community acquired pneumonia (CAP)

3,001 views
2,762 views

Published on

These lecture notes were prepared by Dr. Hamdi Turkey- Pulmonologist- Department of internal medicine - Taiz university

Do Not Forget To Visit Our Pages On Facebook on the following Links:
https://www.facebook.com/groups/569435236444761/
AND
https://www.facebook.com/groups/690331650977113/

Published in: Health & Medicine
0 Comments
17 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total views
3,001
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
297
Comments
0
Likes
17
Embeds 0
No embeds

No notes for slide

community acquired pneumonia (CAP)

  1. 1. Hamdi Turkey- chest physicanHamdi Turkey- chest physican Community acquired pneumonia (CAP)
  2. 2. Pneumonias- classification Nosocomial Pneumonias
  3. 3. Sir William Osler Sir William Osler, known as "the father of modern medicine," appreciated the morbidity and mortality of pneumonia, describing it as the "captain of the men of death" in 1918, as it had overtaken tuberculosis as one of the leading causes of death in his time. Sir William Osler, known as "the father of modern medicine," appreciated the morbidity and mortality of pneumonia, describing it as the "captain of the men of death" in 1918, as it had overtaken tuberculosis as one of the leading causes of death in his time.
  4. 4. Pneumonia classification
  5. 5. Community acquired pneumonia (CAP) An acute infection of the pulmonary parenchyma that isAn acute infection of the pulmonary parenchyma that is associated with some symptoms of acute infection,associated with some symptoms of acute infection, accompanied by the presence of an acute infiltrate on aaccompanied by the presence of an acute infiltrate on a chest radiograph, or auscultatory findings consistentchest radiograph, or auscultatory findings consistent with pneumonia, in a patient not hospitalized or residingwith pneumonia, in a patient not hospitalized or residing in a long term care facility forin a long term care facility for >> 14 days before onset of14 days before onset of symptoms.symptoms. An acute infection of the pulmonary parenchyma that isAn acute infection of the pulmonary parenchyma that is associated with some symptoms of acute infection,associated with some symptoms of acute infection, accompanied by the presence of an acute infiltrate on aaccompanied by the presence of an acute infiltrate on a chest radiograph, or auscultatory findings consistentchest radiograph, or auscultatory findings consistent with pneumonia, in a patient not hospitalized or residingwith pneumonia, in a patient not hospitalized or residing in a long term care facility forin a long term care facility for >> 14 days before onset of14 days before onset of symptoms.symptoms.
  6. 6. CAP - Why do we care about it? 5.6 million cases annually5.6 million cases annually 1.1 million require hospitalization1.1 million require hospitalization Mortality rate =12% in-hospital; nearMortality rate =12% in-hospital; near 40% in ICU patients40% in ICU patients 5.6 million cases annually5.6 million cases annually 1.1 million require hospitalization1.1 million require hospitalization Mortality rate =12% in-hospital; nearMortality rate =12% in-hospital; near 40% in ICU patients40% in ICU patients
  7. 7. Clinical presentations Sudden onset of CAP High fever, shaking chills Pleuritic chest pain, SOB Productive cough Rusty sputum, blood tinge Poor general condition High mortality up to 20% in patients with bacteremia S.pneumoniae causative Sudden onset of CAP High fever, shaking chills Pleuritic chest pain, SOB Productive cough Rusty sputum, blood tinge Poor general condition High mortality up to 20% in patients with bacteremia S.pneumoniae causative Gradual & insidious onset Low grade fever Dry cough, No blood tinge Good GC – Walking CAP Low mortality 1-2%; except in cases of Legionellosis Mycoplasma, Chlamydiae, Legionella, Ricketessiae, Viruses are causative Gradual & insidious onset Low grade fever Dry cough, No blood tinge Good GC – Walking CAP Low mortality 1-2%; except in cases of Legionellosis Mycoplasma, Chlamydiae, Legionella, Ricketessiae, Viruses are causative TypicalTypicalTypicalTypical AtypicalAtypicalAtypicalAtypical
  8. 8. Pathogenesis CAPCAP InhalationInhalation AspirationAspiration HematogenousHematogenous
  9. 9. AgeAge Obesity; Exercise isObesity; Exercise is protectiveprotective SmokingSmoking Asthma, COPDAsthma, COPD Immuno-suppression,Immuno-suppression, HIVHIV Institutionalization, OldInstitutionalization, Old age homes etcage homes etc DementiaDementia AgeAge Obesity; Exercise isObesity; Exercise is protectiveprotective SmokingSmoking Asthma, COPDAsthma, COPD Immuno-suppression,Immuno-suppression, HIVHIV Institutionalization, OldInstitutionalization, Old age homes etcage homes etc DementiaDementia CAP- risk factorsCAP- risk factors
  10. 10. Organism specific risk factors CAP: alcoholism, asthma, immunosuppression, institutionalization, age of 70Y versus 60–69 Y Pneumococcus : dementia, seizure, heart failure, CVA, alcoholism, smoking, COPD, HIV CA-MRSA: Native Americans, homeless youths, men who have sex with men, prison inmates, military recruits, children in day-care centers, and athletes such as wrestlers Enterobacteriaceae: recently hospitalization and/or antibiotic therapy, comorbidities such as alcoholism, heart failure, renal failure P. aeruginosa : as above, severe structural lung disease Legionella: diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection, smoking, male gender, a recent hotel stay or ship cruise CAP: alcoholism, asthma, immunosuppression, institutionalization, age of 70Y versus 60–69 Y Pneumococcus : dementia, seizure, heart failure, CVA, alcoholism, smoking, COPD, HIV CA-MRSA: Native Americans, homeless youths, men who have sex with men, prison inmates, military recruits, children in day-care centers, and athletes such as wrestlers Enterobacteriaceae: recently hospitalization and/or antibiotic therapy, comorbidities such as alcoholism, heart failure, renal failure P. aeruginosa : as above, severe structural lung disease Legionella: diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection, smoking, male gender, a recent hotel stay or ship cruise
