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