Pneumonia in Adults can be community acquired

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1. Pneumonia April 18,2019

2. Outline of the presentation Definition Classification Pathophysiology Etiology Clinical features & Diagnosis Treatment

3. Definition Pneumonia is an infection and inflammation of the pulmonary parenchyma. Classified based on Clinical setting, Etiology, Anatomy One of top 10 cases of outpatient and inpatient diagnosis. New lung infiltrate plus clinical evidence that the infiltrate is of an infectious origin .

4. Anatomic Classification of Respiratory Infections

5. Pneumonia classification Etiologic Types: Infective Viral Bacterial Fungal/Parasitic Tuberculosis Non Infective Toxins Chemical Aspiration Morphologic types : Lobar ( 90% is due to S. pneumoniae ) Multilobar Bronchopneumonia & Interstitial . Duration : Acute Chronic Clinical setting: Typical/Atypical CAP, HCAP, HAP & VAP Primary benefit of classification schemes is to provide framework to guide appropriate management and empiric treatment. Bronchial pneumonia;- affects the lungs in patches around bronchi or bronchioles

6. HCAP (Health Care Associated Pneumonia) Pneumonia that develops in the out patient setting or within 48 hrs of admission to a hospital. In patients at increased risk of exposure to MDR bacteria as a cause of infection.

7. Pathophysiology 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. ─ Aspiration from the oropharynx Gross aspiration (Post op, CNS abn .) Micro aspiration (inhaled droplet - commonest ) ─ H ematogenous spread (endocarditis, UTI) ─ Direct (from pleura, mediastinum)

8. Pathophysiology Protective Factors The hairs and turbinates of the nares (capture larger particles) Branching architecture of the tracheobronchial tree Muco-ciliary clearance Gag reflex and the cough mechanism Local antibacterial factors (Mucosal IgA ) The Normal flora adhering to mucosal cells Resident alveolar macrophages assisted by local proteins with intrinsic opsonizing properties or antibacterial or antiviral activity.

9. Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest. In that situation , the 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 IL-1 and TNF, results in fever. Chemokines , such as IL-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 .

10. Inflammatory mediators released by macrophages and the newly recruited neutrophils create an alveolar capillary leak . Even erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis . The capillary leak results in a radiographic infiltrate and rales detectable on auscultation, and hypoxemia results from alveolar filling . Decreased compliance due to capillary leak, hypoxemia, increased respiratory drive, increased secretions , and occasionally infection-related bronchospasm all lead to dyspnea .

11. 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 . Red hepatization phase ;- due to the presence of erythrocytes . Neutrophil influx is more important with regard to host defense.

12. Gray hepatization ;- no new erythrocytes are extravasating. Those already present RBC have been lysed and degraded . The neutrophil is the predominant cell , fibrin deposition is abundant , and bacteria have disappeared . Resolution = Final phase ;- 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 . This pattern has been described best for lobar pneumococcal pneumonia and may not apply to pneumonia of all etiologies.

13. CAP- Epidemiology Risk factors for CAP RFs for Pneumococcal Pneumonia Alcoholism , Asthma , Immunosuppression , Institutionalization , and An age of >70 years versus 60–69 years. Malnutrition Dementia, Seizure disorders, Heart failure Cerebrovascular D/ rs Alcoholism , Tobacco smoking, COPD, and HIV infection.

14. Pathology Alveolar Macrophages normally efficiently kills microbes. When the capacity of the alveolar m Ф to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest. A lveolar macrophages initiate inflammatory response to bolster lower respiratory tract defenses. ─Host inflammatory response rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia. IL-1,TNF  fever & IL-8,GSF  release of N Ф  ↑WBC, purulent secretion. Inflammatory mediators(N Ф & M Ф ) create an alveolar capillary leak equivalent to that seen in the ARDS  hemoptysis.

15. Patho… The capillary leak results in a radiographic infiltrate and rales detectable on auscultation . Hypoxemia ─ alveolar filling ─ bacterias which interferes with hypoxic vasoconstriction (V/Q mismatch). Increased respiratory drive in the SIRS leads to respiratory alkalosis . Reductions in lung volume & compliance  finally intrapulmonary shunting of blood may cause the patient's death.