  11. 11. 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 • Many pathogens are inhaled as contaminated droplets • pneumonia occurs via hematogenous spread • contiguous extension from an infected pleural or mediastinal space  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 • Many pathogens are inhaled as contaminated droplets • pneumonia occurs via hematogenous spread • contiguous extension from an infected pleural or mediastinal space
  12. 12. Pathophysiology  Mechanical factors are critically important in host defense:  hairs and turbinates of the nares catch larger inhaled particles  branching architecture of the tracheobronchial tree traps particles on the airway lining  mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen  gag reflex and the cough mechanism  normal flora adhering to mucosal cells of the oropharynx  resident alveolar macrophages  Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest »»»»»»»»»»»» the alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses  Mechanical factors are critically important in host defense:  hairs and turbinates of the nares catch larger inhaled particles  branching architecture of the tracheobronchial tree traps particles on the airway lining  mucociliary clearance and local antibacterial factors either clear or kill the potential pathogen  gag reflex and the cough mechanism  normal flora adhering to mucosal cells of the oropharynx  resident alveolar macrophages  Only when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest »»»»»»»»»»»» the alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses
  13. 13. Pathophysiology  The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia  The release of inflammatory mediators, such as IL-1 and TNF »»»»»»»»»»»» fever  Chemokines, such as IL-8 and GCSF, stimulate the release of neutrophils and their attraction to the lung »»»»»»»»»»» peripheral leukocytosis and increased purulent secretions  Even erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis  The capillary leak results in a radiographic infiltrate and rales detectable on auscultation  hypoxemia results from alveolar filling  The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia  The release of inflammatory mediators, such as IL-1 and TNF »»»»»»»»»»»» fever  Chemokines, such as IL-8 and GCSF, stimulate the release of neutrophils and their attraction to the lung »»»»»»»»»»» peripheral leukocytosis and increased purulent secretions  Even erythrocytes can cross the alveolar-capillary membrane, with consequent hemoptysis  The capillary leak results in a radiographic infiltrate and rales detectable on auscultation  hypoxemia results from alveolar filling
  14. 14. Pathophysiology  some bacterial pathogens appear to interfere with the hypoxic vasoconstriction that would normally occur with fluid-filled alveoli, and this interference can result in severe hypoxemia  Increased respiratory drive in the SIRS leads to respiratory alkalosis  Dyspnea due to : Decreased compliance due to capillary leak Hypoxemia Increased respiratory drive Increased secretions Infection-related bronchospasm  Dyspnea due to : Decreased compliance due to capillary leak Hypoxemia Increased respiratory drive Increased secretions Infection-related bronchospasm
  15. 15. Pathology The initial phase »»»»»»»» edema presence of a proteinaceous exudate—and often of bacteria—in the alveoli This phase is rarely evident in clinical or autopsy specimens because it is so rapidly followed by a red hepatization The second stage »»»»»»»»» red hepatization • presence of erythrocytes in the cellular intraalveolar exudate • neutrophils are also present and are important from the standpoint of host defense • Bacteria are occasionally seen in cultures of alveolar specimens The initial phase »»»»»»»» edema presence of a proteinaceous exudate—and often of bacteria—in the alveoli This phase is rarely evident in clinical or autopsy specimens because it is so rapidly followed by a red hepatization The second stage »»»»»»»»» red hepatization • presence of erythrocytes in the cellular intraalveolar exudate • neutrophils are also present and are important from the standpoint of host defense • Bacteria are occasionally seen in cultures of alveolar specimens
  16. 16. Pathology (2) 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 bacteria have disappeared This phase corresponds with successful containment of the infection and improvement in gas exchange The final phase »»»»»»»»» resolution the macrophage is the dominant cell type in the alveolar space the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response
  17. 17. CAP – The Pathogens InvolvedCAP – The Pathogens Involved
  18. 18. CAP – Age wise IncidenceCAP – Age wise Incidence
  19. 19. CAP – Age wise MortalityCAP – Age wise Mortality
  20. 20. Etiology  The extensive list of potential etiologic agents in CAP includes bacteria, fungi, viruses, and protozoa  Newly identified pathogens include hantaviruses, metapneumoviruses, the coronavirus (SARS, MERS, and community-acquired strains of MRSA)  Most cases of CAP are caused by relatively few pathogens  Streptococcus pneumoniae is most common  other organisms must also be considered in light of the patient's risk factors and severity of illness  it is most useful to think of the potential causes as either "typical" or "atypical" organisms
