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Forth stage
Medicine
Lec-7
.د
رامي
1/1/2014
Hospital-acquired pneumonia
Hospital-acquired pneumonia (HAP) or nosocomial pneumonia refers to a pneumonia that
occurs at least 2 days after hospital admission. HAP is the second most common and the
leading cause of death due to hospital-acquired infection. The risk of HAP is higher in
patients admitted to the ICU, especially when mechanically ventilated. HAP occurring in
patients on mechanical ventilation is called ventilator-associated pneumonia (VAP).
Aetiology
HAP occurring within 4-5 days of hospital admission (early onset HAP) is caused by
organisms similar to those causing CAP. However, late onset HAP is more often caused by
Gram negative bacilli (e.g. E. coli, pseudomonas, enterobactor, klebsiella, acinetobactor and
proteus), Staphylococcus aureus (including MRSA) and anaerobes. Factors predisposing to
HAP include:
1. Reduced immune defense (diabetes and corticosteroid therapy)
2. Reduced cough reflex and aspiration of nasopharyngeal secretion (reduced
consciousness and vocal cord and bulbar palsy)
3. Bacteria introduced to the lower airways (endotracheal intubation, tracheostomy
and infected ventilator, nebulizer and bronchoscope)
Clinical features
Although no diagnostic criteria are available, HAP should be considered in any
hospitalized (or ventilated) patient who develops any of the following:
1. Purulent sputum (or endotracheal secretion)
2. New radiological infiltrate
3. Worsening hypoxaemia (or increasing oxygen requirement)
4. Fever (>38.3ºC)
5. Leucocytosis or leucopenia
Investigations
Investigations are similar to CAP, but whenever possible, aetiological confirmation should
be sought. In VAP, endotracheal aspirate or bronchoscope- directed protected brush
specimen or broncho-alveolar lavage (BAL) may be performed to improve the diagnostic
yield.
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Treatment
The choice of empirical antibiotic coverage should be based on:
1. Local knowledge of pathogens in the hospital
2. Drug resistance pattern
3. Recent antibiotic use
4. Co-morbidity
However, protocol should include 2 antibiotics active against Pseudomonas aeruginosa and
1 antibiotic active against MRSA. This would include:
1. A β-lactam with anti-pseudomonal activity (ceftazidime, cefepim, piperacillin-
tozabactam or meropenem)
2. A second agent active against Gram negative bacilli (an aminoglycoside or a
quinolone)
3. An agent active against MRSA (linezolid or vancomycin)
Antibiotics should be given IV at least initially.
Despite appropriate management, the mortality of HAP is around 30%.
Prevention
1. Good hygiene including hand washing and equipment cleansing
2. Measures to reduce the risk of aspiration (elevation of the head of the patient to 30º
- 45º)
Pneumonia in immunocompromised patients
Patients immunocompromised by drugs (cytotoxic or immunosuppressive dugs) or disease
(like AIDS and acute leukaemia) are at high risk of pneumonia. The majority is caused by the
same pathogens that cause pneumonia in immunocompetent individuals, but patients with
more severe immunosuppression are at risk of opportunistic infection caused by organisms
normally considered of low virulence or non-pathogenic.
According to the immunological defect, immunosuppressed patients are at risk of
pulmonary infection caused by Gram negative bacteria (esp. Pseudomonas aeruginosa),
viruses (CMV and herpes viruses), fungi (Pneumocystis jirovecii (PCP), candida and
aspergillus), mycobacteria and nocardia. More than one organism may be responsible.
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Clinical features
Typical features of fever, cough and breathlessness tend to be less specific with more
severe degrees of immunosuppression. Symptom onset is less rapid with opportunistic
organisms such as PCP, CMV and mycobacteria than with bacterial pneumonia.
Investigations
Most of these patients are too ill to withstand invasive investigations such as bronchoscopy
and surgical lung biopsy. Induced sputum is a safe method of obtaining microbiological
sample.
High resolution CT (HRCT) can be helpful in minimizing the differential diagnosis:
1. Focal opacification favours bacteria, mycobacteria and nocardia
2. Bilateral opacification favours PCP, fungi, viruses and nocardia
3. Cavitation suggest mycobacteria, fungi and nocardia
4. Pleural effusion suggests bacteria
Treatment
Treatment is directed to the causative agent if the aetiological diagnosis is confirmed, but
most often the aetiology is at least initially unknown, and broad spectrum antibiotic
coverage is started; examples include a third-generation cephalosporin plus and anti-
staphylococcal antibiotic. The treatment is then tailored according to the results of
investigations and clinical response. Accordingly, antifungal, antiviral or anti-pneumocystis
drugs can be added.
Mechanical ventilation increases the risk of HAP and is associated with higher mortality. It
may be avoided by early use of non-invasive ventilation.
Suppurative pneumonia and lung abscess
Suppurative pneumonia is characterized by destruction of the lung parenchyma by the
inflammatory process with microabscess formation. Lung (or pulmonary) abscess refers to
large collection of pus or a cavity from which pus has escaped by rupture into a bronchus.
Suppurative pneumonia and lung abscess are considered together as their etiology and
clinical features overlap.
Aetiology
1. Inhalation (aspiration) of septic materials during dental or ENT surgery, or vomitus
under general anaesthesia. Aspiration of oropharyngeal secretions in patients with
bulbar or vocal cord palsy, stroke, epilepsy, alcoholism and achalasia.
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Aspiration tends to localize to the dependant area of the lung (such as apical
segments of the lower lobes in supine patients)
2. Bacterial infection of collapsed lobes (caused by tumours or foreign bodies)
3. Bacterial infection of pulmonary infarct
In the above conditions, the infection is caused by mixture of predominantly anaerobic
organisms representing the flora of the mouth and upper airways. These include
bacteroids, fusibacterium, aerobic and microaerophilic cocci.
4. Infection of previously healthy lung by organisms like Staphylococcus aureus and
Klebsiella pneumoniae.
5. Haematogenous lung abscess in injection drug users in association with endocarditis
of the right heart valves.
Clinical features
The patients presents with cough productive of large amount of purulent sputum, which is
sometimes fetid (due to anaerobic infection) or blood stained, associated with high
remittent fever, malaise, fatigue and weight loss (in prolonged cases). Pleuritic pain is
common. Occasionally, sudden expectoration of copious amounts of foul smelling sputum
indicates rupture of the abscess to a bronchus.
Apart from ill-health and fever, examination may show digital clubbing (which may develop
in as rapidly as 10 days). Chest examination may show signs of consolidation (signs of
cavitation is rare). Pleural rub is common (due to surrounding lung and pleural
inflammation)
Investigation
Chest X-ray shows homogenous lobar or segmental opacity consistent with consolidation or
collapse. Abscess is characterized by cavitation and fluid level. Sputum and blood can be
sent for culture.
Treatment
Oral co-amoxiclav 1.2 gm 8 hourly (initially IV in severe cases) is effective. Metronidazole
400 mg 8 hourly can be added (esp. in case of fetid sputum). Clindamycin 600 mg 6 hourly
IV (then orally) is an alternative. Treatment should be continued for 4-6 weeks.
Physiotherapy is of great value.
Surgery is indicated if no improvement occurs on medical therapy and to remove any
obstructing lesion
Complications include empyema and residual fibrosis and bronchiectasis.