16. Pathology Classic pneumonia evolves through a series of pathologic changes: Edema ;- with the presence of a proteinaceous exudate —and often of bacteria—in the alveoli. Red Hepatization Phase;- The presence of erythrocytes in the intra alveolar exudate, neutrophil influx. Bacteria are occasionally seen

17. Gray hepatization RBC lysed and degraded. The neutrophil is the predominant cell , Fibrin deposition is abundant Bacteria have disappeared. Resolution The macrophage reappears and predominant. Debris of neutrophils, bacteria, and fibrin has been cleared .

18. Pathology Classic Pneumococcal Lobar pneumonia stages. 1. Alveolar edema- proteinaceous exudate & bacteria in the alveoli. 2. Red Hepatization - RBCs , Neutrophils starts to appear , Bacterias are occasionally seen. 3. Gray hepatization - Neutrophils is predominant cell, fibrin deposition is abundant,& bacteria disappeared. 4. Resolution - macrophage reappears as the dominant cell type in the alveolar space, debris of neutrophils , bacteria & fibrin has been cleared, as has the inflammatory response.

19. Community Acquired Pneumonia

20. CAP Bacteria, fungi, viruses, and protozoa Most cases of CAP, however, are caused by relatively few pathogens. Although Streptococcus pneumoniae is most common , other organisms also must be considered in light of the patient’s risk factors and severity of illness . 10-15% are polymicrobial and the etiology usually includes a combination of typical and atypical pathogens.

21. CAP- Epidemiology In USA, annually ~ 80% of all CAP cases are treated as outpatient basis and 20 % are treated in the hospital. CAP results in more than 600,000 hospitalizations, 64 million days of restricted activity, and 45,000 deaths annually. The incidence rates are highest at the extremes of age.

22. Etiology…CAP Typical organisms S. pneumoniae (50-90%) H. influenzae (3-38%) , S. aureus (2-5%) and Gram-negative bacilli - K. pneumoniae and - P. aeruginosa . Atypical organisms ─ Mycoplasma pneumonia ─ Chlamydia pneumoniae ( in outpatients) ─ Legionella spp (in inpatients) ─ Respiratory viruses ( influenza viruses, adenoviruses , and RSV ) 50% of cases specific etiology is not found.

23. The atypical organisms:- - C annot be cultured on standard media, - Cannot be seen on Gram's stain. These organisms are intrinsically resistant to all B-lactam agents and must be treated with a macrolide, a fluoroquinolone , or a tetracycline.

24. Anaerobes play a significant role only when an episode of aspiration has occurred days to weeks before presentation for pneumonia . Often complicated by abscess formation and significant empyemas or parapneumonic effusions . Aspiration in patients with unprotected airway (e.g., in pts with alcohol or drug overdose or a seizure & significant gingivitis. S . aureus pneumonia is well known to complicate influenza infection . MRSA, as the primary etiologic agent of CAP , is still relatively uncommon but rates are increasing. N ecrotizing pneumonia MRSA :- Two important developments have led to this problem: The spread of MRSA from the hospital setting to the community and The emergence of genetically distinct strains of MRSA in the community. It is more likely to result in HCAP

25. CAP- Epidemiology Risk factors for CAP RFs for Pneumococcal Pneumonia Alcoholism , Asthma , Immunosuppression , Institutionalization , and An age of >=70 years ;- In the elderly, factors such as decreased cough and gag reflexes as well as reduced antibody and Toll-like receptor responses increase the likelihood of pneumonia. Malnutrition . Dementia, Seizure disorders, Heart failure Cerebrovascular D/ rs Alcoholism, Tobacco smoking, COPD , and HIV infection.

26. CA-MRSA pneumonia:- in patients with skin colonization or infection with CA-MRSA . Enterobacteriaceae :- in patients with recently hospitalized and/or received antibiotic therapy or who have comorbidities such as alcoholism , heart failure , or renal failure . P . aeruginosa :- in patients with severe structural lung disease , such as bronchiectasis , cystic fibrosis , or severe COPD .