  21. 21. Etiology Typical bacterial pathogens includes : S. pneumoniae, Haemophilus influenzae, S. aureus , gram-negative bacilli such as Klebsiella pneumoniae and Pseudomonas aeruginosa Atypical organisms include : Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella spp, respiratory viruses such as influenza viruses, adenoviruses, RSVs The atypical organisms cannot be cultured on standard media, nor can they be seen on Gram's stain are intrinsically resistant to all -lactam agents and must be treated with macrolide, fluoroquinolone, tetracycline Data suggest that a virus may be responsible in up to 18% of cases of CAP In the ~10–15% of CAP cases that are polymicrobial Typical bacterial pathogens includes : S. pneumoniae, Haemophilus influenzae, S. aureus , gram-negative bacilli such as Klebsiella pneumoniae and Pseudomonas aeruginosa Atypical organisms include : Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella spp, respiratory viruses such as influenza viruses, adenoviruses, RSVs The atypical organisms cannot be cultured on standard media, nor can they be seen on Gram's stain are intrinsically resistant to all -lactam agents and must be treated with macrolide, fluoroquinolone, tetracycline Data suggest that a virus may be responsible in up to 18% of cases of CAP In the ~10–15% of CAP cases that are polymicrobial
  22. 22. S. aureus pneumonia is well known to complicate influenza infection. Recently, however, MRSA strains have been reported as primary causes of CAP. While this entity is still relatively uncommon, clinicians must be aware of its potentially serious consequences, such as necrotizing pneumonia. 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. These novel CA-MRSA strains have infected healthy individuals who have had no association with health care Unfortunately, despite a careful history and physical examination as well as routine 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. Nevertheless, it is important to consider epidemiologic and risk factors that might suggest certain pathogens
  23. 23. Influenza A and B viruses, adenoviruses, respiratory syncytial viruses, parainfluenza viruses Anaerobes play a significant role only when an episode of aspiration has occurred days to weeks before presentation for pneumonia. combination of an unprotected airway (alcohol or drug overdose or a seizure disorder) and significant gingivitis constitutes the major risk factor. Anaerobic pneumonias are often complicated by abscess formation and significant empyemas or parapneumonic effusions
  24. 24. First case of deadly MERS-coronavirus confirmed in Yemen Hamdi Turkey
  25. 25. Recent studies support the premise that camels serve as the primary source of the MERS CoV infecting humans and that other‐ livestock are not involved. Although bats may have been the ultimate reservoir of the progenitor virus, epidemiologically it seems much more likely that camels would be the source of infection for humans. The evidence for this includes the frequency with which virus has recently been found in camels to which human cases have been exposed, the serological data that indicate widespread transmission in camels, the similarity of the camel‐ derived virus to human derived virus collected in the same area, and‐ the frequency of either direct or indirect contact between camels and humans in the region. Recent studies support the premise that camels serve as the primary source of the MERS CoV infecting humans and that other‐ livestock are not involved. Although bats may have been the ultimate reservoir of the progenitor virus, epidemiologically it seems much more likely that camels would be the source of infection for humans. The evidence for this includes the frequency with which virus has recently been found in camels to which human cases have been exposed, the serological data that indicate widespread transmission in camels, the similarity of the camel‐ derived virus to human derived virus collected in the same area, and‐ the frequency of either direct or indirect contact between camels and humans in the region.
  26. 26. Microbial causes of CAP by site of care Outpatient Hospitalized Non ICU hospitalized ICU S. pneumoniae Mycoplasma pneumoniae Haemophilus influenzae Chlamydophila pneumoniae Respiratory viruses S. pneumoniae Mycoplasma pneumoniae Chlamydophila pneumoniae Haemophilus influenzae Legionella spp Respiratory viruses S. pneumoniae S. aureus Legionella spp Gram negative organisms Haemophilus influenzae
  27. 27. Distribution of potential etiologies of CAP
  28. 28. Epidemiological factors suggesting the cause of CAP
  29. 29. “I nearly die of double bronchial pneumonia at the age of five” “I nearly die of double bronchial pneumonia at the age of five” –Roger Moore
  30. 30. Diagnosis When confronted with possible CAP, the physician must ask two questions: Is this pneumonia? »»»»»»»»»» answered by clinical and radiographic methods what is the etiology? »»»»»»»» requires the aid of laboratory techniques When confronted with possible CAP, the physician must ask two questions: Is this pneumonia? »»»»»»»»»» answered by clinical and radiographic methods what is the etiology? »»»»»»»» requires the aid of laboratory techniques
  31. 31. Clinical symptoms of acute infectious pneumonia Cough  either nonproductive or productive of mucoid, purulent, or blood-tinged sputum Dyspnea  patient may be able to speak in full sentences or may be very short of breath Chest pain  If the pleura is involved, the patient may experience pleuritic chest pain Constitutio nal symptoms  fever, tachycardia, chills and/or sweats GI symptoms  Up to 20% of patients may have GI symptoms such as nausea, vomiting, and/or diarrhea Other symptoms  fatigue, headache, myalgias, and arthralgias  CAP can vary from indolent to fulminant in presentation and from mild to fatal in severity  CAP can vary from indolent to fulminant in presentation and from mild to fatal in severity
  32. 32. Clinical signs of CAP General examination  Tachypnea, hypotension and shock in severe cases  Tachycardia  Fever, herpis labilais, bulbous maryngitis, erythema multiforme Inspection  Use of accessory muscles of respiration Palpation  increased tactile focal fremitus Percussion  Dullness to percussion over the involved area Auscultatio n  Bronchial breathing, egophony, whispering peqtriloqy, increased vocal resonance , fne crakles ( early) coarse crackers during resolution , pleural friction rub
  33. 33.  The clinical presentation may not be so obvious in the elderly who may initially display new-onset or worsening confusion and few other manifestations.  The clinical presentation may not be so obvious in the elderly who may initially display new-onset or worsening confusion and few other manifestations.
