Lecture 7 - Nosocomial Pneumonia

Health Care Associated
Pneumonia
Respiratory Block
BY PROF .A.M.KAMBAL and
PROF .HANAN HABIB
Department of Pathology, KSU
Health Care Associated
Pneumonia
Definition of Pneumonia:
Infection of the pulmonary Parenchyma

Can be divided in to:

A-Community acquired Pneumonia acquired
in the community, by community acquired
organisms, eg. Streptococcus pneumoniae
usually susceptible to antibiotics.

B-Health care associated Pneumonia acquired
48-72 hours after admission to health care
institutions eg. Hospital, usually caused, by
organisms in hospital which are usually
resistant to antibiotics-eg .Pseudomonas
aeruginosa and Acinetobacter baumanii
Health care associated
Pneumonia
A- Hospital Acquired Pneumonia(HAP)
B- Ventilator Associated
Pneumonia(VAP) in patients who have
assisted respiration for a period of at
least 48 hours.
C Health care associted pneumonia
[HCAP]
In this lecture the three HAP,HCAP and
VAP shall be considered similarly.
Definition
Nosocomial pneumonia: is defined as
hospital associated pneumonia (HAP) or
health care associated pneumonia (HCAP).
Occurring at least 48 hours after admission
and not incubating at the time of
hospitalization.
Introduction
Nosocomial pneumonia is the 2
nd
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 (intensive care unit)
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
Pathogenesis
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.
Pathogenesis
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
Classification
Early-onset nosocomial pneumonia:
Occurs during the first 4 days of admission.
Usually is due to S. pneumoniae, MSSA (Methicillin sensitive
S.aureus ), H. Influenza, or anaerobes.
Late-onset nosocomial pneumonia:
occurs more than 4 days of admission.
More commonly by Gram negative organisms,
especially: P. aeruginosa, Acinetobacter,
Enterobacteriaceae (Klebsiella, Enterobacter, Serratia) or MRSA.
Causative Agent
Enteric Gram negative 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.
Causative Agents

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

Causative Agents
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(methicillin resistant S.aureus) is seen more
commonly in patients who:
Received corticosteroids
Undergone mechanical ventilation >5 days
Presented with chronic lung disease
Had prior antibiotics therapy
Causative Agents
Anaerobes are common in patients
predisposed to aspiration .

Ventilator associated pneumonia (VAP )with
anaerobes occurred more often with
oropharyngeal intubation than nasopharyngeal
intubation.
Ventilator-associated
Pneumonia (VAP)
Ventilator-associated
Pneumonia (VAP)
Definition:
Nosocomial pneumonia that 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
Pathogenesis
Requires 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.
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
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
Preventions for VAP
Pharmacologic strategies
Stress-ulcer prophylaxis
Combination antibiotic therapy
Prophylactic antibiotic therapy
Chlorhexidine oral rinse
Prophylactic treatment of neutropenic patients
Vaccines
Treatment
Most initial therapy is empiric because no
pathogen is identified or results are not
available when antimicrobial decisions are
made in most patients.
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
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
Treatment
The mortality can be reduced with early
appropriate empiric therapy.

(Form 30 % with appropriate therapy to more than 90 % with
inappropriate therapy) .

----
Treatment
Guidelines by American Thoracic Society has
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
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.
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
Treatment
Combination of antipseudomonal drugs is
controversial:
1. 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.
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: congestive heart failure (CHF)
Lung: fibroproliferative acute respiratory distress syndrome
(ARDS), pulmonary emboli, Atelectesis.

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