27. Precipitating factors Viral influenza or parainfluenza :- S.pneumoniae Hospitalized ‘ill’ patients :- Gram negatives Cigarette smoking:- strongest independent risk factor for invasive pneumococcal disease. Bronchiectasis /COPD Bronchial obstruction (lung ca) Immunosuppression ( AIDS/cytotoxic Rx );- PCP, MAC, CMV. IV drug users;- S.aureus Esophageal obstruction ;- anaerobes

28. CAP – Special Features – Pathogen wise Blood tinged sputum - S. pneumoniae , - K. pneumoniae - Legionella spp . Pleural effusion:- H.inflenzae Chronic alcoholism:- K.pneumoniae Structural lung Ds (COPD/bronchiectasis). - P.Aeruginosa (related to smoking) Aspiration:- multiple pathogens Unfortunately , despite a careful hx & P/E as well as radiographic studies, it is usually impossible to predict the pathogen in a case of CAP with any degree of certainty . In more than half of cases , a specific etiology is never determined .

29. Clinical Manifestations CAP can vary from indolent to fulminant in presentation and from mild to fatal in severity . Fever with tachycardia , chills +/- sweats Cough ;- non-productive or productive of mucoid , purulent, or blood-tinged sputum. Gross hemoptysis is suggestive of CA-MRSA pneumonia . Pleuritic chest pain Dyspnea 20% of pts GI sxs ;- nausea, vomiting +/- diarrhea Fatigue , headache , myalgias & arthralgias Signs of Consolidation +/- pleural effusion

30. Physical examination ↑ RR & use of accessory muscles of respiration Palpation - ↑ tactile fremitus :- underlying consolidated lung - ↓ tactile fremitus :- pleural fluid . Percussion note - Dull :- underlying consolidated lung - F lat:- pleural fluid . Auscultation;- Crackles, BBS, pleural friction rub. Elderly s/s may not be obvious - new-onset or worsening confusion. Severely ill patients may have septic shock and evidence of organ failure. The sensitivity and specificity of the findings on P/E are averaging 58 % and 67%, respectively.

31. Lung consolidation :- Consolidation occurs when the normally air filled lung parenchyma becomes engorged with fluid or tissue , most commonly in the setting of pneumonia . If a large enough segment of parenchyma is involved, it can alter the transmission of air and sound. In the presence of consolidation, fremitus becomes more pronounced . Pleural fluid :- Fluid, known as a pleural effusion, can collect in the potential space that exists between the lung and the chest wall, displacing the lung upwards. Fremitus over an effusion will be decreased .

32. Percussion :-  This technique makes use of the fact that striking a surface which covers an air-filled structure (e.g. normal lung) will produce a resonant note . If the normal, air-filled tissue has been displaced by fluid (e.g. pleural effusion ) or infiltrated with white cells and bacteria (e.g. pneumonia ), percussion will generate a deadened/muffled tone . Alternatively , processes that lead to chronic (e.g. emphysema) or acute (e.g. pneumothorax) air trapping in the lung or pleural space, respectively, will produce hyper-resonant (i.e. more drum-like) notes on percussion.

33. Auscultation A healthy individual produces a soft inspiratory sound as air rushes into the lungs, with little noise produced on expiration . These are referred to as vessicular breath sounds . Wheezes are whistling-type noises produced during expiration (and sometimes inspiration) when a ir is forced through airways narrowed by bronchoconstriction , secretions , and/or associated mucosal edema . As this most commonly occurs in association with diffuse processes that affect all lobes of the lung (e.g. asthma and emphysema ) it is frequently audible in all fields. In cases of significant bronchoconstriction, the expiratory phase of respiration (relative to inspiration) becomes noticeably prolonged. 

34. Rales (a.k.a. crackles) are scratchy sounds that occur in association with processes that cause fluid to accumulate within the alveolar and interstitial spaces. The sound is similar to that produced by rubbing strands of hair together close to your ear. Pulmonary edema is probably the most common cause. Pneumonia can result in discrete areas of alveolar filling , and therefore produce crackles restricted to a specific region of the lung.

35. Dense consolidation of the lung parenchyma, as can occur with pneumonia , results in the transmission of large airway noises (i.e. those normally heard on auscultation over the trachea ... known as tubular or bronchial breath sounds ) to the periphery. In this setting, the consolidated lung acts as a terrific conducting medium , transferring central sounds directly to the edges. It's very similar to the noise produced when breathing through a snorkel. Furthermore , if you direct the patient to say the letter ' eee ' it is detected during auscultation over the involved lobe as a nasal-sounding ' aaa '. These ' eee ' to ' aaa ' changes are referred to as egophony .

