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Hospital Acquired Pneumonia (HAP)

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Hospital Acquired Pneumonia (HAP) By Professor Adel Khattab Prof. of Pulmonary Medicine Ain Shams University Definition This infection is with onset of 48-72 hours ... – PowerPoint PPT presentation

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Title: Hospital Acquired Pneumonia (HAP)


1
Hospital Acquired Pneumonia (HAP)
  • By
  • Professor Adel Khattab
  • Prof. of Pulmonary Medicine
  • Ain Shams University

2
Definition
  • This infection is with onset of 48-72
    hours of hospitalization, development of a new or
    progressive infiltrate in CXR, fever,
    leukocytosis and purulent tracheobronchial
    secretions.
  • This infection was neither present nor
    incubating at the time of hospitalization.
  • This definition, however may exclude cases
    that occur in outpatient settings or after
    discharge from the hospital.

3
Definitions
  • HAP refers to pneumonia that occurs ?48 hours
    after
  • admission, which was not incubating at the time
    of
  • admission.
  • HAP is closely related share the same
    principles with
  • Ventilator-associated pneumonia (VAP)
    Healthcare-
  • associated Pneumonia (HCAP).
  • VAP refers to pneumonia that arises more than
    4872
  • hours after endotracheal intubation.
  • (American Thoracic Society, 2005)

4
Incidence of HAP
  • 2nd most common nosocomial infection
  • Rate 5-15 cases/ 1000 hospital admission
  • ? 6- to 20-fold in mechanically ventilated
    patients
  • Increases hospital stay by 7-9 days / patient
  • Excess cost of more than 40,000 / patient
  • Mortality rate is seriously high 30- 50
  • VAP most vigorous type of nosocomial pneumonia
    occurs 927 of all intubated patients
  • Mortality rate is seriously high 30-71

5
Importance of Hospital Acquired Infection ( HAI )
  • HAI are responsible for 44,000 to 98,000
    deaths annually and represent a cost of 17 to
    29 billion.

6
Definitions
  • Early-onset HAP VAP within the first 4 days of
  • hospitalization.
  • Late-onset HAP and VAP 5 days or more of
  • hospitalization.
  • (American Thoracic Society, 2005)

7
Ventilator Associated Pneumonia (VAP )
8
Prevalence of VAP
  • VAP is a common disorder, with a prevalence of
    6-52 cases /100 patients depending on the
    population studied.
  • Crude rate of VAP is usually 1-3 per day of
    intubation mechanical ventilation.
  • Rates are greatly higher in surgical ICU patients
    than in medical ICU ones.

9
Device Associated Infection Rates by Type of ICU
10
Mortality of VAP
  • Crude mortality rates for VAP ranges from 20-71
    , but deaths are often due to other causes in
    critically ill patients.
  • A preferred measure is Attributable mortality
    ,defined as percentage of deaths that would not
    have occurred in the absence of infection.
  • Attributable mortality of VAP ranges from 27-43

11
Respiratory therapy equipment
Host factors
Invassive devices
Medications
Surgery
Gastric colonization
Oropharyngeal colonization
Aspiration Numbers of bacteria virulence
Lung Defenses Mechanical cellular/humoral
Translocation
Bacteremia
Pneumonia
12
Sources of infection
Environment
Devices
Air aspergillus Water legionella Foodenteric
Gram -ve Fomites S. aureus RSV
Endotracheal tube Suction catheters Bronchosc
ope Respiratory therapy equipment Nasogastric tube
Other Patients
Staff
13
Nosocomial pneumonia(NP)risk factors for
cross-transmission
  • Increased risk for NP associated with poor
    hand-washing
  • External colonization
  • - Aerosol inoculation due to colonization of
    respiratory therapy
    equipment
  • Nebulizers
  • Mechanical ventilators
  • Resuscitation bags and portable spirometers
  • Inappropriate airway suctioning

14
Respiratory therapy equipment
Host factors
Invassive devices
Medications
Surgery
Gastric colonization
Oropharyngeal colonization
Aspiration Numbers of bacteria virulence
Lung Defenses Mechanical cellular/humoral
Translocation ?
Bacteremia
Pneumonia
15
Nosocomial pneumoniaClinical risk factors for
Oropharyngeal Colonization
  • Coma
  • Hypotension
  • Renal failure
  • Leucocytosis
  • COPD
  • Alcoholism
  • Clinical underlying condition
  • Period of hospitalization
  • Nutritional status
  • Antibiotic therapy
  • Intubation
  • ICU stay