  34. 34. Hx, PE, CXRHx, PE, CXRHx, PE, CXRHx, PE, CXR Infiltrate or clinicalInfiltrate or clinical evidence of CAPevidence of CAP Infiltrate or clinicalInfiltrate or clinical evidence of CAPevidence of CAP No infiltrateNo infiltrateNo infiltrateNo infiltrate Alternate diagnosisAlternate diagnosisAlternate diagnosisAlternate diagnosis Evaluate the need forEvaluate the need for hospital admissionhospital admission Evaluate the need forEvaluate the need for hospital admissionhospital admission PORT, CURB-65, PSIPORT, CURB-65, PSIPORT, CURB-65, PSIPORT, CURB-65, PSI Out patientOut patientOut patientOut patient Inpatient(ward)Inpatient(ward)Inpatient(ward)Inpatient(ward) Inpatient ( ICU)Inpatient ( ICU)Inpatient ( ICU)Inpatient ( ICU) CAP – Evaluation of a PatientCAP – Evaluation of a PatientCAP – Evaluation of a PatientCAP – Evaluation of a Patient
  35. 35. Radiological classification of pneumonia Lobar pneumonia: homogenous opacity involving a lobe or multi-lobular (streptococcal pneumonia ) Bronchopneumonia: patchy air-space opacities (staphylococcal pneumonia) Interstitial pneumonia: reticular opacities ( viral pneumonias, atypical pneumonias) Lobar pneumonia: homogenous opacity involving a lobe or multi-lobular (streptococcal pneumonia ) Bronchopneumonia: patchy air-space opacities (staphylococcal pneumonia) Interstitial pneumonia: reticular opacities ( viral pneumonias, atypical pneumonias)
  36. 36. Diagnosis
  37. 37. CAP – Laboratory TestsCAP – Laboratory Tests • CXR – PA & lateral • CBC with Differential • BUN and Creatinine • FBG, PPBG • Liver enzymes • Serum electrolytes • Gram stain of sputum • Culture of sputum • Pre Rx. blood cultures • Oxygen saturation • CXR – PA & lateral • CBC with Differential • BUN and Creatinine • FBG, PPBG • Liver enzymes • Serum electrolytes • Gram stain of sputum • Culture of sputum • Pre Rx. blood cultures • Oxygen saturation
  38. 38. Value of CXR • Usually needed to establish diagnosis • It is a prognostic indicator • To rule out other disorders • May help in etiological diagnosis • Usually needed to establish diagnosis • It is a prognostic indicator • To rule out other disorders • May help in etiological diagnosis
  39. 39. CXR Lobar pneumonia. Pneumococcal pneumonia involving the entire left lower lobe. A, Posteroanterior view. B, Lateral view. Lobar pneumonia. Pneumococcal pneumonia involving the entire left lower lobe. A, Posteroanterior view. B, Lateral view.
  40. 40. Diagnosis Diagnosis depends on a good thorough history, physical examination and CXR For cases managed on an outpatient basis, the clinical and radiologic assessment is usually all that is done before treatment is started since most laboratory test results are not available soon enough to influence initial management In certain cases, however (influenza virus infection), the availability of rapid point-of-care diagnostic tests and access to specific drugs for treatment and prevention can be very important. In hospitalized severe cases a more laboratory tests should be performed including: sputum examination, CBC, blood culture, serological tests and urinary antigen testing. Diagnosis depends on a good thorough history, physical examination and CXR For cases managed on an outpatient basis, the clinical and radiologic assessment is usually all that is done before treatment is started since most laboratory test results are not available soon enough to influence initial management In certain cases, however (influenza virus infection), the availability of rapid point-of-care diagnostic tests and access to specific drugs for treatment and prevention can be very important. In hospitalized severe cases a more laboratory tests should be performed including: sputum examination, CBC, blood culture, serological tests and urinary antigen testing.
