Chylopericardium due to Subclavian Vein Thrombosis in the Setting of Protein S Deficiency

Background. Chylopericardium is the accumulation of lymphatic fluid in the pericardial cavity. It can be idiopathic or secondary to trauma, cardiothoracic surgery, neoplasm, radiation, tuberculosis, lymphatic duct dysfunction, thrombosis, or other causes. We present a case of chylopericardium due to subclavian vein thrombosis in a patient with protein S deficiency. Clinical Case. A 48-year-old man with a history of protein S deficiency presented to the emergency department with shortness of breath and a productive cough. CT of the chest showed pulmonary emboli, moderate pericardial effusion, and a large thrombus of the superior vena cava, brachiocephalic vein, and subclavian veins. He developed echocardiographic evidence of cardiac tamponade so he underwent pericardiocentesis with drainage of milky-appearing fluid. Analysis of the fluid showed elevated triglycerides consistent with chylopericardium. The pericardial effusion reaccumulated, likely secondary to lymphatic duct obstruction due to his subclavian vein thrombus. Catheter-assisted thrombolysis was performed with resolution of the patient’s effusion and symptoms. Conclusion. Chylopericardium is a rare but important complication of subclavian vein thrombosis. Management is typically with surgical intervention, although our case represents successful treatment with catheter-assisted thrombolysis.

Trans-cervical thoracic duct embolization for post-surgical left Chylothorax in a patient with multifocal lymphatic malformations

Background Mediastinal and abdominal lymphatic malformations may not be diagnosed until adulthood. Radiologic and pathologic diagnosis is often challenging due to the rarity of the lesion. Surgical excision of these lesions may be curative but lymphatic leak is a known complication. Lymphatic duct embolization may then be required to treat the leak. Case presentation We describe a patient with post-surgical chylothorax where thoracic duct lymphangiography and embolization was performed by catheterizing the thoracic duct at the venous angle where it drains into the subclavian vein. Conclusion Lymphatic duct embolization can be challenging in patients with lymphatic malformations. In these patients, if there is adequate visualization on ultrasound or fluoroscopy, terminal aspect of the thoracic duct can be accessed through the subclavian vein to perform the procedure.

Lymph or Chyle Leak After Neck Dissection in Patients With Thyroid Carcinoma: Results of a Study on 1724 Patients

Background To discuss the prevention and treatment of lymph or chyle leak following neck dissection in patients with thyroid carcinoma. Methods A total of 1724 patients with thyroid carcinoma received neck dissection in the Sun Yat-sen University Cancer Center between November 2009 and October 2014. The incidence and management of leak were analyzed. Results A total of 92 (5.34%) patients developed leak, 28 (1.62%) developed lymph leak, 59 (3.42%) developed chyle leak, and 5 (.29%) developed chylothorax. Medical management to stop postoperative lymph or chyle leak included pressure dressing, reoperation, fasting, or low-fat diet therapy. Conclusions Lymph or chyle leak may occur in thyroid carcinoma patients who underwent neck dissection. Clinicians should alert to leak when there were IV + VI region lymph node metastasis and should become aware of chylothorax after pressure dressing. A careful identification and ligation of lymphatic duct may be an effective way to avoid lymph or chyle leak.

Postoperative External Transabdominal Severe Lymphorrea (Case Report)

Massive lymphorrhea can cause severe dysfunction of organs and systems and result in death due to loss of vital metabolites from the bodyAim. To demonstrate low efficacy of conservative therapy and late lymph duct ligation in continuous massive postoperative lymphorrhea.Results. We treated a patient with previous subtotal gastric resection with single-plane pancreatic resection, D2 lymph node dissection, peritoneal draining due to poorly differentiated carcinoma in the lower third of stomach and total hysterectomy who developed external lymphorrhea through peritoneal drainage tubes 3 days after surgery. A fat-rich diet, endolymphatic sodium etamsylate administration, and lymphatic duct ligation were not successful in terminating the lymph leakage. Despite the intensive care including extracorporeal detoxification, the multi-organ failure progressed and on day 28 after the surgery the patient was pronounced dead.Conclusion. Damage to lymph ducts and lymph nodes can be complicated by massive lymphorrhea. If the source of lymphorrhea can be identified, an urgent surgical intervention is warranted to stop the lymph leakage, as well as the restoration of homeostasis to replenish the lost metabolites and prevent death of the patient.

Management of large congenital chylous ascites in a preterm infant: fetal and neonatal interventions

Congenital chylous ascites is a rare cause of ascites in newborn infants. Its aetiology varies from localised leaky lymphatic duct to genetic syndromes. Most of these cases have transient ascites resolving over time with conservative management but some may progress needing medical as well as surgical treatment. We describe a case of antenatally detected large fetal ascites necessitating abdominal paracentesis and amnioreduction. Marked respiratory distress at birth required urgent abdominal paracentesis to relieve symptoms. The infant initially showed a good response to medium chain triglyceride (MCT) based formula milk feeds. Feeds were discontinued for 3 weeks due to sepsis with ileus. On recovery, recommencement of feeds resulted in reaccumulation of ascites. As the response to MCT-based formula was inadequate, octreotide therapy was initiated. Ascites showed remarkable resolution over the next 2 weeks and was discharged home. Follow-up at 5 years of age revealed normal growth and neurodevelopment.

Endothelial dysfunction and impaired lymphatic drainage of the heart in the pathogenesis of cardiovascular complications in diabetes

Aim. To study the role of activation of lipid peroxidation and endothelial dysfunction in disorders of lymphatic coagulation and lymphatic drainage of the heart in streptozotocin-induced diabetes mellitus. Methods. The experiments were performed on 25 rabbits. To simulate diabetes mellitus, animals were injected intraperitoneally with streptozotocin at a dose of 50 mg/kg. Indicators of lipid peroxidation, coagulation, and endothelial dysfunction were examined in lymph obtained by draining the thoracic lymphatic duct. We also examined the state of lymphatic drainage of tissues at the level of the thoracic lymphatic duct and at the level of the heart, before and after inducing diabetes. Results. On the 5th day after inducing diabetes mellitus, the concentration of diene conjugates in lymph exceeded the initial level by 66.6% (p 0.001), and the concentration of malondialdehyde increased by more than 2.6 times (p 0.001); 30 min later these indicators of diene conjugates and malondialdehyde exceeded the initial values by 3.2 and 2.2 times, respectively (p 0.001), and the concentration of reduced glutathione decreased by 73.8% (p 0.001). At the same time, the indicators of lymph coagulation, activated partial thromboplastin time and thrombin time, were shortened by 42.2 and 32.9%, respectively (p 0.01). The rate of lymphatic drainage from the thoracic duct decreased by 81.8% (p 0.01). Such dynamics persisted throughout the experiment. The duration of the removal of a lymphotropic dye from the heart at stage I was increased on the 30th and 60th days of the study by 28.1% (p 0.05) and 57.9% (p 0.001), respectively. At stage II, this indicator decreased, starting from the 2nd month of the experiment it exceeded the initial level by 22.2% (p 0.05), and subsequently by 32.7% (p 0.001) Conclusion. The activation of lipid peroxidation and intravascular coagulation of lymph, followed by inhibition of lymphatic drainage of tissues at the level of the thoracic lymphatic duct, especially the heart, creates favourable conditions for the accumulation of toxic products of impaired metabolism in the myocardium, contributing to the development of cardiovascular complications.