Hospital Acquired Pneumonia

Ghanem Zoabi
 Pneumonia
• Definition : Infection of the pulmonary parenchyma.
• Despite being the cause of significant morbidity & mortality, it is often mistreated
and underestimated
 Definition
• Infection of the pulmonary parenchyma.
• Despite being the cause of significant morbidity & mortality, it is often mistreated
and underestimated

CAP
Classification
 Definition
• Infection of the pulmonary parenchyma.
• Despite being the cause of significant morbidity & mortality, it is often mistreated
and underestimated

CAP
Classification

HAP
 Definition
• Infection of the pulmonary parenchyma.
• Despite being the cause of significant morbidity & mortality, it is often mistreated
and underestimated

CAP VAP
Classification

HAP
 Definition
• Infection of the pulmonary parenchyma.
• Despite being the cause of significant morbidity & mortality, it is often mistreated
and underestimated

CAP VAP
Classification

HAP HCAP
 Definition
• Infection of the pulmonary parenchyma.
• Despite being the cause of significant morbidity & mortality, it is often mistreated
and underestimated

CAP VAP
Classification

HAP HCAP
Morphology

Lobar pneumonia Bronchopneumonia

Strep. pneumonia M. Pneumonia
Staph
Morphology

Necrotizing pneumonia Interstitial pneumonia

Staph Resp. viruses
Pathophysiology
• Proliferation of microbial pathogens at the alveolar level + the
host’s response

• How do the get there?

- Aspiration from the oropharynx Most common
- Hematogenous spread
- Contiguous extension from an infected Rarely
pleural or mediastinal space

• In order for a clinical pneumonia to become manifest,

pathogens must exceed the following:
Mechanical factors in host defense
• Hairs and turbinates of the nares Nose
 Captures large inhaled particles.

• Branching of bronchoalveolar tree Nose

 Traps microbes in airway lining. (in a
British
accent)
• Mucociliary and antibacterial factors
 Clear or kill potential pathogens.
Nostrils
• Gag & cough reflexes
 Prevent aspirations.

• Normal flora adhering to mucosal cells Nares

 Prevents pathogenic bacteria from binding.
Mechanical factors in host defense
• Hairs and turbinates of the nares
 Captures large inhaled particles.

• Branching of bronchoalveolar tree

 Traps microbes in airway lining.
Can be impaired by:
Alcohol, stroke\ dementia,
• Mucociliary and antibacterial factors
smoking\COPD, long
 Clear or kill potential pathogens. Influenza activity, Viruses…
• Gag & cough reflexes
Unprotected airway + gingivitis –
 Prevent aspirations.
major risk factor
• Normal flora adhering to mucosal cells
 Prevents pathogenic bacteria from binding.
HAP
 Definitions
HAP- Pneumonia that occurs 48 hours or more after admission and did not appear to be
incubating at the time of admission .
VAP- is a type of HAP that develops more than 48 hours after endotracheal intubation .
HCAP- was included in the 2005 American thoracic society guidelines and referred to
pneumonia acquired in health care facilities ( nursing homes,hemodialysis centers ,
outpatients clinics etc..) or during hospitalization for 48 hours or more within 90 days of
the diagnosis .
*Used to identify patients at risk for MDR infections , however , it may have led to
increased , inappropriately broad ABX use . So it was not included in ATS 2016 guidelines .
 HAP vs. VAP
- Most research on HAP was focused on VAP ( the information can be
applied to non-ICU HAP )
Why ?
- The greatest Difference between VAP and HAP studies is the dependence
on expectorated sputum for microbiologic diagnosis for HAP 
complicated by frequent colonization by pathogens in patients with HAP
 literature focused on VAP where access to LRT facilitates an etiologic
diagnosis .
Etiology- HAP
- Can be polymicrobial
- Common pathogens include :
1) aerobic gram negative bacilli ( E.coli[6.9%] , Klebsiella.P[9.8%] , Enterobacter
spp[6.3%], Pseudomonas aeruginosa [21%] , Acinetobacter spp [6.8%]).
2) Gram positive Cocci ( eg, S.aureus [28%] including MRSA , streptococcus spp).
3) Viruses , Fungi ( Immunocompromised )
- non-intubated HAP more microaspiration + Lower oxygen tension in the
lower respiratory tract  more anaerobic infections .
- higher frequency of non-MDR pathogens  allows monotherapy in a
large proportion comparing to VAP .
RISK FACTORS
- The most significant risk factor for HAP is intubation for mechanical
ventilation.
- Aspiration
- Old age
- chronic lung disease
- Depressed consciousness
- Chest \ upper abdominal surgery
- Agents that increase gastric PH
- Previous ABX exposure
- Reintubation or prolonged intubation
- CKD , malnutrition
- - previous hospitalization
Epidemiology- HAP
- HAP is one of the most common and morbid hospital-acquired
infections .
- Most cases of HAP occur in non-ventilated patients , however,
the highest risk for HAP is I
- n patients on mechanical ventilation (VAP) .
- Associated with long hospital stays and significant costs .
Clinical Manifestations
On a physical exam
On a physical exam
On a physical exam
On a physical exam
Diagnosis- HAP
- Clinical Findings are non specific  diagnosis is difficult
- LRT samples appropriate for cultures are more difficult to obtain in
non-intubated patients Diagnosis is harder in HAP than VAP .
So how to diagnose ?
- Clinical diagnosis based upon a new lung infiltrate PLUS clinical
evidence that the infiltrate is of infectious origin ( new onset fever ,
prulent sputum , leukocytosis and decline on oxygenation .
 Diagnosis- HAP
#Good History and Physical exam – fever , productive
cough .

#Blood tests – Leukocytosis , CRP , hypoxemia ,

Procalcitonin

#Chest X-ray – New or progressive lung infiltrate -

#CT- more sensitive , not practical

#Cultures of pulmonary secretions 70-80 % positive –

prone to False positives and False negatives.

# Blood cultures –very low yield , positive in < 15 %

 Treatment- HAP
-Empirical therapy for HAP and VAP –
should include agents with activity against
S.Aureus , P.aeruginosa and other gram
negative bacilli.
-Specific E.therapy should be based upon
knowledge of the pathogen,susceptibility
patterns within health care setting and
patient’s individual risk factors for MDR .
Prevention-HAP
- Avoiding intubation when possible
- Minimizing sedation
- Maintaining and improving physical conditioning
- Prevent aspiration – elevating head of the bed , minimizing sedation , draining
subglottic secretions in ventilated patients , application of PEEP , gastric fluid
monitoring
- Glucocorticoid – stress dose have been proposed as a possible method for
preventing HAP in critically ill patients
Complications- HAP
• death

• Prolongation of mechanical ventilation and duration in ICU.

• Necrotizing pneumonia (Pseudomonas)  Pulmonary hemorrhage.

• Bronchiectasis and parenchymal scarring.

Questions?