommon hospital-acquired infections after UTI.

Accounting for 31 % of all nosocomial infections

Nosocomial pneumonia is the leading cause ofdeath 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 AmericaTherapy 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 oforopharyngeal 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-onsetnosocomial 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 andAcinetobacter arecommon causes of late-onset pneumonia,particularly in the ventilated patients.


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Causative AgentS. aureus is isolated in about 20~40% ofcases and is particularly common in :1. Ventilated patients after head trauma, neurosurgery,

and wound infection2. In patients who had received prior antibiotics or

Prolonged care in ICU

MRSA is seen more commonly in patients

Received corticosteroids

Undergone mechanical ventilation >5 days

Presented with chronic lung disease

Had prior antibiotics therapy


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Causative AgentAnaerobes 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 theintubation 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 glovesSemirecumbent positioning

Avoidance of large gastric volume

Oral (non-nasal) intubation

Continuous subglottic suctioningHumidification with heat and moisture exchanger

Posture change



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Preventions for VAPPharmacologic strategies

Stress-ulcer prophylaxis

Combination antibiotic therapy

Prophylactic antibiotic therapy

Chlorhexidine oral rinse

Prophylactic treatment of neutropenic pt

Vaccines



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Treatment


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TreatmentMost initial therapy is empiric because no

pathogen is identified or results are not

available when antimicrobial decisions aremade in most patients.


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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 % withappropriate 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.

Linezolidis 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-lactamwith 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

NEJMvol.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 diseaseCopyright LWW 2002, 15:387-94


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Thanks for Your Attention!!

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Nosocomial pneumonia.ppt