Pulmonary eosinophilia.pptx

Pulmonary Eosinophilia
D R . M D . S H A F I Q U L I S L A M D E W A N
R E S I D E N T ( P U L M O N O L O G Y )
D E P A R T M E N T O F R E S P I R A T O R Y M E D I C I N E
D H A K A M E D I C A L C O L L E G E H O S P I T A L
April 11, 2023 DR. MD. SHAFIQUL ISLAM DEWAN; RESIDENT (PULMONOLOGY)

Synonymous sentence
Pulmonary Eosinophilia
Eosinophilic pneumonia
Eosinophilic lung diseases

Causes of pulmonary eosinophilia
Idiopathic acute eosinophilic pneumonia
Idiopathic chronic eosinophilic pneumonia
Eosinophilic granulomatosis with
polyangiitis (Churg-Strauss)
Others
 Idiopathic hypereosinophilic syndrome
 Idiopathic interstitial lung diseases
 Neoplasms
 Non-helminthic infections
(eg,Coccidioidomycosis, Mycobacterium
tuberculosis)
Drug- and toxin-induced eosinophilic lung
diseases
 Nonsteroidal antii-nflammatory drugs
(NSAIDs)
 Antimicrobials (nitrofurantoin, minocycline,
sulfonamides, ampicillin, daptomycin)
 Phenytoin
 L-tryptophan

Causes of pulmonary eosinophilia
Helminthic and fungal infection-related
eosinophilic lung diseases
Transpulmonary passage of larvae (Loffler's
syndrome)
◦ Ascaris lumbricoides
◦ Hookworm (Ancylostoma duodenale, Necator
americanus)
◦ Strongyloides stercoralis
Pulmonary parenchymal invasion - mostly
helminths, eg, paragonimiasis
Heavy hematogenous seeding with
helminths
◦ Trichinellosis
◦ Disseminated strongyloidiasis
◦ Cutaneous and visceral larva migrans
◦ Schistosomiasis
Tropical pulmonary eosinophilia
◦ Wuchereria bancrofti
◦ Brugia malayi
Allergic bronchopulmonary aspergillosis

Eosinophilic pneumonia
Eosinophilic pneumonia is a pneumonia in which, on
histopathologic examination, eosinophils are the most prominent
inflammatory cells.
Other inflammatory cells, especially lymphocytes and neutrophils,
are often associated, but eosinophils clearly predominate.

Defining Characteristics
The defining characteristics of pulmonary eosinophilia include the
following_
Peripheral blood eosinophilia (absolute eosinophil count ≥500
eosinophils/microL) with abnormalities on pulmonary imaging
studies
Increased eosinophils in bronchoalveolar lavage (BAL) fluid (eg,
>10 percent)
Lung tissue eosinophilia demonstrated in transbronchial or open
lung biopsies.

Eosinophilia & Hypereosinophila
Blood eosinophilia is defined by an eosinophil blood count greater
than 0.5 × 109/L (500/μl).
Hypereosinophila is defined by an eosinophil blood count greater
than 1.5 × 109/L (1500/μl) on two examinations at least 1 month
apart, and/or tissue hypereosinophilia.

BAL
In normal subjects, BAL eosinophils comprise less than 1% of cells.
In contrast, BAL eosinophilia greater than 40% is found mainly in patients with chronic
eosinophilic pneumonia,
whereas BAL eosinophilia from 3–25% (and especially from 3–9%) may be found in
various conditions, such as idiopathic pulmonary fibrosis, interstitial lung disease
associated with connective tissue disorders, hypersensitivity pneumonitis,
sarcoidosis, radiation pneumonitis, asthma, pneumoconiosis, and infection.

BAL
A conservative cutoff of 40% of eosinophils in the BAL has been adopted
for the diagnosis of ICEP in clinical studies, and a cutoff of 25% has been
proposed for the diagnosis of IAEP.
For clinical practice, a diagnosis of eosinophilic pneumonia is supported
by alveolar eosinophilia when the eosinophils (1) are the predominant cell
population (macrophages excepted) and (2) represent more than 25% of
the differential cell count in the BAL.

BAL
Although BAL is usually useful and safe in patients with suspected
eosinophilic pneumonia, it may not always be mandatory in typical
cases with both pulmonary opacities on imaging and markedly
elevated peripheral blood eosinophilia (>1 × 109/L and preferably 1.5
× 109/L [1500/μL]).

