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Ventilator Associated Pneumonia By Dr.Hanan Ibrahim

Ventilator Associated Pneumonia By Dr.Hanan Ibrahim

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Ventilator Associated Pneumonia

By

Dr.Hanan Ibrahim

NI is any infection that is neither present nor incubating on hospital admission NI is developed -at least 48h after hospital admission , -up to 3 days after hospital discharge , -within 30 days of an operative procedure NI increase by 6% for each day spent in the hospital .

One third of NIs are preventable through infection control programs .This is why NI rates are now included in the criteria used for assessing the quality of patient care in many institutes .

NI in Medical and Surgical ICU NI MedicalICU Surg.ICU

PN 30% UTI 30% BLI 16% Surg. -

33% 18% 13% 14%

Hospital-Acquired Pneumonia (HAP): Definitions

HAP:  Arises 48 hours or more after hospital admission  Is not incubating at the time of admission Ventilator-associated pneumonia (VAP):  Arises 48-72 hours or more after endotracheal intubation Healthcare-associated pneumonia (HCAP):  Arises within 90 days of having been admitted to an acute care facility & pt. has resided in a nursing home or LTCF.

(American Thoracic Society/IDSA. Am J Respir Crit Care Med 2005;171:388-416)

Ventilator-Associated Pneumonia

Ventilator-associated pneumonia is often defined as pneumonia that develops 48 hours or more after intubation with an endotracheal or tracheostomy tube, and which was not present before intubation

Classification: Early-onset pneumonia :VAP that occurs within 48 to 72 hours after tracheal intubation; it often results from aspiration, which complicates the intubation process (Chastre, 2005). late-onset pneumonia VAP that occurs after this period .

Early-onset VAP is most often due to antibiotic-sensitive bacteria (e.g., oxacillinsensitive Staphylococcus aureus, Haemophilus influenza, and Strep-tococcus pneumoniae), whereas late-onset ventilatorassociated pneumonia is frequently caused by antibiotic-resistant pathogens (e.g., oxacillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa, acinetobacter species, and enterobacter species) (Myrianthefs et al, 2004)

Significance of VAP In contrast to infections of more frequently involved organs (e.g., urinary tract and skin), for which mortality is low, ranging from 1 to 4%, the mortality rate for VAP ranges from 24 to 50% and In can reach 76% in some specific settings or when lung infection is caused by high-risk pathogens. ICU ventilated patients with VAP have a 2- to 10-fold higher risk of death than patients without it (Cavalcanti et al., 2005).

Significance of VAP -Increases ventilatory support requirements and ICU stay by 4.3 days -Increases hospital LOS by 4 to 9 days -Increases cost - > $11,000 per episode -Estimates of VAP cost / year for nation > $ 1.2 billion
Heyland et al, Am J Respir Crit Care Med 1999;159:1249 Craven, Chest 2000;117:186-187S Rello et al, Chest 2002;122:2115 Safdar et al, Critical Care Medicine 2005;33:2184-93

Cost of Nosocomial Infection -300 LE /patient/ day -1800LE/ day -54000LE/month -648000LE/year

Pathogens
Mostly Bacilli (56.5%),followed by Cocci (42.1%),and Fungi (1.3%).
(Chastre et al.2003)

Etiologic agent of VAP may differ according to: -patients, units, hospitals or countries. -Length of hospital stay . -Exposition of antimicrobials . -Co morbid conditions .

-(COPD):H.influenzae, Moraxella catarhalis, S. pneumoniae -Steroid Therapy:P.aeruginosa -Chemotherapy: Legionella -Coma Diabetes : S. aureus -Aspiration:Anaerobes

Microorganisms in PICU of Ain Shams University Hospital
70% 60% 50% 40% 30% 29% 20% 10% 0% 18% 8% 1996 32% 19% 9% 1999 2005 15% 47% culture + Gram + Gram 65%

Enterobacter Enterobacter species rarely cause disease in a healthy individual. This opportunistic pathogen, similar to other members of the Enterobacteriaceae family, possesses an endotoxin known to play a major role in the pathophysiology of sepsis and its complications. Enterobacter species, particularly cloacae Enterobacter and Enterobacter aerogenes, are important nosocomial pathogens responsible for various
infections.

