Infiltration of eosinophils in the alveolar spaces, bronchial walls, and, to a lesser extent, in the interstitium. Acute and/or organizing diffuse alveolar damage is present. ,
Most Common Appearance of Acute Eosinophillic Pneumonia Acute Eosinophilic pneumonia is characterised by ground glass opacities (100%) and sometimes consolidation (55%) most commonly with a random distribution 60%. Septal lines (90%) and thickening of the bronchovascular bundles (66%) and bilateral pleural effusions (75%) were common. Ashley Davidoff MD TheCommonvein.net lungs-0775-b (Reference De Giacomi F et al )
Most Common Appearance of Acute Eosinophillic Pneumonia Acute Eosinophilic pneumonia is characterised by ground glass opacities (100%) and sometimes consolidation (55%) most commonly with a random distribution 60%. Septal lines (90%) and thickening of the bronchovascular bundles (66%) and bilateral pleural effusions (75%) were common. Ashley Davidoff MD TheCommonvein.net lungs-0775-bL (Reference De Giacomi F et al )
Eosinophil By Blausen Medical – BruceBlaus
Histopathology of acute eosinophilic pneumonia. Lung biopsy (generally not needed for diagnosis) demonstrating the presence of numerous eosinophils in the alveolar spaces and interstitial septa, in a background of diffuse alveolar damage characterized by confluent intraalveolar fibrinous exudates with hyaline membrane formation (hematoxylin and eosin staining). Scale bar, 50 ?m. From De Giacomi F et al Acute Eosinophilic Pneumonia. Causes, Diagnosis, and Management American Journal of Respiratory and Critical Care Medicine Volume 197, Issue 6
BAL fluid eosinophilia. Markedly increased eosinophils are present in the BAL fluid comprising approximately 25% of the infiltrates (Diff-Quik staining). Some of the eosinophils are indicated with white arrows. Scale bar, 20 ?m. From De Giacomi F et al Acute Eosinophilic Pneumonia. Causes, Diagnosis, and Management American Journal of Respiratory and Critical Care Medicine Volume 197, Issue 6
rare disease inflammatory disease of the small airways and alveoli
characterized by eosinophilic infiltration of the pulmonary parenchyma (alveoli and interstitium)
eosinophil leukocytes
multifunctional cells for
innate and adaptive immunity, including
inflammatory reactions to
parasitic helminth, bacterial, and viral infections
Acute Eosinophillic Pneumonia with Involvement of Small Airways, Alveoli and Interlobular Septa
A collage shows the normal small airway(a) alveoli (b) and secondary lobule (c) and the changes in the airways in acute eosinophillic pneumonia. There is filling of the the small airways (d) alveoli (e) with eosinophils and proteinaceous and fibrinous exudate and also in the interalveolar septa (e) with thickening of the interlobular septa (f) The CT findings include consolidation at the lung bases (g)with thickening of the interlobular septa, centrilobular nodules, and ground glass opacity (g) Ashley Davidoff TheCommonVein.net lungs-0757b
Small Airways Infiltration with Eosinophils and Inflammatory Exudate – Centrilobular Nodules
Small Airways Infiltration with Eosinophils and Inflammatory Exudate – Centrilobular Nodules The diagram shows the small airways of the lung including the respiratory bronchiole, alveolar ducts and alveolar sacs in coronal (a) and in cross section (b) and correlated with an anatomic specimen of a secondary lobule that contains a thickened interlobular septum . The respiratory bronchiole is overlaid in maroon (d), next to the arteriole. Images e and f are magnified views of a CT of the lungs in a patient with acute eosinophillic pneumonia and the centrilobular nodules reflecting small airway disease are highlighted in f. Ashley Davidoff MD The CommonVein.net lungs-0760b
Interlobular Septal Infiltration with Eosinophils and Inflammatory Exudate – Thickening of the Interlobular Septa – Crazy Paving Kerley B lines
