General Thoracic Surgery (General Thoracic Surgery (Shields)) [2 VOLUME SET]

Editors: Shields, Thomas W.; LoCicero, Joseph; Ponn, Ronald B.; Rusch, Valerie W.

Title: General Thoracic Surgery, 6th Edition

Copyright 2005 Lippincott Williams & Wilkins

> Table of Contents > Volume I - The Lung, Pleura, Diaphragm, and Chest Wall > Section XI - The Pleura > Chapter 63 - Anatomy of the Thoracic Duct and Chylothorax

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Chapter 63

Anatomy of the Thoracic Duct and Chylothorax

Joseph I. Miller Jr.

Embryologically, the thoracic duct is a bilateral structure that has the potential to have many varied anatomic patterns. The pattern and anatomy of the thoracic duct is considered standard in only 65% of humans, as reported by Davis (1915). Many anatomic variations occur in lymphatic and lymphaticovenous anastomosis (Fig. 63-1).

TYPICAL PATTERN OF THE THORACIC DUCT

The usual anatomic pattern of the thoracic duct is shown in Fig. 63-2. The thoracic duct is the main collecting vessel of the lymphatic system and is far larger than the right terminal lymphatic duct. Most commonly, the thoracic duct originates from the cisterna chyli in the midline at the level of the second lumbar vertebra. The cisterna chyli is 3 to 4 cm long and 2 to 3 cm in diameter. It is generally found along the vertebral column at the level of L2, but may be found anywhere between T10 and L3, generally to the right side of the aorta.

From the cisterna chyli, the thoracic duct ascends to enter the chest through the aortic hiatus at the level of T10 T12, just to the right of the aorta. Above the diaphragm, the duct lies on the anterior surface of the vertebral column behind the esophagus and between the aorta and the azygos vein. The duct usually lies in front of the right intercostal arteries, with the nerves close by. The duct continues upward on the right side of the vertebral column to approximately the level of the fifth or sixth thoracic vertebra, where it crosses behind the aorta and aortic arch into the left posterior portion of the visceral compartment of the mediastinum. From there, it passes superiorly in close approximation to the left side of the esophagus and the pleural reflection into the neck. Before exiting the mediastinum, the duct receives tributaries from the bronchomediastinal trunk of the right lymphatic duct.

Once the duct enters the neck, it arches 2 to 3 cm above the clavicle and swings laterally anterior to the subclavian artery and thyrocervical arteries. It continues deeper into the neck in front of the phrenic nerve and the scalenus anticus muscle. At this point, it passes behind the left carotid sheath and jugular vein before anastomosing with the left subclavian jugular junction (Fig. 63-3). The anatomic manner in which the thoracic duct ends varies. It may enter the jugular vein as a single trunk or as multiple trunks. It most commonly enters at the junction of the left internal jugular and subclavian veins.

MAJOR VARIATIONS OF THE THORACIC DUCT

The only thing constant about the anatomy of the thoracic duct is the numerous anatomic variations. Davis (1915) reported 9 major variations, and Anson (1950) listed 12 different anatomic variations of the lower portion of the thoracic duct (Fig. 63-4).

Major variations of the thoracic duct include doubling, left-sidedness, and right or bilateral termination, as well as the rare azygos vein termination. The embryologic basis for these variations is the plexiform nature of the trunks from which the duct arises. Doubling was reported in 4.7% of patients by Adachi (1953) and in 39% in a larger series by Van Pernis (1949); the lower figure is probably correct for extensive duplication. In a few instances, the abdominal components of the trunk may pass upward to both sides or only to the left of the aorta. Rarely, as noted by Adachi (1953) as well as Davis (1915), the duct may be left-sided throughout its course. Adachi also reported that only the upper part of the duct may be double, so that it terminates in both the right and left sides of the neck (1.8%) or the right side alone (1.6%). At its termination, the duct may enter into a short plexus with its tributary trunks so that in approximately 20% of people it enters the vein by two or more branches. Termination of the duct in the azygos system is rare. Edwards (1972) reported, in an autopsy subject, that he had observed the duct to enter the hemiazygos vein. In its cervical course, Adachi (1953) noted that the duct may run posterior rather than anterior to the vertebral or the subclavian artery.

