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Lymphangiographic evaluation of experimentally induced chylothorax after ligation of the cranial vena cava in dogs.

Fossum Tw, Birchard Sj

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Abstract

Ligation of the cranial vena cava (CrVC) distal to the entrance of the azygous vein resulted in chylothorax in 7 of 10 dogs. Of the remaining 3 dogs, 1 developed a serosanguineous effusion that did not become chylous, and 2 dogs did not develop pleural effusion. In 2 of the 7 dogs developing chylothorax, the pleural effusion became serosanguineous within 2.5 weeks after CrVC ligation. Mesenteric lymphangiography was performed 2 to 6 weeks after ligation of the CrVC. Lymphangiectasia was seen in 4 dogs with chylothorax, but was not seen in the 3 dogs with serosanguineous effusions or the 2 dogs that did not develop effusions. One dog with chylothorax died prior to repeat lymphangiography. Less dye entered the thoracic duct, and alternate lymphaticovenous communications to the caudal vena cava were evident in the dogs without chylothorax. Ligation of the thoracic duct at the lymphaticovenous junction was performed in 3 dogs. These dogs did not develop pleural effusion. Lymphangiography was performed immediately after ligation and indicated filling of abdominal lymphatics but not of the thoracic duct. Lymphangiographic findings 6 weeks after ligation also indicated filling of intestinal lymphatics. Results of the present study indicated that ligation of the CrVC causes chylothorax, and that thoracic lymphangiectasia is a consistent finding in animals with experimental chylothorax. Obstruction of the thoracic duct did not induce lymphangiectasia or chylothorax. Impedence of thoracic duct flow into the CrVC may be a cause of clinical chylothorax in the dog.

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What this paper is about

Ligation of the cranial vena cava (CrVC) distal to the entrance of the azygous vein resulted in chylothorax in 7 of 10 dogs. Of the remaining 3 dogs, 1 developed a serosanguineous effusion that did not become chylous, and 2 dogs did not develop pleural effusion. In 2 of the 7 dogs developing chylothorax, the pleural effusion became serosanguineous within 2.5 weeks after CrVC ligation. Mesenteric lymphangiography was performed 2 to 6 weeks after ligation of the CrVC. Lymphangiectasia was seen in 4 dogs with chylothorax, but was not seen in the 3 dogs with serosanguineous effusions or the 2 dogs that did not develop effusions. One dog with chylothorax died prior to repeat lymphangiography. Less dye entered the thoracic duct, and alternate lymphaticovenous communications to the caudal vena cava were evident in the dogs without chylothorax. Ligation of the thoracic duct at the lymphaticovenous junction was performed in 3 dogs. These dogs did not develop pleural effusion. Lymphangiography was performed immediately after ligation and indicated filling of abdominal lymphatics but not of the thoracic duct. Lymphangiographic findings 6 weeks after ligation also indicated filling of intestinal lymphatics. Results of the present study indicated that ligation of the CrVC causes chylothorax, and that thoracic lymphangiectasia is a consistent finding in animals with experimental chylothorax. Obstruction of the thoracic duct did not induce lymphangiectasia or chylothorax. Impedence of thoracic duct flow into the CrVC may be a cause of clinical chylothorax in the dog.

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Available abstract

Ligation of the cranial vena cava (CrVC) distal to the entrance of the azygous vein resulted in chylothorax in 7 of 10 dogs. Of the remaining 3 dogs, 1 developed a serosanguineous effusion that did not become chylous, and 2 dogs did not develop pleural effusion. In 2 of the 7 dogs developing chylothorax, the pleural effusion became serosanguineous within 2.5 weeks after CrVC ligation. Mesenteric lymphangiography was performed 2 to 6 weeks after ligation of the CrVC. Lymphangiectasia was seen in 4 dogs with chylothorax, but was not seen in the 3 dogs with serosanguineous effusions or the 2 dogs that did not develop effusions. One dog with chylothorax died prior to repeat lymphangiography. Less dye entered the thoracic duct, and alternate lymphaticovenous communications to the caudal vena cava were evident in the dogs without chylothorax. Ligation of the thoracic duct at the lymphaticovenous junction was performed in 3 dogs. These dogs did not develop pleural effusion. Lymphangiography was performed immediately after ligation and indicated filling of abdominal lymphatics but not of the thoracic duct. Lymphangiographic findings 6 weeks after ligation also indicated filling of intestinal lymphatics. Results of the present study indicated that ligation of the CrVC causes chylothorax, and that thoracic lymphangiectasia is a consistent finding in animals with experimental chylothorax. Obstruction of the thoracic duct did not induce lymphangiectasia or chylothorax. Impedence of thoracic duct flow into the CrVC may be a cause of clinical chylothorax in the dog.

Key concepts: Chylothorax, Thoracic duct, Medicine, Ligation, Lymphangiectasia, Effusion, Pleural effusion, Lymphatic system

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Lymphangiographic evaluation of experimentally induced chylothorax after ligation of the cranial vena cava in dogs. — Research Paper | ScholarLens