Interlobular Septal Infiltration with Eosinophils and Inflammatory Exudate – Thickening of the Interlobular Septa – Crazy Paving Kerley B lines The diagram shows the thickened septum surrounding the secondary lobule due to an inflammatory process, cellular infiltrate and congestion of the venules and lymphatics in the septum (a) . An anatomic specimen of a secondary lobule from a patient with thickened interlobular septa is shown in c and overlaid in d. CT of the lungs in a patient with acute eosinophillic pneumonia shows thickened interlobular septa and centrilobular nodules and the thickened septa are overlaid in red (e). Ashley Davidoff MD The CommonVein.net lungs-0761
Alveolar and Interalveolar Interstitial Infiltration with Eosinophils and Inflammatory Exudate – Ground Glass Changes
The ground glass changes are a combination of the cellular and exudative inflammatory response in the small airways, alveoli, interalveolar septa and interstitium, and thickened alveolar septum
Alveolar and Interalveolar Interstitial Infiltration with Eosinophils and Inflammatory Exudate – Ground Glass Changes The ground glass changes are a combination of the cellular and exudative inflammatory response in the small airways, alveoli, interalveolar septa and interstitium, and thickened alveolar septum The diagram shows the abnormal secondary lobule (a) The involved components include the small airways(b) alveoli and interalveolar interstitium (c) and the thickened interlobular septum (d) surrounding the secondary lobule due to an inflammatory process, cellular infiltrate and congestion of the venules and lymphatics in the septum. An anatomic specimen of a secondary lobule from a patient with thickened interlobular septa and interstitial thickening is shown in image e, and is overlaid in red (f) . A magnified view of an axial CT of the lungs in a patient with acute eosinophillic pneumonia shows thickened interlobular septa and centrilobular nodules (g) The inflammatory changes in the aforementioned structures result in an overall increase in density of the lung manifesting as ground glass changes (g) and overlaid in red (h) Ashley Davidoff MD The CommonVein.net lungs-0762
Infiltration of eosinophils and exudation into the alveoli and interalveolar septa and interstitium Ashley Davidoff TheCommonVein.net lungs-0756b01
The Secondary Lobule in Acute Eosinophilic Pneumonia (AEP) This diagram reveals the important structural changes in the secondary lobule that includes filling of the alveoli with eosinophils and proteinaceous and fibrinous exudate as well as infiltration into the alveolar septa and interstitium (red walls of alveoli) . An important component of the disease is the thickening of the interlobular septa (maroon) which results in Kerley B lines and an interstitial pattern on the CXR and CT that is reminiscent of cardiogenic interstitial edema. Ashley Davidoff TheCommonVein.net lungs-0758
Chest CT demonstrated diffuse ground glass opacities, reticular shadows, and alveolar septal thickening.Matsuno O et al Respiratory Medicine Volume 101, Issue 7, July 2007, Pages 1609-1612
Advancing Acute Eosinophilic Pneumonia which may go onto Diffuse Alveolar Damage and ARDS
Advancing Acute Eosinophilic Pneumonia As the disease advances the small airways, and alveoli, get progressively filled with eosinophils, inflammatory cells and fluids resulting in consolidation. This image reveals progressive filling of the small airways, (a) alveoli, (b) and secondary lobules (c) with eosinophils and products of inflammation resulting in multi-segmental consolidations (d), in the lung bases, with air bronchograms at the right base (e), and less dense consolidation at the left base (f) Ashley Davidoff MD The CommonVein.net lungs-0763
The ground glass changes are a combination of the cellular and exudative inflammatory response in the small airways, alveoli, interalveolar septa and interstitium, and thickened alveolar septum
