pneumonia.pptx respiratory system mbbs nepal coms college

Mukesh presentation

1. Pneumonia Dr Deepak Sharma

2. Lower respiratory and pleural disease 2 Pneumonia -- infection of alveoli (viral or bacterial) vs. Pneumonitis -- immune-mediated inflammation of alveoli Bronchitis -- inflammation of bronchi, may be immune-mediated , e.g. asthma, COPD, or infectious (usually viral but can be bacterial) Empyema: purulent exudate in the pleural cavity Abscess : circumscribed collection of pus within the lung parenchyma Bronchiolitis : inflammation of bronchioles (often viral but can be bacterial)

3. DEFINITION Pneumonia is an infection of the pulmonary parenchyma. Despite being the cause of significant morbidity and mortality, it is often misdiagnosed, mistreated, and underestimated. Pneumonia historically was typically classified as community-acquired (CAP), hospital-acquired (HAP), or ventilator-associated (VAP). A fourth category, health care–associated pneumonia (HCAP), was introduced recently. This category was meant to encompass those cases of CAP that were caused by multidrug-resistant (MDR) pathogens typically associated with HAP

4. Lobar pneumonia is a radiological and pathological term referring to homogeneous consolidation of one or more lung lobes, often with associated pleural inflammation Bronchopneumonia refers to more patchy alveolar consolidation associated with bronchial and bronchiolar inflammation, often affecting both lower lobes

5. Hospital-acquired pneumonia (HAP) or nosocomial pneumonia refers to a new episode of pneumonia occurring at least 2 days after admission to hospital. Health-care-associated pneumonia (HCAP) refers to the development of pneumonia in a person who has spent at least 2 days in hospital within the last 90 days, or has attended a haemodialysis unit, or received intravenous antibiotics, or been resident in a nursing home or other long-term care facility

6. PATHOPHYSIOLOGY Pneumonia results from the proliferation of microbial pathogens at the alveolar level and the host’s response to those pathogens. Microorganisms gain access to the lower respiratory tract in several ways. The most common is by aspiration from the oropharynx. Small-volume aspiration occurs frequently during sleep (especially in the elderly) and in patients with decreased levels of consciousness. Rarely, pneumonia occurs via hematogenous spread (e.g., from tricuspid endocarditis) or by contiguous extension from an infected pleural or mediastinal space

7. CLEARANCE vs. COLONIZATION Microbes constantly enter airways but many factors prevent colonization: mucous entrapment ciliary clearance immune surveillance intact epithelial barrier secreted factors such as: secretory IgA surfactant proteins (SP-a, SP-d) defensins 7 Disrupting or overwhelming these defense mechanisms can allow microbes to colonize the lungs, resulting in PNEUMONIA

8. Mechanical factors are critically important in host defense. The hairs and turbinates of the nares capture larger inhaled particles before they reach the lower respiratory tract. The branching architecture of the tracheobronchial tree traps microbes on the airway lining, where mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen. The gag and cough reflexes offer critical protection from aspiration. In addition, the normal flora adhering to mucosal cells of the oropharynx, whose components are remarkably constant, prevents pathogenic bacteria from binding and thereby decreases the risk of pneumonia

9. When these barriers are overcome or when microorganisms are small enough to be inhaled to the alveolar level, resident alveolar macrophages are extremely efficient at clearing and killing pathogens. Once engulfed by the macrophage, the pathogens—even if they are not killed—are eliminated via either the mucociliary elevator or the lymphatics and no longer represent an infectious challenge. Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest.

10. T he alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses. The host inflammatory response, rather than proliferation of microorganisms, triggers the clinical syndrome of pneumonia. The release of inflammatory mediators, such as interleukin 1 and tumor necrosis factor, results in fever.

11. Chemokines, such as interleukin 8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils and their attraction to the lung, producing both peripheral leukocytosis and increased purulent secretions. Inflammatory mediators released by macrophages and the newly recruited neutrophils create an alveolar capillary leak equivalent to that seen in acute respiratory distress syndrome, although is pneumonia this leak is localized (at least initially).

