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Healthcare associated pneumonia
Definition
Pneumonia developing more than 2-3 days after admission to healthcare
facility.
Epidemiology
- 0.5-5% of hospital patients
- higher incidence in certain groups, eg postoperative patients and patients
in ICU.
Risk factors
Click here
Pathogenesis
- Thought to result from micro-aspiration of bacteria colonizing the upper
respiratory tract and stomach. Microaspiration has been shown to occur in 45%
of humans when asleep and the upper airway of 75% of critically ill patients
is colonized by enteric gram -ve bacilli.
- Other routes of infection include:
- macro-aspiration of gastric contents
- inhaled aerosols
- haematogenous spread
- spread from pleural space
- direct innoculation from ICU personnel
- translocation from gut followed by haematogenous spread (unproven)
- Infected biofilm in endotracheal tube, with subsequent embolization to
distal airways, may be important
Aetiology
- Gram -ve bacilli have been predominant causes but recent data suggest that
gram +ve bacteria (particularly S. aureus) are becoming more common
- Certain factors associated with multi-drug resistant organisms (eg
Pseudomonas aeruginosa, Acinetobacter spp and Stenotrophomonas
maltophilia):
- antimicrobial therapy in previous 90 days
- current hospitalization for 5 days or more
- high frequency of antibiotic resistance of in the specific hospital unit
- hospitalization for 2 days or more in previous 90 days
- residence in nursing home or extended care facility
- home infusion therapy (including antibiotics)
- chronic dialysis within 30 days
- home wound care
- family member with multi-drug resistant pathogen
- immunosuppression
- bronchiectasis
- NB causative organisms differ from hospital to hospital, ICU to ICU and at
different times in the same ICU
- Legionella should be considered in patients receiving steroids who
are not intubated at the time they develop pneumonia
- Pneumonia caused by multiple organisms common
- Virus and fungi are uncommon causes
Investigations
- Similar to those required for community acquired pneumonia
- Sampling of lower respiratory secretions
- non-invasive approach: sputum or tracheal aspirate
- invasive approach: protected specimen brush or bronchoalveolar lavage
specimen
- some organisms are virtually always pathogens when recovered from
respiratory secretions
- Blood cultures identify aetiological agent in 8-20% of patients
- Bacteraemia
is associated with a worse prognosis
- A large proportion of patients with severe hospital
acquired pneumonia and positive blood cultures have another source of
sepsis.
Diagnosis
May be difficult:
- clinical features of pneumonia are nonspecific
- many non-infectious conditions (eg atelectasis, pulmonary embolus,
aspiration, congestive heart failure and cancer) can cause infiltrates on a
chest X-ray
- bacteriological diagnosis is difficult due to the high incidence of
colonization of the oropharynx by gram negative bacteria (~70-75% of
moribund and chronically ill patients become colonized within 48 hours
- semi-quantitive culture of sputum increases specificity and may be
helpful in diagnosing pneumonia but may not be sufficiently specific in
identifying the responsible organisms
- invasive techniques for collection of distal airway secretions associated
with higher specificity but lower sensitivity and considerably greater cost (needs to weighed
against cost of unnecessary antibiotic treatment for patients who do not
actually have pneumonia).
- techniques include aspiration,
brushing and bronchoalveolar lavage. Can be performed blindly via an
endotracheal tube or under direct vision using a bronchoscope
- false negative results due to:
- sampling at an early stage of infection when bacterial load low
- sampling from an unaffected segment of lung
- incorrect processing
- sampling after starting antimicrobial
- recent randomized controlled trial
demonstrated an improved outcome amongst patients investigated by invasive
bronchoscopic sampling and quantitative microbiology compared to those
investigated with conventional sputum sampling and conventional microbiology.
Although these data are used to support the use of invasive sampling it
may have been the quantitative culture that was the key difference
- although bronchoscopic techniques are probably most accurate non-bronchoscopic
(blind) protected specimen brushing and mini-bronchoalveolar lavage
associated with good sensitivity and acceptable specificity (~75%)
- blind techniques have the advantage of being less invasive, available
to non-bronchoscopists, available to patients with small diameter endotracheal
tubes and of having less effect on gas exchange.
Management
Initial management based on clinical approach
- Early treatment with antimicrobials that cover all likely pathogens is
thought to result in a reduction in morbidity and mortality, although not
all studies have shown a difference in survival amongst those who were
treated with adequate antibiotic therapy compared with inadequate antibiotic
therapy
- Initial selection of
antimicrobials should be made on the basis of:
- risk factors for multi-drug resistant pathogens
- local bacterial flora and resistance patterns
- antimicrobial therapy in past 2 weeks: try to avoid using the same
class of antibiotic
- in the absence of local guidelines the regimes given in tables 1 & 2 may
help
- Do not delay initiation of antibiotic therapy to obtain lower respiratory
tract specimens
- Antibiotic treatment of acute tracheobronchitis may reduce the duration
of mechanical ventilation but there is no evidence it alters mortality
Subsequent management based on clinical approach
Reassess management after 2-3 days or sooner if patient deteriorates.