In 1922, Lee reported a detailed study of the collateral circulation of the lymphatic system in the mediastinum. He

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Lymph from the right side of the head, neck, and chest wall, as well as from the right lung and the lower half of the left lung (through the bronchomediastinal trunk), drains into the right lymphatic duct. This duct also carries lymph from the heart and the dome of the liver and from the right diaphragm. Bessone and colleagues (1971) pointed out that the right lymphatic duct is small and is rarely visualized.

COMPOSITION OF CHYLE

The term chyle comes from the Latin chylus, meaning juice. It is the lymph that originates in the intestine. The fat contained in the intestinal lymph gives chyle its characteristic appearance. Thoracic duct lymph is not pure chyle, but a mixture of lymphatic fluid originating in the intestine, liver, abdominal wall, and lower extremities. Ninety-five percent of the volume of the thoracic duct lymph originates in the liver and the intestinal tract. Under normal circumstances, the amount of lymph originating in the extremities is negligible.

The primary function of the thoracic duct is the transport of digestive fat to the venous system. Munk and Rosenstein (1891) observed a thoracic duct fistula and recognized that the thoracic duct lymph was clear during fasting but became milky after a fatty meal. Approximately 60% to 70% of the ingested fat is absorbed by the intestinal lymphatic system and conveyed to the bloodstream by the thoracic duct. The composition of chyle is listed in Table 63-1. The main component of chyle is fat.

Thoracic duct lymph contains from 0.4 to 5.0 g of fat per 100 mL, and 50% to 70% of absorbed fat is conveyed to the bloodstream by way of the thoracic duct. This amount is made up of neutral fat, free fatty acids, sphingomyelin, phospholipids, cholesterol, and cholesterol esters.

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Those fatty acids with fewer than 10 carbon atoms in the chain are absorbed directly by the portal venous system. This particular fact forms the basis for the use of medium-chain triglycerides as an oral diet in the conservative management of chylothorax. Neutral fat, as Ross (1961) noted, is found in the lymph in the form of minute globules that are smaller than 0.5 mm in diameter. Ingested fat passes from the intestine to the systemic circulation in approximately 1.5 hours, with a peak absorption at 6 hours after ingestion.

Ross (1961) and Roy and associates (1967) reported that the total protein content of thoracic duct lymph ranges from 2.2 to 5.9 g per 100 mL, approximately one-half of that found in the plasma. Thoracic duct lymph contains as much as 4% protein, consisting of albumin, globulin, fibrinogen, and prothrombin, with an albumin ratio of 3:1. Sugar concentration in thoracic duct lymph ranges from 40 to 200 g per 100 mL. The electrolyte composition is similar to that found in plasma, with sodium, potassium, chloride, calcium, and inorganic phosphorus being the predominant electrolyte components.

Antithrombin globulin, prothrombin, and fibrinogen are all present in human thoracic duct lymph in concentrations greater than 25% of plasma levels. Stuttman and associates (1965) reported that factors V and VIII are present in concentrations of approximately 8.9% and 4.5%, respectively, in thoracic lymph.

The main cellular elements of thoracic duct lymph are lymphocytes. They range from 400 to 6,800 cells per L. As Hyde and colleagues (1974) noted, most of these lymphocytes are T lymphocytes. Thoracic duct lymphocytes differ qualitatively and quantitatively from peripheral blood lymphocytes in their reactivity to antigenic stimulation.

In clear lymph, approximately 50 red cells per L exist, whereas in the postabsorptive states, as Shafiroff and Kau (1959) reported, the number may increase to 600 red cells per L of thoracic duct lymph. In addition, fat-soluble vitamins, antibodies, enzymes (including pancreatic lipase, alkaline phosphatase, serum glutamic-oxaloacetic transaminase, and serum glutamic-pyruvic transaminase), and urea nitrogen are present in thoracic duct lymph. Because of the numerous constituents of thoracic duct lymph, it is readily apparent why the persistent loss of this fluid can interfere with nutrition and immunity.

