1. Pneumonia In the name of GOD Hassan Ghobadi MD. Pulmonologist
Assistant Professor of Internal Medicine
Ardabil University of Medical Science

2. Pneumonia Definition: Classification:
Pneumonia is an infection of the pulmonary parenchyma
Classification:
Community-acquired (CAP),
Health care – associated pneumonia (HCAP)
Hospital-acquired (HAP)
Ventilator-associated (VAP)

3. Pneumonia
Over the last decade or two, however, patients presenting to the hospital have often been found to be infected with multi drug-resistant (MDR) pathogens previously associated with hospital-acquired pneumonia
Widespread use of potent oral antibiotics
Earlier transfer of patients out of acute-care hospitals to their homes
Increased use of outpatient IV antibiotic therapy
General aging of the population
More extensive immunomodulatory therapies

4. Pathogens in HCAP

5. Host Defenses Mucociliary clearance Local antibacterial factors
Gag reflex
Cough mechanism
Normal flora
Mucosal barriers
Alveolar macrophages
Intrinsic opsonizing properties

6. Pathophysiology
Proliferation of microbial pathogens at the alveolar level .
when the capacity of the alveolar macrophages to ingest or kill the microorganisms is exceeded does clinical pneumonia become manifest.
The host inflammatory response, rather than the proliferation of microorganisms, triggers the clinical syndrome of pneumonia
The release of inflammatory mediators, such as interleukin (IL) 1 and tumor necrosis factor (TNF), results in fever
Chemokines, such as IL-8 and granulocyte colony-stimulating factor, stimulate the release of neutrophils

7. Pathophysiology
Newly recruited neutrophils create an alveolar capillary leak
The capillary leak results in a radiographic infiltrate and rales detectable on auscultation
Hypoxemia results from alveolar filling
Increased respiratory drive in the systemic inflammatory response syndrome (SIRS) leads to respiratory alkalosis
Reductions in lung volume and compliance and the intrapulmonary shunting of blood may cause the patient's death.

8. Access of microorganisms to the lower respiratory tract
Aspiration
Inhalation
Contaminated droplets
Hematogenous spread
Contiguous extension
Reactivation of occult infection

9. Aspiration The most common route is by aspiration from the oropharynx.
Small-volume aspiration occurs frequently during sleep.
Patients with decreased levels of consciousness are at risk of aspiration.
The gag reflex and the cough mechanism offer critical protection from aspiration.

10. Pathology
The initial phase is one of edema, in clinical or autopsy specimens it is so rapidly followed by
Red hepatization phase (The presence of erythrocytes in the cellular intraalveolar exudate )
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
Resolution, the macrophage is the dominant cell type in the alveolar space, and the debris of neutrophils, bacteria, and fibrin has been cleared

11. Etiology Streptococcus pneumonia is the most common pathogen.
Typical bacterial pathogens includes :
S. pneumoniae, Haemophilus influenzae,
and (in selected patients) S. aureus and gram-negative bacilli such as Klebsiella pneumoniae and Pseudomonas aeruginosa
Atypical organisms include :
Mycoplasma pneumoniae, Chlamydophila pneumoniae, and Legionella spp. as well as respiratory viruses such as influenza viruses, adenoviruses, and respiratory syncytial viruses (RSVs).
The atypical organisms cannot be cultured on standard media, nor can they be seen on Gram's stain

12. Etiology
Bacteria, fungi, protozoa and viruses (responsible in up to 18% of cases of CAP)
Etiology of pneumonia usually cannot be determined on the basis of clinical presentation.
Treatment directed at a specific pathogen is not superior to empirical therapy.
Identification of an unexpected pathogen allows narrowing of the initial empirical regimen.

13. Microbial Causes of CAP

14. Microbial Causes of CAP
Anaerobes play a significant role only when an episode of aspiration has occurred
The combination of
(1) An unprotected airway (e.g., in patients with alcohol or drug overdose or a seizure disorder) and
(2) significant gingivitis constitutes the major risk factor
Anaerobic pneumonias are often complicated by abscess formation and significant empyemas or parapneumonic effusions.