36. Secretions that form/collect in larger airways , as might occur with bronchitis or other mucous creating process, can produce a gurgling-type noise , similar to the sound produced when you suck the last bits of a milk shake through a straw . These noises are referred to as ronchi . Auscultation over a pleural effusion will produce a very muffled sound . If , however, you listen carefully to the region on top of the effusion , you may hear sounds suggestive of consolidation , originating from lung which is compressed by the fluid pushing up from below .

37. Most of the above techniques are complimentary . Dullness detected on percussion may represent either lung consolidation or a pleural effusion . Auscultation over the same region should help to distinguish between these possibilities;- - C onsolidation generates BBS while - Effusion :- a relative absence of sound . Fremitus will be:- - I ncreased over consolidation and - Decreased over an effusion .

38. Diagnosis Two questions to ask: Is this pneumonia? It is typically answered by clinical and radiographic methods. If so, what is the etiology? It requires the aid of laboratory techniques . Differential DX Acute bronchitis A cute exacerbations of chronic bronchitis H eart failure P ulmonary embolism Hypersensitivity pneumonitis R adiation pneumonitis

39. The benefits of establishing a microbial etiology be questioned as there is no difference b/n specific Vs empirical treatment . No data exist to show that txt directed at a specific pathogen is statistically superior to empirical therapy. Decreases antibiotic selection pressure and may lessen the risk of resistance. The benefit of establishing a microbial etiology can therefore be questioned, particularly in light of the cost of diagnostic testing . Except for the 2% of CAP patients who are admitted to the intensive care unit (ICU).

40. Clinical Diagnosis Sensitivity and specificity of the findings on physical examination are less than ideal, averaging 58% and 67 %, respectively . Therefore , chest radiography is often necessary to differentiate CAP from other conditions . Radiographic findings may include risk factors for increased severity (e.g., cavitation or multi-lobar involvement ). Occasionally , radiographic results suggest an etiologic diagnosis. For example;- - P neumatoceles suggest infection with S. aureus , and - An upper-lobe cavitating lesion suggests secondary TB . - Pleural effusion  H. Influenzae - CT may be of value in a patient with suspected postobstructive pneumonia caused by a tumor or foreign body or suspected cavitary disease .

41. Investigation CXR – PA & lateral CBC with Differential CRP BUN and Creatinine FBG, PPBG Liver enzymes Serum electrolytes Gram stain of sputum Culture of sputum Pre Rx. blood cultures Oxygen saturation

42. Investigation CBC : High WBC or low WBC , Increased ESR CXR may show areas of consolidation , x-ray usually lags behind clinical response, may stay upto SIX WEEKs . suggest an etiologic dx (Eg. Pneumatoceles  S. aureus, & upper-lobe cavitating lesion  TB, Pleural effusion  H. Influenzae ). CXR Usually needed to establish diagnosis It is a prognostic indicator ( multi-lobar infiltrates ) To rule out other disorders May help in etiological diagnosis

43. Infiltrate Patterns and Pathogens CXR Pattern Possible Pathogens Lobar S.pneumo , Kleb , H. influ , Gram Neg Patchy Atypicals , Viral, Legionella Interstitial Viral, PCP, Legionella Cavitatory Anerobes , Kleb , TB, S.aureus , Fungi Large effusion Staph, Anaerobes, Klebsiella

44. CXR Bronchopneumonia Lobar Pneumonia

45. Interstitial Pneumonia

46. CT Scan Post-obstructive pneumonia caused by a tumor or foreign body. Recurrent pneumonia and unresponsive to therapy. To define questionable CXR findings Guide to biopsy.

47. Etiologic DX No strong evidence exist that show RX directed at a specific pathogen is statistically superior to empirical therapy. Gram's stain & culture of sputum:- The main purpose of the sputum Gram’s stain is to ensure that a sample is suitable for culture. However, Gram’s staining may also identify certain pathogens (e.g., S. pneumoniae, S . aureus , and gram-negative bacteria ) ─ Sputum sample must have >25 neutrophils and <10 squamous epithelial cells per low-power field. ─ Sensitivity of Sputum culture is low (proven bacteremic pneumococcal pneumonia < = 50%). ─ Deep-suction aspirate or BAL has high yield .