The diagram shows the abnormal secondary lobule (a) The involved components include the small airways(b) alveoli and interalveolar interstitium (c) and the thickened interlobular septum (d) surrounding the secondary lobule due to an inflammatory process, cellular infiltrate and congestion of the venules and lymphatics in the septum. An anatomic specimen of a secondary lobule from a patient with thickened interlobular septa and interstitial thickening is shown in image e, and is overlaid in red (f) . A magnified view of an axial CT of the lungs in a patient with acute eosinophillic pneumonia shows thickened interlobular septa and centrilobular nodules (g) The inflammatory changes in the aforementioned structures result in an overall increase in density of the lung manifesting as ground glass changes (g) and overlaid in red (h)
Ashley Davidoff MD The CommonVein.net lungs-0762
36 year old Patient in Second Phase of Disease showing Multicentric Infiltrates
36 year old female presents with dyspnea CXR shows bibasilar patchy infitrates She was treated with antibiotics Ashley Davidoff MD TheCommonVein.net dx acute eosinophillic pneumonia
Following treatment with antibiotics for 1 week the CXR shows progression of the left upper lobe infiltrate Ashley Davidoff MD TheCommonVein.net dx acute eosinophillic pneumonia
CT scan a few days later shows progressive pneumonic changes Ashley Davidoff MD TheCommonVein.net dx eosinophillic pneumonia
36f-esosinophilli-pneumonia-3-08-12b.jpg
CT scan a few days later shows progressive pneumonic changes
Ashley Davidoff MD
TheCommonVein.net
dx eosinophillic pneumonia
CXR 1 month later shows resolution of previously identified infiltrates Ashley Davidoff MD TheCommonVein.net dx eosinophillic pneumonia
Cause
unknown
?acute hypersensitivity reaction to an unidentified inhaled antigen in an otherwise healthy individual
Of all inhalational causes of AEP, tobacco smoking has been the most frequently implicated trigger
smoke
cigarettes
marijuana
electronic cigarettes
water pipe cigarettes
cocaine and other drugs
immune therapy
result
degranulation of activated eosinophils
granules release
cationic proteins into the
extracellular space,
direct toxicity to the
heart,
brain, and
bronchial epithelium
Also release
proinflammatory cytokines
Structural
extensive disease
eosinophils
marked numbers of interstitial eosinophils
lesser numbers of alveolar eosinophils
intraalveolar fibrinous exudate (100 percent of cases),
perivascular and intramural inflammation without necrosis
DAD
hyaline membranes
edema
fibrosis
Clinical
acute/subacute illness of
less than four weeks duration
cough
dyspnea
fever (often high)
may require ventilation
Lab
leukocytosis
eosinophils not initially but
becomes markedly elevated subsequently
may be absent or delayed, especially in smoking-related AEP.
IgE elevated
Some ANCA positive
some positive sputum eosinophilia
At the onset
Radiology
diffuse disease
unlike chronic eosinophilic pneumonia, in which the opacities are typically localized to the lung periphery.
CXR
early chest radiograph
AEP mimics
hydrostatic pulmonary edema,
subtle reticular or ground glass opacities,
Kerley B lines
evolving
ground glass
bilateral diffuse diffuse parenchymal opacities
CT
bilateral, random, and patchy ground-glass or reticular opacities
show random cephalocaudal distribution
centrilobular nodules and air-space consolidation are seen in approximately 50 and 40 percent, respectively
bilateral ground-glass areas: common
interlobular septal thickening : common
pleural effusions: can be present in ~80% (range 60-100%) of cases
thickening of bronchovascular bundles: present in around two-thirds of cases
air-space consolidation: present in around half of the cases
ill-defined centrilobular nodules : present in around one-third of cases
Bronchoscopy BAL
Crucial for the diagnosis
pulmonary eosinophilia in the BAL fluid
Links and References
Cottin V et al Eosinophilic Pneumonia Orphan Lung Diseases. 2014 Dec 11 : 227?251.
Daimon T et al Acute eosinophilic pneumonia: Thin-section CT findings in 29 patients Volume 65, Issue 3 , March 2008, Pages 462-467
De Giacomi F et al Acute Eosinophilic Pneumonia. Causes, Diagnosis, and Management American Journal of Respiratory and Critical Care Medicine Volume 197, Issue 6
Johkoh T , Müller NL , Akira M , Ichikado K , Suga M , Ando M , et al . Eosinophilic lung diseases: diagnostic accuracy of thin-section CT in 111 patients . Radiology 2000 ;216:773 ?780
TCV