12. Some bacterial pathogens appear to interfere with the hypoxemic vasoconstriction that would normally occur with fluid filled alveoli, and this interference can result in severe hypoxemia. Increased respiratory drive in the systemic inflammatory response syndrome leads to respiratory alkalosis. Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased secretions, and occasionally infection-related bronchospasm all lead to dyspnea. If severe enough, the changes in lung mechanics secondary to reductions in lung volume and compliance and the intrapulmonary shunting of blood may cause respiratory failure and death.

13. The presence of a normal alveolar microbiota raises the possibility of an alternative pathway for development of pneumonia. Rather than invasion of a sterile lower respiratory tract by pathogens to cause pneumonia, alterations in host defense may allow overgrowth of one or more components of the normal bacterial flora. The fact that many CAP pathogens are components of the normal alveolar microbiota supports this alternative-pathogenesis model. The two most likely sources of an altered alveolar microbiota are viral upper respiratory tract infections for CAP and antibiotic therapy for HAP/VAP

14. PATHOLOGY Classic pneumonia evolves through a series of pathologic changes. The initial phase is one of edema, with the presence of a proteinaceous exudate—and often of bacteria—in the alveoli. This phase is rarely evident in clinical or autopsy specimens because of the rapid transition to the red hepatization phase. The presence of erythrocytes in the cellular intra-alveolar exudate gives this second stage its name, but neutrophil influx is more important with regard to host defense. Bacteria are occasionally seen in pathologic specimens collected during this phase.

15. In the third phase, gray hepatization, no new erythrocytes are extravasating, and those already present have been lysed and degraded. The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. This phase corresponds with successful containment of the infection and improvement in gas exchange. In the final phase, resolution, the macrophage reappears as the dominant cell type in the alveolar space, and the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response.

16. ETIOLOGY

17. Streptococcus pneumoniae is most common Typical bacterial pathogens: S. pneumoniae, Haemophilus influenzae, and (in selected patients) S. aureus and gram-negative bacilli such as Klebsiella pneumoniae and Pseudomonas aeruginosa. Atypical organisms: Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella species as well as respiratory viruses such as influenza viruses, adenoviruses, human metapneumovirus, and respiratory syncytial viruses.

18. Atypical organisms cannot be cultured on standard media or seen on Gram’s stain. They are intrinsically resistant to all β-lactam agents and must be treated with a macrolide, a fluoroquinolone, or a tetracycline. Anaerobes play a significant role only when an episode of aspiration has occurred days to weeks before presentation for pneumonia. Anaerobic pneumonias are often complicated by abscess formation and by significant empyemas or parapneumonic effusions.

19. Effects and patterns of microbial colonization: where and how inflammation appears can be informative 20 Alveolar In alveolar lumen Purulent exudate of RBCs and PMNs Interstitial Mostly in alveolar wall Mononuclear WBCs Fibrinous exudate Lobar pneumonia lobar distribution “typical” CAP S. pneumo , H. flu. Bronchopneumonia patchy distribution aspiration, intubation, bronchiectasis Staph, enterics , Pseudomonas Atypical pneumonia diffuse infiltrate w/ perihilar concentration Mycoplasma, Chlamydophila , Legionella Respiratory viruses, e.g. influenza

20. CLINICAL MANIFESTATIONS: CAP can vary from indolent to fulminant in presentation and from mild to fatal in severity. Febrile with tachycardia or may have a history of chills and/or sweats. Cough: nonproductive or productive of mucoid, purulent, or blood-tinged sputum. Gross hemoptysis (CA-MRSA pneumonia) Depending on severity, the patient may be able to speak in full sentences or may be very short of breath. Pleuritic chest pain if the pleura is involved Gastrointestinal symptoms: nausea, vomiting, and/or diarrhea. Other symptoms may include fatigue, headache, myalgias, and arthralgias.

21. Findings on physical examination vary with the degree of pulmonary consolidation and the presence or absence of a significant pleural effusion. An increased respiratory rate and use of accessory muscles of respiration are common. Palpation may reveal increased or decreased tactile fremitus Percussion note can vary from dull to flat, reflecting underlying consolidated lung and pleural fluid, respectively.