48. Factors affecting culture results Unable to produce an appropriate expectorated sputum sample (aging, dehydration) Initiation of a course of antibiotics before sampling For patients admitted to the ICU and intubated, a deep-suction aspirate or BAL ( broncho -alveolar lavage) sample has a high yield on culture The greatest benefit of staining and culturing respiratory secretions is to alert the physician of unsuspected and/or resistant pathogens and to permit appropriate modification of therapy .

49. Blood culture yield is very low (~5–14% ) and the most frequently isolated pathogen is S. pneumonia Since recommended empirical regimens all provide pneumococcal coverage , a blood culture positive for this pathogen has little, if any, effect on clinical outcome. However , susceptibility data may allow narrowing of antibiotic therapy in appropriate cases. Blood cultures are no longer considered for all hospitalized CAP patients . But in Certain high-risk patients including : Neutropenia secondary to pneumonia Asplenia , or complement deficiencies CLD or Severe CAP should have blood cultured.

50. Antigen testing & Serology :- Two commercially available tests detect pneumococcal and Legionella antigen in urine. The sensitivity and specificity of the Legionella urine antigen test are as high as 90% and 99%, respectively. The pneumococcal urine antigen test is also quite sensitive and specific (80% and >90%, respectively). Although false-positive results can be obtained with samples from pneumococcus-colonized children, the test is generally reliable. Both tests can detect antigen even after the initiation of appropriate antibiotic therapy. PCR :- amplify a microorganism’s DNA or RNA. PCR of nasopharyngeal swabs has become the standard for diagnosis of respiratory viral infection . - Limited to research studies.

51. Serology :- A fourfold rise in specific IgM antibody titer between acute- and convalescent-phase serum samples is generally considered diagnostic of infection with the pathogen in question . Biomarkers :- The 2 currently in use biomarkers are;- - C-reactive protein ( CRP ) and - Pro-calcitonin ( PCT ) . Levels of these acute-phase reactants increase in the presence of an inflammatory response , particularly to bacterial pathogens . CRP may be of use in the identification of worsening disease or treatment failure . PCT may play a role in determining the need for antibacterial therapy.

52. CAP – Evaluation of a Patient

53. CAP – Management Guidelines Rational use of microbiology laboratory . Pathogen directed antimicrobial therapy whenever possible. Prompt initiation of Antibiotic therapy. Decision to hospitalize based on prognostic criteria - PORT or CURB-65. Initial therapy is usually empirical and is designed to cover the most likely pathogens including the pneumococcus and the atypical pathogens .

54. Treatment Where to Manage?/Site of care There are currently two sets of criteria: The Pneumonia Severity Index (PSI) = a prognostic model used to identify patients at low risk of dying & The CURB-65 criteria = a severity-of-illness score.

55. PSI;- 20 variables including age , coexisting illness , and abnormal P/E and lab findings . Classified into 5 d/t mortality rates Class 1 = 0.1 %; Class 2 = 0.6 %; Class 3 = 2.8 %; Class 4 = 8.2 %; and Class 5 = 29.2%. PSI is often impractical in a busy emergency-department setting because of the number of variables that must be assessed .

56. CURB-65 criteria include 5 variables: Confusion (C) BUN >20mg/dl (U) RR > 30/min (R) BP : SBP < 90 mmHg or DBP < 60 mmHg (B); and Age > 65 years (65). Score of 0 The 30-day MR is 1.5%, can be treated outside the hospital . Score of 2 The 30-day MR is 9.2%, and pts should be admitted to the hospital. Scores of > 3 MR are 22% overall; These may require admission to an ICU.

57. It is not clear which assessment tool is superior . Neither PSI nor CURB-65 is accurate in determining the need for ICU admission . Septic shock or respiratory failure in the emergency department is an obvious indication for ICU care .

58. A variety of scores have been proposed to identify patients most likely to have early deterioration. Most factors in these scores are similar to the minor severity criteria proposed by the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) in their guidelines for the management of CAP.

