acute eosinophilic pneumonia

Eosinophilic PneumoniaAbdalmohsen AbabtainSenior Resident

Saudi Board for Emergency Medicine

March 31st 2013

Supervised by :Dr Ghassan Alghamdi

Case19 Years old Presented to ER with

SOB and Sore throat and fever for 2 Days after coming Back from Makkah

Has a Hx of atopy (SOB from Dust) with positive Family history too

He Started to smoke cigarettes a week ago (a cigarette/day)

ExamT 36.8 P:122 BP 120/65

RR 30SpO2 79% RA Patient looks in Respiratory

DistressIn Tripod PositionEqual Bilatral AirentryNo Wheeze, No Stridor nor

drooling

LabsWBC 25.6 (mostly Nuetrophilic)

Lactate 12.3Urine Tox NegativeBG :PH 7.27 Co2 30 Po2 85 Hco3

14

In ERAsthma Management Started In

ERPatient continue to Deteriorate Tubed ! HIGH Peak and Airway Pressure !

In ICUH1N1 & Influenza & Parainfluenza

and AFB NegativeLactate started to NormalizedBAL Done and Showed Eos

14%

Acute Eosinophilic Pneumonia !!!

What’s the Fastest Legal Street Car on Earth ?

Bugatti Veyron Super Sport

Max Speed 430km/hr

0-100 km in 2.4 Seconds !!

1200 hp !!

Base Price $2,400,000

Eosinophilic Lung DiseasesGroup of Disorders with high

eosinophils in Lung Parenchyma The Defining Characteristics

include either:1. Peripheral Blood Eosinophilia

with Radiological Pulmonary Abnormality

2. Lung tissue eosinophilia in Biopsy

3. High eosinophils in BAL

Eosinophilic Lung DiseasesAcute Eosinophilic Pneumonia (AEP)Chronic Eosinophilic Pneumonia (CEP)Helminthic Infections (Löffler's syndrome)Non-Helminthic Infection (Coccidioidal

infection)Medications (NSAID)ToxinsChurg-Strauss SyndromeAllergic Bronchopulmonary Aspergellousis

(ABPA)

ToxinsScorpion stingsInhalation of heroin or crack

cocaineInhalation of organic chemicals

during rubber manufactureInhalation of dust or smokeAbuse of 1,1,1-trichloroethane

(Scotchguard)

Acute eosinophilic pneumoniaAcute febrile illness with

Severe hypoxaemia,Diffuse pulmonary infiltratesIncrease in bronchoalveolar

lavage (BAL) eosinophilsNo evidence of infection or

Drug ingesion

Less than 100 cases of AEP have been reported to date

The largest series including only 33 patients

An epidemiologic study of this disease identified 18 patients with AEP among183,000 US military personnel deployed in Iraq, all of them were smokers, with 78% of them recently beginning to smoke

Chest 2008; 133: 1174–1180JAMA 2004; 292:2997–3005

Inhalational exposures associated with AEPSmoke (Most common specially

first time)Passive smoking* !!World Trade Center demolition dustFireworkTear gas bomb explosionGasoline tank cleaningCave explorationWoodpile moving

Chest 2000;117:277–279*Allergology International. 2010;59:421-423

Approach

History :Chief complain and Associated

symptomsMedicationChemical and occupational Exposure

(NSAID, Dust, Smoke)Travel Hx (Fungal inf.)Respiratory Hx (Asthma)Extrapulmonary Involvment

Physical ExamFeverTachypneaBibasilar inspiratory crackles or

could be clear in 20% of PatientsHypoxemic respiratory

insufficiency is frequently identified at presentation and often requires mechanical ventilation

Semin Respir Crit Care Med. 2006 Apr;27(2):142-7.

LabsPatients generally present with an initial

neutrophilic leukocytosisBlood eosinophilia, However, the absence

of it does not exclude these conditions.Any concomitant glucocorticoid therapy

will suppress blood eosinophiliaThe magnitude of blood eosinophilia

is not a reliable means to distinguish the possible etiologies of pulmonary eosinophilia.

High ESR !

ImagingAt the Start, Subtle reticular or

ground glass opacities, often with Kerley B lines

Small pleural effusions are common

ImagingHigh resolution CT ground-glass

attenuation, airspace consolidation, poorly defined nodules.

The triad of • Interlobular septal thickening, • Bronchovascular bundle

thickening, and • Pleural effusions

are most suggestive AEP

Eur Respir J 2013; 41: 402–409

BAL

BiopsyIf BAL is not RevealingBiopsy, via a transbronchial or

open lung biopsy or VATS approach depending upon the clinical and radiographic findings

CulturesIf there have been appropriate

geographic exposures for coccidioidomycosis or clinical and radiographic findings suggestive of ABPA, fungal cultures should be obtained

AEP is a diagnosis of exclusion and Requires :An acute febrile illness of short duration

(usually less than one week)Hypoxemic respiratory failureDiffuse pulmonary opacities on chest

radiographBAL eosinophilia >25 percentLung biopsy evidence of eosinophilic

infiltrates (acute and/or organizing diffuse alveolar damage with prominent eosinophilia is the most characteristic finding)

Absence of known causes of eosinophilic pneumonia, including drugs, infections.

Treatment1. Glucocorticoid administration (preferably

after blood extraction) is medically indicated if:

Hypoxemia and in respiratory distress If the etiology is either AEP or a medication

or toxin-elicited AEPRegimens : In the absence of respiratory failure, initial

treatment is with oral prednisone (40 to 60 mg daily).

In the presence of respiratory failure, methylprednisolone (60 to 125 mg every 6 hours)

Optimal Duration is not yet clear (2-4 wks no diff)*

*Eur Respir J 2013; 41: 402–409

After Improvment

Continue oral prednisone in a dose of 40-60 mg per day for 2-4 weeks

2. Supportive Therapy3. Smoking Cessation

Recurrence Relapse is uncommon and is

usually associated with resumption of cigarette smoking after initial cessation

RefrencesUp to dateEur Respir J 2013; 41: 402–409Chest 2008; 133: 1174–1180JAMA 2004; 292:2997–3005Chest 2000;117:277–279Semin Respir Crit Care Med. 2006

Apr;27(2):142-7.

Thank You