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Idiopathic Eosinophilic Pneumonia Dr. Hadil Alotair KKUH History A 18 Y/O saudi lady living in Riyadh. she is a student – C/O •Fever •productive cough •Chest pain •Dizziness+syncope 8 days 8 days 2 days 2 days – She was seen in a private hospital and was given Augmentin and azithromycin for five days without any improvement. Past H/O – BA – Eczema – Allergic rhinitis – WPW Drug Hx •Budesonide •Flexinase •Ventolin •Singulare Examination • looked sick. • Pulse 125/minute, BP 108/67 mm Hg. • Temperature 37. 8c. • Respiratory rate 22/minute. • No lymphadenopathy. • 02 saturation was 88% on room air. • Chest – Decreased chest expansion on the right side – Dull ness – Bronchial breathing Rt. Infrascapular – Coarse crepitations – Pleural rub • Other systemic examination- NAD Investigations • CBC: – – – – – WBC 29,000 RBC 4.5 Hb 137 Plt 327 ESR 14. • Differential: neut 51, lymph 14,mono 5, eos 30% • Urea and electrolytes: Normal • LFT – Normal. • ABG: – pH – PC02 – Po2 – HC03 – 02 saturation 7.43 36 51.9 23.2 87.9 on RA Hospital course • The patient was admitted initially with the impression of - CAP • on the following day – increasing SOB , cough -- Desaturated. • she was transferred to the MICU MICU • In MICU -- Ceftriaxone increased (2 g iv BD) – CIarithromycin – along with 02 10 lt – active nebulization with Ventolin, Atrovent and Pulmicort, • ABG on 10 l o2 via NRBM – PH 7.39 Pco2 41 Po2 88 HCo3 24 • She was put on non invasive ventilation BIPAP 60% O2 IPAP-10 EPAP-4 • Her blood culture - Streptococcus pneumoniae • Meropenem and levoftoxacin • she was not responding to BiPAP • hemodynamically unstable – inotropes • She was Intubated • Her ventilator mode was – ACMV ,PEEP 10, FIO2 60%, Vt 350, RR 22 pH – 7.49 PCO2- 42 PO2- 85 HCO3 – 31 %O2Sat-97 – CT scan showed •Large pneumonic consolidation of the right lung with para pneumonic effusion •Dense opacification in the apical segment of left lower lobe •Early ARDS. • At this stage the DDx was: – CAP – ABPA – Churg Strauss Syndrome – Pulmonary eosinophilic syndrome such as •Loffler’s syndrome •Acute eosinophillic pneumonia •Hyper eosinophilic syndrome – Drug induced Investigation results • PLF – Negative for malignant cells • – Inflammatory infiltrate consists mainly of neutrophil mixed with moderate no. of eosinophil & few plasma cells & lymphocytes Bronchial lavage : Eosinophils – 35% Negative for malignant cells. Negative for fungal element and gram staining and AFB • Endobronchial biopsy: Marked eosinophilic infiltration in bronchial mucosa. •Skin biopsy: Drug related dermatitis. Methylprednisolone 40 mg iv q8h • Improved • Extubated - 5 days Results of pending investigations • Serum Aspergillus antibodies: Negative for all variants. • Serum anti-mycoplasma IgM: Negative • ANA, Anti DNA – Negative • ANCA – Negative Etiology • Acute hypersensitivity reaction to inhaled antigen in a previously healthy Individual • Enviromental factors • Cigarette smoking • World trade centre • Military personnel in Iraq • HIV Clinical presentation • • • • • Cough Dyspnea Pleuritic chest pain Myalgia Night sweats Physical exam • • • • • Fever Tachypnea Tachycardia Bibasilar crackers rhonchi Complication • Hypoxemic respiratory failure • 14 of 22 patients(63%) required MV • Hyper dynamic Shock Lab • • • • Neutrophilia Eosinophilia IgE ESR CXR • • • • • Reticular infiltrate Kerly B line Bil.diffuse alveolar &reticular opacities Isolated reticular or alveolar Small bil effusion)Eosinophilic) HRCT • Bil.patchy ground glass or reticular opacities • Effusion BAL • • • • • Eosinophilia >25%(mean 37%) IL-5 GM-CSF IL-1ra VEGF Pathology • Acute &organising diffuse alveolar damage • Interstitial&alveolar &bronchiolar infiltration of eosinophil • Hyaline membranes and interstitial widening • Organising intra alveolar fibrinous exudate Treatment • • • • • Spontaneous improvement rare Resp. failure (50-60%) Steroids Clinical response 12-48 hrs Continue steroids for 2-4 wks after plain Xray normalises (2-6wks) ACR – Classification Critera: Asthma Eosinophilia of > 10% Mono or poly-neuropathy Migratory or transient pulmonary opacities Para-nasal sinus abnormalities Biopsy containing blood vessel –extra vascular eosinophils