The thoracic duct, a primary central common drainage pathway for the lymphatic system of the trunk and lower extremities, exists in close anatomic proximity to the esophagus. Roughly 0.5% to 2.0% of patients undergoing thoracic surgery, especially esophagectomy, will suffer iatrogenic thoracic duct disruption, an injury that can result in intractable high-volume chylous pleural effusions. The thoracic duct carries 2 to 4 liters of lymph daily, the major components of which include proteins, lipids, and lymphocytes. The clinical sequelae of persistent high-volume lymph loss can be severe and life threatening and include respiratory compromise, immune compromise, dehydration, and severe nutritional depletion. Unremitting chylous effusions can be associated with up to 50% mortality.1 Conservative treatment with parenteral nutrition, cessation of oral intake, and pleural fluid drainage may help resolve some leaks, but these maneuvers are frequently unsuccessful. In one review of 11,315 patients undergoing thoracic surgery, 47 (0.42%) developed postoperative chylothorax, of which only 13 (27.7%) resolved with nonoperative treatment; the remaining 34 (72.3%) required reoperation. In this series, reoperation was associated with a mortality rate of 2.1% and a complication rate of 38.3%.2 Recently, thoracic duct embolization (TDE) has been described as a minimally invasive treatment for persistent chylous effusions, either by direct thoracic duct cannulation and embolization (type 1) or cisterna chyli maceration (type 2).3,4 The primary indication for TDE is unremitting true chylous effusion in the clinical setting of suspected thoracic duct injury. Typical predisposing events include pulmonary or esophageal surgery or penetrating thoracic trauma. If lymph production can be minimized by restricting oral and fat intake, thoracic duct leaks with an output of less than 500 mL/day can sometimes heal spontaneously. However, the process can take 2 to 3 weeks, during which the patient may become nutritionally depleted, and many of these effusions may not ultimately resolve. The decision to proceed to intervention in chylous effusions of less than 500 mL/day depends on the clinical status of the patient, duration of the effusion, and daily output trends. Successful nonoperative management of chylous effusions with more than 500 mL/day output is questionable, and with more than 1000 mL/day output, unlikely. Accepted criteria for operative intervention include over 1000 mL chyle output per day for 48 hours, increasing output on conservative management over 5 days, and persistent chylothorax after 2 weeks of conservative management.5 Chylous effusions typically have a milky appearance and are categorized as either true chylous effusions or pseudochylous effusions. True chylous effusions can be confirmed by the presence of pleural fluid chylomicrons and/or a pleural fluid triglyceride level above 110 mg/dL. Causes of true chylous effusions include thoracic duct injury and lymphatic disruption by tumor (e.g., lymphoma). Pseudochylous effusions may have a milky appearance, but chemical analysis demonstrates cholesterol to be the dominant lipid component with triglyceride level less than 50 mg/dL and the absence of chylomicrons.6 The most common causes of pseudochylous effusions include tuberculosis and rheumatoid disease. Pseudochylous effusions do not reflect thoracic duct disruption and are not an indication for TDE. • 21- or 22-gauge 15- to 20-cm Chiba needle (Cook Medical Inc., Bloomington, Ind.) • Stiff 0.018-inch 150-cm guidewire (V-18 Control Wire [Boston Scientific, Natick, Mass.]) • 4F inner dilator and stiffening cannula from a nonvascular access kit (MAK-NV Introducer System [Merit Medical Systems, South Jordan, Utah]) • Microcatheter (Slip-Cath 3F 80-cm Infusion Catheter [Cook Medical]) • Platinum-fibered microcoils (Nester Embolization Microcoils, 4- to 6-mm, 14-cm [Cook Medical]) • Liquid embolic adhesive (TRUFILL NBCA Liquid Embolic System [Codman & Shurtleff Inc., Raynham, Mass.]) The lymphatic system of the lower extremities coalesces in the pelvis with the internal and external iliac lymphatic chains. These in turn join the common iliac lymphatics and coalesce to join the paraaortic and paracaval lymphatic chains. At the level of T12-L2, the paraaortic and paracaval chains join the intestinal trunk to form the cisterna chyli, a fusiform or saclike channel that is distinctly larger than the surrounding lymphatics and visible on lymphography in 80% of patients. In the majority of patients, the cisterna chyli is located to the right posterior aspect of the abdominal aorta. The thoracic duct arises from the cisterna chyli at its cephalad terminus and courses superiorly posterior to the esophagus and slightly right of midline in the lower thorax, crossing to left of midline around T5-T6. It continues cephalad to terminate variably in the region of confluence of the left subclavian and internal jugular veins. The thoracic duct can be a single-channel or multichannel structure, and 10% of patients will have a bilateral duplicated thoracic duct system.7
Thoracic Duct Embolization for Postoperative Chylothorax
Indications
Equipment
Technique
Anatomy and Approaches
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