Johanson et al, celis et al
16
Respiratory therapy equipment
Host factors
Invassive devices
Medications
Surgery
Gastric colonization
Oropharyngeal colonization
Aspiration Numbers of bacteria virulence
Lung Defenses Mechanical cellular/humoral
Translocation ?
Bacteremia
Pneumonia
17
Nosocomial pneumonia risk factors for gastric
colonization
  • Advanced age .
  • Achlorhydria.
  • Alterations in gastric juice secretion.
  • Antacids and H2 blockers.
  • Increased concentration of conjugated bilirubin
    in gastric content.

18
Respiratory therapy equipment
Host factors
Invassive devices
Medications
Surgery
Gastric colonization
Oropharyngeal colonization
Aspiration Numbers of bacteria virulence
Lung Defenses Mechanical cellular/humoral
Translocation ?
Bacteremia
Pneumonia
19
Nosocomial pneumonia risk factors for aspiration
  • Alterations of consciousness- Trauma, sedative
    drugs
  • Nasogastric intubation
  • Supine position
  • Endotracheal tube
  • - Direct pass to the lower airway- Leakage
    around the cuff- Bacterial biofilm/dislodgement
    to distal airway

20
(American Thoracic Society, 2005)
21
Microbiology of HAP
  • Bacterial ( 80-90)
  • - Gram ve bacilli (50-70)
  • Pseudomonas aeruginosa
  • Enterobacteriaceae
  • Staphylococcus aureus (15-30)
  • Anaerobic bacteria (10-30)
  • Haemophilus influenzae (10-20)
  • Streptococcus pneumoniae (10-20)
  • Legionella speecies (4)

22
Microbiology of HAP (con.)
  • Viral (10-20 )
  • - Cytomegalovirus
  • - Influenza
  • - Respiratory syncytial virus
  • Fungal (lt 1 )

23
Bacterial pathogens associated with HAP
  • Early-onset HAP
  • First 4 days
  • Strept. pneumoniae.
  • Hemophilus influenzae.
  • Moraxella catarrhalis.
  • Anaerobes (uncommon).
  • Late-onset HAP
  • After 4 days
  • Pseudomonas aeruginosa.
  • Acinetobacter.
  • Enterobacter sp.
  • MRSA.

24
DIAGNOSTIC TECHNIQUES
  • Blood, Pleural Fluid Analysis, and Culture
  • Nonbronchoscopic evaluations
  • Percutaneous needle aspiration
  • Endotracheal aspiration
  • Blind bronchial sampling
  • Bronchoscopic techniques
  • PSB
  • BALTissue diagnosis

25
Problems in Diagnosis of HAP
  • Contamination by the upper airways Solved by
    protecting the sampling fluid.
  • Separation of infection from colonization Solved
    by using quantitative cultures.

26
Diagnostic strategies approaches
  • HAP is suspected The presence of a new or
    progressive
  • radiographic infiltrate plus at least two of
    three clinical
  • features (fever gt38C, leukocytosis or leukopenia
  • purulent secretions).
  • Lower respiratory tract sample for microscopy
  • culture from all patients, ideally before
    antibiotic started .
  • Bronchoscopic or nonbronchoscopic.
  • endotracheal aspirate (ETA), bronchoalveolar
    lavage (BAL),
  • or protected specimen brush (PSB).
  • Semi-quantitative or quantitative In
    quantitative cultures the diagnostic threshold
    is
  • ETA 106 cfu/ml, BAL 104 or 105 cfu/ml, PSB 103
    cfu/ml.

27
Hospitalized patient
No further Investigations observe
Clinical features Suggest Infection?
NO
Yes
Order/review recent CXR
Observe investigate for other sources
Abnormal ?
No
Yes
28
Yes
Option A Quantitative culture
Option B Emperic treatment Qualitative culture
If clinically unstable
Nonbronchoscopic EA ,BAL ,PSB
Bronchoscopic BAL, PSB, PBAL
Adjust treatment According to Culture results
or Clinical response
Treat based on results Of diagnostic testing
29
I will prevent disease whenever I can,
prevention is preferable to cure.Modem Versoin
(1964)
30
Prevention of HAP
  • (A) Regimens for specific indications
  • Hand washing between patient contact.
  • Pneumococcal and influenza vaccination for
    population at risk.
  • Isolating patients with highly resistant
    organisms such as MRSA.