22. Crackles, bronchial breath sounds, and possibly a pleural friction rub may be heard on auscultation. The clinical presentation may not be so obvious in the elderly, who may initially display new-onset or worsening confusion and few other manifestations. Severely ill patients may have septic shock and evidence of organ failure. Cardiac complications like myocardial infarction, congestive heart failure, and arrhythmias, particularly in the elderly. secondary to enhanced inflammation and procoagulant activity is increased.

23. Investigations

24. Differential diagnosis

25. Pleural effusion inflammation leads to exudation of fluid into pleural space can compromise lung function Empyema purulent exudate in pleural space necrosis/breakdown of visceral pleura and/or spread of infection into pleura Pleural adhesions, lung fibrosis 31 Complications of pneumonia

26. Abscess / cavitary lesion circumscribed focus of liquefactive necrosis within lung tissue associated with necrotizing Staph or Strep infections or Gram- neg rods (e.g. aspiration) 32 Complications of pneumonia

27. TREATMENT

28. Oxygen: Oxygen should be administered to all patients with tachypnoea, hypoxaemia , hypotension or acidosis Aim of maintaining the PaO2 ≥ 8 kPa (60 mmHg) or SaO2 ≥ 92%. High concentrations (≥ 35%), preferably humidified, should be used in all patients who do not have hypercapnia associated with COPD. Continuous positive airway pressure (CPAP) should be considered in those who remain hypoxic despite high-concentration oxygen therapy, Mechanical ventilation may be employed.

29. Fluid balance: Intravenous fluids should be considered in those with severe illness, in older patients and those with vomiting. Discontinue hypertensive agents temporarily. Otherwise, an adequate oral intake of fluid should be encouraged. Inotropic support in patients with shock Treatment of pleural pain: For the majority, simple analgesia with paracetamol, co-codamol or NSAIDs is sufficient. In some patients, opiates may be required Physiotherapy: May be helpful to assist expectoration in patients who suppress cough because of pleural pain.

30. ICU referral criteria

31. Empirical Antibiotic Treatment of CommunityAcquired Pneumonia Outpatients Previously healthy and no antibiotics in past 3 months •  A macrolide [clarithromycin (500 mg PO bid) or azithromycin (500 mg PO once, then 250 mg qd )] or •  Doxycycline (100 mg PO bid) 2. Comorbidities or antibiotics in past 3 months: select an alternative from a different class •  A respiratory fluoroquinolone [moxifloxacin (400 mg PO qd ), gemifloxacin (320 mg PO qd ), levofloxacin (750 mg PO qd )] or •  A β- lactam [preferred: high-dose amoxicillin (1 g tid ) or amoxicillin/ clavulanate (2 g bid); alternatives: ceftriaxone (1–2 g IV qd ), cefpodoxime (200 mg PO bid), or cefuroxime (500 mg PO bid)] plus a macrolidea 3. In regions with a high rate of “high-level” pneumococcal macrolide resistance,b consider alternatives listed above for patients with comorbidities.

32. Inpatients, Non-ICU •  A respiratory fluoroquinolone [e.g., moxifloxacin (400 mg PO or IV qd ) or levofloxacin (750 mg PO or IV qd )] •  A β- lactamc [e.g., ceftriaxone (1–2 g IV qd ), ampicillin (1–2 g IV q4–6h), cefotaxime (1–2 g IV q8h), ertapenem (1 g IV qd )] plus a macrolided [e.g., oral clarithromycin or azithromycin as listed above or IV azithromycin (1 g once, then 500 mg qd )] Inpatients, ICU •  A β- lactame [e.g., ceftriaxone (2 g IV qd ), ampicillin-sulbactam (2 g IV q8h), or cefotaxime (1–2 g IV q8h)] plus either azithromycin or a fluoroquinolone (as listed above for inpatients, non-ICU)

