We present a case of a 35-year-old male with a history of HIV (CD4 < 100, viral load undetectable) and no known history of underlying malignancy. The patient initially presented to an outside hospital for acute shortness of breath, and subsequently underwent placement of a right sided chest tube for treatment of a pleural effusion seen on chest X-ray. Initial output was 4 L. Sampling of the effusion demonstrated transudative fluid without malignant cells, and a triglyceride level of 272 mg/dL, consistent with chlyothorax. He was then found to have ascites, and a diagnostic paracentesis yielded fluid with a borderline triglyceride level of 110 mg/dL. Additional testing of the fluid demonstrated the presence of chlyomicrons, suggestive of chylous ascites. MR lymphangiography revealed dilated lymphatic channels peripheral to a non-visualized thoracic duct, and a suspicion of chronic thrombosis of the left brachiocephalic vein and left subclavian vein, possibly contributing to bilateral chylothorax. Lymphangiogram (Fig. 1A) demonstrated diminutive inguinal lymph nodes, limiting adequate opacification of the left iliac lymphatic network. Opacification of the right inguinal, iliac, and paravertebral lymphatics up to approximately L3 level was observed; however, the cisterna chyli and thoracic duct were not visualized and venous migration of lipiodol was demonstrated. Transvenous thoracic duct access was attempted, but unsuccessful due to chronic venous thrombosis. The patient subsequently underwent left video-assisted thoracoscopic surgery for thoracic duct ligation and pleurodesis. Post-operatively the patient had four right chest tubes and one left chest tube. The patient continued to have a high amount of chylous output from all drains, with the left chest tube producing up to 3.1 L/day. The four right chest tubes had a cumulative output of up to 3 L/day. At this point, alternative approaches to explain and manage the patient’s symptoms were pursued. A CT scan of the abdomen and pelvis (Fig. 2A–D) revealed a severe, short-segment occlusion of the proximal superior mesenteric vein with extensive mesenteric collateral formation. The patient presented to our department to attempt SMV recanalization and stenting. Portal and SMV venography demonstrated the SMV occlusion (Fig. 3), which was crossed with a 5 French Cobra catheter and 035 Glidewire achieving distal access. Venography performed distal to the occlusion demonstrated extensive mesenteric collateral veins with retrograde flow directed to a splenic vein shunt. Venoplasty was performed with a 4 mm angioplasty balloon. A 14 mm × 80 mm Abre venous stent was then deployed, and post-stenting venography revealed brisk appropriate redirection of flow from the mesenteric veins toward the portal vein through the SMV stent. Following SMV stenting, output from the left and right chest tubes changed from chylous to serousanguinous and markedly decreased to 0.2 L and 0.0 L, respectively, over 24 h. The patient’s shortness of breath also subsequently improved. Shortly after chest tube removal, the patient was discharged home. There was no evidence of pleural or peritoneal fluid accumulation at 6 month follow-up.
Fig. 1
A Lymphangiogram demonstrating lipiodol migration of the pelvic and lower lumbar lymphatic network and non-visualization of cisterna chyli and thoracic duct. B Left upper extremity venogram demonstrating complete central venous occlusion with extensive collateralization. C Intraoperative photograph from thoracic duct ligation
Fig. 2
Axial and coronal contrast enhanced CT abdomen and pelvic pre-SMV stenting, demonstrating focal SMV occlusion and dilated collaterals (A and C) and post-stenting, demonstrating patent SMV stent and absence of contrast in the previously seen mesenteric collaterals (B and D)
Fig. 3
SMV occlusion pre-stenting demonstrating SMV occlusion and dilated collaterals with retrograde flow (A and B) and post-stenting with non-visualization of the mesenteric collaterals and appropriate redirection of flow (C)
