NON-RESOLVING PNEUMONIA

1. NON-RESOLVING
PNEUMONIA

2. • PNEUMONIA is defined as inflammation of lung parenchyma
caused by an infectious agent.

3. • Clinical features & Signs : Fever, pleurisy, cough , expectoration,
SOB, Tachypnoea, Tachycardia
• In case of severe pneumonia : Hypotension, reduced SPO2, altered
sensorium, cyanosis, use of accessory muscles.

7. • A non-resolving pneumonia (NRP) is a common clinical dilemma
and the concept of NRP is difficult to define.
• In 1987, Fein and colleagues defined non-resolving pneumonia as
a clinical syndrome in which focal infiltrates begins with clinical
association of acute pulmonary infection (that is fever,
expectoration, malaise and/or dyspnea) and do not resolve in the
expected time.

8. • In 1991, Kirtland and Winterbauer defined slowly resolving
pneumonia as a clearing of the radiographic features by less than
50% in two weeks or complete clearance in 4 weeks.
• Another criteria includes a minimum of 10 days of antibiotic
therapy and a radiographic infiltrate that has not resolved in an
expected period of time.

9. • Non resolving pneumonia is defined as the persistence of clinical
symptoms & signs and failure of resolution of the radiographic
features, despite adequate antimicrobial therapy.

10. Causes of Non-Resolving Pneumonia
• Inappropriate antimicrobial therapy
• Super-infection
• Complication of initial pneumonia
• Host factors
• Defects in defense
• Presence of resistant organisms
• Inadequate host response
• Non-infectious process or Diseases mimicking Pneumonia

11. Inappropriate Anti-Microbial Therapy
• Inadequate dosing
• Agents that fail to penetrate infected lung tissue (Eg:
aminoglycosides)
• Use of agents to which organisms are resistant.

12. Common examples of resistance
• Amoxicillin in the case of beta-lactamase producing H. influenzae
• Azithromycin or Doxycycline resistant S. pneumoniae
• Infection with Pseudomonas or MRSA

13. Super infection
• Failure to respond could represent progression of a viral
pneumonia to bacterial superinfection, often with MRSA.

14. • Non-resolving pneumonia may also result from infections with
Mycobacteria(MTB, NTM), endemic mycoses( Blastomyces
dermatitidis, Histoplasma capsulatum) or less common bacteria
including Nocardia and Actinomycetes.
• These infections are more difficult to diagnose and treat.
• Nocardia and Aspergillus should be considered in
immunosuppressed patients.

15. • Untreated endovascular infections, intra-abdominal abscess, or
septic pulmonary emboli may cause persistent, evolving lung
infections.

16. Host factors :
• Age esp. greater than 50
• Co-morbid illnesses- Diabetes , COPD
• Immunosuppressive/cytotoxic therapy
• Bacteremia
• Intubated patients ( colonized with resistant microorganisms)

17. RISK FACTORS FOR MDR VAP
• Prior iv antibiotic use within 90 days
• Septic shock at time of VAP
• H/o Acute renal replacement therapy prior to occurrence of VAP
• > or = 5 days of hospitalization prior to occurrence of VAP
• ARDS proceeding VAP
• eg : P. aeruginosa, MRSA

18. MRSA suspected if
• Advanced age
• Recurrent skin infection
• Prior antibiotic coverage
• Contact with pts having MRSA
Around 50% of non responding VAP are due to MRSA, P. aeruginosa

19. TIME OF CLEARANCE CAUSATIVE AGENTS
2WEEKS-2MONTHS MYCOPLASMA
1-3 MONTHS PNEUMOCOCCUS(NON-BACTEREMIC)
CHLAMYDIA
MORAXELLA
1-5 MONTHS H. INFLUENZAE
2-6 MONTHS LEGIONELLA
3-5 MONTHS PNEUMOCOCCUS (BACTEREMIC)
STAPHYLOCOCCUS AUREUS,
GRAM NEGATIVE ORGANISMS

20. • Presence of Unusual organisms - Nocardia, Atypical mycobacteria
• Fungi: aspergillus , cryptococcus, mucor,
histoplasma,coccidiodomycosis.
• Exposure to animals-Francisella, Yersinia, Leptospira, Chlamydia
• Travel to Endemic areas- Hantavirus, Paragognimiasis.

21. Defects in defence
• Impaired cough-(sedatives, neuromuscular illness, stroke.)
• Mucociliary transport
• ET tube , tracheostomy
• Bacterial adherence to airway epithelium and decreased function
of alveolar macrophages.
• Immuno-deficiency

22. Disease mimicking pneumonia
• Non infectious causes : Neoplasia mimicking infiltrative process:
*Bronchoalveolar cell carcinoma.
• Lobar Atelectasis-Bronchogenic CA
• Carcinoid, metastatic disease.
• Hypersenstivity pneumonitis.

23. • CTD(connective tissue diseases)
• Granulomatous polyangiitis
• BOOP(Bronchiolitis obliterans with organizing pneumonia.)
• PAP (Pulmonary alveolar proteinosis )
• Sarcoidosis
• AIP (Acute interstitial pneumonia)

26. Hypersensitivity Pneumonitis

29. NSIP

30. • Drugs induced lung disease
• Nitrofurantoin
• Amiodarone
• Methotrexate
• Bleomycin
• Mitomycin
• Paclitaxel,Docetaxel
• Cyclophosphamide
• IL-2 (Aldesleukin)

31. • By 2 mechanisms : i) Direct, dose-dependent toxicity. ii) Immune-
mediated. Cytotoxic lung injury may result from direct injury to
pneumocytes or the alveolar capillary endothelium

33. Diagnostic evaluation
• Re-evaluate host factors
• Possibility of antimicrobial failure :
• patient noncompliance
• improper dosage.
• review antibiotic resistant pathogen
• unusual pathogen
• Infectious complications :
• empyema Rpt CXR/chest CT
• endocarditis. Echo
• super infection

34. • Look for atypical organisms
• Blood cultures
• Urine- antigen test for detection of legionella

35. Radiology
• CXR -infiltrates, pleural effusion, cavitation
• CT scans -detailed study of parenchyma, interstitium, pleura &
mediastinum.

36. Bronchoscopy :
• PSB(protected specimen brush)
• BAL(bronchoalveolar lavage )
• TBLB ( transbronchial lung biopsy)
• Biopsies seldom useful in achieving bacterial diagnosis. Invaluable
in TB, neoplasms, BOOP
• Also of important role in Immuno-suppressed.

37. Protected brush specimens
• Reported sensitivities of 50-80%
• Specificity >80%
• Gram, ZN, and C/S of the specimen
• However it is of limited utility due to:
• lack of standardization of the tests
• paucity of studies demonstrating benefit in morbidity or mortality.

38. CT/USG guided FNAC
• Establishes the diagnosis in 93.7% of cases.
• Specially useful in peripheral lesions.
• Also helpful when FOB cannot establish any diagnosis.

40. THANK YOU