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![……..CAP
• Relatively few pathogens cause most cases
• Typical bacterial pathogens:
– S. pneumoniae, Haemophilus influenzae, Staphylococcus
aureus [ (CA-MRSA)], gram-negative bacteria such as
Klebsiella pneumoniae and Pseudomonas aeruginosa
• Atypical organisms:
– Mycoplasma pneumoniae, Chlamydophila pneumoniae,
Legionella spp., respiratory viruses (e.g., influenza viruses)
• Anaerobes play a significant role in CAP only when
aspiration occurs days to weeks before presentation.](https://image.slidesharecdn.com/pneumonia-2-1-240208210236-9475d4bc/75/Pneumonia-2-1-pptx-11-2048.jpg)
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Pneumonia-2-1.pptx
- 1.
- 2. Introduction • Pneumonia isan infection of the pulmonary parenchyma • Between 5 and 10 million cases of infectious pneumonia occur annually in the US and result in more than 1 million hospitalizations. • Pneumonia is a leading cause of death worldwide( 6th leading cause of death in US) • the most common lethalfatal infectious disease • The top 10 cause of morbidity & mortality in our setup.
- 3. ………………contd • In thepast, pneumonia was typically classified as community-acquired, hospital-acquired, or ventilator-associated. • Increases prevalence of MDR pathogens has led to a revised classification system as community-acquired pneumonia (CAP) or health care–associated pneumonia (HCAP), • HCAP subclassified into: hospital-acquired pneumonia (HAP) and ventilator- associated pneumonia (VAP).
- 5. Microbial Pathogen thatcause Pneumonia • depend on the setting in which pneumonia is acquired: 1. Community-acquired pneumonia – Streptococcus pneumoniae ( pneumococcal pneumonia ) commonest cause – Haemophilus influenza, Mycoplasma pneumoniae, Chlamydia pneumoniae – Oral anaerobic bacteria, Staphylococcus aureus – Legionella pneumophila, Mycobacterium tuberculosis 2. Aspiration pneumonia • It is often polymicrobial – Anerobic organisms in the oral cavity – Enterobateriacae – S. pneumoniae – S.aureus
- 6. …………….contd 3. Community acquiredPneumonia in Immunocompromised hosts: – Common bacterial causes of CAP : St. Pneumoniae , H.influenzae, Mycoplasma – Gram negative organisms : enterobacteriaceae – Funguses : PCP, C. neoformans , Histoplasmosis , Aspergillus – Mycobaterium tuberculosis – Viruses : HSV , CMV 4. Hospital-acquired pneumonia – Gram-negative bacilli :Pseudomonas aeroginosa, K.pneumoniae – Staphylococcus aureus ( may be drug resistant ) – Oral anaerobes
- 7. PATHOPHYSIOLOGY • Microorganisms gainaccess to the lower respiratory tract via – Micro-aspiration from the oropharynx (the most common route), – inhalation of contaminated droplets, – hematogenous spread, or – contiguous extension from an infected pleural or mediastinal space
- 8. ……………contd • Mechanical factorsare critically important in host defense – The hairs and turbinates of the nares catch larger inhaled particles – the branching architecture of the T-B tree traps particles – mucociliary clearance and – local antibacterial factors clear or kill the potential pathogen – the normal flora adhering to mucosal cells of the oropharynx prevents pathogenic bacteria from binding • The gag reflex and the cough mechanism offer critical protection from aspiration
- 9. Predisposing factors • Precedingrespiratory viral infections • Alcoholism • Cigarette smoking • Underlying diseases such as Heart failure, COPD • Age extremes • Immunosuppressive therapy and disorders • Decreased consciousness, comma , seizure etc • Surgery and aspiration of secretions
- 10. Community Acquired Pneumonia(CAP) •CAP, which affects ~4 million adults each yr. • is more common among pts with severe underlying illness. • Many factors (e.g., alcoholism, asthma, age >70 years, immunosuppression, smoking, and HIV infection) influence the types of pathogens that should be considered in identifying the etiologic agent.
- 11. ……..CAP • Relatively fewpathogens cause most cases • Typical bacterial pathogens: – S. pneumoniae, Haemophilus influenzae, Staphylococcus aureus [ (CA-MRSA)], gram-negative bacteria such as Klebsiella pneumoniae and Pseudomonas aeruginosa • Atypical organisms: – Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella spp., respiratory viruses (e.g., influenza viruses) • Anaerobes play a significant role in CAP only when aspiration occurs days to weeks before presentation.