PHYSIOLOGY OF THE THORACIC DUCT

The function of the thoracic duct is the transport of ingested fat to the venous system. Volume and weight of flow of lymph have been estimated to be 1.38 mL/kg of body weight per hour. Crandall and associates (1943) found that the rate of flow increases after ingestion of food and water and during abdominal massage, with a maximum flow of 3.9 mL/min and a minimum flow of 0.38 mL/min. Hepatic lymph increases by 150% after meals, whereas intestinal lymph increases to up to 10 times the basal flow after fatty meals. Starvation and complete rest decrease the flow of thoracic duct lymph.

The forward flow of chyle from the cisterna chyli to the entrance into the left subclavian internal jugular vein junction is influenced by several factors:

• The inflow of chyle into the lacteal system creates a vis a tergo, which is in turn produced by the intake of food and liquid into the intestine and is augmented by intestinal movement.

• Negative intrathoracic pressure on inspiration and the resultant gradient between this negative pressure and positive intraabdominal pressure help the upward flow of chyle.

• Muscular contractions of the thoracic duct wall are probably the most important factor. Contractions of the duct wall occur every 10 to 15 seconds independent of respiratory movements. The intraductal pressure ranges from 10 to 25 cm H₂O, and with obstruction, as Shafiroff and Kau (1959) observed, it may increase to 50 cm H₂O. These rhythmic contractions cause the duct to empty into the subclavian vein. The thoracic duct valves, located throughout its course but mostly in the upper portion, permit only upward unidirectional flow.

The flow of chyle varies greatly with the content of the meal and is particularly increased when the fat content of the food is high. Volumes up to 2,500 mL of chyle in 24 hours have been collected from the cannulated human thoracic duct. Most of the body's lymphocytes are transported through the thoracic duct system back to the venous system.

The lymph circulation performs the vital function of collecting and transporting excess tissue fluid, extravasated plasma protein, absorbed lipids, and other large molecules from the interstitial spaces back to the bloodstream.

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ETIOLOGY OF CHYLOTHORAX

Chylothorax is the presence of lymphatic fluid in the pleural space resulting from a leak of the thoracic duct or one of its major divisions. This condition is being recognized more frequently, after both cardiac and general thoracic surgery. Increased understanding of the physiology, pathogenesis, diagnosis, and management of chylothorax has decreased the initial 50% mortality to a mortality of 10% in major medical centers.

Numerous classifications of chylothorax have been suggested. Most have been based on information obtained at postmortem examination. In 1971, Bessone and colleagues suggested classifying chylothorax as follows: congenital chylothorax, postoperative traumatic chylothorax, nonsurgical traumatic chylothorax, and nontraumatic chylothorax. DeMeester (1983), however, has published a more thorough classification (Table 63-2).

Congenital Chylothorax

Chylothorax in the neonate, although rare, is the leading cause of pleural effusion in this age group. In most cases, the exact cause cannot be ascertained. Birth trauma or congenital defects in the duct wall, or both, may be precipitating factors. Increased venous pressure in birth trauma, causing thoracic duct rupture, has been suggested as a possible cause. In rare instances, malformations of the lymphatic system, particularly in the thoracic duct itself, have been shown to be the cause of congenital chylothorax. The thoracic duct may be absent or atretic, and, in occasional instances, multiple, dilatated lymphatic channels with abnormal communications have been noted, as well as multiple fistulae between the thoracic duct and pleural space.

Traumatic Chylothorax

The second major cause of chylothorax is traumatic chylothorax, which may occur with either blunt or penetrating trauma or after a surgical procedure. The most common form of nonpenetrating injury to the thoracic duct is produced by a sudden hyperextension of the spine with rupture of the duct just above the diaphragm. Sudden stretching over the vertebral bodies may be enough in itself to tear the duct, but usually the duct has been fixed as a result of prior disease or malignancy. This may be secondary to a blast or blunt trauma. Episodes of vomiting or a violent bout of coughing also can result in tearing of the thoracic duct. Biet and Connolly (1951) believe this is generally caused by a shearing of the thoracic duct by the right crus of the diaphragm. These are the most commonly mentioned causes of chylothorax resulting from nonpenetrating injuries to the chest. Penetrating injury from a gunshot or a stab wound to the thoracic duct is unusual and is apt to be overshadowed by damage to other structures of more immediate importance.

