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. ,

• 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 

Small Airways Infiltration with Eosinophils and Inflammatory Exudate – Centrilobular Nodules

Interlobular Septal Infiltration with Eosinophils and Inflammatory Exudate – Thickening of the Interlobular Septa – Crazy Paving Kerley B lines

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

 

Advancing Acute Eosinophilic Pneumonia which may go onto Diffuse Alveolar Damage and ARDS

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

 

• 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