- 12. Clinical Features OfCAP • Typical symptoms are – fever, chills, sweats, – cough (non-productive or productive of mucoid, purulent, or blood-tinged sputum), – pleuritic chest pain, and – dyspnea. • Other common symptoms – nausea, vomiting, diarrhea, fatigue, headache, myalgias, and arthralgias. • Elderly pts may present atypically with confusion. • Physical examination: tachypnea, increased or decreased tactile fremitus, dull to flat percussion reflecting consolidation or pleural fluid, crackles, BBSs, pleural friction rub
- 13. …………..c/f • The “atypical”pneumonia present with – More gradual onset of symptoms, dry cough, shortness of breath. – Prominence of systemic symptoms like headache, myalgia, fatigue, nausea, vomiting and diarrhea. – Chest findings on physical examination are minimal even though X-ray changes are marked
- 14. Lab. CBC: – leucocytosis with↑ed neutrophils is seen in most cases CXR – is usually adequate for diagnosis, but CT of the chest may be required in some cases. – Some patterns suggest an etiology; e.g., pneumatoceles suggest S. aureus Sputum stains and culture – The presence of >25 white blood cells and <10 squamous epithelial cells per high-power field suggests that a sample is appropriate for culture. • Blood cultures – optional – positive in 5–14% of cases
- 15. Diagnosis: • Pneumonia shouldbe suspected in patients with acute febrile illness, associated with chest pain, dyspnea and cough. • Presumptive diagnosis can be made from history, changes on chest x-ray, blood and sputum culture and sputum Gram stains. • An absolute diagnosis requires demonstration of S. pneumoniae or other etiologic agents in pleural fluid, blood, lung or transtracheal aspirate.
- 16. Complications: • Local: – Parapneumoniceffusion or – pus in the pleural space (empyema). • Distant complications: – septic arthritis and meningitis. – Pneumonia can progress to sepsis, sometimes with septic shock
- 17. Severe forms ofCAP • If patients are seriously ill they should be admitted and treated as inpatient. Criteria for Hospitalization – RR of >28/min ( Tachypnea ) tachycardia >140/min – Systolic blood pressure <90mm Hg (hypotension) – Hypoxemia (PO2 < 60mm Hg) with room air or SaO2 < 90 % – New onset of confusion or impaired level of consciousness – Unstable /Significant co-morbidity (e.g. HF , uncontrolled DM, Chronic RF ,alcoholism , immunosuppresion ) – Multi-lobar pneumonia if Hypoxemia is present – Complicated Pleural effusion
- 18. ……..admission ……contd • Otherconditions in which inpatient management may be advisable – Elderly patient >65 yrs of age – Leukopenia <5000 WBC/ml – Pneumonia caused by S. aureus or Gram negative bacilli – Suppurative complications e.g. empyema, arthritis, meningitis, endocarditis – Failure of Outpatient treatment – Inability to take oral medication or persistent vomiting
- 19. Treatment of CAP •Mild form of CAP- uncomplicated cases can be treated at OPD level. • uncomplicated “typical” pneumonia – Amoxicillin 500 mg PO TID or Ampicillin 500 mg PO QID for 7 to 10 days OR – Procaine penicillin 600,000 IU IM every 12 hrs. – amoxicillin/clavulanate(Augmentin) – oral clarithromycin or azithromycin for penicillin allergic pts • If “atypical” pneumonia is suspected, – Erythromycin 500 mg PO QID for 7-10 days or – Doxycycline100 mg PO BID • Supportive Therapy: – Patients should also get bed rest, adequate fluids and analgesics for pleuritic chest pain and fever • Response – In mildly ill pts, fever subsides in 24 to 48 hrs. – Some may require 4 days to respond
- 20. Management of severeCAP • Supportive management – Ensure adequate oxygenation to patients with cyanosis, significant hypoxemia, sever dyspnea, circulatory disturbance or delirium. – Patients should be well hydrated – Fever and pain should be managed
- 21. Antibiotic Therapy forsevere CAP • Should be started on antibiotics empirically • High dose of crystalline penicillin 3-4 million IU IV every 4-6 hours • Alternatives are – Ceftriaxone 1gm IV daily or 2X /day or – Ampicillin 500 mg IV QID Or – Cefotaxime • In severely ill pts erythromycin or a flouroquinolone can be added. • Choice of Antibiotics may be modified based on culture and sensitivity results, if available. • If the patient improves, IV treatment can be changed to oral after 3-4 days to complete a 7-10 days course.