31
It is not enough to produce satisfactory soap it
also necessary to induce people wash.
32
Prevention of HAP
  • (B) Regimens used widely in some clinical
    settings
  • Nutritional support with careful attention to the
    route and volume of feeding.
  • Intestinal bleeding prophylaxis, sucralfate
    compared with either antacids or H-2 blockers.
  • Careful handling of ventilator tubing and
    associated equipments.
  • Subglottic secretion drainage.
  • Lateral rotation bed therapy.

33
Prevention of HAP
  • Intervention to decrease risk
  • Single use non-sterile used for suction and
    change catheter between patients after each
    use.
  • Single-use disposable or wash with detergent
  • Single-use or disposable mouthpiece clean
    according to manufacture recommendations.
  • Procedure or device
  • Suction catheter
  • Suction bottle
  • Spirometry

34
Prevention of HAP
  • Breathing circuit
  • Nebulizers Humidifiers
  • Change MV circuit every 48 hours. Periodically,
    drain breathing-tube condensation trap, taking
    care not to spill it back to patient trachea.
  • Change reprocess device between patients by
    sterilization or high level of disinfection
    fill with sterile water only.

35
Classification of HAP Patients
  • Is pneumonia mild to moderate or severe?
  • Are specific host or therapeutic risk factors
    predisposing to specific pathogens present?
  • Is pneumonia early onset (within 4 days of
    admission) or late onset?

36
ATS DEFINITION OF SEVERE HAP
  • Admission of ICU
  • Resp. failure, defined as need for mechanical
    ventilation or the need for gt 35 oxygen to
    maintain an arterial oxygen saturation gt90
  • Rapid radiographic multilobar pneumonia, or
    cavitation of a lung infiltrate
  • Evidence of severe sepsis with hypotension and/or
    end-organ dysfunction
  • Shock (systolic BP lt 90mmHg or diastolic Bp
    lt 60 mmHg) Requirement for vasopressors for gt 4 h
  • Urine output lt20mL/h or total urine output
    lt80mL in 4 h(unless another explanation is
    available).
  • Acute renal failure requiring dialysis

37
(American Thoracic Society, 2005)
38
(American Thoracic Society, 2005)
39
(American Thoracic Society, 2005)
40
previously
41
  • (American Thoracic Society, 2005)

42
Duration of Therapy
  • Efforts should be made to shorten the duration of
  • therapy from the traditional 14 to 21 days to
    periods as
  • short as 7 days, provided that the etiologic
    pathogen is
  • not P. aeruginosa, and that the patient has a
    good
  • clinical response with resolution of clinical
    features of Infection.

43
  • Control of antibiotic resistance requires
    aggressive implementation of several strategies
  • 1- Ongoing surveillance of resistance.
  • 2- when the rate of resistance increases using
    hygienic controls to limit spread of single
    (colonial)strains
  • a-Hand hygiene (30-120 sec).
  • b-Alcohol-based hand rubs (10-30 sec ).
  • c-Use of disposable examination gloves during
    contacts with pts to decrease the problem of
    colonization pressure.

44
  • 3-Hospitals should use (closed formularies) for
    prescription of antibiotics to limit prescribing
    options to one or two drugs per class.
  • 4-Restriction of the use of antibiotics has been
    effective in reducing cost and excessive empiric
    use of broad spectrum drugs .
  • 5-Rotational use of antibiotics (antibiotic
    cycling program).

45
  • (American Thoracic Society, 2005)

46
Clinical Resolution of HAP
47
Clinical Pulmonary Infection Score
  • For every item give score 0 ,1, 2 .
  • For temperature normal 0 , up to 38.5 give 1,
    but if higher give 2 .
  • Count the final score of all items if lt ,or 6
    means clinical resolution but if gt 6 means
    clinical unresolution and unimprovement.

48
  • (American Thoracic Society, 2005)

49
Unresolved HAP
  • Clinical re-assessment of the patient .
  • Consider differential diagnosis .
  • Exclude another site of infection ( UTI, vascular
    lines, bed sores, wounds).
  • Re-collect another samples ( ET aspirate,
    bronchoscopic, pleural fluid, blood).
  • Use multiple antibiotics instead of monotherapy.
  • Consider steroids and open lung biopsy.

50
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