33. Special Concerns If Pseudomonas is a consideration: •  An antipseudomonal β- lactam [e.g., piperacillin/tazobactam (4.5 g IV q6h), cefepime (1–2 g IV q12h), imipenem (500 mg IV q6h), meropenem (1 g IV q8h)] plus either ciprofloxacin (400 mg IV q12h) or levofloxacin (750 mg IV qd ) •  The above β- lactams plus an aminoglycoside [amikacin (15 mg/kg qd ) or tobramycin (1.7 mg/kg qd )] plus azithromycin •  The above β- lactams plus an aminoglycoside plus an antipneumococcal fluoroquinolone If CA-MRSA is a consideration: •  Add linezolid (600 mg IV q12h) or vancomycin (15 mg/kg q12h initially, with adjusted doses) plus clindamycin (300 mg q6h)

34. FOLLOW-UP: Fever and leukocytosis usually resolve within 2–4 days in otherwise healthy patients with CAP, physical findings may persist longer. Chest radiographic abnormalities are slowest to resolve (4–12 weeks) follow-up radiograph ~4–6 weeks later If relapse or recurrence is documented, particularly in the same lung segment, the possibility of an underlying neoplasm must be considered.

35. PREVENTION: A pneumococcal polysaccharide vaccine (PPSV23) and a protein conjugate pneumococcal vaccine (PCV13) The influenza vaccine is available in an inactivated or recombinant form.

36. Hospital Acquired Pneumonia (HAP) Ventilator Associated Pneumonia (VAP) Healthcare Associated Pneumonia (HCAP)

37. HAP: pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admit. VAP: A type of HAP acquired at 48-72 hours after intubation. HCAP: non hospital patient with healthcare contact: IV therapy, wound care, chemotherapy within 30 days Nursing home or long term care facility (SNF/LTAC) Hospitalization >2 days ore more in past 90 days Attendance at hospital or HD within 30 days

38. HCAP Added as a category of pneumonia in the 2005 ATS/IDSA guidelines as an increased risk for patients who may have been exposed to multidrug-resistant (MDR) pathogens from community settings.

39. Four Major Principles Underlie the Management of HAP, VAP and HCAP Avoid untreated or inadequately treated HAP, VAP or HCAP, failure to do so is a consistent factor associated with increased mortality. Recognize the variability of bacteriology from one hospital to another, one department from another and one time period to another. Avoid the overuse of antibiotics by focusing on accurate diagnosis, tailoring therapy and limit duration of therapy to the minimal effective period. Apply prevention strategies aimed at modifiable risk factors.

40. Epidemiology HAP is the second most common nosocomial infection in the US HAP increased hospital stay by an average of 7-9 days per patient Estimated occurrence of 5-10 cases per 1,000 hospital admissions HAP accounts for up to 25% of all ICU infections and more than 50% of antibiotics prescribed

41. Epidemiology Early onset HAP and VAP (first 4 days) carries a better prognosis with better bacterial sensitivities. Patients with hospitalization or prior antibiotic use within last 90 days should be treated as late onset HAP or VAP due to risk of MDR bacteria. • Late onset HAP and VAP (5 days plus) MDR pathogens Increased morbidity/mortality

42. Epidemiology HAP-associated mortality remains the leading cause of death among hospital-acquired infections: estimated at 20-50%. Studies not relating co-founding factors- age, debility, stroke, MI, etc.

43. Epidemiology Crude mortality of HAP is 30-70%, but may be due to underlying disease rather than pneumonia. Attributable mortality is 33-50%. Worse outcomes in patients with bacteremia ( esp Pseudomonas aeruginosa or Acinetobacter species), medical rather than surgical illness, ineffective antibiotic therapy.

44. Etiology: HAP, VAP and HCAP Aerobic gram-negative bacteria: P. aeruginosa, Escherichia coli, Klebsiella pneumoniae, and Acinetobacter species Gram-positive cocci: Staphylococcus aureus (50% in ICU due to MRSA) More common in patients with diabetes mellitus, head trauma and those hospitalized in the ICU. Oropharyngeal commensals ( viridans group streptococci, coag -negative Staph, Neisseria species and Corynebacterium) may be relevant in mostly immunocompromised patients.

45. Etiology: Special Circumstances HAP involving anaerobic organisms may follow aspiration in non-intubated patients, rare in VAP. Patients who have used NIPPV. HCAP in elderly patients of long term care facilities have pathogens that more closely resemble late-onset HAP and VAP.

