Interventional Radiology in Management of Postoperative Chylous Ascites

Abstract

Postoperative chylous ascites is a rare condition that can be caused by abdominal and pelvic surgery. The mortality rate associated with untreated postoperative lymphorrhea is as high as 50%. Conservative management is the primary treatment, and most patients improve. However, some patients continue to exhibit high-volume chylous ascites and need invasive intervention. Many surgical series have shown that the outcomes of patients with chylous ascites were unfavorable. Therefore, the need for minimally invasive interventional radiology procedures, such as intranodal lymphangiography, thoracic duct, lymphatic pseudoaneurysm, lymph node, hepatic lymphatic embolization, and peritoneovenous shunting, is increasing. This review describes the anatomy, physics, and diagnosis related to interventional radiology for postoperative chylous ascites as well as interventional radiology treatment options and strategies for this condition referring to recent literature.

Keywords: chylous ascites; embolization; interventional radiology; lymphatic; postoperative.

Figure 1.

Anatomic variation of the CC described by Loukass et al. Type I; CC was formed by the union of the left LT and the IT. Type II; CC was formed where the IT opened into the TD and the right and left LT, retroaortic nodes and branches from the intercostal lymphatics joined in a variable manner. Type III; CC was formed by the junction of the right LT and IT. Type IV; could not classified. CC: cisterna chyli; IT: intestinal trunk; LT: lumber trunk

Figure 2.

Treatment algorithm for postoperative chylous ascites.

Figure 3.

IR algorithm for postoperative chylous ascites. *Leak points were presumed to be the intestinal trunk, branches near the cisterna chyli, or hepatic lymphatic ducts. IR: Interventional radiology; TD: thoracic duct

Figure 4.

A 50-year-old female with CA after left radical nephrectomy. (a) Intranodal lymphangiography was performed, and contrast extravasation was confirmed in the left lumber lymphatic tract (black arrow). (b) Enlarged view near the extravasation. (c) A small lymphatic duct (white arrow) connecting to extravasation (black arrow) was recognized, and lymphatic duct puncture and embolization were attempted but failed. (d) RTV was attempted but the catheter could not be inserted into the terminal TD due to a lymph node-like structure present in the terminal TD (white arrow). (e) CT was then acquired, and a chylocele (white arrow) was found in the left posterior of the abdominal aorta. (f) Percutaneous drainage and embolization with NBCA were performed. NBCA casts spreading in the longitudinal direction can be seen due to repeated embolization (white arrow). Contrast enhancement from the inserted catheter just before embolization (black arrow). The chyle leak was stopped after this embolization. CA: chylous ascites; NBCA: n-butyl-2-cyanoacrylate; RTV: retrograde transvenous approach; TD: thoracic duct

Figure 5.

A 60-year-old female with CA after adnexectomy and retroperitoneal lymphadenectomy. Intranodal lymphangiography was invalid due to disruption of the bilateral pelvic lymph tract. (a) RTV and retrograde ductography were performed and recognized normal type TD (black arrow). (b) A microcatheter was advanced to below the diaphragm and contrast extravasation was recognized in the left lumber tract (black arrow). Embolization was then performed using 50% NBCA; Lipiodol and CA were improved. CA: chylous ascites; NBCA: n-butyl-2-cyanoacrylate; RTV: Retrograde transvenous approach; TD: thoracic duct

Figure 6.

A 70-year-old female with invasive clear cell carcinoma who had undergone right nephrectomy with total tumor removal, including the removal of retroperitoneal and intra-IVC lesions. Five days after surgery, chylous ascites were observed, which did not improve with conservative treatment. Lymphoscintigraphy did not show leakage, and CT did not show lymphopseudoaneurysm. (a) Eighteen days post-surgery, we attempted retrograde transvenous thoracic duct cannulation with inguinal intranodal lymphangiography; however, this failed due to the plexiform shape of the terminal TD. (b) Then, we attempted hepatic lymphangiography using iodine contrast material. (c, d) Posthepatic lymphangiography CT showed the lymphatic duct in the hepato-duodenal ligament (white arrow) and contrast accumulation in the peritoneal cavity (black arrow). Therefore, embolization was performed through the hepatic lymphatic ducts using 20% NBCA, and the chylous ascites subsequently improved. IVC: inferior vena cava; NBCA: n-butyl-2-cyanoacrylate; TD: thoracic duct