15. Microbial Causes of CAP
It is usually impossible to predict the pathogen in a case of CAP
It is important to consider epidemiologic and risk factors that might suggest certain pathogens

16. Epidemiology
80% of the CAP cases are treated on an outpatient basis, and ~20% are treated in the hospital
The incidence rates are highest at the extremes of age
The risk factors for CAP in general and for pneumococcal pneumonia in particular have implications for treatment regimens
Risk factors for CAP include alcoholism, immunosuppression, institutionalization, asthma, and an age of >70 years
Risk factors for pneumococcal pneumonia include dementia, seizure disorders, heart failure, cerebrovascular disease, alcoholism, tobacco smoking, chronic obstructive pulmonary disease, and HIV infection

17. Epidemiology
CA-MRSA infection is more likely in Native Americans, homeless youths, men who have sex with men, military recruits, children in day-care centers, and athletes such as wrestlers.
P. aeruginosa may also infect these patients as well as those with severe structural lung disease.
Risk factors for Legionella infection include diabetes, hematologic malignancy, cancer, severe renal disease, HIV infection, smoking, male gender, and a recent hotel stay or ship cruise .

18. Epidemiologic Factors

19. Clinical Manifestations
SYMPTOMS :
Fever & Chill & Sweats
Tachycardia
Cough (nonproductive or productive )
Blood-tinged sputum (Hemotysis)
Short of breath
Pleuritic chest pain
nausea, vomiting, and diarrhea (up to 20%)
fatigue, headache, myalgias, and arthralgias

20. Clinical Manifestations
SIGNS :
Inspection : Use of accessory muscles of respiration,
Palpation : Increased or decreased tactile fremitus,
Percussion : Dull to flat ( consolidated lung and pleural fluid ),
Auscultation : Crackles, bronchial breath sounds,

21. Diagnosis (clinical and radiographic methods ) what is the etiology?
Is this pneumonia?
(clinical and radiographic methods )
what is the etiology?
( laboratory techniques )

22. Differential diagnosis
Acute bronchitis
Acute exacerbations of COPD
Chronic bronchitis
Heart failure
Pulmonary embolism
Radiation pneumonitis

23. Diagnosis
The main purpose of the sputum Gram's stain is to ensure that a sample is suitable for culture
Gram's staining may also help to identify certain pathogens
To be adequate for culture, a sputum sample must have >25 neutrophils and <10 squamous epithelial cells per low-power field
For patients admitted to the ICU and intubated, a deep-suction aspirate or bronchoalveolar lavage sample should be sent to the microbiology laboratory as soon as possible
For suspected tuberculosis or fungal infection, specific stains are available
Cultures of pleural fluid obtained from effusions >1 cm in height on a lateral decubitus CXR

24. Diagnosis
Blood Cultures: Only ~5–14% of cultures of blood from patients hospitalized with CAP are positive .
Antigen Tests: Detect pneumococcal and Legionella antigens in urine The sensitivity 90% and specificity 99% ,
Serology: A fourfold rise in specific IgM antibody titer,

25. Imaging

26. Imaging

27. Abscess-staph

28. Pneumonia-lingula

29. Treatment 2- CURB-65 criteria 1- Confusion (C);
2- Urea >7 mmol/L (U);
3- Respiratory rate 30/min (R);
4- SBP < 90 mmHg or DBP < 60 mmHg (B);
5- Age > 65 years ,
Patients With a score of 2 should be admitted to the hospital .
Patients With a score of >3 may require admission to an ICU.

30. Treatment Site of Care 1-PSI class 1 to class 5 home or hospital
Points are given for 20 variables, including age, coexisting illness, and abnormal physical and laboratory findings
class 1 to class 5
Patients in classes 4 and 5 should be admitted to the hospital

31. Treatment
pneumococcal resistance to penicillin associated with reduced susceptibility to other drugs, such as macrolides, tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX)
For strains of S. pneumoniae with intermediate levels of resistance, higher doses of the drug should be used
Risk factors for drug-resistant pneumococcal infection include recent antimicrobial therapy, an age of <2 years or >65 years, attendance at day-care centers, recent hospitalization, and HIV infection .