Interstitial lung disease associated with BAL eosinophilia

When we suspect Pulmonary Eosinophilia?
Diagnosis of eosinophilic pneumonia is suspected in patients
presenting with_
Respiratory symptoms (dyspnea, cough, or wheezing),
Pulmonary opacities on chest imaging, and
Demonstration of eosinophilia in the peripheral blood or,
preferably, in the lung.

History and physical examination
Medication and chemical exposures, including aspirin, nonsteroidal anti-
inflammatory drugs (NSAIDs), anticonvulsants, and antibiotics, as well as
exposures to dust, smoke (eg, firefighting, tobacco smoke, vaping), or chemicals.
Travel and immigration histories, including residence in or travel to regions
endemic for Coccidioides and varied parasites.
History of ingestion of poorly cooked pork, wild boar, or other wild animal
meats associated with complaints of muscle pain, tenderness, swelling, and
weakness.

Respiratory history and findings, including antecedent or concomitant asthma,
as found inallergic bronchopulmonary aspergillosis/mycosis (ABPA/ABPM),
eosinophilic granulomatosis with polyangiitis (EGPA, Churg-Strauss), and
sometimes chronic eosinophilic pneumonia (CEP) or helminthic etiologies.
Duration of any antecedent symptoms should be considered. Acute
eosinophilic pneumonia (AEP) is characteristically abrupt in onset, whereas CEP
develops insidiously over months.
 Asthma in EGPA may begin years before the development of vasculitic lung
involvement.

Presence of symptoms or signs of extrapulmonary organ involvement, since
these may be indicative of systemic diseases, including EGPA, hyper-eosinophilic
syndromes, and neoplasms.
Physical examination is looking for cutaneous lesions that might indicate a
certain diagnosis or provide an opportunity for a less invasive biopsy site.
Stigmata of rheumatic diseases (eg, muscle weakness, joint swelling, or
erythema) should be sought.
Lung examination is nonspecific, although wheezes would be more consistent
with EGPA, CEP,or ABPA, while crackles would be more likely with drug-induced
pulmonary eosinophilia, AEP, or less commonly CEP.

Transbronchial biopsy
In general, transbronchial biopsy is less likely to secure a confident diagnosis
than surgical lung biopsy. However, when EGPA (Churg-Strauss) is suspected, a
definitive diagnosis can sometimes be made on a transbronchial biopsy, thus
avoiding a more invasive lung biopsy procedure.

Lung biopsy
For causes of pulmonary eosinophilia other than infection, medication, or toxin, it is important to
establish and document the nature of the disease.
While EGPA, AEP, CEP, and often HES will respond to glucocorticoid therapy, establishing a firm
pathologic diagnosis upfront is prudent given the side effects of long-term glucocorticoid treatment
and the options for second-line therapy in glucocorticoid-refractory disease.
Moreover, since EGPA has the potential to involve and damage other organs, documenting this
vasculitis has important implications for the future management of the patient.
As with the general evaluation of interstitial lung disease a surgical approach is typically preferred
over a transbronchial biopsy due to the small size of transbronchial specimens. Video-assisted
thoracoscopic surgery (VATS) can substitute for a thoracotomy to provide tissue.

The three diseases that could be diagnosed with greatest
certainty by HRCT were CEP, ABPA, and AEP.

CT findings of CEP
Characteristic CT findings of CEP include: bilateral consolidative
opacities and areas of ground-glass attenuation, involving
predominantly the peripheral regions of the middle or upper lung
zones.

CT findings in AEP
CT findings in AEP include: ground-glass attenuation,
consolidation, poorly defined nodules, interlobular septal thickening,
and pleural effusions.
The triad of interlobular septal thickening, bronchovascular
bundle thickening, and pleural effusions are most suggestive of this
diagnosis

CT findings of ABPA
Common CT findings of ABPA consist of bronchiectasis, mucous
plugging, bronchial wall thickening, atelectasis, consolidation, areas
of ground-glass attenuation, and upper and central lung
predominance.
 The first three of these findings are the most indicative of ABPA.

Thank You

Pulmonary eosinophilia.pptx

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Pulmonary eosinophilia.pptx