Enterobacter in ICU : Infection control is poor (little hand-washing) many infections are acquired through crosstransmission. Ready transmission occurs - for example, rapid disinfection of rectal thermometers with 80% alcohol does NOT prevent transmission of E. cloacae. Enterobacter infection has also been traced to contaminated albumin concentrates, prefilled saline syringes, multidose vials and contaminated infant formulae (in the tin), with consequent necrotising enterocolitis. Total parenteral nutrition solutions have been contaminated during preparation.

Haemodialysis machines with defective waste-handling ports have also been responsible for haematogenous infection. Strains have even been found that can grow in drinks containing methylparaben (and will even grow in concentrations of 3000mg/L)! Enterobacter meningitis in adults has been reported following neurosurgery, presumably consequent on the usual predisposing causes!

Specific risk factors for infection with nosocomial multidrug-resistant strains of Enterobacter species include the recent use of broad-spectrum cephalosporins or aminoglycosides and ICU care . These "ICU bugs" cause significant morbidity and mortality, and infection management is complicated by multiple antibiotic resistance(MEREA)

Treatment Carbapenems (imipenem, meropenem)are at present probably the treatment of choice, although cefepime may be used. Quinolone sensitivity is variable, and resistance may develop during treatment (this can also occur with carbapenems). Some organisms are sensitive to cotrimoxazole .

(Egyptian Journal of Pediatrics 2007)

Acinetobacter enters into the body through open wounds, catheters, and breathing tubes. It usually infects those with compromised immune systems, such as the wounded, the elderly, children or those with immune diseases. Colonisation poses no threat to people who aren't already ill, but colonized health care workers and hospital visitors can carry the bacteria into neighboring wards and other medical facilities. The number of nosocomial infections caused by A. baumannii has increased in recent years.

Multi-resistant A. baumannii infections are currently treated with imipenem and an older class of drugs known as polymyxins. These, along with stricter infection-control measures, such as monitored hand washing, have lowered infection rates in some military hospitals. MDRAB infections are difficult and costly to treat. A study at a public teaching hospital found that the mean total hospital cost of patients who acquired MDRAB was $98,575 higher than that of control patients who had identical burn severity of illness indices.

PATHOGENESIS

- Low or absent LESP due to many

factors ( Sepsis-HypotensionMedications-Sedation ). -Impaired clearance of the esophagus. -Supine body position. -Nasogastric feeding and high

29th International Symposium on Intensive Care and Emergency Medicine, March 19, 2009

ASPIRATION OF PATHOGENIC ORGANISMS FROM THE OROPHARYNX

The percentage of matching between microorganisms cultivated from pharyngeal swab in relation to BAL microorganisms. (Egyptian Journal of Pediatrics 2007) PATHOGENESIS

PATHOGENESIS

Diagnosis
For many years, VAP has been diagnosed by the clinical criteria published by Johanson et al. in 1972, which include the appearance of a new or progressive pulmonary infiltrate, fever, leukocytosis, and purulent tracheobronchial secretions ; however, these criteria are nonspecific .

Use of a clinical pulmonary infection score (CPIS) has improved the diagnostic utility of clinical criteria. CPIS includes the following six weighted clinical and microbiological variables: temperature, white blood cell count, character and volume of tracheobronchial aspirate, Gram stain and culture of tracheobronchial aspirate, gas exchange ratio and chest radiograph infiltrates. This score proved to achieve 72% sensitivity and 85% specificity in a post mortem study. (Baughman, 2005)

CPIS Used for the Diagnosis of VAP*
1.

Temperature °C

Points
0 1 2 0 1 1 0 1 1

≥ 36.5 and ≤ 38.4 ≥ 38.5 and ≤ 38.9 ≥ 39.0 or ≤ 36.0 ≥ 4,000 and ≤ 11,000 < 4,000 or > 11,000 + band forms 500 Absence of tracheal secretions Presence of tracheal secretions Purulent secretions
Sensitivity: 93%

1.

