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pneumonia for C-1.pptx

  2. PNEUMONIA DEFINITION • Pneumonia is an infection of the pulmonary par enchyma. • To the pathologist, pneumonia is an infection of t he alveoli ,distal airways, and interstitium of the l ung that is manifested by increased weight of th e lungs, replacement of normal lung’s spongines s by consolidation ,and alveoli filled with white bl ood cells ,red blood cells and fibrin .
  3. • To the clinician, pneumonia is a constellation of symptoms and signs in combination with at least one opacity on CXR. Epidemiology • Between 5 and 10 million cases of infectious pne umonia occur annually in the United States and r esult in more than 1 million hospitalizations. • Pneumonia is a leading cause of death worldwid e, the sixth leading cause of death in the United States, and the most common lethal infectious di sease.
  4. CLASSIFICATION • ETIOLOGIC 1.Infections 2.Inhala tion of gastric contents 3.Immunological reactio ns 4.Inhalation of other toxic substanc es • ANATOMIC 1.Lobar or segmental : process is confined to th ese division of the lung 2.Bronchopneumonia : small areas of the lung al veoli and lobule around small terminal bronchi ar e affected
  5. • Revised classification system 1.Community-acquired pneumonia (CAP) –includes - Cases of infectious pneumonia in patients l iving independently in the community - Patients who have been hospitalized for ot her reasons for less than 48 hours before t he development of respiratory symptoms
  6. 2.Health care–associated pneumonia (HCAP) -Patients who have previously been hospitalized for at least 2 days within the 90 days before infe ction -Patients from nursing homes who received intrav enous antibiotic therapy, chemotherapy, or woun d care within the past 30 days -Patients from hemodialysis centers -Patients contracting pneumonia greater than 48 hours after the institution of endotracheal intubat ion and mechanical ventilation a. Hospital-acquired pneumonia (HAP) b. Ventilator-associated pneumonia (VAP).
  7. PATHOPHISIOLOGY • Pneumonia results from the proliferation of microbial pat hogens at the alveolar level and the host's response to t hose pathogens. 1.Microorganism • How do micro organisms gain access to the lower respir atory tract ? a .Aspiration from the oropharynx or nasopharynx b .Direct inhalation from ambient air c .Haematogenous dissemination d .Penetrating chest trauma e .Local spread from contagious site
  8. 2 . Host defence • What are the host defence mechanisms? A. mechanical factors - Hairs and turbinates of the nares & airway cilia -The gag reflex and -The cough mechanism B. Cellular immunity - Alveolar macrophage and neutrophils C. Humoral immunity - IgG and IgA
  9. PATHOLOGY • Classic pneumonia evolves through a series of p athologic changes. A. Congestion or Edema B. Red hepatization C. Gray hepatization D. Resolution * This pattern has been described best for pneum ococcal pneumonia and may not apply to pneum onias of all etiologies, especially viral or Pneumo cystis pneumonia.
  10. CLINICAL MANIFESTATION -Cough that is either non-productive or prod uctive of mucoid, purulent, or blood-tinged sputum -Fever -Pleuritic chest pain -Shortness of breath -Gastrointestinal symptoms (20%) -Other symptoms may include fatigue, head ache, myalgias, and arthralgias.
  11. PHYSICAL FINDINGS • Findings on physical examination vary with the degree of pulmonary consolidation and the presence or absence of a significant pl eural effusion. -Increased respiratory rate and use of ac cessory muscles of respiration -In creased or decreased tactile fremitus - Relative or stony dullness - Crackles, bronchial breath sounds
  12. INVESTIGATION • Clinical diagnosis -Chest radiography • Etiologic diagnosis -Gram stain and culture of sputum -Blood culture -Antigen tests -PCR -Serology -Bronchoscopy
  13. DIFFERENTIAL DIAGNOSIS • Acute bronchitis • Acute exacerbations of chronic bronchitis, • Heart failure • Pulmonary embolism
  14. COMPLICATIONS • Respiratory failure • Shock and multiorgan failure • Exacerbation of comorbid illnesses • Metastatic infection (e.g., brain abscess or endocarditis) • Lung abscess • Complicated pleural effusion (Empyema)
  15. MANAGEMENT • The principles of treatments are 1.To treat non complicated pneumonia as outpatient and complicated pneumonia an d severely ill patients as inpatients 2.To kill the organism with appropriate anti biotics 3.To recognize and treat complications
  16. Criteria for hospitalization • Age >65 • Co morbidity • Leukopenia (<5000/ul) not attributable to a known conditi ons • S.aures ,G-ve bacilli, anaerobes suspected causes of p neumonia • Suppurative complications • Failure of PO treatment • RR >30’ ,PR >120’ ,SBP<90/mmhg • Po2 < 60mmhg , acute alteration in mental status • Multiple lobe involvement
  17. FOLLOW UP • Fever and leukocytosis usually resolve wit hin 2 and 4 days, respectively . • Physical findings may persist longer. • Chest radiographic abnormalities are slow est to resolve and may require 4–12 week s to clear.
