DR MUHAMMAD AKRAM

HOSPITAL ACQUIRED PNEUMONIA

BY

PNEUMONIA

Infection of the alveoli, distal airways, and interstitium.

S&S OF PNEUMONIA

Cough

Tachycardia HR > 100

Tachypnea RR > 20

Fever T >37.8C

At least one abnormal chest findings- diminished breath sounds, rhonchi, crackles or wheeze

New x-ray infiltrate with no clear alternative such as lung cancer or pulmonary edema

CHEST RADIOGRAPH

Confirm the diagnosis of pneumonia

Assess severity of disease and presence of complication

CLASSIFICATION (OLD)

Community acquired pneumonia (CAP) - Typical

- Atypical*Aspiration

Hospital Acquired (NOSOCOMIAL) Pneumonia (HAP) - Early onset- Late onset- Ventilator associated

CURRENT CLASSIFICATION

Community acquired pneumonia (CAP)

Health Care-Associated Pneumonia (HCAP) - Hospital-Acquired Pneumonia (HAP)

- Ventilator-Associated pneumonia (VAP)

DEFINITIONS

Health Care-Associated Pneumonia (HCAP)- Hospitalization for 2 or more days within 90 days of the present infection

- Resident of a nursing home or long-term care facility

- Received recent IV antibiotic therapy, chemotherapy or wound care in the past 30 days of the current infection

- Attended a hospital or hemodialysis clinic

DEFINITIONS

Hospital Acquired Pneumonia (HAP)

-Defined as pneumonia that occurs 48 hours or more after admission, which was not incubating at the time of admission

DEFINITIONS

Ventilator Associated Pneumonia (VAP)

- Pneumonia that arises more than 48-72 hours after endotracheal intubation

EPIDEMIOLOGY

HAP is the second most common nosocomial infection in the United States.

It carries an associated mortality rate of 30% to 70%.

HAP lengthens the hospital stay by 7 to 9 days and is associated with a higher cost of medical care.

HAP is the most common infection occurring in patients requiring care in an intensive care unit (ICU)

This increased incidence is because patients located in an ICU often require mechanical ventilation, and mechanically ventilated patients are 6 to 21 times more likely to develop HAP than nonventilated patients.

Mechanical ventilation is associated with high rates of HAP The development of HAP in mechanically ventilated patients portends a

poor prognosis, with a rate of mortality 2 to 10 times higher for this group than for mechanically ventilated patients without HAP.

PATHOGENESIS

Gram-negative bacteria (Pseudomonas,K.Pneumonia, H.Influenza.Acenatobacter…) account for 55% to

85% of HAP infections, and gram-positive cocci (Staph and Streptococci)account for 20% to 30%.

Microaspiration of contaminated oropharyngeal secretions is the most common cause of HAP

The oropharynx of hospitalized patients becomes colonized by GNB in as many as 35% of moderately ill and 73% of critically ill patients, often within the first 4 days of admission.

PATHOGENESIS

Colonization of the oropharynx with pathogenic microorganisms

Aspiration from the oropharynx into the lower respiratory tract

Compromise of the normal host defense mechanisms

MICROBIOLOGIC CAUSES OF HCAP

Non-MDR Pathogens MDR Pathogens

Streptococcus pneumoniae Pseudomonas aeruginosa

Other Streptococcus spp. MRSA

Haemophilus influenzae Acinetobacter spp.

Escherichia coli

Klebsiella pneumoniae Klebsiella spp.

Proteus spp. Legionella pneumophila

Enterobacter spp. Burkholderia cepacia

Serratia marcescens Aspergillus

Risk factors for hospital-acquired pneumonia

Intrinsic risk factors Age 60-65 yr Gender: male Season: fall, winter Prolonged mechanical

ventilation APACHE II score 16-20 Coma Aspiration COPD/pulmonary disease Surgery Organ system failure index 3

of 7

Extrinsic risk factors Supine position Nasogastric tube Enteral nutrition Re-intubation Tracheotomy Intra-cuff pressure <20

cmH2O Gastric alkalization Heated humidifiers (open

systems)

RISK FACTORS FOR MULTIDRUG-RESISTANT PATHOGENS

Antimicrobial therapy was initiated within the preceding 90 days.

Onset of pneumonia occurred after 4 days of hospitalization.

Known MDR pathogens are circulating in the community or hospital.

Immunosuppressive disease is present or immunosuppressive therapy has been initiated.

Increased use of outpatient IV antibiotic therapy General aging of the population

HAP RISK INDEX

Pao2/Fio2 = ratio of arterial O2 pressure to fraction of inspired O2; ARDS = acute respiratory distress syndrome.