Operative Injuries

Injury at operation is fairly common. Chylothorax has been reported after almost every known thoracic surgical procedure, including operations on the aorta, esophagus, heart, lungs, and sympathetic nervous system. Injury also has been reported after surgery in the neck, after such operations as radical neck resection and scalene node biopsy. It has been reported also after abdominal operations of sympathectomy and radical lymph node dissection. In addition, it has been reported with translumbar aortography and subclavian venous catheterization. An occasional instance has been reported after an attempt to introduce a cannula into the left internal jugular vein.

Often, a latency interval of 2 to 10 days passes between the time of injury and the development of a chylothorax that becomes clinically evident. This is because lymph accumulates in the posterior mediastinum until the mediastinal pleura ruptures, usually on the right side at the base of the pulmonary ligament. Once established, the thoracic duct pleural fistula does not tend to close, in contrast to the dictum that in the absence of obstruction a fistula closes. Spontaneous sealing of a fistula after a closed injury may be expected in only approximately 50% of patients, and death generally ensues in the remaining patients unless the fistula is surgically closed.

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Intraoperatively, the duct is most vulnerable to damage in the upper part of the left chest, particularly, as Higgins and Mulder (1971) noted, with procedures involving mobilization of the aortic arch, the left subclavian artery, or the esophagus. The classically described course of the duct explains why damage to it below the level of the fifth or sixth thoracic vertebra usually results in a right-sided chylous effusion, and why damage above this level usually results in effusion on the left side.

Neoplastic Chylothorax

Ross (1961) stated that the thoracic duct can be involved in both benign and malignant disease by direct lymphatic permeation in continuity with the primary growth, by direct invasion of the duct by the primary growth, or by tumor embolus in the main duct. The chylothorax may be either unilateral or bilateral. DeMeester (1983) reported that the predominant mechanism of the leak is by rupture of distended tributaries because of back pressure from the neoplastic obstruction or actual erosion of the duct itself. Chylothorax has been most frequently reported after lymphosarcoma, retroperitoneal lymphoma, or primary carcinoma of the lung. Rarely, malignant chylous leaks may fill the pericardial sac with chyle and produce signs and symptoms of cardiac tamponade.

Miscellaneous Causes

Infections, filariasis, pancreatic pseudocysts, thrombosis of the jugular and subclavian veins, cirrhosis of the liver, and tuberculosis can all cause chylothorax. Benign lymphangiomas arising in the thoracic duct also may produce single or multiple cystlike spaces filled with chyle.

Pulmonary lymphangioleiomyomatosis, as reported by Corrin (1975) and Silverstein (1974) and their associates, is a rare cause of chylothorax. This condition is seen in women of reproductive age who have shortness of breath as the major complaint. Pneumothorax and hemoptysis can be seen in addition to chylothorax, and these women usually die of pulmonary insufficiency within 10 years of presentation.

PATHOLOGIC PHYSIOLOGY

Chylothorax can cause cardiopulmonary abnormalities, as well as serious metabolic and immunologic deficiencies. The accumulation of chyle in the chest can result in compression of the underlying lung with a reduction of vital capacity and mediastinal shift, resulting in shortness of breath and, occasionally, symptoms of marked respiratory distress. In general, the development is insidious, and symptoms occur gradually. In contrast, with rapid accumulation, shock, tachypnea, tachycardia, and hypotension can occur. Chyle is thought to be bacteriostatic because of its lecithin and fatty acid content and therefore is usually sterile. Because it is nonirritating, chyle does not tend to form a peel that can result in a trapped lung.

The loss of protein, fat-soluble vitamins, and fat contained in chyle can lead to serious metabolic defects and death in patients with chylothorax. Shafiroff and Kau (1959) emphasized that the loss of lymphocytes and antibodies can also interfere with the immunologic status of a patient with chylothorax.