59. CAP – Criteria for ICU Admission Major criteria - Respiratory failure - Septic shock with the need of vasopressors. Minor criteria ( at least 3 ) - Confusion/disorientation - Blood urea nitrogen ≥ 20 mg/dl - Respiratory rate ≥ 30 / min; Core temperature < 36ºC - Severe hypotension; PaO2/FiO2 ratio ≤ 250 - Multi-lobar infiltrates - WBC < 4000 cells; - Platelets <100,000

60. Severity Signs of CAP RR>28 PR>140 SBP<90 Hypoxemia (PaO2<60 or SaO2<90%) New onset of confusion Significant comorbidity Multi-lobar Pneumonia Complications Failure of OPD Rx Elderly >65yrs Unable to take PO medications or persistent vomiting Leukopenia <5000/ml S.aureus or G - ves

61. CAP- Supportive Rx Oxygen therapy for hypoxemic Assisted ventilation when needed Adequate hydration Persistent hypotension despite fluid Rx  ? Adrenal Involvement Corticosteroids Pleuritic pain should be relieved using simple analgesia such as Paracetamol

62. The selection of antimicrobial regimens for empiric therapy is based upon a number of factors, including: The most likely pathogen(s ). Risk factors for antimicrobial resistance . Medical comorbidities Additional factors pharmacokinetic and pharmacodynamic properties, safety profile, and cost . The exact reason is unknown for combination treatment, but possible explanations include: An additive or synergistic antibacterial effect , antimicrobial tolerance, Atypical co-infection, or the immunomodulatory effects of the macrolides .

63. Duration of Therapy For patients initially treated IV, a switch to oral treatment is appropriate as long as the patient can ingest and absorb the drugs, is hemodynamically stable , and is showing clinical improvement. Minimum of 5-7 days Afebrile for at least 48-72 h Longer duration of therapy : If initial therapy was not active against the identified pathogen or complicated by extra pulmonary infection . Bacteremia , Metastatic infection , or Infection with a virulent pathogen such as P. aeruginosa or CA-MRSA.

64. Follow-Up - Response to Rx Generally, clinical improvement is seen in 48-72 hours. No response by 72 hrs  Non responders Features Time Fever 2-4 days Cough 4-9 days Crackles 3-6 days Leukocytosis 3-4 days CRP 1-3 days Radiology 1-4 weeks (up to 12 weeks ) 1st week- 25% of patients 4th week- 78% of patients Response can lag to 12 weeks if patients has underlying lung disease

65. Fever and leukocytosis usually resolve within 2–4 days in otherwise healthy patients with CAP, but physical findings may persist longer. Chest radiographic abnormalities are slowest to resolve (4–12 weeks) , with the speed of clearance depending on the patient’s age and underlying lung disease. For a hospitalized patient, a follow-up radiograph ∼4–6 weeks later is recommended . If relapse or recurrence is documented, particularly in the same lung segment, the possibility of an underlying neoplasm must be considered.

66. Failure to improve Patients slow to respond to therapy should be re-evaluated at about day 3 . Non-bacterial pathogen Resistant bacteria Wrong drug or the correct drug at the wrong dose or frequency of administration Weakened Immunity of host Complications:- Empyema, lung abscess… Non-infectious:- Neoplastic D/O, drugs , CT D/O, PE, Pulmonary edema Unsuspected pathogen;- (e.g., CA-MRSA, M. tuberculosis , or a fungus):- consider serologic tests The patient must be carefully reassessed and appropriate studies initiated, possibly including such diverse procedures as CT or bronchoscopy .

67. CAP – Complications 3 particularly noteworthy conditions are;- - M etastatic infection ( e.g., brain abscess or endocarditis ) - L ung abscess , and - C omplicated pleural effusion . Hypotension and septic shock 3-5% Pleural effusion ; Clear fluid + pus cells 1% Empyema thoracis pus in the pleural space Lung abscess;- destruction of lung Single (aspiration) anaerobes, Pseudomonas Multiple (metastatic) Staphylococcus aureus Septicemia ;- Brain abscess, Liver Abscess

68. A significant pleural effusion should be tapped for both diagnostic and therapeutic purposes. If the fluid has the following on the tapped pleural effusion, it should be completely drained and a chest tube is often required :- - A pH of <7, - A glucose <2 . 2 mmol /L (<40mg/dl ) and - A LDH >1000 U/L or - If bacteria are seen or cultured

69. Prognosis The prognosis of CAP depends on the;- - P atient’s age, - C omorbidities, and - S ite of treatment (inpatient or outpatient). Young patients without comorbidity do well and usually recover fully after ~2 weeks . Older patients and those with comorbid conditions can take several weeks longer to recover fully.