Blood leukocytes, mm-3
– –

1.

Tracheal secretions
– – –

*CPIS score > 6

Specificity: 100%

(Pugin J et al. Am Rev Respir Dis 1991;143:1121-1129)

CPIS Used for the Diagnosis of VAP* (cont’d)
4.

Oxygenation: PaO2/FiO2, mm Hg

> 240 or ARDS ≥ 240 and no evidence ARDS

0 2

5.

Pulmonary radiography
– – –

No infiltrate Diffuse or patchy infiltrate Localized infiltrate

0 1 2

6.

Culture of tracheal aspirate (semiquantitative 0-1-2-3 +)
– – –

Pathogenic bacteria cultured ≤ 1+ or no growth Pathogenic bacteria cultured > 1+ Same pathogenic bacteria on Gram Stain > 1+ Sensitivity: 93%

0 1 1

*CPIS score > 6

Specificity: 100%

(Pugin J, et al. Am Rev Respir Dis 1991; 143:1121-1129)

Tracheal Aspirates TA cultures have high sensitivity and very low specificity. The negative culture of TA can be used to exclude pneumonia but a positive culture cannot be used to confirm the diagnosis of pneumonia . The diagnostic accuracy of TA cultures can be improved by : 1- Microscopic Analysis 2- Quantitative Cultures

In 1979, a fiberoptic bronchoscopic technique was introduced for obtaining uncontaminated lower respiratory tract secretions, which were cultured quantitatively . The causative microorganisms were recovered at >1000 CFU/mL from six patients with clinical evidence of lower respiratory tract infection. In 1987, a correlation was observed between pneumonia and >100000 CFU/mL in bronchoalveolar lavage (BAL) fluid . Kahn and Jones noted that BAL fluid with >100000CFU/mL and <1% squamous epithelial cells had 100% sensitivity and specificity for the diagnosis of bacterial pneumonia.

Bronchoscopically Directed Techniques for Diagnosis of VAP PSB = protected specimen brush; BAL = bronchoalveolar lavage Nonbronchoscopically Directed (Blind) Diagnostic Techniques

Quantitative Cultures To Predict VAP Onset and Monitor
Therapy
The 89% positive predictive value of lower respiratory tract colonization for pneumonia further substantiates the accuracy of quantitative culture of lower respiratory tract secretions for the diagnosis of VAP. Quantitative culture of lower respiratory tract secretions can also be used to monitor the progress of antimicrobial therapy for VAP.

VAP AND ARDS ARDS and VAP have very similar clinical manifestations. About 10% of ARDS cases are due to VAP. VAP is more common in patients with ARDS (50%)than in those with other causes of respiratory failure ; it occurs later and is caused by more resistant microorganisms. Chastre et al. observed no significant differences in temperature, leukocyte count, Pao2/Fio2 ratio, or radiologic score in patients with ARDS with and without VAP .

Prevention
General Preventive Strategy Nonpharmacologic Strategies Effective Hand Washing and the Use of Protective Gowns and Gloves Semirecumbent Positioning of Patients Avoidance of Large Gastric Volumes Oral (Non-Nasal) Intubation Routine Maintenance of Ventilator Circuits Continuous Subglottic Suctioning Type of Suction Catheter and Its Replacement Humidification with Heat and Moisture Exchangers Postural Changes

HOB Elevation
HOB at 30-45º

CDC Guideline for Prevention of Healthcare Associated Pneumonias 2004 ATS / IDSA Guidelines for VAP 2005

Pharmacologic Strategies Stress-Ulcer Prophylaxis Administration of Antibiotics Combination Antibiotic Therapy Prophylactic Antibiotic Therapy Chlorhexidine Oral Rinse Selective digestive decontamination Administration of Immune Globulin Prophylactic Treatment of Patients with Neutropenia

Treatment
Initial empiric therapy -The timing of onset of VAP relative to mechanical ventilation (early vs. late VAP). -The prior administration of antibiotics during the current hospitalization . -Specific institutional epidemiological data .