DIAGNOSIS

Diagnosis of a chylothorax is suggested by the presence of a nonclotting, milky fluid, which is obtained from the pleural space at thoracentesis or chest tube insertion. The diagnosis is confirmed by the finding of free microscopic fat and fat content in the fluid higher than that in the plasma. In traumatic chylothorax, the chyle may initially appear bloodstained, which may be misleading. On microscopic examination, the presence of fat globules that clear with alkali and ether, or stain with Sudan-3, is diagnostic. Lymphocytes are the predominant cells found in chyle, whereas in traumatic chylus effusion, red blood cells are at least initially present.

Chylous effusions must be distinguished from pseudochyle and cholesterol pleural effusions. Boyd (1986) noted that pseudochyle occurs with malignant tumors or infection and is milky in appearance because of the presence of lecithin globulin complex. Pseudochyle contains only a trace of fat, and fat globules cannot be seen with Sudan-3 stain smears. Milky pleural effusions also can be seen secondary to tuberculosis, and Bower (1968) reported milky pleural effusions to occur in rheumatoid arthritis. Cholesterol pleural effusions that are seen in these two disease entities acquire their milky appearance from a high concentration of cholesterol crystals.

If it is still difficult to distinguish chyle from pseudochyle or cholesterol pleural fluid, feeding a patient a fat stained with green No. 6 dye, which stains the chylous effusion approximately 1 hour after ingestion of the dye, is a helpful diagnostic test. Obtaining cholesterol and triglyceride levels of the fluid can help because most chylous effusions have a cholesterol-to-triglyceride ratio of less than 1, whereas nonchylous effusions have a ratio greater than 1. In addition, if the fluid has a triglyceride level of more than 110 mg per 100 mL, a 99% chance exists that the fluid is chyle. If the triglyceride level is less than 50 mg per 100 mL, Staats and colleagues (1980) noted that only a 5% chance exists that the fluid is chyle.

Another helpful index in determining if a leak is related to a chylous leak is the rate of fluid accumulation in the chest. The rate of accumulation in the chest from a chylous fistula exceeds 400 to 500 mL/day and averages approximately 700 to 1,200 mL/day in a 70-kg adult. The flow rate is obviously proportionately less in infants and children, depending on the body surface area. A detailed analysis of

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Once a chylothorax is diagnosed, a complete history and physical examination should be performed to discern the etiology. Chylothorax in a postoperative period generally develops 7 to 14 days postoperatively. Surgery in the region of the aorta, esophagus, or posterior mediastinum should suggest the presence or the possibility of a chylothorax. Blunt trauma 2 to 6 weeks earlier also should suggest the presence of a potential chylothorax.

In nontraumatic chylothorax, an extensive search for the cause of the pleural effusion must be undertaken. Computed tomography (CT) and lymphangiography are diagnostic techniques that are helpful in the study of chylothorax. Occasionally, lymphangiography details the exact site of leakage and also the anatomic abnormalities of the thoracic duct. A CT examination of the chest is a good way to demonstrate the presence of mediastinal disease that could cause a chylothorax. A mediastinal mass or enlarged mediastinal nodes, as well as primary lung cancer, could easily be demonstrated by this technique.

MANAGEMENT

The ideal management of the patient with chylothorax is unknown. The disease occurs in various situations, and opinions are diverse about which types of chylothorax should be treated operatively: the postsurgical or posttraumatic types only, or the nontraumatic types as well. Whether young children should undergo surgery is also controversial. The development of a lymphatic leak in the thorax certainly necessitates decisive management if considerable morbidity and mortality are to be avoided. Well-standardized guidelines have emerged that have enhanced the understanding and treatment of this difficult clinical problem.

Table 63-3 lists the various modalities used in the treatment of chylothorax. They can be divided into conservative therapy, operative therapy, and radiation therapy. Current treatment of chylothorax is thoracic duct ligation, introduced by Lampson and associates (1948). They showed that the mortality from chylothorax decreased from 50% to 15% using this approach. Before this report of successful control of traumatic chylothorax by direct ligation of the thoracic duct, the mortality for this condition was 45%; nontraumatic chylothorax had a mortality of 100%. Treatment of the condition before 1948 consisted of thoracentesis or closed chest tube thoracostomy and a low-fat diet. Today, the crucial decision in the management of these patients is when to advocate surgical intervention. No unanimous opinion exists on whether to operate or, if surgery is not undertaken initially, on how long conservative management should be used before resorting to surgical intervention.

