PMC10333516_01
Ventrodorsal (A) and lateral (B) radiographic projections of an 11-week old, sexually intact, female Catahoula Leopard dog with congenital lobar emphysema. Noted in image (A), is a left mediastinal shift, and images (A, B) depict a hyperlucent right lung lobe and displacement of the cardiac silhouette.
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F1
At 8 weeks of age, the primary veterinarian performed thoracic radiographs to investigate for causes of exercise intolerance and respiratory distress (Figures 1A, B).
PMC10333516_02
Thoracic CT dorsal reconstruction images from an 11-week old, sexually intact, female Catahoula Leopard dog with congenital lobar emphysema. Note the hyperinflated right middle lung lobe (RM) with an abrupt narrowing of the main stem bronchus (asterisk); leftward deviation of the heart, mediastinal structures, and accessory lung lobe (Ac); and diffuse increased attenuation/ground glass pattern within remaining right cranial (RCr) and right caudal (RCd) lung lobes as well as left lung.
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F2
Distension of the right middle lung lobe resulted in a marked leftward displacement of the heart and other mediastinal structures as well as the right cranial, right caudal and accessory lung lobes (Figure 2).
PMC10333516_03
PMC10333516_04
(A-D) Intraoperative images from an 11-week old, sexually intact, female Catahoula Leopard dog with CLE. The head is to the right and dorsal is on the bottom of all images. The right middle lung lobe (asterisk in all images) is occupying a majority of the right thoracic cavity (A) and is hyperinflated (A, B). A lung lobectomy was performed with a DST Series TA Stapler using a 30 mm V3 vascular stapler (C). The right middle lung hilus can be seen with the staple line (white arrow) following lobectomy, and the right caudal lung lobe has an area of atelectasis (+) (D).
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F3
The markedly inflated right middle lung lobe was manipulated to access the hilus, resulting in a majority of the lobe being externalized from the thoracic cavity (Figure 3).
Gross (A) and histopathologic (B) images of the right middle lung lobe affected by CLE are depicted. Ruptured alveoli are present in the lung lobe: grossly this is visible as air pockets within the lung tissue (surrounding the arrow, A) and microscopically as discontinuity of the alveolus wall (arrow within alveolus, B). In image (B), bronchial cartilage is present as a small discontinuous basophilic band (arrow head), which should fully surround a normal bronchus. This represents bronchial cartilage hypoplasia and is the cause of the bronchus in image (B) (star) being partially collapsed instead of rounded.
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F4
Histopathology was performed including hematoxylin and eosin (H&E) stain, Masson's trichrome stain to identify collagen, and immunohistochemistry antibodies for AE1/AE3 cytokeratin to identify epithelial cells and alpha-smooth muscle actin (alpha-SMA) to evaluate bronchial smooth muscle of the resected right middle lung lobe (Figures 4-7). Results revealed bronchial cartilage hypoplasia characterized by variable quality cartilage to the absence of cartilage, dilated and coalescing alveoli consistent with marked emphysema, abnormal bronchial smooth muscle architecture, and expanded connective tissues and collagen with pleural fibrosis (Figures 4-7).
Masson's trichrome staining of the right middle lung lobe highlights the abundant collagen/connective tissues (arrow) surrounding the bronchus B with no cartilage present. A, alveolus.
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F5
Histopathology was performed including hematoxylin and eosin (H&E) stain, Masson's trichrome stain to identify collagen, and immunohistochemistry antibodies for AE1/AE3 cytokeratin to identify epithelial cells and alpha-smooth muscle actin (alpha-SMA) to evaluate bronchial smooth muscle of the resected right middle lung lobe (Figures 4-7). Results revealed bronchial cartilage hypoplasia characterized by variable quality cartilage to the absence of cartilage, dilated and coalescing alveoli consistent with marked emphysema, abnormal bronchial smooth muscle architecture, and expanded connective tissues and collagen with pleural fibrosis (Figures 4-7).
Immunohistochemistry AE1/AE3 cytokeratin of the right middle lung lobe highlights the bronchial epithelium with multilayered columnar to cuboidal epithelium and invaginations (arrowheads). The bronchus is identified as B. The alveoli are identified as A and contain ruptured septa with clubbed ends (double arrow).
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F6
Histopathology was performed including hematoxylin and eosin (H&E) stain, Masson's trichrome stain to identify collagen, and immunohistochemistry antibodies for AE1/AE3 cytokeratin to identify epithelial cells and alpha-smooth muscle actin (alpha-SMA) to evaluate bronchial smooth muscle of the resected right middle lung lobe (Figures 4-7). Results revealed bronchial cartilage hypoplasia characterized by variable quality cartilage to the absence of cartilage, dilated and coalescing alveoli consistent with marked emphysema, abnormal bronchial smooth muscle architecture, and expanded connective tissues and collagen with pleural fibrosis (Figures 4-7).
Immunohistochemistry alpha-SMA for smooth muscle of the right middle lung lobe highlights the abnormal bronchial smooth muscle architecture as the discontinuous smooth muscle bundles (asterisks) surrounding the bronchus B. A, alveoli.
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F7
Histopathology was performed including hematoxylin and eosin (H&E) stain, Masson's trichrome stain to identify collagen, and immunohistochemistry antibodies for AE1/AE3 cytokeratin to identify epithelial cells and alpha-smooth muscle actin (alpha-SMA) to evaluate bronchial smooth muscle of the resected right middle lung lobe (Figures 4-7). Results revealed bronchial cartilage hypoplasia characterized by variable quality cartilage to the absence of cartilage, dilated and coalescing alveoli consistent with marked emphysema, abnormal bronchial smooth muscle architecture, and expanded connective tissues and collagen with pleural fibrosis (Figures 4-7).