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.
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.
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.
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).
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.
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).
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.
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.
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.
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.