Conservative therapy consists of maintaining effective thoracostomy tube drainage with good expansion of the lung. The most important aspect is to maintain adequate nutrition, because loss of chylous fluid causes electrolyte imbalance and increases nutritional needs. Central hyperalimentation is routinely used, while giving the patient nothing by mouth. Any oral feedings increase output through the fistula. No standard exists for how long conservative therapy should be tried before considering operative intervention. Williams and Burford (1964), as well as Selle and associates (1973), recommended 14 days as a maximum limit for conservative therapy before surgical intervention. In approximately 50% of patients, the thoracic duct leak closes spontaneously; the other 50% require surgical intervention. When chest tube drainage is consistently greater than 500 mL/day for 2 weeks, surgical intervention is definitely indicated, except for those patients for whom thoracotomy is contraindicated, such as those with vertebral fractures or with nonresectable tumors. If a lung is entrapped and pleural synthesis cannot be achieved with reexpansion by closed chest tube thoracostomy, then early surgical intervention is indicated. If chylous drainage is still present after a period of carefully supervised nonoperative conservative therapy, patients with congenital, traumatic, or postoperative chylothorax should undergo surgical treatment.

OPERATIVE THERAPY OF A CHYLOUS FISTULA

Several techniques may be used to control a chylous fistula, singly or in combination: direct ligation of the thoracic duct, mass ligation of the thoracic duct, pleuroperitoneal shunting, and pleurectomy. Occasionally, decortication may be required when the lung is entrapped. Stenzel and colleagues (1983) suggested that fibrin glue be applied in some instances.

In unilateral chylothorax, the chest should be opened on the side of the effusion. When the effusion is bilateral, it is more prudent to explore the right side first, with ligation of the duct low in the right chest. Exploration of the left side is done later, if necessary. Ross (1961) stated that the easiest way to find the duct and the leakage point is to give the patient 100 to 200 mL of olive oil through a nasogastric tube 2

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Ligation of the thoracic duct just above the diaphragm through the right chest is currently favored by most authors, including Selle (1973), Patterson (1981), and Milson (1985) and their associates, regardless of the site of the chylous leak. As noted, the thoracic duct is a single structure from T12 T8 in more than 75% of all patients.

The three techniques used to control the leak of chyle are direct closure of the fistula, suture of the leaking mediastinal pleura, and supradiaphragmatic ligation of the duct. The best method is to find the actual point of leakage and to close it with nonabsorbable sutures with the use of Teflon pledgets, compressing the leakage point in the adjacent tissue between the two pledgets, and, if possible, allowing the main portion of the duct to remain patent. Either of the first two techniques, and particularly the second, should be combined with supradiaphragmatic ligation of the duct. This alone is entirely effective in instances in which no attempt has been made to directly close the fistula. The most favorable site for elective ligation is low in the right chest just above the right crus of the diaphragm where the duct lies on the vertebral column between the aorta and the azygos vein (Fig. 63-5).

If a definite source of leakage cannot be identified when the right side of the chest is explored, despite use of the previously described ingestion of fat (milk or cream) or olive oil before surgery, then supradiaphragmatic ligation of the duct should be performed. This method was originally described by Murphy and Piper (1977) and subsequently championed by Patterson and colleagues (1981).

Supradiaphragmatic Ligation of the Thoracic Duct

A standard posterolateral thoracotomy incision is made, going through the bed of the resected right sixth rib. Generally, the pleura has a shaggy appearance because of fibrin deposits. After these deposits are cleaned off, the pulmonary ligament is divided between clamps and the pulmonary ligament is swept upward to the level of the inferior pulmonary vein. The retropleural area is often thickened up to 1 to 2 cm. If this is the case, it should be biopsied. It is best to ligate the duct en masse by going around the duct, taking a generous bite of tissue around the duct and going close to the vertebral bodies, but avoiding the esophagus, aorta, and azygos vein. This suture should be tied with large pledgeted sutures on either end, as shown in Fig. 63-6. This effects a mass ligature in the area between the azygos vein and the aorta just above the diaphragm. One must take care not to enter the wall of the esophagus. In effect, all tissue between the azygos vein and the aorta is ligated in the mass ligature.