  41. 41. Diagnosis  The etiology of pneumonia usually cannot be determined on the basis of clinical presentation  Except for the 2% of CAP patients who are admitted to the ICU, no data exist to show that treatment directed at a specific pathogen is statistically superior to empirical therapy.  The benefits of establishing a microbial etiology can therefore be questioned, particularly in light of the cost of diagnostic testing.  a number of reasons can be advanced for attempting an etiologic diagnosis:  Identification of an unexpected pathogen allows narrowing of the initial empirical regimen, which decreases antibiotic selection pressure and may lessen the risk of resistance  Pathogens with important public safety implications, such as TB and influenza virus  without culture and susceptibility data, trends in resistance cannot be followed accurately  The etiology of pneumonia usually cannot be determined on the basis of clinical presentation  Except for the 2% of CAP patients who are admitted to the ICU, no data exist to show that treatment directed at a specific pathogen is statistically superior to empirical therapy.  The benefits of establishing a microbial etiology can therefore be questioned, particularly in light of the cost of diagnostic testing.  a number of reasons can be advanced for attempting an etiologic diagnosis:  Identification of an unexpected pathogen allows narrowing of the initial empirical regimen, which decreases antibiotic selection pressure and may lessen the risk of resistance  Pathogens with important public safety implications, such as TB and influenza virus  without culture and susceptibility data, trends in resistance cannot be followed accurately
  42. 42. Sputum examination- gram stain and culture  a sputum sample must have >25 neutrophils and <10 squamous epithelial cells per low-power field  sensitivity / specificity of the sputum Gram's stain and culture are highly variable »»»»»»»»» in cases of proven bacteremic pneumococcal infection the yield of positive cultures from sputum samples is 50%  Some patients, particularly elderly individuals, may not be able to produce an appropriate expectorated sputum sample.  The inability to produce sputum can be a consequence of dehydration, and the correction of this condition may result in increased sputum production and a more obvious infiltrate on radiography  For patients admitted to the ICU and intubated, a deep-suction aspirate or BAL sample  a sputum sample must have >25 neutrophils and <10 squamous epithelial cells per low-power field  sensitivity / specificity of the sputum Gram's stain and culture are highly variable »»»»»»»»» in cases of proven bacteremic pneumococcal infection the yield of positive cultures from sputum samples is 50%  Some patients, particularly elderly individuals, may not be able to produce an appropriate expectorated sputum sample.  The inability to produce sputum can be a consequence of dehydration, and the correction of this condition may result in increased sputum production and a more obvious infiltrate on radiography  For patients admitted to the ICU and intubated, a deep-suction aspirate or BAL sample
  43. 43. Good sputum samples is obtained only from 39% 83% show only one predominant organism Good sputum samples is obtained only from 39% 83% show only one predominant organism CAP – Gram’s Stain of SputumCAP – Gram’s Stain of SputumCAP – Gram’s Stain of SputumCAP – Gram’s Stain of Sputum
  44. 44. Blood culture 1) The yield from blood cultures, even those obtained before antibiotic therapy, is disappointingly low  Only ~5–14% of cultures of blood from patients hospitalized with CAP are positive  the most frequently isolated pathogen is S. Pneumoniae 2) Since recommended empirical regimens all provide pneumococcal coverage, a blood culture positive for this pathogen has little effect on clinical outcome ************* susceptibility data may allow a switch from a broader-spectrum regimen to penicillin in appropriate cases  Because of 1) the low yield and 2) the lack of significant impact on outcome, blood cultures are no longer considered for all hospitalized patients.  CAP patients should have blood cultured :  neutropenia secondary to pneumonia  Asplenia  complement deficiencies  chronic liver disease  severe CAP
  45. 45. Pathogens Retrieved from Blood CulturePathogens Retrieved from Blood Culture
  46. 46. Antigen detection tests  Two commercially available tests detect a) pneumococcal b) certain Legionella antigens in urine  The test for Legionella pneumophila detects only serogroup 1, but this serogroup accounts for most CAP cases of Legionnaires' disease a) The sensitivity and specificity of the Legionella urine antigen test are as high as 90% and 99%  The pneumococcal urine antigen test is also quite sensitive and specific 80% and >90%  false-positive results can be obtained with samples from colonized children,but the test is reliable  Both tests can detect antigen even after the initiation of appropriate antibiotic therapy and after weeks of illness a) Other antigen tests include a rapid test for influenza virus and direct fluorescent antibody tests for influenza virus and RSV b) the test for RSV is only poorly sensitive
  47. 47. PCR PCR tests are available for a number of pathogens, including :  L. Pneumophila  Mycobacteria a multiplex PCR can detect the nucleic acid of  Legionella spp.  M. Pneumoniae  C. pneumoniae PCR tests are available for a number of pathogens, including :  L. Pneumophila  Mycobacteria a multiplex PCR can detect the nucleic acid of  Legionella spp.  M. Pneumoniae  C. pneumoniae
