Hospital-Acquired
(Nosocomial) Pneumonia
Hospital-acquired (nosocomial)
pneumonia (HAP) including ventilator-associated
pneumonia (VAP) and healthcare-associated pneumonia (HCAP) affects
0.5-2% of hospital patients and is a leading cause of nosocomial infection
(i.e. with wound, urinary tract and bloodstream). Pathogenesis, causative
organisms and outcome differ from community-acquired pneumonia (CAP).
Preventative measures and early antibiotic therapy, guided by awareness of the
role of multidrug-resistant (MDR) pathogens, improve outcome.
Definitions
HAP: pulmonary infection developing more than 48 hours
after hospital admission that was not incubating at the time of admission. VAP:
pneumonia developing more than 48-72 hours after endotracheal intubation. HCAP:
includes any patient admitted to hospital for more than 2 days within 90
days of the infection, residing in a nursing home, receiving therapy (e.g.
wound care and intravenous therapy) within 30 days of the current infection, or
attending a hospital or haemodialysis clinic.
Epidemiology
Incidence: varies between 5 and 10 episodes per 1000
discharges and is highest on surgical and ICU wards and in teaching hospitals.
It lengthens hospital stay by between 3 and 14 days per patient. The risk of
HAP increases 6- to 20-fold during mechanical ventilation (MV), and in ICU, it
accounts for 25% of infections and approximately 50% of prescribed antibiotics.
VAP accounts for more than 80% of all HAP and occurs in 9-27% of intubated
patients. Risk factors: include those that predispose to CAP and factors
associated with HAP pathogenesis, some of which can be prevented (Table
1). Mortality: between 30 and 70%. Early-onset HAP/VAP (<4
days in hospital) is usually caused by antibiotic-sensitive bacteria and
carries a better prognosis than late-onset HAP/VAP (>4 days in
hospital), which is associated with MDR pathogens. In early-onset HAP/VAP,
prior antibiotic therapy or hospitalization predisposes to MDR pathogens and is
treated as late- onset HAP/VAP. Bacteraemia, medical rather than surgical
illness, VAP and late or ineffective antibiotic therapy also increase
mortality.
Pathogenesis
Oropharyneal colonization with enteric
Gram-negative bacteria occurs in most hospital patients due to immobility,
impaired consciousness, instrumentation (e.g. nasogastric tubes), poor hygiene
or inhibition of gastric acid secretion. Subsequent aspiration of
nasopharyngeal secre-tions (± gastric contents) causes HAP (Fig. 37b).
Aetiology
Time of onset (early/late) and risk
factors for infection with MDR organisms (Table 2) determine potential
pathogens (Fig. 37c). Aero- bic Gram-negative bacilli (e.g. Klebsiella
pneumoniae, Pseudomonas aeruginosa, Escherichia coli) cause
approximately 60-70% of infections and Staphylococcus aureus approximately
10-15%. Streptococcus pneumoniae and Haemophilus influenza may
be isolated in earlyonset HAP/VAP. In ICU, more than 50% of S. aureus infections
are methicillin-resistant (MRSA). S. aureus is more common in diabetics
and ICU patients.
Diagnosis
Requires both clinical and microbiological
assessment. It may be diffcult as (i) clinical features are non-specifi or
confused with concurrent illness (e.g. acute respiratory distress syndrome
(ARDS)); and (ii) pre- vious antibiotics limit microbiological evaluation. Clinical:
HAP is suspected when new radiographical infiltrate occur with features
suggestive of infection (e.g. fever >38◦C, purulent sputum,
leucocytosis and hypoxaemia). Diagnostic tests: confir infection and
determine the causative organism ( ± antibiotic sensitivity). They include routine
blood counts, blood gases, serology, blood cultures, pleural effusions
aspiration, sputum, endotracheal aspirate and bronchoalveolar lavage
microbiology and CXR. CT scanning (Fig. 37a) aids diagnosis and detects complications
(e.g. abscesses).
Management
Early diagnosis and treatment improves
morbidity and mortality and requires constant vigilance in hospital patients.
Antibiotic therapy must not be delayed while awaiting microbiological results.
Supportive therapy
This includes supplemental oxygen to
maintain Pao2 of more than 8 kPa (Sao2
<90%), intravenous fluids ( ± vasopressors/inotropes) for haemodynamic stability and ventilatory
support (e.g. continuous positive airway pressure (CPAP), MV) in
respiratory failure. Physiotherapy and analgesia aid sputum
clearance postoperatively and in the immobilized patient. Semi-recumbent (i.e.
30◦ bed-head elevation) nursing of bed-bound patients reduces aspiration risk.
Strict glycaemic control and attention to other modifiabl risk factors (Table
1) may improve outcome.
Antibiotic therapy
This is empirical while awaiting
microbiological guidance. The key decision is whether the patient has risk
factors for MDR organisms. Figure 37c illustrates the American Thoracic Society
(ATS) guidelines for initial, intravenous antibiotic therapy. Local patterns of
antibiotic resistance are used to modify these protocols.
|
.
|
In early-onset HAP/VAP with no
risk factors for MDR organ- isms, monotherapy with a β-lactam/β-lactamase,
third-generation cephalosporin or fluoroquinolon antibiotic is advised.
In late-onset HAP/VAP with risk
factors for MDR pathogens (Table 2), combination therapy with
broad-spectrum antibiotics to cover MDR Gram-negative bacilli and MRSA (e.g. vancomycin)
is required (Fig. 37c). Adjunctive therapy with inhaled aminoglycosides or
polymyxin is considered in patients not improving with systemic therapy.
A short course of therapy (e.g. 7
days) is appropriate if the clinical response is good. Aggressive or resistant
pathogens (e.g. P. aeruginosa, S. aureus) may require 14-21 days'
treatment. Therapy is focused on causative organisms when culture data are
available and unnecessary antibiotics are withdrawn. Sterile cultures (in the
absence of new antibiotics for >72 hours) virtually rules out HAP.
Other pneumonias
Aspiration/anaerobic pneumonia: Bacteroides and other anaerobic infections follow aspiration of oropharyngeal contents
due to laryngeal incompetence or reduced consciousness (e.g. cerebrovascular
accident; CVA, drugs). Lung abscesses are common. Antibiotic therapy should
include anaerobic coverage (e.g. metronidazole).
Pneumonia during immunosuppression (Chapter 39): HIV, transplant and chemotherapy
patients are susceptible to viral (e.g. cytomegalovirus), fungal (e.g. Aspergillus)
and mycobacterial infections, in addition to the normal range of organisms. HIV
patients with CD4 counts of less than 200/mm3 also develop opportunistic
infections such as Pneumocystis carinii pneumonia (PCP) or toxoplasma.
Severely immunocompromised patients require broad-spectrum antibiotic,
antifungal and antiviral regimens. PCP is treated with steroids and high-dose co-trimoxazole.