*Criteria applicable 72 h after initial diagnosis. Score ≥ 6 suggests hospital-acquired pneumonia. Score < 6 suggests alternative process.

American Journal of Respiratory and Critical Care Medicine 162:505–511, 2000.

HOSPITAL ACQUIRED PNEUMONIA RISK INDEX

Factor PointsTemperature (°C)

≥ 36.5 and ≤ 38.4 0≥ 38.5 and ≤ 38.9 1≥ 39 and ≤ 36 2

Blood leukocytes, μL≥ 4,000 and ≤ 11, 000 0< 4,000 or > 11,000 1Band forms ≥ 50% 1

Tracheal secretionsNone 0Nonpurulent 1Purulent 2

Oxygenation: Pao2/Fio2, mm Hg> 240 or ARDS 0≤ 240 and no ARDS 2

Pulmonary radiographyNo infiltrate 0Diffuse (or patchy) infiltrate 1Localized infiltrate 2

Progression of infiltrate*None 0Progression (heart failure and ARDS excluded) 2

Growth of pathogenic bacteria on tracheal aspirate culture*

No, rare, or light growth 0Moderate or heavy growth 1Same bacteria as on Gram stain 1

DIAGNOSTIC TESTS

Blood Cultures: gold standard Gram stain and cultures of

appropriate pulmonary secretions Serology PCR Urine antigen test Direct antibody test

DIAGNOSTIC TESTS

Blood Culture

- Only 5-14% of cultures of blood are positive

- No longer considered necessary for all hospitalized CAP patients

- Should be done in certain high-risk patients (i.e. severe CAP; chronic liver disease

DIAGNOSTIC TESTS

Sputum Culture

- Sensitivity and specificity is highly variable (< 50%)

- Greatest benefit is to alert the physician of unsuspected and/or resistant pathogens

DIAGNOSTIC TESTS

Gram Stain

- May help identify pathogens by their appearance

DIAGNOSTIC TESTS

Antigen tests

- Two commercially available tests detect pneumococcal and Legionella antigens in urine

- Sensitivity and specificity are high for both tests

- Can detect antigen even after the initiation of appropriate antibiotic therapy

- Limited availability

DIAGNOSTIC TESTS

SPUTUM DIRECT FLUORESCENT ANTIBODY (DFA)

A test that looks for microorganisms in lung secretions

Abnormal results may be due to an infection such as Legionnaire's disease, mycoplasma pneumonia , or chlamydia pneumonia.

GENERAL CONSIDERATIONS

Adequate hydration Oxygen therapy for hypoxemia Assisted ventilation when necessary

EMPIRICAL ANTIBIOTIC TREATMENT OF HCAP

PATIENTS W/O RISK FOR MDR PATHOGENS

- Ceftriaxone 2g IV q24 hours or

- Moxifloxacin 400mg IV q24 hours, Ciprofloxacin 400mg IV q8 hours, Levofloxacin 750mg IV q24 hours or

- Ampicillin/Sulbactam 3 gm IV q6 hours or

- Ertapenem 1gm IV q24 hours

EMPIRICAL ANTIBIOTIC TREATMENT OF HCAP

PATIENTS WITH RISK FOR MDR PATHOGENS1. A beta-lactam:Ceftazidime 2 gm IV q8 hours or Cefepime 2 gm IV q8-q12 hours orPiperacillin/Tazobactam 4.5 gm IV q6 hours, Imipinem 500mg IV q6

hours or 1 gm IV q8 hours, Meropenem 1 gm IV q8 hours plus

2. A second agent active against gram-negative bacterial pathogens:Gentamicin or Tobramycin 7 mg/kg IV q24 hours or Amikacin 20 mg/kg

IV q24 hours orCiprofloxacin 400mg IV q8 hours or Levofloxacin 750mg IV q24 hours

plus

3. An agent active against gram-positive bacterial pathogens:Linezolid 600 mg IV q 24 hours orVancomycin 15mg/kg q12 hoursAdapted from Niederman MS, Craven DE, Bonten MJ, et al: Guidelines for the management of adults with

hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 2005;171:388-416.

STREAMLINING OF EMPIRIC ANTIBIOTIC THERAPY

Switch of oral antibiotic agent

1. There is less cough and resolution of respiratory distress (normalization of RR)

2. The patient is afebrile for > 24 hours.

3. The etiology is not a high risk (virulent/resistant) pathogen.

4. There is no unstable co-morbid condition or life-threatening complication such as MI, CHF, complete heart block, new atrial fibrillation, supraventricular tachycardia, etc.