Some studies recommended ciprofloxacin to be used as a single empirical treatment in patients with suspected VAP (Singh et al., 2000). Ciprofloxacin is usually effective against enterobactericeea species, Haemophilus influenzae, and some Staphylococcus species, on the other hand it is ineffective against streptococcus species, Pseudomonas aeruginosa and Acinetobacter species (Michalopoulos & Geroulanos, 2003).

No further investigation, observe

NO

Clinical features suggest infection? YES
Clinical pulmonary infection score (CPIS) CPIS > 6

Decision tree proposed by Singh et al. AJRCCM 2000;162:505

YES

Antibiotics for 10-21 days

NO Ciprofloxacin for 3 days
Re-evaluate at 3 days

CPIS > 6

YES

Treat as pneumonia

NO
Discontinue ciprofloxacin

De-escalation Strategy for Antimicrobial Treatment of VAP De-escalation refers to a strategy of aggressive broad spectrum initial empiric antimicrobial therapy, followed by narrowing or discontinuation of antimicrobial drugs after the results of antimicrobial susceptibility tests become available This general strategy is fully endorsed by the new American Thoracic Society/Infectious Diseases Society of America guidelines for the management of VAP (Park, 2005) (Rello et al, 2004).

Treatment of VAP:

No risk factors for resistance, early onset (<5 days of hospitalization) & moderate presentation

Treatment: 3rd generation non-pseudomonal cephalosporin (eg. ceftriaxone 1 g q24h IV, cefotaxime 1 g q8h IV) or 4th generation cephalosporin (cefepime 2 g q12h IV) OR beta-lactam/beta-lactamase inhibitor (eg. piperacillin-tazobactam 4.5 g q6h IV) OR fluoroquinolone (levofloxacin 750 mg IV qd, moxifloxacin 400 mg IV qd] → po
New Canadian Guidelines for Hospital-Acquired Pneumonia (HAP) & Ventilator-Associated Pneumonia (VAP),2008

Therapy of VAP:

Risk factors for antimicrobial resistance present, late onset and/or severe presentation
Risk factors for antimicrobial resistance present: - Prolonged hospitalization - Prior hospital antimicrobial therapy within 90 d - ICU stay ≥ 5 days - Structural lung disease - P. aeruginosa or Acinetobacter spp. Severe presentation - hypotension, intubation, severe sepsis, rapid progression of infiltrates or organ dysfunction

Risk factors for resistance present +/- severe presentation (Cont’d)

Treatment of VAP:

Treatment: ceftazidime 2 g q8h IV or cefepime 2g q8h IV OR imipenem-cilastatin 1 g q8h IV OR meropenem 1 g q8h IV OR piperacillin-tazobactam 4.5 g q6h IV PLUS ciprofloxacin 400 mg q8h IV or levofloxacin 750 mg q24h IV OR gentamicin or tobramycin 5-7 mg/kg q24h IV or amikacin 15-20 mg/kg q24h IV +/vancomycin 1 g q12h IV or linezolid 600 mg q12h IV

For how long ?

The traditional duration of antibiotic therapy has been 14 to 21 days.
(American Thoracic Society and Infectious Disease of America 2005)

VAP: 8 Day vs. 15 Day Antibiotic Therapy – Shorter may be Better
80 70 60

76.2

57.1

% or Days

50 40 30 20 10 0

40.6 28.9 26 18.8 17.2 *P=.01 28.9 18.4 d 15.3 d
BSA Free days NFGN I nfections Unfavorable Outcome MRSA

8 Day Treatment 15 Day Treatment

Mortality

Lung Infection Recurrence

Primary Outcomes
(Chastre J et al. JAMA 2003;290:25882598)

Antibiotic cycling Scheduled changes of antibiotic regimens or routine microbiological surveillance-guided changes of antibiotic policy may also reduce the risk of emerging of resistant strains (Kollef et al, 1997).

Recommendation -Proper infection control .
-Semisetting position and evaluation of GER status of the mechanically ventilated patient -Avoid unnecessary use of antibiotics . -Regular evaluation of the prevelant organisms . -Bronchoscopically directed methods to diagnose VAP is more accurate than TA cultures however this does not affect mortality , but depending on TA will result in excessive use of antibiotics .

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