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  Hospital-acquired (nosocomial) pneumonia (HAP)

Definition of Hospital-acquired (nosocomial) pneumonia (HAP)

HAP is a pulmonary infection that develops >48 hours after hospital admission and which was not incubating at the time of admission. VAP is pneumonia >48–72 hours after endotracheal intubation. HCAP includes patients residing in nursing homes, receiving therapy (e.g. wound care, intravenous therapy) within 30 days or admitted to hospital for >2 days within 90 days of the current infection, or attending a hospital or haemodialysis clinic. 

Epidemiology of Hospital-acquired (nosocomial) pneumonia (HAP)

Incidence varies between 5 and 10 episodes per 1000 discharges and is highest on surgical and intensive care unit (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 is responsible for 25% of infections and ∼50% of prescribed antibiotics. VAP accounts for >80% of all HAP and occurs in 9–27% of intubated patients. Risk factors include CAP risk factors and those associated with HAP pathogenesis, some of which can be prevented (Figure 39b). Mortality is 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 increase mortality.

Pathogenesis of Hospital-acquired (nosocomial) pneumonia (HAP)

The oropharynx is colonized by enteric gram-negative bacteria 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 oral secretions (±gastric contents) causes HAP. 

Aetiology of Hospital-acquired (nosocomial) pneumonia (HAP)

Early or late-onset risk factors for infection with MDR organisms determine likely pathogens. Aerobic gram-negative bacilli (e.g. Klebsiella pneumoniae, Pseudomonas aeruginosa, Escherichia coli) cause ∼60–70% and Staphylococcus aureus ∼10–15% of infections. Streptococcus pneumoniae and Haemophilus influenza may be isolated in early-onset HAP/VAP. In intensive care, >50% of S. aureus infections are methicillin-resistant (MRSA). S. aureus is more common in diabetics and ICU patients. 

Diagnosis of Hospital-acquired (nosocomial) pneumonia (HAP)

This requires both clinical and microbiological assessment. Non-specific clinical features, concurrent illness (e.g. acute respiratory distress syndrome [ARDS]) and previous antibiotics, which limit microbiological evaluation, can make diagnosis difficult. Clinical: suspect HAP when new chest radiograph (CXR) infiltrates occur with features suggestive of infection (e.g. fever > 38°C, purulent sputum, leukocytosis, hypoxaemia). Diagnostic tests: confirm infection and establish the causative organism (±antibiotic sensitivity). They include blood tests and gases, serology, blood cultures, pleural fluid aspiration, sputum, endotracheal aspirates and bronchioalveolar lavage. CXR and CT scanning aid diagnosis and detect complications (e.g. cavitation, abscesses). 

Continuous Positive Airway Pressure (CPAP): Indication and Procedure

Management of Hospital-acquired (nosocomial) pneumonia (HAP)

Early diagnosis and treatment improve morbidity and mortality. Do not delay antibiotic therapy while awaiting microbiological results. 

Supportive therapy of Hospital-acquired (nosocomial) pneumonia (HAP)

Supplemental oxygen maintains Pao2 >8 kPa (Sao2 <90%), intravenous fluids (±inotropes) preserve haemodynamic stability and ventilatory support (e.g. MV) corrects respiratory failure. Physiotherapy and analgesia aid sputum clearance post-operatively 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 avoidable risk factors may improve outcomes. 

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Antibiotic therapy for  Hospital-acquired (nosocomial) pneumonia (HAP)

This is empirical while awaiting microbiological guidance. The key factor is whether the patient is at risk of MDR organisms. Figure 39e illustrates the American Thoracic Society guidelines for initial, empiric, 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 organisms, use monotherapy with a β-lactam/β-lactamase, third generation cephalosporin or fluoroquinolone antibiotic.

• In late-onset HAP/VAP or with risk factors for MDR pathogens, start combination therapy with broad-spectrum antibiotics to cover MDR gram-negative bacilli and MRSA (e.g. vancomycin). Consider adjunctive therapy with inhaled aminoglycosides or polymyxin in patients not improving with systemic therapy.

A short course of therapy (e.g. 7 days) is appropriate if the clinical response is good. Resistant pathogens (e.g. Pseudomonas aeruginosa, S. aureus) may require 14–21 days’ treatment. Focus therapy on causative organisms when culture data are available and withdraw unnecessary antibiotics. Sterile cultures (without new antibiotics for >72 hours) virtually rule out HAP.

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Other pneumonias

• Aspiration/anaerobic pneumonia: anaerobic infection (e.g. Bacteroides) follows aspiration of oropharyngeal contents due to laryngeal incompetence or reduced consciousness (e.g. drugs). Lung abscesses are common. Antibiotic therapy should include anaerobic coverage (e.g. metronidazole).

• Pneumonia during immunosuppression: 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 <200/mm3, may also develop opportunistic infections such as Pneumocystis (carinii) jiroveci pneumonia (PCP) or toxoplasma. Severely immunocompromised patients require broad-spectrum antibiotic, anti-fungal and antiviral regimes. PCP is treated with steroids and high-dose co-trimoxazole.