70. Early treatment better outcome Poor outcome- severe/HAP/etiology Risk factor for mortality- Age , alcohol, Extent on CXR, Bactermia , (for S. pneumoniae) Immunosuppression

71. Prevention The main preventive measure is vaccination Vaccination is recommended for influenza and pneumococcus. Polyvalent Pneumococcal vaccine Influenza vaccine Prevent aspiration Prophylaxis Stop smoking

72. VAP and HAP

73. HCAP represents a transition b/n classic CAP & typical HAP . HCAP = Pneumonia that develops in the out patient setting or within 48 hrs of admission to a hospital. The incidence of MDR pathogens in HCAP was as high as or higher than in HAP/VAP . MRSA in particular was more common in HCAP The patients at greatest risk for HCAP are not well defined . - Recently received antibiotics - Recent hospitalization (i.e., in the preceding 90 days ) - P atients receiving home infusion therapy or undergoing chronic dialysis are probably at particular risk for MRSA pneumonia.

74. In general, the management of HCAP due to MDR pathogens is similar to that of MDR HAP/VAP. The prognosis of HCAP is intermediate between that of CAP and VAP and is closer to that of HAP.

75. Epidemiology PNEUMONIA IS A common complication among pts requiring MV = mechanical ventilation. Being on MV for 30 days… MR is 70 %. On any given day in the ICU, an average of 10% of patients will have pneumonia — VAP in the overwhelming majority of cases. The frequency of diagnosis is not static but changes with the duration of mechanical ventilation , with the highest hazard ratio in the first 5 days and a plateau in additional cases (1% per day) after ~2 weeks.

76. Etiology

77. VAP Potential etiologic agents of VAP include both MDR and non-MDR bacterial pathogens. The non-MDR group is nearly identical to the pathogens found in severe CAP. Most hospitals have problems with P. aeruginosa and MRSA, but other MDR pathogens are often institution-specific . Less commonly, fungal & viral pathogens cause VAP , usually affecting severely immunocompromised patients.

78. MDR Risk Factors Host risk factors for infection with MDR pathogens include: Receipt of antibiotics within the preceding 90 days Current hospitalization of ≥5 days High frequency of antibiotic resistance in the community or in the specific hospital unit. Immunosuppressive disease  and/or therapy

79. Pathogenesis 3 factors are critical in the pathogenesis of VAP C olonization of the oropharynx with pathogenic microorganisms. A spiration of these organisms from the oropharynx into the lower respiratory tract C ompromise of the normal host defense mechanisms.

80. The most obvious risk factor is the endotracheal tube, which bypasses the normal mechanical factors preventing aspiration. While the presence of an ETT may prevent large-volume aspiration, microaspiration is actually exacerbated by secretions pooling above the cuff. The ETT and the concomitant need for suctioning can damage the tracheal mucosa, thereby facilitating tracheal colonization.

81. In a high percentage of critically ill patients, the most important risk factors are;- - Antibiotic selection pressure - Cross-infection from other infected/colonized patients or contaminated equipment, and - Malnutrition . Of these factors, antibiotic exposure poses the greatest risk by far. Pathogens such as P. aeruginosa almost never cause infection in patients without prior exposure to antibiotics.

82. Almost all intubated patients experience micro-aspiration and are at least transiently colonized with pathogenic bacteria . However , only around one-third of colonized patients develop VAP . Severely ill patients with sepsis and trauma appear to enter a state of immunoparalysis several days after admission to the ICU. Mechanism is not known but Hyperglycemia affects neutrophil function , and exogenous insulin may have beneficial effects, including a decreased risk of infection .

83. The clinical manifestations are generally the same in VAP as in all other forms of pneumonia: - F ever , - Leukocytosis - Tachypnea , - Tachycardia - Worsening oxygenation, - I ncrease in respiratory secretions, and - P ulmonary consolidation on PE, along with - A new or changing radiographic infiltrate .

84. Diagnosis HAP and VAP should be suspected in patients with a new or progressive infiltrate on lung imaging as well as clinical characteristics such as: Fever Purulent sputum Leukocytosis Decline in oxygenation No single set of criteria is reliably diagnostic of pneumonia in a ventilated patient.