46. Pathogenesis Number and virulence of organisms entering the lower respiratory tract and response of the host. microaspiration of organisms which have colonized the upper respiratory/gastrointestinal tract Hospitalized patients tend to become colonized with organisms in the hospital environment within 48 hours. Common mechanisms include: mechanical ventilation, routine nursing care, lack of hand washing of all hospital personnel. Disease state also plays a role: alteration in gastric pH due to illness, certain medications, malnutrition and supplemental feedings.

47. Multi-drug resistance Gram negative bacilli MDR: variably defined as resistance to at least 2-8 antibiotics that are usually used to treat common infections. Pan-resistance: Gram negative organisms resistant to cephalosporins, beta-lactams and fluoroquinolones.

48. Microbiology Common pathogens: aerobic gram-negative rods: E coli, Klebsiella, Enterobacter, Pseudomonas, Acinetobacter gram positive cocci: Staphylococcus aureus-MRSA, MSSA, Streptococcus Nosocomial pneumonia most often seen in immunocompromised patients which include viruses and fungal infections.

49. MDR: Pseudomonas Aeruginosa Most common MDR gram-negative causing HAP/VAP. Increasing resistance to piperacillin, ceftazidime, cefepime, imipenem and meropenem. Currently, some MDR isolates of P. aeruginosa are susceptible to only polymyxin B.

50. MDR: Klebsiella, Enterobacter, and Serratia Species Klebsiella are resistant to ampicillin and can acquire resistance to cephalosporins and aztreonam by producing extended-spectrum beta-lactamases (ESBLs). ESBLs remain susceptible to carbapenems. Citrobacter and Serratia may also produce ESBLs

51. MDR: Acinetobacter species, Stenotrophomonas Maltophilia and Burkholderia Cepacia Acinetobacter has recently showed increased resistance to common antimicrobials. More than 85% are susceptible to carbapenems, but resistance is increasing. Sulbactam has become an alternative therapy. S. maltophilia and B. cepacia are common colonizers of the respiratory tract. Uniformly resistant to carbapenems Usually susceptible to Bactrim, Timentin ( ticarcillin+clavulanic ), or fluoroquinolone. B. cepacia is also usually susceptible to ceftazidime and carbapenems.

52. MDR: Methicillin-Resistant Staphylococcus Aureus (MRSA) Vancomycin-intermediate: MIC 8-16 mcg/ml High-level vancomycin-resistant: MIC of 32-1024 mcg/ml All have been sensitive to linezolid Linezolid resistance has emerged, but currently is rare

53. MDR: Streptococcus pneumoniae and Haemophilus influenzae Most likely associated with early-onset HAP in patients without other risk factors. Frequently community acquired Many strains or S. pneumoniae are penicillin resistant (penicillin binding proteins), these can also be resistant to cephalosporins, macrolides, tetracyclines, and clindamycin. Despite in vitro resistance, usually have good outcomes with penicillins and cephalosporins. All MDR strains are sensitive to vancomycin or linezolid and fluoroquinolones. MDR resistance is rare in Haemophilus influenzae

54. Microbiology Fungal pathogens: most common is Candida and Aspergillus Most commonly in organ transplant or immunocompromised, neutropenic patients. Aspergillus- contaminated air ducts or local construction. Candida- common airway colonizer and rarely requires treatment.

55. Microbiology Viral Pathogens: low incidence in immunocompetent hosts. Influenza A is the most common viral cause of HAP and HCAP in adults. Risk for secondary bacterial infection “super-infection” Streptococcus, H. influenza, Group A Streptococcus, S. aureus

56. VAP and HAP Leading infectious causes of VAP include MSSA (9%), MRSA (18%), P. aeruginosa (18%), S. maltophilia (7%), Acinetobacter spp (8%) and others (9%) HAP include, MSSA (13%), MRSA (20%), P. aeruginosa (9%), S. maltophilia (1%), Acinetobacter spp (3%), and others (18%)

57. MDR risk factors Host risk factors for infection with MDR pathogens include: Treatment with antibiotics within the preceding 90 days. Current hospitalization of >4 days High frequency of antibiotic resistance in the community or hospital unit Immunosuppressive disease and/or therapy

