Nosocomial Pneumonia Powerpoint Presentation

Nosocomial Pneumonia

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Slide 1 :

Nosocomial Pneumonia Presented by Ri ???

Slide 2 :

Definition Nosocomial pneumonia: Occurring at least 48 hours after admission and not incubating at the time of hospitalization

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Introduction Nosocomial 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 is highest in ICU.

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Introduction The incidence of nosocomial pneumonia in ventilated 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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Pathogenesis For pneumonia to occur, at least one of the following three conditions must occur: 1. Significant impairment of host defenses 2. Introduction of a sufficient-size inoculum to overwhelm the host's lower respiratory tract defenses 3. The introduction of highly virulent organisms into the lower respiratory tract Most common is microaspiration of oropharyngeal secretions colonized with pathogenic bacteria.

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Pathogenesis --- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM

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Classification Early-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 Agent Enteric G(-) bacilli are isolated most frequently particularly in patients with late-onset disease and in patients with serious underlying disease often already on broad-spectrum antibiotics. Prior use of broad-spectrum antibiotics and an immunocompromised state make resistant gram-negative organisms more likely.

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Causative Agent P. aeruginosa and Acinetobacter are common causes of late-onset pneumonia, particularly in the ventilated patients.

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Causative Agent S. aureus is isolated in about 20~40% of cases and is particularly common in : 1. Ventilated patients after head trauma, neurosurgery, and wound infection 2. 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 Agent Anaerobes are common in patients predisposed to aspiration VAP with anaerobes occurred more often with oropharyngeal intubation than nasopharyngeal intubation.

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Causative Agent Legionella pneumophilia occurs sporadically but may be endemic in hospitals with contaminated water systems. The incidence is underestimated because the test to identify Legionella are not performed routinely. Because the incubation period of Legionella infection is 2 to 10 days. cases that occur more than 10 days after admission are considered to be nosocomial, and cases that develop between 4 and 10 days are considered as possible nosocomial. Patients who are immunocompromised, critically ill, or on 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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Pathogenesis Require 2 important processes: 1. Bacterial colonization of the aerodigestive tract 2. Aspiration of contaminated secretion into the Lower airway Prevents mechanical clearance by cough and the mucociliary escalator.

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Prevention for VAP The 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 VAP Non-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 VAP Pharmacologic 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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Treatment Most initial therapy is empiric because no pathogen is identified or results are not available when antimicrobial decisions are made in most patients.

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Treatment Initially be treated with a broad-spectrum antibiotic regimen aimed at covering all likely bacterial pathogen This regimen should subsequently be narrowed, according to the result of culture

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Treatment The pathogen may be influenced by coexisting illnesses, prior treatment, and length of hospitalization. The frequency of ICU-acquired P. Aeruginosa carriage 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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Treatment The mortality can be reduced with early appropriate empiric therapy.(Form 30 % with appropriate therapy to more than 90 % with inappropriate therapy) Inappropriate initial antibiotic therapy was associated 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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Treatment Guideline was published in 1996 by American thoracic society and separated patients into three groups, each with a set of probable pathogens. 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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Treatment For mild-to-moderate HAP, monotherapy has been shown to be effective. For severe HAP in which infection with resistant organisms is likely, combination therapy probably should be instituted until culture result are available.

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Treatment Patients for S. aureus infection, agents against this organism are necessary, including Vancomycin if MRSA is suspected. Linezolid is comparable with Vancomycin. The advantage of Linezolid is less possible nephrotoxicity ---- current opinion in infectious disease 2002, 15:387-94, copyright LWW

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Treatment Combination of antipseudomonal drugs is controversial: 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.

Slide 32 :

Treatment Results: 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 Therapy Because of the delays in clinical response of treatment, it is thought that unless there is significant clinical deterioration or new microbiologic information, therapy should not be changed for at least the first 48 to 72 hours Measured by quantitating the bacterial load in the lower 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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Reference The 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

Slide 37 :

Thanks for Your Attention!!

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Nosocomial pneumonia is the 2nd most common hospital-acquired infections after UTI. Accounting f more Nosocomial pneumonia is the 2nd most common hospital-acquired infections after UTI. Accounting for 31 % of all nosocomial infections ... less