- 22. Prognosis • Poor prognosticfactors – Extremes of age, especially < 1 yr or >60yrs, – Positive blood culture – Involvement of more than one lobe – Peripheral WBC < 5000/ml – Presence of associated diseases (e.g. cirrhosis, CHF, immunosuppression) – Development of extrapulmonary complications like meningitis and endocarditis
- 23. HEALTH CARE–ASSOCIATED PNEUMONIA VENTILATOR-ASSOCIATED PNEUMONIA •VAP is a common complication in pts on mechanical ventilation. • Three factors important in the pathogenesis of VAP are – colonization of the oropharynx with pathogenic microorganisms, – aspiration of these organisms to the lower respiratory tract, and – compromise of normal host defense mechanisms • Potential etiologic agents include MDR and non-MDR pathogens • Clinical manifestations are similar to those in other forms of pneumonia. • Diagnosis is difficult
- 26. Hospital-Acquired Pneumonia • HAPmore commonly involves non-MDR pathogens • The definition of HAP includes the presence of a new or progressive infiltrates of Chest X-ray ,plus at least two of the following – Fever >37.8 oC – Leukocytosis > 10,000/mm3 – Production of purulent sputum • Other findings: dyspnea, hypoxemia and chest pain • The only pathogens that may be more common in the non-VAP population are anaerobes because of the increased risk of macroaspiration in pts who are not intubated.
- 27. Treatment of HAP •Antibiotics should cover at least gram negatives and S. aureus – Ceftriaxone 1gm IV daily or BID plus Cloxacillin or meticillin Or – Levofloxacin 500 mg IV /day • When resistant organisms are suspected – Cefotaxime 750 mg IV TID plus Vancomycin 1gm IV BID
- 28. Suppurative lung diseases Disease of the lungs that are xed by pus formation 1-Lung Abscess • it is defined as pulmonary parenchymal necrosis and cavitation resulting from infection • The development of a lung abscess implies a high microorganism burden as well as inadequate microbial clearance from the airways • It may develop following – necrotizing infections of the lung (bacterial pneumonia, TB, fungi), – loss of blood supply to a part of the lung causing cavitary – infarction due to septic or bland embolism, obstruction to airways or cavitations of malignancy The anaerobic abscess is the commonest and usually follows periodontal diseases or aspiration of oropharyngeal/gastric contents.
- 29. Etiology of Lungabscess • Anaerobic bacteria are the most common causative organisms for lung abscess • Aerobic or facultative bacteria such as S. aureus, Klebsiella pneumoniae, Nocardia sp., and gram-negative organisms may also cause abscess formation • In the immunocompromised host, aerobic bacteria and opportunistic pathogens may predominate. • Multiple isolates are more commonly seen in all patients • Common risk factors include – alcoholism, – immunodeficiency, – loss of consciousness,and – periodontal diseases
- 30. Clinical features: • Thesymptoms of LA are typical of pulmonary infection in general and may include cough of massive purulent & foul smelling sputum production, pleuritic chest pain, high grade fever, sweating and hemoptysis. • More acute presentations are typical of infection with aerobic bacteria. • anaerobic infectionover an extended period of time • Physical examination – is often unrevealing. – Rales or evidence of consolidation may be present – Clubbing. – Poor dental hygiene is a clue
- 31. Diagnosis: • The diagnosisof lung abscess is based on clinical symptoms, identification of predisposing conditions, and chest radiographic findings • Blood cultures CXR – parenchymal infiltrates . – cavity containing air-fluid level Gram stain and culture of the sputum help to make etiologic diagnosis Others: CBC(leukocytosis, N=predominant),CT-of the chest
- 32. Treatment • Pts shouldbe admitted • Medical therapy is the main stay of treatment. 1-Antibiotics – Penicillin was the mainstay of empiric antibiotic therapy for lung abscess in the past. – clindamycin (150 mg–300 mg every 6 h) is now standard therapy – Metronidazole alone is associated with a high treatment failure rate.
