Dr. FIROZ A HAKKIM

Dept. CHEST MEDICINE

MMCHRI

PNEUMONIA Pneumonia is defined as inflammation of the

pulmonary parenchyma caused by an infectious agent.

The clinical syndrome include fever, sweats ,rigor/chills, and pulmonary symptoms like cough, sputum, dyspnea, pleurisy or pulmonary lesions observed on radiographic examination.

Diagnosis and management of pneumonia has been complicated by the discovery of newer pathogens, expanded antimicrobial resistance ,

increased populations of immunocompromisedpatients and by newer diagnostic tools and antimicrobial agents.

Pneumonia – anatomic classification Lobar pneumonia

Segmental pneumonia

Subsegmental pneumonia

Bronchopneumonia

10% -CAP,60% of HAP have inadequate

responses to the empirical therapy initiated.

Necessitates Pulmonary specialist opinion &

bronchoscopic evaluation.

Rate of resolution of physical and laboratory abnormalities

Abnormalities Duration

Fever 2 to 4 days

Cough 4 to 9 days

Crackles 3 to 6 days

Leukocytosis 3 to 4 days

C-reactive protein 1 to 3 days

CXR abnormalities 4-12 weeks

Patient is considered to have responded if:1. Fever declines within 72 hrs2. Temperature normalizes within 5 days3. Respiratory signs (tachypnea) return to normal

•The expected time course for resolution" is controversial,

In 1975, Hendin defined slowly resolving as pulmonary consolidation persisting more than 21 days.

•In 1991, Kirtland and Winterbauer defined slowly resolving CAP in immunocompetent patients based upon radiographic criteria.>50% clearing by 2 weeks or > complete clearing at 4 weeks.

The terms non-resolving and slowly resolving pneumonia have been used interchangeably to

refer to “persistence of radiographic abnormalities beyond the expected time course”.

Non responding pneumonia-absence of clinical response antibiotic treatment after 3-5 days.

Progressive pneumonia- increase in radiographic abnormalities and clinical deterioration during first 72 hours of treatment.

NON RESOLVING PNEUMONIA Non resolving pneumonia is defined as a clinical

syndrome in which focal infiltrates begin withsome clinical association of acute pulmonaryinfection and despite a minimum of 10 days ofantibiotic therapy patients either don’t improveor worsen or radiographic opacities fail to resolvewithin 12 weeks

Causes of non resolution :•Inappropriate antimicrobial therapy.•Superinfection.• Complications of initial pneumonia. • Host factors.• Delayed radiological recovery• Presence of resistant organisms• Presence of unusual organisms.• Defects in defense. • Diseases mimicking pneumonia.

1)Inappropriate antimicrobialtherapy.

Includes inadequate dosing

Agents that fail to penetrate infected lung tissue (often aminoglycosides)

Use of agents to which organisms are or have become resistant.

2)Superinfection. Superinfection with resistant microorganisms

Including fungi, mycobacterium tuberculosis

Viral co infection with community – acquired respiratory viruses.

3)Complications from initial pneumonia: Sequestered foci of infection may prevent adequate amount of antibiotic from reaching site of infection.

• Empyema/Para pneumonic effusion• Abscess• Metastatic focus of infection eg:Infective endocarditis( Require drainage and appropriate antibiotic

therapy and addressal of the basic disease.)

4)Host factors :• Age esp. greater than 50• Co morbid illnesses- DiabetesCOPD• Alcoholism• Immunosuppressive/cytotoxic therapy• Bacteremia .• Multi-lobar pneumonia•Intubated patients ( colonized with resistant microorganisms)

5)Delayed Radiological recovery :• Non resolving pneumonia encompasses failure of clinical or radiological recovery.• Many will have clinical improvement but radiological recovery lags. • Important to know what time it takes for radiological recovery.

Causative agent time to clearance1) Pneumococcus

*bacteremic 3-5 months*non bacteremic 1-3 months

2)Legionella 2-6 months3)Mycoplasma 1/2-2 months4)Chlamydia 1-3 months5)Virus variable

6)Presence of Resistant pathogens :1- Drug-Resistant Streptococcus pneumonia (DRSP) suspected if :Treated with betalactams within 6 month.Close exposure to young children.Pneumonia in last one year.Hospitalized in last 3 month.HAP in last 2 months.