32. Treatment CAP due to MRSA resistance to all beta-lactam drugs
Gram-Negative Bacilli
Enterobacter spp. are resistant to cephalosporins
the drugs of choice are fluoroquinolones or carbapenems

33. Empirical Treatment (CAP)

34. Empirical Treatment (CAP)

35. Treatment The duration of treatment for CAP : 10–14 days
with fluoroquinolones and telithromycin a 5-day course is sufficient for otherwise uncomplicated CAP
A longer course for patients with bacteremia, metastatic infection, or infection with P. aeruginosa or CA-MRSA
Longer-term therapy should also be considered if initial treatment was ineffective and in most cases of severe CAP
Patients with severe CAP who remain hypotensive despite fluid resuscitation may have adrenal insufficiency

36. Failure to Improve
Respond to therapy should be reevaluated at about day 3
(1) Is this a noninfectious condition?
(2) If this is an infection, is the correct pathogen being targeted?
( e.g., M. tuberculosis or a fungus )
(3) Is this a superinfection with a new nosocomial pathogen?
(4) If this is an infection, is the complicated pneumonia
(e.g., a lung abscess or empyema )
Noninfectious conditions can mimic pneumonia, including pulmonary edema, pulmonary embolism, lung carcinoma, radiation and hypersensitivity pneumonitis, and connective tissue disease involving the lungs

37. Complications Respiratory failure Shock and multiorgan failure
Bleeding diatheses
Exacerbation of comorbid illnesses
Lung abscess
Complicated pleural effusion
If the fluid has a pH of <7, a glucose level of <2.2 m mol/L, and a LDH concentration of >1000 U/L or if bacteria are seen or cultured, then the fluid should be drained; a chest tube is required.( complicated para pneumonic effusion )

38. Follow-Up & Prevention
Fever usually resolve within 2 days.
Leukocytosis usually resolve within 4 days.
Physical findings may persist longer.
CXR abnormality resolve with in 4–12 Weeks.
The main preventive measure is vaccination.
( for influenza and pneumococcal vaccines )

39. Ventilator-Associated Pneumonia
VAP
Ventilator-Associated Pneumonia
The pathogens and treatment strategies for VAP are more similar to those for HAP than to those for pure CAP
Etiologic agents of VAP include both MDR and non-MDR bacterial pathogens

40. Microbiologic Causes of VAP

41. Prevention Strategies for VAP

42. Prevention Strategies for VAP

43. Clinical Manifestations of VAP
Are the same as other forms of pneumonia
Fever
Leukocytosis
Increase in respiratory secretions
Pulmonary consolidation on physical examination
New or changing radiographic infiltrate
Tachypnea, tachycardia,
Worsening oxygenation,
Increased minute ventilation.

44. Diagnosis of VAP
No single set of criteria is reliably diagnostic of pneumonia in a ventilated patient
The differential diagnosis of VAP includes: atypical pulmonary edema, pulmonary contusion and/or hemorrhage, hypersensitivity pneumonitis, ARDS, and pulmonary embolism , antibiotic-associated diarrhea, sinusitis, urinary tract infection, pancreatitis, and drug fever.
The recent IDSA/ATS guidelines for HCAP suggest that either approach is clinically valid.

45. Diagnosis of VAP Quantitative-Culture Approach
Discriminate between colonization and true infection
The diagnostic threshold is 106 cfu/mL
The PSB method has a threshold of 103 cfu/mL
With sensitive microorganisms, a single antibiotic dose can reduce colony counts
After > 3 days of consistent antibiotic therapy for another infection prior to suspicion of pneumonia, the accuracy of diagnostic tests for pneumonia is unaffected.
Colony counts above the diagnostic threshold during antibiotic therapy suggest that the current antibiotics are ineffective

46. Diagnosis of VAP The Clinical Pulmonary Infection Score (CPIS)

47. VAP Treatment
Frequent use of beta-lactam drugs, especially cephalosporins, is the major risk factor for infection with MRSA and ESBL-positive strains.
Treatment should be started once diagnostic specimens have been obtained
A negative tracheal-aspirate culture or growth below the threshold for quantitative cultures strongly suggests that antibiotics should be discontinued
Combination therapy with a beta-lactam and an aminoglycoside for Pseudomonas infection

48. Empirical Antibiotic Treatment (VAP)

49. Empirical Antibiotic Treatment (VAP)

50. Prevention (VAP)
Avoid endotracheal intubation or at least to minimize its duration
Minimizing the amount of microaspiration around the ET cuff
Simply elevating the head of the bed (at least 30° but preferably 45°) decreases VAP rates
Emphasis on the avoidance of agents that raise gastric pH

51. Hospital-Acquired Pneumonia
HAP is similar to VAP
The main differences are in the higher frequency of non-MDR pathogens and the better underlying host immunity
The lower frequency of MDR pathogens
As in the management of CAP, specific therapy targeting anaerobes probably is not indicated unless gross aspiration is a concern.
Blood cultures are infrequently positive (<15% of cases).