5. There is no obvious reason for continued hospitalization such as hypotension, acute mental changes, BUN: Cr of >10:1, hypoxemia, metabolic acidosis, etc.

Rate of resolution of physical and laboratory abnormalities

Abnormalities Duration

Fever 2 to 4 days

Cough 4 to 9 days

Crackles 3 to 6 days

Leukocytosis 3 to 4 days

C-reactive protein 1 to 3 days

CXR abnormalities 4-12 weeks

Patient is considered to have responded if:1. Fever declines within 72 hrs2. Temperature normalizes within 5 days3. Respiratory signs (tachypnea) return to normal

Failure to improve within 48 to 72 hours following therapy

Noninfectious conditions

- Cancer, embolus, hemorrhage Resistant pathogen Wrong drug Right drug, wrong dose Unusual pathogens

- Mycobacterial, anaerobic(Bacteroides, Actinomyces…) viral, fungal

Nosocomial superinfections

FAILURE TO IMPROVE

Due to MDR pathogens Reintroduction of the microorganisms Superinfection Extrapulmonary infections Drug toxicity

COMPLICATIONS

Death Prolonged mechanical ventilation Prolonged hospital stay Development of necrotizing pneumonia Long-term pulmonary complications Inability of the patient to return to

independent function

PROGNOSIS

HCAP is associated with significant mortality (50%-70%)

Presence of underlying diseases increases mortality rate

Causative pathogen also plays a major role

PREVENTION

Decreasing likelihood of encountering the pathogen- hand washing- use of gloves- Use of face mask- Negative pressure room- Prompt institution of effective chemotherapy for patients with contagious

illnesses- Correction of condition that facilitate aspiration- Maintenance of gastric acidity- FOLLOW VAP PREVENTION PROTOCOLS

Strengthening the host’s response once the pathogen is encountered- Chemoprophylaxis- Immunizing of patients at risk

PATHOGENIC MECHANISMS AND CORRESPONDING PREVENTION STRATEGIES FOR VENTILATOR-

ASSOCIATED PNEUMONIA

Pathogenic Mechanism Prevention StrategyOropharyngeal colonization withpathgenic bacteria Elimination of normal flora Avoidance of prolonged antiobiotic

courses Large-volume oropharyngeal

aspiration around time of Short course of prophylactic antibiotics intubation for comatose patients

Gastroesophageal reflux Post pyloric enteral feeding; Avoidance of high gastric residuals

Bacterial overgrowth of stomach Avoidance of gastrointestinal bleeding

due to prophylactic agents that raise gastric pH; selective decontamination

of digestive tract with nonabsorbable antibiotics

Pathogenic Mechanism Prevention StrategyCross-infection from other Hand washing, especially with alcohol colonized patients based hand rub; intensive infection control education; isolation; proper cleaning of reusable equipmentLarge-volume aspiration Endotracheal intubation; avoidance of sedation; decompression of small-bowel obstructionMicroaspiration around endotracheal tube Endotracheal intubation Noninvasive ventilation Prolonged duration of Daily awakening from sedation ventilation weaning protocols Abnormal swallowing function Early percutaneous tracheostomy Secretions pooled above Head of bed elevated; continuous endotracheal tube aspiration of subglottic secretions

Pathogenic Mechanism Prevention Strategy

with specialized endotracheal tube

avoidance of reintubation;

minimization of sedation and

patient transport

Altered lower respiratory host Tight glycemic control; lowering of

defenses hemoglobin transfusion threshold;

specialized enteral feeding formula

REFRENCE

Treatment of hospital-acquired, ventilator-associated, and healthcare-associated pneumonia in adults UpToDate.com Octobar 2009

Author

Thomas M File, Jr, MD European Respiratory Society 2007 Adapted from Singh N, Rogers P, Atwood CW, et al: Short-course empiric antibiotic therapy

for patients with pulmonary infiltrates in the intensive care unit. American Journal of Respiratory and Critical Care Medicine 162:505–511, 2000.

Hospital-Acquired Pneumonia by John G. Bartlett, MD, May 2008 Hospital-Acquired, Health Care Associated, and Ventilator-Associated Pneumonia BY Justin

L. Ranes Steven Gordon Alejandro C. Arroliga ,CLEVELAND CLINIC

Hospital-acquired pneumonia: Epidemiology, etiology, and treatment. Infect Dis Clin North Am. 12: 1998; 761-779

Hospital-acquired pneumonia: Risk factors, microbiology, and treatment. Chest. 119: 2001; 373S-384S

David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine 5/23/2010