  48. 48. 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  Recently, however, they have fallen out of favor because of the time required to obtain a final result for the convalescent-phase sample  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  Recently, however, they have fallen out of favor because of the time required to obtain a final result for the convalescent-phase sample
  49. 49. Management
  50. 50. Assessment of severity  Site of Care  cost of inpatient management exceeds that of outpatient treatment by a factor of 20  There are currently two sets of criteria:  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  The PSI is less practical in a busy emergency-room setting because of the need to assess 20 variables  Site of Care  cost of inpatient management exceeds that of outpatient treatment by a factor of 20  There are currently two sets of criteria:  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  The PSI is less practical in a busy emergency-room setting because of the need to assess 20 variables
  51. 51. ConfusionConfusion UreaUrea Respiratory rate > 30Respiratory rate > 30 BP ( systolic BP < 90 mmHg, diastolic BP < 60)BP ( systolic BP < 90 mmHg, diastolic BP < 60) Age > 65Age > 65 ( give one point for each feature present)( give one point for each feature present) ConfusionConfusion UreaUrea Respiratory rate > 30Respiratory rate > 30 BP ( systolic BP < 90 mmHg, diastolic BP < 60)BP ( systolic BP < 90 mmHg, diastolic BP < 60) Age > 65Age > 65 ( give one point for each feature present)( give one point for each feature present) CURB-65 score Severity Where to treat 0 Low Home 1 Low Home 2 Moderate Hospital 3-5 Severe Hospital assess for ICU admission CURB-65 scoreCURB-65 score
  52. 52. PORT Scoring –PORT Scoring – PSIPSI Pneumonia Patient Outcomes Research Team
  53. 53. < 70< 70Predictor absentPredictor absent 71-9071-90 90-13090-130 > 130> 130 Mortality 0.1-0.4Mortality 0.1-0.4 Out patientOut patientOut patientOut patient MortalityMortality 0.6-0.70.6-0.7 Out patientOut patientOut patientOut patient MortalityMortality 0.9-2.60.9-2.6 BriefBrief hospitalizationhospitalization BriefBrief hospitalizationhospitalization MortalityMortality 8.5-9.38.5-9.3 InpatientInpatientInpatientInpatient MortalityMortality 27-31.127-31.1 Inpatient-ICUInpatient-ICUInpatient-ICUInpatient-ICU
  54. 54. Who Should be Hospitalized?Who Should be Hospitalized? Class I and IIClass I and II Usually do not require hospitalizationUsually do not require hospitalization Class IIIClass III May require brief hospitalizationMay require brief hospitalization Class IV and VClass IV and V Usually do require hospitalizationUsually do require hospitalization Class I and IIClass I and II Usually do not require hospitalizationUsually do not require hospitalization Class IIIClass III May require brief hospitalizationMay require brief hospitalization Class IV and VClass IV and V Usually do require hospitalizationUsually do require hospitalization Severity of CAP with poor prognosisSeverity of CAP with poor prognosis RR > 30; PaORR > 30; PaO22/FiO2 < 250, or PO/FiO2 < 250, or PO22 < 60 on room air< 60 on room air Need for mechanical ventilationNeed for mechanical ventilation Multi lobar involvementMulti lobar involvement HypotensionHypotension Need for vasopressorsNeed for vasopressors • OliguriaOliguria Altered mental statusAltered mental status Severity of CAP with poor prognosisSeverity of CAP with poor prognosis RR > 30; PaORR > 30; PaO22/FiO2 < 250, or PO/FiO2 < 250, or PO22 < 60 on room air< 60 on room air Need for mechanical ventilationNeed for mechanical ventilation Multi lobar involvementMulti lobar involvement HypotensionHypotension Need for vasopressorsNeed for vasopressors • OliguriaOliguria Altered mental statusAltered mental status
  55. 55. CAP – Criteria for ICU AdmissionCAP – Criteria for ICU Admission Major criteriaMajor criteria Invasive mechanical ventilation requiredInvasive mechanical ventilation required Septic shock with the need of vasopressorsSeptic shock with the need of vasopressors Minor criteria (least 3)Minor criteria (least 3) Confusion/disorientationConfusion/disorientation Blood urea nitrogen ≥ 20 mg%Blood urea nitrogen ≥ 20 mg% Respiratory rate ≥ 30 / min; Core temperature < 36ºCRespiratory rate ≥ 30 / min; Core temperature < 36ºC Severe hypotension; PaO2/FiO2 ratio ≤ 250Severe hypotension; PaO2/FiO2 ratio ≤ 250 Multi-lobar infiltratesMulti-lobar infiltrates WBC < 4000 cells; Platelets <100,000WBC < 4000 cells; Platelets <100,000 Major criteriaMajor criteria Invasive mechanical ventilation requiredInvasive mechanical ventilation required Septic shock with the need of vasopressorsSeptic shock with the need of vasopressors Minor criteria (least 3)Minor criteria (least 3) Confusion/disorientationConfusion/disorientation Blood urea nitrogen ≥ 20 mg%Blood urea nitrogen ≥ 20 mg% Respiratory rate ≥ 30 / min; Core temperature < 36ºCRespiratory rate ≥ 30 / min; Core temperature < 36ºC Severe hypotension; PaO2/FiO2 ratio ≤ 250Severe hypotension; PaO2/FiO2 ratio ≤ 250 Multi-lobar infiltratesMulti-lobar infiltrates WBC < 4000 cells; Platelets <100,000WBC < 4000 cells; Platelets <100,000
  56. 56. New Treatment ParadigmNew Treatment Paradigm Hit hard and early with appropriate antibiotic(s) Hit hard and early with appropriate antibiotic(s) Short Rx. Duration; De-escalate where possibleShort Rx. Duration; De-escalate where possible
