The thoracic cavity is lined entirely by a serous membrane known as pleura. The pleura is divided into visceral pleura which
covers the lungs and parietal pleura which covers the remaining thoracic cavity. The pleura is composed of a single layer
of mesothelial cells supported by a delicate network of elastic connective tissue. The visceral and parietal pleura contain
a rich capillary network that originates from the pulmonary and systemic circulations, respectively. In addition, the parietal
pleura contains a rich lymphatic network responsible for lymphatic drainage of the pleural space. Under normal conditions,
the pleural space is only a potential cavity. The visceral and parietal pleura are separated by a thin layer of pleural fluid,
the average volume of which is 2.4 ml in a 10 kg dog. Liquid coupling between the thoracic wall and lungs provides instantaneous
transmission of thoracic volume changes to the lungs, and yet allows low friction sliding between the pleural surfaces.
Because high pleural permeability causes the pleural space to be continuous with the interstitial fluid of the thoracic wall,
the dynamics of pleural fluid formation and absorption are controlled by Starling's forces. Since hydrostatic pressure in
the systemic capillaries that supply the parietal pleura is a 30 cm of water and hydrostatic pressure of the pulmonary capillaries
that supply the visceral pleura is approximately 11 cm of water, one theory suggests pleural fluid is formed by the parietal
pleura and absorbed by the visceral pleura under physiologic conditions. More recent evidence suggests that pleural fluid
filters through the parietal pleura and is drained by parietal lymphatics.
Anatomy of thoracic duct
Chylothorax results when chyle from the cisterna chyli-thoracic duct system gains access to the pleural space. In the dog,
the caudal thoracic duct courses dorsal and to the right of the aorta, lateral to the intercostal arteries, and ventral to
the azygos vein. The duct crosses to the left side of the aorta ventral to the body of the fifth thoracic vertebra and continues
cranioventral across the left side of the esophagus to empty at the junction of the left jugular vein and cranial vena cava.
Although this description of the thoracic duct is considered "normal", few dogs exhibit this pattern without some variation.
Variations included multiple collaterals of the caudal and middle portions of the duct, and double duct systems. In the cat,
the caudal thoracic duct typically courses dorsal and to left of the aorta.
The etiology of chylothorax is poorly understood in the dog and cat. The incidence of chylothorax in Afghan is inordinately
high, but it is unknown if this predisposition is hereditary. Trauma is an often cited cause of chylothorax in dogs and cats.
Thoracic duct rupture might result from blunt or penetrating injuries, traumatic diaphragmatic herniation , thoracic surgery,
or severe coughing or vomiting episodes. Recent evidence suggests that traumatic rupture of the thoracic duct may be an uncommon
cause of chylothorax in animals. The role that obstruction of the thoracic duct plays in the development of chylothorax is
unclear. Experimental obstruction of the thoracic duct alone rarely results in chylothorax, but ligation of the cranial vena
cava produces lymphangiectasia of the thoracic duct and a high incidence (> 50%) of chylothorax in dogs and cats. It is speculated
that lymphangiectasia may allow extravasation of chyle through the lymphatic vessel wall. Malignancies or thrombosis that
occludes the cranial vena cava might induce chylothorax by such a mechanism. Elevations in systemic venous pressure secondary
to congestive heart failure likely explain why chylothorax occurs with cardiomyopathy, tricuspid dysplasia, and heartworm
disease. Lymphangiectasia of unknown origin has been demonstrated in dogs and cats with spontaneous chylothorax.
Debilitation associated with chylothorax is caused primarily by loss of chyle from the body after pleural drainage is instituted.
Water and electrolyte losses can be sufficient to cause dehydration and electrolyte imbalance. Loss of lipid and protein can
lead to protein-calorie malnutrition and hypoproteinemia. Malnutrition is compounded by the loss of fat soluble vitamins.
Immunocompetence becomes impaired due to loss of antibodies, lymphopenia, and malnutrition.