2- MRSA suspected if –Advanced age .Indwelling IV catheters.Prior antibiotic coverage.Contact with pts having MRSA.Dialysis.Burns.Surgical wounds.Tertiary care centers.

7)Presence of Unusual organisms :• Tuberculosis .• Nocardia (Nocardia as an oral microflora)• Atypical mycobacteria.• Fungi: aspergillus , cryptococcus, mucor, histoplasma,coccidiodo.• Exposure to animals-Francisella,yersinialeptospira,chlamydia psittaci.• Travel to Endemic areas- Hantavirus, Paragonimiasis.

8)Defects in defense. Nasal filtration-( ET tube , tracheostomy)

Oral adherence- (aging ,smoking, severe

illnesses, viral illness.)

Epiglottitis-( stroke,ET,sedatives.)

Impaired cough-(sedatives, neuromuscular illness, stroke.)

mucociliary transport- (ch bronchitis,

ET, dehydration, alcohol, vit A def.)

• Ig or complement def-specific disorders, (aging malnutrition,B6,folate ,zinc def.)• Bacterial adherence to airway epithelium and decreased function of alveolar macrophages.• Immune deficiency states-primary and secondary, (B cell and T cell.)

Non infectious causes :• Neoplasia mimicking infiltrative process:

*Bronchoalveolar cell carcinoma.*Lymphoma.*Lymphangitic carcinoma.

• Lobar Atelectasis-Bronchogenic CA, carcinoid,metastatic.

9)Diseases mimicking pneumonia

Inflammatory disorders:• Systemic vasculitis – CTD(connective tissue diseases) • Wegeners including DAH(Diffuse alveolar hemorrhage)• BOOP.(Bronchiolitis obliterans with organizing pneumonia.) • AEP,CEP(Acute &chronic eosinophilic pneumonia) •PAP (Pulmonary alveolar proteinosis ) • Sarcoidosis•AIP (Acute interstitial pneumonia)

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

Drug-induced interstitial lung disease (DILD) is not uncommon. Causing either benign infiltrates to life-threatening acute respiratory distress syndrome. By 2 mechanisms :

1 ) Direct, dose-dependent toxicity.2 ) Immune-mediated. Cytotoxic lung injury

may result from direct injury to pneumocytes or the alveolar capillary endothelium. DILD can be difficult to diagnose; diagnosis is often possible by exclusion alone.

Diagnostic evaluation :• Re evaluate host factors.• Possibility of antimicrobial failure :

*patient noncompliance*improper dosage.*review antibiotic resistant pathogen.*review sensitivities.*unusual pathogen.

• Infectious complications :*empyema . Rpt CXR/chest CT*endocarditis. Echo.*super infection

• Gram stain and culture of sputum is neither sensitive nor specific due to :* contamination by upper airway flora

failure to get secretions from lower airway* previous use of antibiotics

• Look for atypical organisms• Hence the role of secretions is from endotracheal aspirate and protected brush specimens,.

Radiology :• CXR repeated -infiltrates,pleuraleffusion,lymphadenopathy,cavitation• CT scans -detailed study of parenchyma,interstitium,pleura & mediastinum.

Bronchoscopy : • Simpler procedures no yield-Invasive• PSB.(protected specimen brush).

BAL (bronchoalveolar lavage )

TBLB ( transbronchial lung biopsy)

• Sensitivity of PSB 40% -non responding• Gram stain of cytocentrifuged BAL-identifies intracellular organisms.• Biopsies seldom useful in achieving bacterial diagnosis.Invaluable in TB, fungal, neoplasms, BOOP,histocytosis.• Also of important role in Immuno-suppressed.

Protected brush specimens:• Reported sensitivities of 50-80%• Specificity >80%• Gram,ZN,Giemsa,IF and C/S of the specimen• However it is of limited utilitylack of standardization of the testspaucity of studies demonstrating benefit in morbidity or mortality.