- 33. …..Rx….contd • Our setup(DACA2014) First line • Benzyl penicillin, 1-2 million IU I.V. OR I.M. every 4-6 hours for about 4-6wks. PLUS • Metronidazole, 500 mg I.V. every 8-12 hours for 10-14 days • Alternative • Amoxicillin + clavulanic acid, 500 mg + 125 mg, P.O. TID + Clindamycin, 600mg I.V. TID
- 34. ………..contd 2-Drainage of abscess –postural drainage can be effective but bronchoscopic drainage may be used when airway obstruction by foreign body or mass hinders drainage of pus by postural means. – Bronchoscopes and experts. 3) Surgical treatment : has limited role Indications are: – Persistent or massive hemoptysis – Empyema or bronchopleural fistula – Failure of medical treatment – Lung cancer
- 35. Outcome • prognosis – Patientswith classic anaerobic lung abscess, cure rate is 90–95%. – Higher mortality rates in immunocompromised patients, those with significant comorbidities, and infection with P. aeruginosa, S. aureus, and K. pneumoniae • Complications include – Metastatic brain abscess – Fatal hemoptysis – Empyema
- 36. 2-Bronchiectasis • Bronchiectasis isa pathologic, irreversible destruction and permanent dilatation of bronchi. • Usually resulting from suppurative infection in an obstructed bronchus • The walls of medium-sized airways are involved. • It may be either focal or diffuse • It is a disorder that typically affects older individuals. • Approximately 2/3 of patients are women.
- 37. Etiology and pathogenesis •BE is a consequence of inflammation and destruction of the structural components of the bronchial wall. • Infection is the usual cause of the inflammation • bacterial pneumonia is the commonest cause of BE • obstruction by foreign body, lymph node, or impacted secretions, all of which lead to persistent infection and the development of BE • Micro organisms – Adenovirus and influenza virus, HIV – Staphylococcus aureus, Klebsiella, and anaerobes – TB (by its necrotizing effect or AW obstruction by LAP)
- 38. Clinical Manifestations • Patientstypically present with persistent or recurrent cough and purulent sputum production Repeated, purulent respiratory tract infections should raise clinical suspicion for bronchiectasis • Hemoptysis occurs in 50–70% of cases • Systemic symptoms such as fever, fatigue, weight loss, and myalgias can also occur • Physical examination – variable – Any combination of crackles, rhonchi, and wheezes may be heard – May have clubbing , cor-pulmonale & right ventricular failure
- 39. Diagnosis • Diagnosis islargely based on clinical features. – Obtaining a history of recurrent pulmonary infections ultimately followed by chronic recurrent cough and production of copious purulent sputum may suggest a diagnosis of BE • Chest x-ray non specific – usually shows peribronchial fibrosis – Segmental lung collapse may be observed in parts of the lung affected by BE. • CT scanning often identifies the lesions, eliminating the need for bronchoscopy and contrast studies • Definitive diagnosis of bronchiectasis is made by bronchography.
- 40. Treatment • Therapy hasseveral major goals: treatment of infection, particularly during acute exacerbations improved clearance of tracheobronchial secretions reduction of inflammation; and treatment of an identifiable underlying problem • Antibiotics are the cornerstone of bronchiectasis management
- 41. ……….Treatment of BE……contd 1)Control of respiratory infections • Broad spectrum antibiotics that should be given – empiric coverage (e.g., with amoxicillin, Ampicillin, trimethoprim-sulfamethoxazole, or levofloxacin) – If P. aeruginosa suspected, use of oral therapy with a quinolone or parenteral therapy with an aminoglycoside, carbapenem, or third-generation cephalosporin • Length of therapy no firm guidelines 10–14 day course or longer is typically administered.
- 42. Rx of BE…………contd 2)Improve drainage of secretion: – using postural drainage, liquefaction and bronchodilators. 3) O2 therapy: for hypoxemic pts 4) Surgical resection – For localized BE – recurrent massive hemoptysis that fails to respond to conservative treatment.