  57. 57. Risk assessment approachRisk assessment approach Early Antibiotic selectionEarly Antibiotic selection Change treatment driven by local surveillanceChange treatment driven by local surveillance Hit hard and hit earlyHit hard and hit early As short a duration as possibleAs short a duration as possible De-escalate when and where possibleDe-escalate when and where possible Risk assessment approachRisk assessment approach Early Antibiotic selectionEarly Antibiotic selection Change treatment driven by local surveillanceChange treatment driven by local surveillance Hit hard and hit earlyHit hard and hit early As short a duration as possibleAs short a duration as possible De-escalate when and where possibleDe-escalate when and where possible CAP Treatment ConsensusCAP Treatment ConsensusCAP Treatment ConsensusCAP Treatment Consensus
  58. 58. Antibiotics of choice for CAPAntibiotics of choice for CAPAntibiotics of choice for CAPAntibiotics of choice for CAP
  59. 59. Empiric Treatment – OutpatientEmpiric Treatment – Outpatient Healthy and no risk factors for DRHealthy and no risk factors for DR S.pneumoniaeS.pneumoniae 1. Macrolide or Doxycycline1. Macrolide or Doxycycline Presence of co-morbidities, use of antimicrobialsPresence of co-morbidities, use of antimicrobials within the previous 3 months, and regions with awithin the previous 3 months, and regions with a high rate (>25%) of infection with Macrolidehigh rate (>25%) of infection with Macrolide resistantresistant S. pneumoniaeS. pneumoniae 1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox 2. Beta-lactam (High dose Amoxicillin, Amoxicillin-2. Beta-lactam (High dose Amoxicillin, Amoxicillin- Clavulanate is preferred; Ceftriaxone, Cefpodoxime,Clavulanate is preferred; Ceftriaxone, Cefpodoxime, Cefuroxime)Cefuroxime) plus a Macrolideplus a Macrolide or Doxycyclineor Doxycycline Healthy and no risk factors for DRHealthy and no risk factors for DR S.pneumoniaeS.pneumoniae 1. Macrolide or Doxycycline1. Macrolide or Doxycycline Presence of co-morbidities, use of antimicrobialsPresence of co-morbidities, use of antimicrobials within the previous 3 months, and regions with awithin the previous 3 months, and regions with a high rate (>25%) of infection with Macrolidehigh rate (>25%) of infection with Macrolide resistantresistant S. pneumoniaeS. pneumoniae 1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox1. Respiratory FQ – Levoflox, Gemiflox or Moxiflox 2. Beta-lactam (High dose Amoxicillin, Amoxicillin-2. Beta-lactam (High dose Amoxicillin, Amoxicillin- Clavulanate is preferred; Ceftriaxone, Cefpodoxime,Clavulanate is preferred; Ceftriaxone, Cefpodoxime, Cefuroxime)Cefuroxime) plus a Macrolideplus a Macrolide or Doxycyclineor Doxycycline
  60. 60. 1.1. A Respiratory Fluoroquinolone (FQ) LevoA Respiratory Fluoroquinolone (FQ) Levo oror 2.2. A Beta-lactamA Beta-lactam plusplus a Macrolide (or Doxycycline)a Macrolide (or Doxycycline) (Here Beta-lactam agents are 3 Generation(Here Beta-lactam agents are 3 Generation Cefotaxime, Ceftriaxone, Amoxiclav)Cefotaxime, Ceftriaxone, Amoxiclav) 3.3. If Penicillin-allergic Respiratory FQ orIf Penicillin-allergic Respiratory FQ or Ertapenem is another optionErtapenem is another option 1.1. A Respiratory Fluoroquinolone (FQ) LevoA Respiratory Fluoroquinolone (FQ) Levo oror 2.2. A Beta-lactamA Beta-lactam plusplus a Macrolide (or Doxycycline)a Macrolide (or Doxycycline) (Here Beta-lactam agents are 3 Generation(Here Beta-lactam agents are 3 Generation Cefotaxime, Ceftriaxone, Amoxiclav)Cefotaxime, Ceftriaxone, Amoxiclav) 3.3. If Penicillin-allergic Respiratory FQ orIf Penicillin-allergic Respiratory FQ or Ertapenem is another optionErtapenem is another option Empiric Treatment – Inpatient – Non ICUEmpiric Treatment – Inpatient – Non ICUEmpiric Treatment – Inpatient – Non ICUEmpiric Treatment – Inpatient – Non ICU
  61. 61. Empiric Treatment: Inpatient inEmpiric Treatment: Inpatient in ICUICU 1.1. A Beta-lactam (Cefotaxime, Ceftriaxone,A Beta-lactam (Cefotaxime, Ceftriaxone, or Ampicillin-Sulbactam)or Ampicillin-Sulbactam) plusplus eithereither AzithromycinAzithromycin oror FluoroquinoloneFluoroquinolone 2.2. For penicillin-allergic patients, a respiratoryFor penicillin-allergic patients, a respiratory Fluoroquinolone and AztreonamFluoroquinolone and Aztreonam 1.1. A Beta-lactam (Cefotaxime, Ceftriaxone,A Beta-lactam (Cefotaxime, Ceftriaxone, or Ampicillin-Sulbactam)or Ampicillin-Sulbactam) plusplus eithereither AzithromycinAzithromycin oror FluoroquinoloneFluoroquinolone 2.2. For penicillin-allergic patients, a respiratoryFor penicillin-allergic patients, a respiratory Fluoroquinolone and AztreonamFluoroquinolone and Aztreonam
  62. 62. Empiric Rx. – SuspectedEmpiric Rx. – Suspected PseudomonasPseudomonas 1.1. Piperacillin-Tazobactam, Cefepime, CarbapenumsPiperacillin-Tazobactam, Cefepime, Carbapenums (Imipenem, or Meropenem)(Imipenem, or Meropenem) plus eitherplus either Cipro or LevoCipro or Levo 2.2. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ AzithromycinAzithromycin 3.3. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ anan antipseudomonal and antipneumococcal FQantipseudomonal and antipneumococcal FQ 4.4. If Penicillin allergic - Aztreonam for the Beta-lactamIf Penicillin allergic - Aztreonam for the Beta-lactam 1.1. Piperacillin-Tazobactam, Cefepime, CarbapenumsPiperacillin-Tazobactam, Cefepime, Carbapenums (Imipenem, or Meropenem)(Imipenem, or Meropenem) plus eitherplus either Cipro or LevoCipro or Levo 2.2. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ AzithromycinAzithromycin 3.3. Above Beta-lactamAbove Beta-lactam ++ AminoglycosideAminoglycoside ++ anan antipseudomonal and antipneumococcal FQantipseudomonal and antipneumococcal FQ 4.4. If Penicillin allergic - Aztreonam for the Beta-lactamIf Penicillin allergic - Aztreonam for the Beta-lactam
