PNEUMONIA ( TYPICAL/ATYPICAL) Dr. AISHA SIDDIQUI.

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PNEUMONIA ( TYPICAL/ATYPICAL) Dr. AISHA SIDDIQUI

PNEUMONIA Insults Tissue response Mode of spread Classification Causative agents Clinical features Complications Differential diagnosis Investigations Treatment Poor prognosis References

INSULTS Viral>>>Staph.aureus, G-ve bacilli Cigarettes/C.O.P.D>>>Impair mucociliary function & phagocytosis Alcohol Head trauma Anasthaesia C.N.S lesions>>>dec conciousness,dec gag reflex>>>>>>>>>>ASPIRATION Foreign body/ tumours>>>Impair bronchial drainage>>>Infection

INSULTS Dec leucocytes/ dec Ig>>>Recurrent Pneumonia Steroids/Immunosuppression>>>opportunisti c infections Severely ill Ventillators I.C.U N.G tubes A/B Surgery>>>Nosocomial infections

TISSUE RESPONSE. Strep. Pneumoniae/ H. Influenza: lobar consolidation (NO tissue necrosis). Staph. Aureus/ G-ve bacilli: Necrosis>>>cavitation (abcess), peribonchial. Atypical: Viruses Mycoplasma Pneumonia Chlamydia Pneumonia/ Psittica Legionella Pneumophila Coxella Burnetti>>>>>> Intrestitial, diff, bilateral. Mycobacterium Tuberculosis/ Fungi: Slow granulation.

MODE OF SPREAD Inhalation Aspiration Bld. stream

CLASSIFICATION Community Nosocomial Radiological Microbiological Immunocompromized Aspiration Recurrent

COMMUNITY AQUIRED PNEUMONIA Increase in winter( viruses & close contact) Strep.pneumonia 60% (G + C) H.influenza 10% (G-CB) >C.O.P.D Moraxella Catarrhalis (G-C) >C.O.P.D ATYPICAL: Legionella pneumophila(G-B) Mycoplasma pneumonia Chlamydophila Viruses Staph. Aureus & G-ve Bacilli>>> less common Staph (influenza), Klebsiella & G-ve (alcohol)

HOSPITAL ACQUIRED PNEUMONIA Second most common nosocomial infection Very ill>>> Increased mortality Polymicrobial: G-B (pseudomonas, Klebsiella, E.Coli) Anaerobes Staph. Aureus Pneumococci & others also

PNEUMONIA IN IMMUNOCOMPROMIZED Opportunistic organisms : Bact. : Nocardia/ Legionella Mycobacterium :M. Avium/ Intercellularae Viruses:CMV/ Herpes zoster Fungi: Candida/ Aspergillus Protozoa: Pneumocystis carinii(Jeroveci)/ Toxoplasma gondii

CLINICAL FEATURES Symptoms: Fever, chills, cough, haemoptysis, pleurisy, s.o.b, toxic. Examination: Consolidation. VS. Atypical pneumonia.

COMPLICATIONS Hypoxia. Cardiopulmonary failure. Lung abcess. Empyema. Spread of infection. Lobar collapse Thromboembolism ARDS, renal failure, multiorgan failure

DIFFERENTIAL DIAGNOSIS Pulmonary infarction Tuberculosis Atelectasis Lung tumors Bronchiectasis Pulmonary oedema Hypersensitivity reactions: chemicals/ drugs Sarcoidosis Vasculitis Pulmonary hge

INVESTIGATIONS C.B.C: WBC/ differential C.X.R: consolidation/abcess/ effusion Sputum Pleural tap/ biopsy Bronchoscopy/ Lavage/ Biopsy ABG Bld. culture UE/LFT Cold agglutinins Urinalysis

TREATMENT Hydration Analgesics/ antipyretics Oxygen Physiotherapy Antibiotics (clinical setting & CXR): 1- Community acquired ( bact.): Penicillins- Amoxicillin- Clavulanic acid 2 nd generation Cephalosporins Trimethoprim- Sulphamethoxazole Macrolides Fluoroquinolones (Ciprofloxacin)

TREATMENT (cont’d) Antibiotics (cont ’ d): 2- Atypical : Erythromycin 3- G-ve : 3 rd generation Cephalosporins + Gentamycin, Pipracillin- tazobactam, meropenum, imipenum- cilastatin. 4- Staph. Aureus : Augmentin/ cefuroxime/ Flucloxacillin, Vancomycin 5- Aspiration : Penicillin/ Clindamycin

RISK FACTORS FOR MORTALITY Age >65 y. Presence of coexisting dis. : DM, COPD, CRF, CCF, CLD, aspiration, altered mental status, post splenectomy, alcohol. Physical : BP 38.3, Extrapulm. Infection Lab findings : Leucocytes 30,000, PaO2 50, mech. Vevt., Creatinine>1.2, Multilobar, spread, Sepsis.

REFERENCES Davidson ’ s principles & practice of medicine Scientific American Medicine UptoDate 2009