- 43. 3-Empyema( pyothorax) • Thoracicempyema is an accumulation of pus in the pleural cavity • Most pleural empyemas arise from an infection within the lungs(e.g. pneumonia) • Common organisms – S.pneumonea, S.aureus, H.infulenzae, E.coli, K.pneumonea……..MTB • Typical symptoms include: cough, fever,chest pain, sweating and shortness of breath – Empyema is likely if fluid is present and fever and leukocytosis (even low-grade) persist after 4–5 days of appropriate antibiotic treatment for pneumococcal pneumonia • Clubbing may be present in chronic cases
- 44. Diagnosis • Diagnosis isconfirmed by thoracentesis; – frank pus or merely cloudy fluid may be aspirated from the pleural space • Pleural fluid analysis typically shows: – leukocytosis, – low pH (<7.20), – low glucose (<60 mg/dL), – a high LDH (lactic dehydrogenase), – elevated protein Gram stain & AFB stain
- 45. treatment • Therapy includesall of the following: – Sterilization of the empyema cavity with appropriate antibiotics; at least 4-6 weeks of therapy are required, a longer course may be necessary Follow for resolution of fever and leukocytosis – Complete pleural fluid drainage – Obliteration of the empyema cavity by adequate lung expansion
- 46. Pleural Effusion • Thepleural space lies between the lung and chest wall and normally contains a very thin layer of fluid • A pleural effusion is present when there is an excess quantity of fluid in the pleural space • a pleural effusion may develop when there is – excess pleural fluid formation (from the interstitial spaces of the lung, the parietal pleura, or the peritoneal cavity) or – decreased fluid removal by the lymphatics.
- 47. Diagnostic Approach • 1ststep is the effusion a transudate or an exudate(?) – distinguished by measuring the lactate dehydrogenase (LDH) and protein levels in the pleural fluid. • Exudative pleural effusions meet at least one of the following criteria (Light's criteria ): – 1. pleural fluid protein/serum protein >0.5 – 2. pleural fluid LDH/serum LDH >0.6 – 3. pleural fluid LDH >2/3 normal upper limit for serum • The above criteria misidentify ~25% of transudates as exudates • the difference b/n the protein levels in the serum and the pleural fluid should be determined – If Gradient is > 31 g/L (3.1 g/dL), almost all such pts have a transudative pleural effusion
- 48. ………….contd • A transudativepleural effusion occurs when systemic factors that influence the formation and absorption of pleural fluid are altered. – The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis. • An exudative pleural effusion occurs when local factors that influence the formation and absorption of pleural fluid are altered. • The leading causes of exudative pleural effusions are – bacterial pneumonia, – TB – malignancy, – viral infection, and pulmonary embolism
- 50. Effusion Due toHeart Failure • The most common cause of pleural effusion is left ventricular failure • occurs because the increased amounts of fluid in the lung interstitial spaces • Usually bilateral • Isolated right-sided pleural effusions are more common than left-sided effusions in heart failure
- 51. Parapneumonic Effusion • Parapneumoniceffusions are associated with: – bacterial pneumonia, – Lung abscess, or – bronchiectasis • are probably the most common cause of exudative pleural effusion in the USA. • Patients with aerobic bacterial pneumonia and pleural effusion present with an acute febrile illness consisting of chest pain, sputum production, and leukocytosis • Parapneumonic pleural effusions are divided into three groups or stages based on pathogenesis – Uncomplicated parapneumonic effusion(Simple Pl. effusion) – Complicated parapneumonic effusion – Thoracic empyema
- 52. ……………………contd • Uncomplicated parapneumoniceffusion – is characterized by "exudative" pleural fluid chemistries and an influx of neutrophils into the pleural space – they resolve with resolution of the infections. • Complicated parapneumonic effusion – There is persistent bacterial invasion of the pleural space – are often sterile because bacteria can be cleared rapidly from the pleural space – increased number of neutrophils and the development of pleural fluid acidosis – have a variable response to appropriate antibiotic therapy alone – Pts are treated as though they have thoracic Empyema(Most experts recommend fluid drainage) • Empyema – pus in the pleural space or an effusion with organisms seen on Gram stain, invariably requires drainage
- 53. ………..parapneumonic…….contd • Factors indicatingthe likely need for a invasive procedure (chest tube insertion) (in increasing order of importance) include: – loculated pleural fluid – pleural fluid pH < 7.20 – pleural fluid glucose < 3.3 mmol/L (<60 mg/dL) – positive Gram stain or culture of the pleural fluid – the presence of gross pus in the pleural space
- 54. Tuberculous Pleuritis • Worldwide,the most common cause of an exudative pleural effusion is tuberculosis (TB), • are usually associated with primary TB • Patients with tuberculous pleuritis present with fever, weight loss, dyspnea, and/or pleuritic chest pain. Pl. fluid analysis – exudate with predominantly small lymphocytes – high levels of TB markers in the pleural fluid adenosine deaminase > 40 IU/L, interferon γ > 140 pg/mL, or positive polymerase chain reaction (PCR) for tuberculous DNA – culture of the pleural fluid, needle biopsy of the pleura • Treatment anti TB