Subsequent management should be based on results of microbiological
investigations and response to therapy.
Assessing response to treatment
Assessing response is a vital part of the use of an empirical treatment
strategy
- Clinical improvement usually not apparent for 48-72 h and therapy should not
be changed in this time unless progressive deterioration occurs or unless
dictated by initial microbiological results
- Abnormal clinical parameters (fever, white cell count, oxygenation and
temperature) have usually resolved by 7 days. Persistence of abnormalities
should prompt a search for an alternative cause
- CXR
- Limited value for assessing response
- Initial CXR deterioration is common
- CXR improvement often lags behind clinical response
- Rapidly deteriorating CXR pattern, >50% increase in size of infiltrate in
48h, new cavitation or significant new pleural effusion should raise concern
- If patient fails to respond consider:
- Is it pneumonia?
- In particular consider the possibility of acute lung injury due to
infection at another site
- Host factors (eg immunosuppressed, debilitated)
- Consider unrecognized immunosuppression (eg AIDS) and the possibility
of Pneumocystis carinii infection
- Bacterial factors (eg virulent organism)
- In patients with ventilator associated pneumonia due to Pseudomonas
aeruginosa or Acinetobacter species the mortality approaches
90% in some series
- Unusual organism eg Mycobacterium tuberculosis, virus,
fungus
- Therapeutic factors (eg wrong drug, inadequate dose)
Management of non-responder
- consider broadening antimicrobial cover while waiting for results of
investigations
- repeat sampling of lower respiratory tract secretions
- repeat blood cultures
- consider invasive microbiology: BAL/PSB
- ultrasound or CT may be helpful to demonstrate a pleural effusion.
Diagnostic aspiration of pleural fluid should be carried out to exclude an
empyema
- CT can demonstrate empyema, abscesses, lymphadenopathy and pulmonary masses
- consider other source of infection
- open lung biopsy
- value in non-immunocompromised patient is controversial
- should only be considered if bronchoscopic cultures and other
diagnostic testing is not helpful
- empiric alteration of antibiotics or initiation of corticosteroid
therapy may be preferable if the patient remains haemodynamically stable
Duration of antibiotic therapy
- Little data to guide duration of therapy
but a randomized controlled trial demonstrated that patients who received
appropriate initial empiric therapy for ventilator associated pneumonia for
8 days had similar outcomes to those who received treatment for 14 days
(Click
here to view abstract)
- Disadvantages of prolonged course of antibiotics:
- selection of resistant bacteria
- increased risk of toxicity
- cost (needs to be balance against cost of relapse)
-
American Thoracic Society recommend shortening the antibiotic course to
as short as 7 days provided that the aetiological agent is NOT
Pseudomonas aeruginosa and the patient has a good clinical response with
resolution of clinical features of infection
Prevention
CDC guidelines for preventing healthcare associated pneumonia can be
downloaded by clicking here
General measures
- hand washing: the most effective.
- isolation of patients with multi-drug resistant pathogens
- nurse patients in semi-recumbent position (30-45º),
particularly when receiving enteral feed to prevent aspiration
- selective decontamination of the digestive tract may be useful in
environments where the incidence of multi-drug resistant pathogens is low
- minimize blood transfusion
Intubation and ventilation
- Avoid intubation and re-intubation where possible
- Orotracheal intubation and orogastric tubes are associated with a lower
risk of nosocomial sinusitis and may reduce the risk of ventilator
associated pneumonia
- Maintain tracheal cuff pressure >20 cmH2O to minimize leakage
of bacterial pathogens around the cuff
- Careful handling of ventilator tubing and associated equipment
- Subglottic drainage of secretions. Aspiration of subglottic secretions which
pool above the cuff of the endotracheal tube is thought to decrease aspiration
of oropharyngeal organisms and has been shown in to be associated with a lower
incidence of early-onset ventilator associated pneumonia
Prognosis
- mortality is higher in patients with ventilator associated pneumonia than
those without
- increased mortality may be due to association of VAP with increased
severity of illness rather than due to VAP itself however it is likely
that VAP does have a direct effect on outcome
- mortality higher for VAP due to aerobic gram -ve bacilli compared to
VAP due to gram +ves (when organisms are fully susceptible to antibiotics).
Further reading
Click here
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