A parietal pleurectomy is performed to achieve pleural synthesis. At the same time, if the underlying lung is trapped, it is decorticated. Two chest tube catheters are placed into the thoracic cavity, and the chest is closed in the usual fashion. In general, the chest tubes can be removed in 5 to 7 days, and recovery is rapid.

Other Techniques to Control Chylothorax

Milson and associates (1985) and Weese and Schouten (1984) reported the successful use of pleuroperitoneal

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Stenzel and colleagues (1983) reported the successful use of fibrin glue in one case of postsurgical chylothorax after an extrapleural ligation of the patent ductus arteriosus.

In selected cases of chylothorax, a thoracoscopic approach may be utilized. This is best restricted to traumatic cases of chylothorax, such as hyperextension of the thoracic spine with traumatic rupture of the duct, in which an isolated tear may be found. This can be closed by suture ligation. Others have reported the use of various types of sealants and glues in this situation. In general, a thoracoscopic approach is best reserved for when the case is well defined and decortication and en masse ligation is not thought to be required.

In nontraumatic chylothorax, the cause must be determined, and if neoplasm or infection is the cause, it must be treated specifically with radiation therapy, chemotherapy, or antibiotic therapy. If chylous drainage persists in these situations, pleural synthesis by catheter drainage of the pleura with instillation of nitrogen mustard or other irritants can be tried. In some cases, even though not desirable, thoracic duct ligation or pleurectomy may be needed to control the chylothorax. Radiation therapy has been successful in managing chylothorax in patients with mediastinal lymphoma and carcinoma. Irradiation of the pleural lymphatics to 2,000 rads causes closure of the thoracic duct leak in most cases. I have observed four patients with nontraumatic chylothorax in whom no malignancy could be found and who received radiation therapy to the pleural lymphatics to 2,000 rads, with success in all cases.

GUIDELINES FOR MANAGEMENT

In an excellent review of the indications for surgery, Selle and colleagues (1973) established the following guidelines:

• Idiopathic cases in the neonate usually respond well to thoracentesis.

• Nontraumatic chylothorax, exclusive of the neonatal group, usually suggests a widespread fatal illness. Operative intervention is usually ineffective and should therefore be avoided.

• In cases resulting from trauma, an initial trial of nonoperative therapy is indicated. Transthoracic ligation of the duct is indicated when the average daily chyle loss has exceeded 1,500 mL/day in adults for more than 5 days.

• If the chyle flow has not diminished within 14 days or if nutritional complications appear imminent, surgery is indicated.

Figure 63-7 outlines my approach to the management of chylothorax. Thoracentesis is performed to confirm the diagnosis.

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If the drainage is less than 250 mL/day and appears to be decreasing, I may continue to try conservative therapy for 1 more week. If the leakage stops, the chest tube is removed. If this is to be done, one should give a trial of a high-fat diet before removing the chest tube. If leakage persists at this time, pleuroperitoneal shunting could be performed if the patient is a medically compromised candidate; otherwise, thoracotomy and the previously mentioned procedures can be performed. If conservative therapy fails to control the chylothorax after 2 weeks, and the underlying condition is a malignancy, then irradiation is administered. Generally, radiation therapy to the amount of 2,000 rads controls most cases of this variety of chylothorax.

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Reading References

Blalock A, Cunningham RS, Robinson CS: Experimental production of chylothorax by occlusions of the superior vena cava. Ann Surg 104:359, 1936.

Cerfolio RJ, et al: Postoperative chylothorax. J Thorac Cardiovasc Surg 112:1361, 1996.

Donini I, Batteggati M: The Lymphatic System. London: Piccin Medical Books, 1972, pp. 11 26.

Goorwitch J: Traumatic chylothorax and thoracic duct ligation. J Thorac Surg 29:467, 1955.

Klepser RG, Berny JF: The diagnosis and surgical management of chylothorax with the aid of lipophilic dyes. Dis Chest 25:409, 1954.

Miller JI Jr: Diagnosis and management of chylothorax. Chest Surg Clin N Am 6:139, 1996.