58. HCAP and MDR Specific risk factors for MDR pathogens associated with HCAP: Hospitalization for >/= 2 days within the last 90 days severe illness antibiotic therapy in the past 6 months poor functional status as defined by ADL score Immunosuppression

59. Modifiable Risk Factors Strict infection control Alcohol-based hand disinfection Microbiologic surveillance with timely data on local MDR pathogens Removal of invasive devices Programs to reduce or alter antibiotic-prescribing practices

60. Modifiable Risk Factors: Intubation and Mechanical Ventilation Intubation and mechanical ventilation increase the risk of HAP 6-21 fold. NIPPV, data shows use to avoid reintubation may be associated with more incidence of HAP. Sedation protocols to accelerate ventilator weaning. Reintubation increases the risk of VAP Oral gastric and tracheal tubes rather than nasal may reduce incidence of sinusitis and subsequent lower respiratory tract infection (HAP). Limiting use of sedative and paralytic agents that depress cough. Keep endotracheal cuff to >20 cm H2O

61. Modifiable Risk Factors: Aspiration, Body Position and Enteral Feeding HOB >30 degrees during enteral feedings decreases risk for aspiration. Post-pyloric feeding appears to be superior in a meta-analysis at reducing ICU-acquired HAP.

62. Modifiable Risk Factors: Modulation of Colonization: Oral Antiseptics and Antibiotics Oropharyngeal colonization is an independent risk factor for ICU-acquired HAP by enteric gram-negative bacteria and P. aeruginosa Oral antiseptic chlorhexidine significantly reduced rates of nosocomial infection in post-operative patients and is routinely used in the ICU as part of “oral care”. Selective decontamination of the digestive tract (SDD): using non-absorbable antibiotics either orally or through GT has shown benefit in reducing HAP/VAP. However not widely used due to risk for drug resistance.

63. MDR: Stress Bleeding Prophylaxis, Transfusion, and Glucose Control H2 blockers have shown an increased risk for VAP, risk vs. benefit for stress bleeding should be considered Multiple studies have identified allogeneic blood products as a risk factor for post-operative pneumonia, and the time length of blood storage as another risk factor. Blood transfusion is usually limited to Hb <7 in the patient who has no active bleeding. Hyperglycemia is an additional risk for blood stream infection, increased duration of mechanical ventilation increasing risk for HAP/VAP.

64. Diagnosis Difficult because the clinical findings are nonspecific. 2005 ATS/IDSA guidelines on the management of adults with HAP, VAP and HCAP do not provide specific criteria.

65. Diagnosis HAP, VAP or HCAP should be suspected in patients with a new or progressive infiltrate on lung imaging and clinical characteristics such as: • Fever • Purulent sputum • Leukocytosis • Decline in oxygenation • Radiographic findings plus two of the clinical findings. • 69% sensitivity and 75% specificity for pneumonia.

66. Diagnosis A lower respiratory tract culture needs to be collected from all patients before antibiotic therapy, but collection of cultures should not delay the initiation of therapy in critical ill patients. semiquantitative or quantitative culture data can be used for management of patients with HAP. Lower respiratory tract cultures from bronchoscopy or tracheal aspirate, mostly applies to VAP.

67. Diagnosis Quantitative cultures increase specificity of the diagnosis of HAP. Negative lower respiratory tract cultures can be used to stop antibiotic therapy in a patient who has had cultures obtained in the absence of an antibiotic change in the past 72 hours.

68. Diagnosis Comprehensive medical history Chest x-ray (preferably PA and Lat) to identify infiltrate and possible complication such as effusion or cavitation Arterial oxygenation saturation +/- ABG Blood cultures Patients with moderate/severe pleural effusion should undergo thoracentesis to rule out empyema or parapneumonic effusion. Lower respiratory tract samples: sputum culture, BAL or tracheal aspirate. A sterile culture of respiratory secretions in the absence of new antibiotic in the past 72 hours virtually rules out the presence of bacterial pneumonia. (Viral and Legionella still possible)