Thoracic Duct Embolization for Postoperative Chylothorax


The thoracic duct, a primary central common drainage pathway for the lymphatic system of the trunk and lower extremities, is anatomically close 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. 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%. 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).

Indications

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 more than 1000 mL of chyle output per day for 48 hours, increasing output on conservative management over 5 days, and persistent chylothorax after 2 weeks of conservative management.

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. 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.

Contraindications

Contraindications to TDE include absence of a true chylous effusion, chylothorax that is responding positively to conservative management, allergy to lymphangiographic contrast agents (methylene blue and ethiodized oil), and anatomic unsuitability. Some patients lack a distinct cisterna chyli or suitable upper lumbar lymphatic channel for cannulation. A completely retroaortic position may make the thoracic duct inaccessible to percutaneous cannulation. Prior low ligation of the thoracic duct limits the effectiveness of TDE, although embolization or maceration of the cisterna chyli may still be beneficial. Because passage of the needle and catheter through visceral organs cannot be avoided during TDE, bleeding diatheses and uncorrectable coagulopathies are contraindications as well.

Equipment

  • 25-gauge ×3.5-inch spinal needle (Becton Dickinson Company, Franklin Lakes, NJ)

  • Microbore extension set, 36-inch (Braun Medical, Bethlehem, PA)

  • Medallion syringe, 1 mL (Merit Medical, South Jordan, UT)

  • Metal three-way stopcock (Merit Medical)

  • 21- or 22-gauge 15- to 20-cm Chiba needle (Cook Medical Inc., Bloomington, IN)

  • Stiff 0.018-inch 150-cm guidewire (V-18 control wire [Boston Scientific, Natick, MA])

  • 4F inner dilator and stiffening cannula from a nonvascular access kit (MAK-NV introducer system [Merit Medical])

  • 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 N -butyl cyanoacrylate Liquid Embolic System [Codman & Shurtleff, Raynham, MA])

Technique

Anatomy and Approaches

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 most 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.

TDE is a two-phase procedure. In the initial phase, direct inguinal lymphangiography is performed to visualize the cisterna chyli or dominant upper lumbar lymphatics as potential cannulation targets. The cisterna chyli has a predilection for right-sided location in the upper abdomen, and in our experience, for the purposes of TDE, right-sided lymphography results in more efficient and definitive visualization of the cisterna chyli than left-sided lymphography. Intranodal lymphangiography allows for rapid opacification of the lumbar lymphatics ( Fig 86.1 ), but it requires sonographic guidance for needle placement in a suitable lymph node, which can be challenging in patients with anasarca or obese body habitus. In these patients a bipedal approach can be performed. Lastly, retrograde cannulation of the thoracic duct can be achieved by accessing the ostium of the thoracic duct near the left angulus venosus, using a 5F reverse curve or angled catheter and a coaxial microcatheter delivered from a left brachial or basilic vein approach. Of these three methods, the retrograde transvenous approach is the least reliable because of the primary difficulty of locating and seating a catheter in the ostium of the thoracic duct and the secondary difficulty of passing a wire and microcatheter through competent terminal valves.

Fig. 86.1, Intranodal lymphangiography. The equipment utilized for intranodal lymphangiography (A) and successful bilateral inguinal lymphangiography (B) is shown.

The second phase of TDE involves cannulation and embolization of the thoracic duct, typically from a right anterior oblique transabdominal approach to avoid the aorta, although a right posterior oblique transhepatic approach is also feasible. If the thoracic duct cannot be cannulated, a secondary strategy of needle maceration and disruption of the cisterna chyli can be performed to divert chyle flow into the retroperitoneum. This results in decompression of the thoracic duct and promotes healing of the breach.

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