  18. Failure to improve • Noninfectious conditions • Correct diagnosis but that a different patho gen • The pathogen may be resistant to the drug selected • Wrong drug or the correct drug at the wron g dose or frequency of administration • Nosocomial superinfections
  19. Suppurative Lung diseases • Lung Abscess • Bronchectasis • Empyema
  20. LUNG ABCESS • Is defined as pulmonary parenchymal necrosis and cavit ation resulting from infection. Conditions that predispose to lung abscess • any cause of aspiration or decreased ciliary action reduced levels of consciousness alcoholism seizure disorders general anesthesia cerebrovascular accidents drug addiction
  21. • Periodontal disease, gingivitis, sinus infecti on, and bronchiectasis • septic pulmonary embolism • Bronchial obstruction – neoplasm , foreign bodies • Lung infarction • Fluid-filled cysts or bullae • Pulmonary contusion
  22. MICROBIOLOGY • Anaerobic bacteria ( most common )-strept occoci, H.influenza • Aerobic or facultative bacteria - S. aureus, Klebsiella pneumoniae, Nocardia sp., and gram-negative organisms • Fungi • parasites
  23. CLINICAL MANIFESTATION • Clinical course -acute presentations - aerobic bacteria -evolve over an extended period of time - anaerobic infection • Presentation -Asymptomatic -Symptomatic - cough, copious foul smelli ng purulent sputum production, pleuritic ch est pain, fever, and hemoptysis
  24. PHYSICAL EXAMINATION • Unrevealing • Fetid breath and poor dentition • Dullness to percussion • Reduced breath sounds or criptation • Clubbing or hypertrophic pulmonary osteo arthropathy
  25. INVESTIGATION • Chest radiograph - cavity with an air-fluid level, with or wi thout surrounding infiltrate -Lung abscess occur commonly in dependent segment s of the lung .The posterior segments of the upper lobes and .The superior segments of the lower lobes • CT of the chest - to define the size and location of the ab scess • Gram stain and culture of sputum • Blood culture • Pleural fluid cultures • Bronchoscopy
  26. complications • Empyema, with or without bronchopleural f istula • Massive hemoptysis • Septicemia
  27. MANAGEMENT The principles of treatments are 1.To kill the organism with appropriate antibiotics - Clindamycin (150 mg–300 mg every 6 h) 4-8wks - Metronidazole 400mg tid plus penicillin 2. To drain the pus -Postural -Bronchoscopical 3.Surgical resection of affected segment Indications -refractory hemoptysis -inadequate response to medical therapy -Empyema or bronchopleural fistula -the need for a tissue diagnosis when there is concern fo r a noninfectious etiology (lung ca).
  28. BRONCHECTASIS • is an abnormal and permanent dilatation of bronchi. • It may be either focal, involving airways su pplying a limited region of pulmonary pare nchyma, or diffuse, involving airways in a more widespread distribution .
  29. PATHOLOGY • Three different patterns of bronchiectasis have been described 1. Cylindrical bronchiectasis 2. Varicose bronchiectasis 3. Saccular (cystic) bronchiectasis
  30. PATHOGENESIS • Bronchiectasis is a consequence of inflammation and destruction of the structural components of t he bronchial wall. • The induction of bronchiectasis requires several factors: (1) an infectious insult (2) airway obstruction (3) reduced clearance of mucus and other mate rial from the airways (4) a defect in host defense
  31. CLINICAL MANIFESTATION • Persistent or recurrent cough and purulent sputum production • Hemoptysis • Asymptomatic or nonproductive cough ("dr y" bronchiectasis ) • Systemic symptoms (fatigue, weight loss, myalgias,fever) • Dyspnea or wheezing
  32. PHYSICAL EXAMINATION • Crackles, rhonchi, and wheezes • Clubbing
  33. MANAGEMENT • The principles of treatment (1) treatment of infection, particularly during acute exacerbations • empiric coverage (e.g., with amoxicillin, t rimethoprim-sulfamethoxazole, or levoflox acin) (2) improved clearance of tracheobronchial s ecretions
  34. (3) reduction of inflammation; and (4) treatment of an identifiable underlying pr oblem
  35. Empyema • Is defined as grossly purulent pleural effusion. • Causes Extension of infection from infected lung ( pnemonia,lung abcess) Subphrenic abcess Chest trauma Esophageal perforation Iatrogenic
  36. MANAGEMENT • Principles of treatment 1.Removal of pus – chest tube drainage 2.Antibiotic 3.Decortication