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The thoracic cavity is lined entirely by a serous membrane known as pleura.
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.
Diagnosis of chylothorax is based on recognition of characteristic clinical and radiographic findings of pleural effusion and by demonstration of chyle on fluid analysis. Chylous effusions are typically opaque and milky white to yellow in color. Chyle retains its milky appearance upon standing and may form a creamy top layer. Physicochemical properties of chylous effusions are similar to obstructive transudates since lymph composes a large portion of thoracic duct chyle. Total protein ranges from 3 to 5 gm/dl. Cytological examination reveals a predominance of small and large lymphocytes. Chronic chylous effusions will show increased neutrophils, macrophages, and mesothelial cells. Total cell counts generally do not exceed 20 X 103 cells/ul. Chylomicrons within an effusion confirms its chylous nature. Chylomicrons can be visualized on direct smears or with supravital stains such as Sudan III or IV. The presence of chylomicrons is most reliably confirmed by determination of triglyceride levels in the serum and fluid. Chylous fluids typically show triglyceride levels that are 12 to 100 times greater than levels measured in the serum. Cholesterol levels in chylous effusions are not elevated when values are compared to values from serum. Anorectic animals with chylous effusion may have greatly reduced levels of chylomicrons. Pleural fluid from such animals may easily be mistaken for a modified transudate or obstructive effusion. Feeding a fatty meal is often necessary to demonstrate the chylous nature of a pleural effusion in these animals.Pleural effusions high in cholesterol or lecithin-globulin complexes appear grossly similar to chylous effusions, but are due to degenerating cells associated with chronic inflammatory or malignant processes. These effusions are termed pseudochylous effusions. Pseudochylous effusions will be low in triglycerides and may have a high cholesterol level.
Once chylothorax is diagnosed, an attempt to determine its cause should be undertaken. Owners should be questioned regarding the possibility of recent trauma. Thoracic radiographs taken after complete pleural drainage should be evaluated for the presence of masses particularly in the cranial mediastinum. Echocardiography and ultrasound examination of the mediastinum also can be undertaken. Animals with chylothorax should be evaluated for dirofilariasis using microfilaria concentration techniques or serum adult antigen detection tests, or both. Cytologic examination of the chylous effusion for the presence of neoplastic cells helps rule out neoplasia. Often, a cause for chylothorax is not found and the clinician is left with a diagnosis of idiopathic chylothorax. Direct lymphangiography may provide information on the etiology of idiopathic chylothorax (i.e rupture versus lymphangiectasia), but generally is of academic interest only since it usually does not change the therapeutic plan.
Treatment of chylothorax may be medical or surgical. Medical management is directed at draining the pleural space and reducing the formation of chyle. Pleural drainage is indicated to relieve respiratory distress and may either be intermittent or continuous. Low-fat diets decrease the triglyceride content of chyle, but there is no evidence that the volume of chyle is similarly decreased. Animals with chylothorax should receive aggressive nutritional support and be supplemented with fat soluble vitamins.
Surgical management of chylothorax involves ligation of the caudal thoracic duct. The rationale for ligation of the thoracic duct is based on formation of lymphaticovenous anastomoses that divert chyle flow away from the thoracic duct system. Absolute indications for surgical intervention are not established in animals. The following indications for surgery are suggested: 1) failure to significantly diminish the flow of chyle after 5 to 10 days of medical management, 2) losses of chyle exceeding 20 ml/kg/day over a five day period, or 3) protein-calorie malnutrition and hypoproteinemia. Transthoracic ligation of the thoracic duct is accomplished through a right ninth or tenth intercostal thoracotomy in the dog. Failure to ligate all collateral branches of the caudal thoracic duct is thought to be a most common cause of operative failure. For this reason, en bloc ligation of all structures in the caudal mediastinum dorsal to the aorta is recommended. Intraoperative lymphangiograms performed to ensure complete ligation of the thoracic duct have been advocated, however this approach substantially increases operative time and requires facilities for taking intraoperative radiographs. The success rate for surgical management of chylothorax alone is generally less than 60%. Combined mechanical pleural pleurodesis and thoracic duct ligation, both performed via median sternotomy, is currently undergoing clinical evaluation and shows early promise for improving the success of surgery.
Despite vigorous attempts at medical and surgical management, a significant number of animals with chylothorax will fail to respond to therapy. Pleuroperitoneal shunting and chemical pleurodesis have been advocated as palliative treatments for refractory chylothorax. Chronic chylothorax can cause a constrictive pleuritis that may require decortication.