Idiopathic Eosinophilic Pneumonia Dr. Hadil Alotair KKUH.

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Idiopathic Eosinophilic Idiopathic Eosinophilic Pneumonia Pneumonia Dr. Hadil Alotair Dr. Hadil Alotair KKUH KKUH

Transcript of Idiopathic Eosinophilic Pneumonia Dr. Hadil Alotair KKUH.

Idiopathic Eosinophilic PneumoniaIdiopathic Eosinophilic Pneumonia

Dr. Hadil Alotair Dr. Hadil Alotair

KKUHKKUH

HistoryHistory

A 18 Y/O saudi lady living in Riyadh. she is a student

–C/O •Fever 8 days•productive cough 8 days•Chest pain 2 days•Dizziness+syncope 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 HxDrug Hx

•Budesonide•Flexinase•Ventolin•Singulare

ExaminationExamination • 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 –Coarse crepitations –Pleural rub

•Other systemic examination- NAD

Rt. InfrascapularRt. Infrascapular

InvestigationsInvestigations • 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 7.43–PC02 36–Po2 51.9–HC03 23.2– 02 saturation 87.9 on RA

Hospital courseHospital 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

MICUMICU• 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 resultsInvestigation 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 Results of pending investigationsinvestigations

• Serum Aspergillus antibodies: Negative for all variants.

• Serum anti-mycoplasma IgM: Negative

• ANA, Anti DNA – Negative• ANCA – Negative

EtiologyEtiology

• Acute hypersensitivity reaction to inhaled antigen in a previously healthy Individual

• Enviromental factors

• Cigarette smoking

• World trade centre

• Military personnel in Iraq

• HIV

Clinical presentationClinical presentation

• Cough

• Dyspnea

• Pleuritic chest pain

• Myalgia

• Night sweats

Physical examPhysical exam

• Fever

• Tachypnea

• Tachycardia

• Bibasilar crackers

• rhonchi

ComplicationComplication

• Hypoxemic respiratory failure

• 14 of 22 patients(63%) required MV

• Hyper dynamic Shock

LabLab

• Neutrophilia

• Eosinophilia

• IgE

• ESR

CXRCXR

• Reticular infiltrate

• Kerly B line

• Bil.diffuse alveolar &reticular opacities

• Isolated reticular or alveolar

• Small bil effusion)Eosinophilic)

HRCTHRCT

• Bil.patchy ground glass or reticular opacities

• Effusion

BALBAL

• Eosinophilia >25%(mean 37%)

• IL-5

• GM-CSF

• IL-1ra

• VEGF

PathologyPathology

• Acute &organising diffuse alveolar damage

• Interstitial&alveolar &bronchiolar infiltration of eosinophil

• Hyaline membranes and interstitial widening

• Organising intra alveolar fibrinous exudate

TreatmentTreatment

• Spontaneous improvement rare

• Resp. failure (50-60%)

• Steroids

• Clinical response 12-48 hrs

• Continue steroids for 2-4 wks after plain X-ray normalises (2-6wks)

ACR – Classification CriteraACR – 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