Understanding Hospital-Acquired Pneumonia: Epidemiology, Etiology, Diagnosis & Treatment

Slide Note
Embed
Share

Hospital-acquired pneumonia is a serious infection occurring at least 2 days after hospital admission, leading to complications and mortality. It can be classified into VAP and HCAP, with various predisposing factors and microbiological causes. Recognizing clinical features and prompt treatment are crucial for managing HAP.


Uploaded on Oct 01, 2024 | 0 Views


Download Presentation

Please find below an Image/Link to download the presentation.

The content on the website is provided AS IS for your information and personal use only. It may not be sold, licensed, or shared on other websites without obtaining consent from the author. Download presentation by click this link. If you encounter any issues during the download, it is possible that the publisher has removed the file from their server.

E N D

Presentation Transcript


  1. a.c. 6/12/2018 1440

  2. Hospital-acquired pneumonia

  3. OBJECTIVES To know the epidemiology ,etiology, pathogenesis ,clinical presentation, investigation ,diagnosis ,treatment ,complication ,prognosis

  4. Hospital-acquired pneumonia Hospital-acquired or nosocomial pneumonia is a new episode of pneumonia occurring at least 2 days after admission to hospital It is the second most common hospital- acquired infection (HAI) and the leading cause of HAI-associated death.

  5. Classification of HAP Ventilator-associated pneumonia (VAP) Pneumonia occurred patients in intensive care units, especially when mechanically ventilated; Healthcare-associated pneumonia (HCAP) pneumonia in a person who has spentat least 2 days in hospital within the last 90 days, has attended a haemodialysis unit, received intravenous antibiotics . been resident in a nursing home or other long-term care facility

  6. Factors predisposing to hospital-acquired pneumonia Reduced host defences against bacteria Reduced immune defences (e.g.corticosteroid treatment, diabetes, malignancy) Reduced cough reflex (e.g. post-operative) Disordered mucociliary clearance (e.g. anaesthetic agents) Bulbar or vocal cord palsy Aspiration of nasopharyngeal or gastric secretions Immobility or reduced conscious level Vomiting, dysphagia (N.B. stroke disease), achalasia or severe reflux Nasogastric intubation Bacteria introduced into lower respiratory tract Endotracheal intubation/tracheostomy Infected ventilators/nebulisers/bron- choscopes Dental or sinus infection Bacteraemia Abdominal sepsis IV cannula infection Infected emboli

  7. Microbiology The early-onset HAP (occurring within 4 5 days of admission) are similar to those involved in CAP. Late onset HAP Gram-negative bacteria (e.g. Escherichia, Pseudomonas, Klebsiella species and Acinetobacterbaumannii), Staph. aureus (including the meticillinresistant type (MRSA)) and anaerobes

  8. Clinical features The hospitalised or ventilated patient purulent sputum (or endotracheal secretions), new radiological infiltrates, unexplained increase in oxygen requirement, a core temperature of more than 38.3 C, a leucocytosis or leucopenia. differential diagnosis Venous thromboembolism . ARDS . pulmonary oedema. Pulmonary haemorrhage. drug toxicity.

  9. Investigations microbiological confirmation . the full blood count (FBC). urea and electrolytes (U&E), Erythrocyte sedimentation rate (ESR) and C- reactive protein (CRP). arterial blood gas. chest X-ray.

  10. Management adequate oxygenation, Appropriate fluid balance antibiotics.

  11. Treatment In early-onset HAP, 1-If not received antibiotics treated with co-amoxiclav or cefuroxime. 2- Received antibiotics piperacillin/tazobactam or a third generation Cephalosporin.. In late-onset HAP, the antibiotics must cover the 1-Gram-negative bacteria 2-Staph. aureus (including MRSA) 3- anaerobes.

  12. Prevention the mortality from HAP is approximately 30%, Good hygie regard to handwashing and any equipment used. The risk of aspiration should be minimised, ventilator associated pneumonia by limiting use of proton pump inhibitors. decontaminate the upper airway, by Oral antiseptic (chlorhexidine 2%) selective decontamination of the digestive tract.

  13. Suppurative pneumonia, aspiration pneumonia and pulmonary abscess These conditions are considered together, as their aetiology and clinical features overlap

  14. Suppurative pneumonia is characterised by destruction of the lung parenchyma by the inflammatory process . Microabscess formation is a characteristic histological feature. Pulmonary abscess is usually taken to 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.

  15. Risk Inhalation septic material during operations on the nose, mouth or throat under general anaesthesia, vomitus during anaesthesia coma, particularly if oral hygiene is poor. bulbar palsy vocal cord palsy, stroke, achalasia oesophageal reflux, alcoholism. local bronchial obstruction from a neoplasm or foreign body.

  16. Aetiology of lung abscess

  17. Microbilogy mixture of anaerobes and aerobes from flora in the mouth and upper respiratory tract. in a previously healthy lung, Staph. aureus Klebsiella pneumoniae. pulmonary infarct or a collapsed Strep. pneumoniae, Staph. aureus, Strep. pyogenes, H. influenzae and, in some cases, anaerobic bacteria. In many cases, no pathogen can be isolated, particularly when antibiotics have been given.

  18. Clinical features of suppurative pneumonia Symptoms Cough with large amounts of sputum, sometimes fetid and blood- stained Pleural pain common 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; signs of cavitation rarely found Pleural rub common Rapid deterioration in general health, with marked weight loss if not adequately treated

  19. Investigations Radiological features Abscesses are characterised by cavitation and fluid level. Occasionally, a preexisting emphysematous bulla becomes infected and appears as a cavity containing an air fluid level

  20. Managment Intravenousco-amoxiclav 1.2 g 3 times daily. Metronidazole 400 mg 3 times daily If an anaerobic bacterial infection is suspected (e.g. from fetor of the sputum), oral CA-MRSA is usually susceptible to a variety of oral non- -lactam antibiotics, such as trimethoprim/sulfamethoxazole, clindamycin, others Parenteral therapy with vancomycin or daptomycin and to metronidazole, or clindamycin and third-generation cephalosporins. Prolonged treatment for 4 6 weeks may be required in some patients with lung abscess. Physiotherapy

  21. Prognosis In most patients, there is a good response to treatment and, although residual fibrosis and bronchiectasis Surgery may be required.

  22. Pneumonia in the immunocompromised patient Patients immunocompromised by drugs or disease are at high risk of pulmonary infection. The majority of cases are caused by the same pathogens that cause pneumonia Patients with more profound immunosuppression, unusual organisms or those normally considered to be of low virulence or non-pathogenic may become opportunistic pathogens

  23. Clinical features fever, cough breathlessness,

  24. Diagnosis Invasive investigations, such as Bronchoscopy. BAL. transbronchial biopsy. surgical lung biopsy.

  25. Management Broad-spectrum antibiotic a third-generation cephalosporin or aquinolone, plus an antistaphylococcal antibiotic, Or an antipseudomonal penicillin plus an aminoglycoside.

  26. Respiratory infection in old age Increased risk of and from respiratory infection. Predisposing factors: . Atypical presentation . Mortality Influenza TB

  27. THANK YOU To know the epidemiology ,etiology, pathogenesis ,clinical presentation, investigation ,diagnosis ,treatment ,complication ,prognosis

Related


More Related Content