85. Application of clinical criteria consistently results in over-diagnosis of VAP , largely because of 3 common findings in at-risk patients : Tracheal colonization with pathogenic bacteria in patients with ETT, Multiple alternative causes of radiographic infiltrates in mechanically ventilated patients, and The high frequency of other sources of fever in critically ill patients .

86. The differential diagnosis of VAP includes Alveolar hemorrhage , Hypersensitivity pneumonitis , ARDS Pulmonary edema P ulmonary embolism . Fever and/or leukocytosis may have alternative causes

87. Diagnostic Evaluation Quantitative-Culture Approach   Discriminate b/n colonization & true infection by determining the bacterial burden. The more distal in the respiratory tree the diagnostic sampling, the more specific the results and therefore the lower the threshold of growth necessary to diagnose pneumonia and exclude colonization.  

88. Clinical Approach The Clinical Pulmonary Infection Score (CPIS) was developed by weighting of the various clinical criteria usually used for the diagnosis of VAP. Use of the CPIS allows the selection of low-risk patients who may need only short-course antibiotic therapy or no treatment at all.

89. sensitivity and specificity of only 60 and 59 percent, respectively Initial validation of the CPIS found that a score greater than six correlated with VAP

90. Treatment of VAP Frequent use of β-lactam drugs, especially cephalosporins , appears to be the major risk factor for infection with MRSA and extended-spectrum β-lactamase–positive strains . Treatment should be started once diagnostic specimens have been obtained . The major factor in the selection of agents is the presence of risk factors for MDR pathogens. Choices among the various options listed depend on local patterns of resistance and—a very important factor—the patient’s prior antibiotic exposure. The majority of patients without risk factors for MDR infection can be treated with a single agent.

91. The major difference from CAP is the markedly lower incidence of atypical pathogens in VAP ; the exception is Legionella , which can be a nosocomial pathogen, especially with breakdowns in the treatment of potable water in the hospital . The standard recommendation for patients with risk factors for MDR infection is for 3 antibiotics: - T wo directed at P. aeruginosa and - O ne at MRSA.

92. SPECIFIC TREATMENT Once an etiologic diagnosis is made For patients with MDR risk factors, antibiotic regimens can be reduced to a single agent in more than one-half of cases and to a two-drug combination in more than one-quarter of cases. Only a minority of cases require a complete course with three drugs . A negative tracheal-aspirate culture or growth below the threshold, strongly suggests that antibiotics should be discontinued .

93. COMPLICATIONS Apart from death , the major complication of VAP is prolongation of mechanical ventilation , with corresponding increases in length of stay in the ICU and in the hospital . In rare cases, some types of necrotizing pneumonia (e.g., that due to P. aeruginosa ) result in significant pulmonary hemorrhage. More commonly, necrotizing infections result in the long-term complications of bronchiectasis and parenchymal scarring leading to recurrent pneumonias .

94. Prognosis Crude mortality rates is 50–70% Pts who develop VAP are at least twice as likely to die as those who do not. The causative pathogen also plays a major role S . maltophilia is simply a marker for severe immunocompromisation that death is almost inevitable

95. Prevention Because of the significance of the ETT as a RF for VAP, the most important preventive intervention is;- - T o avoid endotracheal intubation or - M inimize its duration . Short-course antibiotic prophylaxis can decrease the risk of VAP in comatose patients requiring intubation. Minimizing the amount of micro-aspiration around the ETT cuff also is a strategy for avoidance of VAP. Simply elevating the head of the bed (at least 30° above horizontal but preferably 45 °) decreases VAP rates.

96. HOSPITAL-ACQUIRED PNEUMONIA HAP in non-intubated patients—both inside and outside the ICU—is similar to VAP. The main differences are;- - T he higher frequency of non-MDR pathogens and - T he better underlying host immunity in non-intubated pts . The lower frequency of MDR pathogens allows monotherapy in a larger proportion of cases of HAP The only pathogens that may be more common in the non-VAP population are anaerobes due to;- - The greater risk of macro-aspiration by non-intubated patients & - T he lower oxygen tensions in the lower respiratory tract

97. Diagnosis is even more difficult for HAP in the non-intubated patient than for VAP. Lower respiratory tract samples appropriate for culture are considerably more difficult to obtain from non-intubated patients . Many of the underlying diseases that predispose a patient to HAP are also associated with an inability to cough adequately.

98. Thank you!