  63. 63. Strategies for Prevention of CAPStrategies for Prevention of CAP •Cessation smokingCessation smoking •Influenza Vaccine (Flu shot – Oct through Feb)Influenza Vaccine (Flu shot – Oct through Feb) It offers 90% protection and reduces mortality by 80%It offers 90% protection and reduces mortality by 80% •Pneumococcal Vaccine (Pneumonia shot)Pneumococcal Vaccine (Pneumonia shot) It protects against 23 types of PneumococciIt protects against 23 types of Pneumococci 70% of us have Pneumococci in our RT70% of us have Pneumococci in our RT It is not 100% protective but reduces mortalityIt is not 100% protective but reduces mortality Age 19-64 with co morbidity of high for pneumoniaAge 19-64 with co morbidity of high for pneumonia Above 65 all must get it even without high riskAbove 65 all must get it even without high risk •Starting first dose of antibiotic with in 4 h & OStarting first dose of antibiotic with in 4 h & O22 statusstatus
  64. 64. Switch to Oral TherapySwitch to Oral Therapy Four criteriaFour criteria Improvement in cough, dyspnea & clinical signsImprovement in cough, dyspnea & clinical signs Afebrile on two occasions 8 h apartAfebrile on two occasions 8 h apart WBC decreasing towards normalWBC decreasing towards normal Functioning GI tract with adequate oral intakeFunctioning GI tract with adequate oral intake If overall clinical picture is otherwise favorable,If overall clinical picture is otherwise favorable, hemodynamically stable; can switch to oral therapyhemodynamically stable; can switch to oral therapy while still febrile.while still febrile. Four criteriaFour criteria Improvement in cough, dyspnea & clinical signsImprovement in cough, dyspnea & clinical signs Afebrile on two occasions 8 h apartAfebrile on two occasions 8 h apart WBC decreasing towards normalWBC decreasing towards normal Functioning GI tract with adequate oral intakeFunctioning GI tract with adequate oral intake If overall clinical picture is otherwise favorable,If overall clinical picture is otherwise favorable, hemodynamically stable; can switch to oral therapyhemodynamically stable; can switch to oral therapy while still febrile.while still febrile.
  65. 65. CAP- complications Hypotension and septic shockHypotension and septic shock 3-5% Pleural effusion; Clear fluid + pus cells3-5% Pleural effusion; Clear fluid + pus cells 1% Empyema thoracis pus in the pleural space1% Empyema thoracis pus in the pleural space Lung abscess – destruction of lungLung abscess – destruction of lung Single (aspiration) anaerobes,Single (aspiration) anaerobes, PseudomonasPseudomonas Multiple (metastatic)Multiple (metastatic) Staphylococcus aureusStaphylococcus aureus Septicemia – Brain abscess, Liver AbscessSepticemia – Brain abscess, Liver Abscess Multiple Pyemic AbscessesMultiple Pyemic Abscesses Hypotension and septic shockHypotension and septic shock 3-5% Pleural effusion; Clear fluid + pus cells3-5% Pleural effusion; Clear fluid + pus cells 1% Empyema thoracis pus in the pleural space1% Empyema thoracis pus in the pleural space Lung abscess – destruction of lungLung abscess – destruction of lung Single (aspiration) anaerobes,Single (aspiration) anaerobes, PseudomonasPseudomonas Multiple (metastatic)Multiple (metastatic) Staphylococcus aureusStaphylococcus aureus Septicemia – Brain abscess, Liver AbscessSepticemia – Brain abscess, Liver Abscess Multiple Pyemic AbscessesMultiple Pyemic Abscesses
  66. 66. CAP – So How Best to Win theCAP – So How Best to Win the War?War? Early antibiotic administration within 4-6 hoursEarly antibiotic administration within 4-6 hours Empiric antibiotic Rx. as per guidelines (IDSA / ATS)Empiric antibiotic Rx. as per guidelines (IDSA / ATS) PORT – PSI scoring and Classification of casesPORT – PSI scoring and Classification of cases Early hospitalization in Class IV and VEarly hospitalization in Class IV and V Change Abx. as per pathogen & sensitivity patternChange Abx. as per pathogen & sensitivity pattern Decrease smoking cessation - advice / counselingDecrease smoking cessation - advice / counseling Arterial oxygenation assessment in the first 24 hArterial oxygenation assessment in the first 24 h Blood culture collection in the first 24 h prior to Abx.Blood culture collection in the first 24 h prior to Abx. Pneumococcal & Influenza vaccination; SmokingPneumococcal & Influenza vaccination; Smoking XX Early antibiotic administration within 4-6 hoursEarly antibiotic administration within 4-6 hours Empiric antibiotic Rx. as per guidelines (IDSA / ATS)Empiric antibiotic Rx. as per guidelines (IDSA / ATS) PORT – PSI scoring and Classification of casesPORT – PSI scoring and Classification of cases Early hospitalization in Class IV and VEarly hospitalization in Class IV and V Change Abx. as per pathogen & sensitivity patternChange Abx. as per pathogen & sensitivity pattern Decrease smoking cessation - advice / counselingDecrease smoking cessation - advice / counseling Arterial oxygenation assessment in the first 24 hArterial oxygenation assessment in the first 24 h Blood culture collection in the first 24 h prior to Abx.Blood culture collection in the first 24 h prior to Abx. Pneumococcal & Influenza vaccination; SmokingPneumococcal & Influenza vaccination; Smoking XX

×