5 th lecture Hospitalacquired pneumonia Nosocomial pneumonia It

5 th lecture : Hospital-acquired pneumonia Nosocomial pneumonia • It is a new episode of pneumonia occurring at least 2 days after admission to hospital. • It is: the 2 nd most common hospital-acquired infection (HAI) & the leading cause of HAI-associated death It risky in: • The elderly • In intensive care units, • When mechanically ventilated

Factors predisposing to HAP Reduced host defences against bacteria • Reduced immune defenses (corticosteroid , diabetes, malignancy) • Reduced cough reflex (post-operative) • Disordered mucociliary clearance ( anaesthetic agents) • Bulbar or vocal cord palsy Aspiration of nasopharyngeal or gastric secretions • Immobility or reduced conscious level • Vomiting, dysphagia (stroke disease) • Nasogastric intubation Bacteria introduced in to lower respiratory tract • Endotracheal intubation/tracheostomy • Infected ventilators/nebulisers/bronchoscopes • Dental or sinus infection Bacteraemia • Abdominal sepsis, IV cannula infection, Infected emboli

Organisms implicated In early-onset HAP ( 4– 5 days ) are similar to those in CAP Late onset HAP different organism , with more: Gram-negative (e. g. Escherichia, Pseudomonas, Klebsiella ) Staph. aureus (including meticillin resistant (MRSA)) Anaerobes

Clinical features & investigations The diagnosis should be considered in any hospitalized or ventilated patient who develops: Ø Ø Ø Purulent sputum (or endotracheal secretions) New radiological infiltrates Unexplained increase in oxygen requirement Temperature of more than 38. 3°C Leucocytosis or leucopenia

differential diagnosis • • • Venous thromboembolism ARDS Pulmonary oedema Pulmonary haemorrhage Drug toxicity. • Therefore, microbiological confirmation should be sought whenever possible

Management • The principles are similar to those for CAP, focusing on: adequate oxygenation, fluid balance & antibiotics • The choice of empirical antibiotic therapy is more challenging (diversity of pathogens & drug resistance) In early-onset HAP, pats. received no previous antibiotics, treated with: • co-amoxiclav or cefuroxime If the patient has received a course of recent antibiotics, • piperacillin/tazobactam • third generation cephalosporin.

In late-onset HAP the choice of antibiotics must cover Gram-negative Staph. aureus ( MRSA) & anaerobes Anti pseudomonal cover by: • carbapenem (meropenem) • a third-generation cephalosporin with aminoglycoside MRSA cover by glycopeptides (vancomycin)

The choice of agent Guided by: • knowledge of local patterns of microbiology & antibiotic resistance • It is usual to commence broad-based cover, discontinuing less appropriate antibiotics as culture results become available. duration of antibiotic therapy a matter for clinical judgments Physiotherapy aid expectoration in the immobile & elderly nutritional support is often required.

Pneumonia in the Immuno-compromised patients Patients immunocompromised by drugs or disease ( HIV) are at high risk of pulmonary infection. Ø The majority caused by the same pathogens that cause pneumonia in normal individuals, Ø in more profound immunosuppression, • unusual organisms • low virulence • non-pathogenic may become ‘opportunistic’ pathogens. Gram-negative bacteria, Pseudomonas viral agents fungi mycobacteria, & less common Nocardia asteroides has to be considered • Infection is often due to more than one organism.

Causes of immune suppression-associated lung infection Defective type Causes Infecting organisms phagocytic function Acute leukaemia Cytotoxic drugs Agranulocytosis Gram-positive bacteria, Staph. aureus Gram-negative bacteria Fungi, e. g. Candida & Aspergillus Immunosuppressive drugs Cytotoxic Chemotherapy Lymphoma Viruses: Cytomegalo, Herpes, Adenovirus, Influenza Fungi Pneumocystis jirovecii ( carinii) Candida , Aspergillus Multiple myeloma Chronic lymphocytic leukaemia Haemophilus influenzae Mycoplasma pneumoniae cell-mediated immunity antibody production

Clinical features • typically include fever, cough & breathlessness, but • less specific in the more profoundly immunosuppressed • The onset tends to be less rapid with opportunistic organisms as Pneumocystis jirovecii & mycobacterial than with bacterial infections. • In P. jirovecii pneumonia: cough and breathlessness proceed onset of systemic symptoms or CX-ray abnormalities

Diagnosis Invasive investigations: ü bronchoscopy ü bronchoalveolar lavage (BAL) ü transbronchial biopsy ü surgical lung biopsy are often impractical, as many patients are too ill to undergo these safely However, ‘induced sputum’ offers a relatively safe method of obtaining microbiological samples

High resolution computed tomography HRCT is useful in differentiating the likely cause: • Focal unilateral airspace opacification favours bacterial infection, mycobacteria or Nocardia • Bilateral opacification favours P. jirovecii pneumonia, fungi, viruses and unusual bacteria • ‘halo sign’ may suggest Aspergillus • Pleural effusions suggest a pyogenic bacterial infection & are uncommon in P. jirovecii pneumonia

HRCT

Management • In theory, treatment should be based on the identified causative organism but, • In practice, this is frequently unknown and broad-spectrum antibiotic therapy is required, such as : • third-generation cephalosporin or a quinolone, plus an • antistaphylococcal , or • antipseudomonal penicillin plus aminoglycoside • treatment may be tailored according to the results of investigations and the clinical response. • These may dictate the addition of antifungal or antiviral therapies

Supportive pneumonia, Aspiration pneumonia & pulmonary Abscess • These conditions are considered together, as their aetiology and clinical features overlap. • Suppurative pneumonia is a destruction of the lung parenchyma by the inflammatory process & microabscess formation • Pulmonary abscess’ is refer to lesions in which there is a large localised collection of pus, or a cavity lined by chronic inflammatory tissue, from which pus has escaped by rupture into a bronchus.

Risk factor • Aspiration localize to dependent areas • Bronchial obstruction by a neoplasm, foreign body. • Infections due to a Mixture of anaerobes & aerobes Ø the most likely infecting organism is Staph. Aureus or Klebsiella pneumoniae. Ø Bacterial infection of a: pulmonary infarct or a collapsed lobe.

Clinical features of suppurative pneumonia Symptoms • Cough with large amounts of sputum, sometimes fetid and bloodstained • Pleural pain • Sudden expectoration of copious amounts of foul sputum if abscess ruptures into a bronchus Clinical signs • High remittent pyrexia • Profound systemic upset • Digital clubbing may develop quickly (10– 14 days) • Consolidation on chest examination; rarely signs of cavitation • Pleural rub common • Rapid deterioration in general health, with marked weight loss if not adequately treated

I investigations and management CXR: Ø homogeneous lobar or segmental opacity consistent with consolidation or collapse. Ø Abscesses (cavitation and fluid level) Ø Occasionally, a preexisting emphysematous bulla infected and appears as a cavity containing an air–fluid level. treated with • Intravenous co-amoxiclav 1. 2 g 3 times daily. • oral metronidazole 400 mg 3 times daily If an anaerobic. • Further modification of antibiotics may be required, depending on the clinical response and the microbiological results.