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Chylothorax and Chylopericardium: a Complication of Long-Term Central Venous Catheter Use

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Chylothorax and Chylopericardium: a Complication of Long-Term Central Venous Catheter Use Hindawi Case Reports in Pulmonology Volume 2019, Article ID 4908259, 5 pages https://doi.org/10.1155/2019/4908259 Case Report Chylothorax and Chylopericardium: A Complication of Long-Term Central Venous Catheter Use James Livesay , Isaac Biney, and J. Francis Turner Jr. Department of Medicine, University of Tennessee Graduate School of Medicine, Knoxville, TN, USA Correspondence should be addressed to J. Francis Turner Jr.; [email protected] Received 30 April 2019; Accepted 1 July 2019; Published 11 July 2019 Academic Editor: Reda E. Girgis Copyright © 2019 James Livesay et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Te development of chylothorax and chylopericardium is an uncommon complication of the long-term use of central venous catheters. We describe a unique case of an end stage renal disease patient on hemodialysis with a lef jugular tunneled catheter who developed superior vena cava syndrome. Our patient presented with both a large pleural and pericardial efusion that despite drainage continued to reaccumulate. Further imaging with CT scan of the thorax revealed stenosis of the superior vena cava leading to recurrent chylothorax and chylopericardium. 1. Introduction best defned as a diameter reduction >50% with or without upstream collaterals [5]. We report a case of SVC stenosis in Chylothorax and chylopericardium refer to the accumulation an end stage renal disease (ESRD) patient on hemodialysis ofchyleinthepleuralandpericardialspace,respectively. with a chronically indwelling lef jugular central catheter Chyle is a milky-appearing fuid containing high levels of leading to both chylothorax and chylopericardium. fat, proteins, and immunoglobulins, which is carried back to the venous system from the cisterna chyli via the thoracic 2. Case Presentation duct [1]. Te thoracic duct originates from the cisterna chyli and terminates at the junction of the lef subclavian and A 45-year-old male was admitted to the hospital with internaljugularveins.Tevolumeofchylerangesfrom10 a one-day history of abdominal pain and dyspnea. Te to 100 mL/kg body weight, in a normal adult, impacted by abdominal pain started the day of admission; however, he factors including diet, intestinal absorption, and degree of noted worsening shortness of breath and a productive cough physical activity [2]. with clear sputum over the course of several days. He also Both chylothorax and chylopericardium can be a direct noted a 20-pound weight loss occurring over a three-month result of superior vena cava (SVC) syndrome, which is best period but denied fevers, chills, or night sweats. Physical described as obstruction of the SVC interrupting normal exam was notable for tachycardia, distant heart sounds, and venous return of blood from the head, upper extremities, decreased breath sounds of the lung bases bilaterally. Vitals ∘ and thorax to the right atrium [3]. Causes of SVC syndrome at presentation included a temperature of 99.2 F, heart rate of include direct trauma, surgical injury to the thoracic duct, 104, respiratory rate of 20, blood pressure 182/106 mmHg, and malignancy, or as in this case central venous lines [4]. SVC an oxygen saturation of 95% of 2 liters via nasal cannula. syndrome secondary to central venous lines is typically a Our patient has a past medical history signifcant for direct result of either thrombosis or vessel wall thickening hypertension, chronic anemia, and end stage renal disease, leading to stenosis. Many cases present as a result of thrombo- due to focal segmental glomerular nephritis, on hemodialysis sis around the catheter leading to SVC obstruction requiring three times per week. He has required hemodialysis for removal of the catheter and long-term anticoagulation. Te approximately four years and unfortunately does not have an other common cause of SVC syndrome is SVC stenosis arteriovenous fstula due to fnancial restraints; therefore, his 2 Case Reports in Pulmonology Figure 1: Initial chest x-ray demonstrating pleural efusion and abnormal cardiac silhouette. Table 1: Light’s Criteria. > Pleural Fluid PF/Serum PF/Serum PF LDH Upper 2/3 Limit Protein Ratio LDH Ratio of Normal Transudative <0.5 <0.6 <2/3 Exudative ≥0.5 ≥0.6 ≥2/3 dialysis access is via a lef jugular tunneled catheter. He has protein ratio of 0.5 and pleural fuid LDH/serum LDH ratio required multiple tunneled catheters over the past four years. of 0.445. Acid fast smear and cultures were obtained and Initial metabolic panel was within normal limits except resulted negative. Cytology was negative for malignancy but for his creatinine of 7.99 mg/dL. Complete blood cell count showed many small mature lymphocytes, mesothelial cells, revealed anemia with a hemoglobin of 10.6 g/dL and hema- and a few acute infammatory cells. tocrit of 33.7% but otherwise within normal limits. Chest Following thoracentesis, he had signifcant improvement x-ray was remarkable for bilateral pleural efusions and in dyspnea and oxygen saturation improved to the upper 90s prominence of the cardiopericardial silhouette consistent on room air. Regarding the pericardial efusion, a transtho- with pericardial efusion (Figure 1). Given his abdominal racic echocardiogram was obtained revealing a large circum- pain a CT of the abdomen and pelvis without intravenous ferential pericardial efusion measuring 1.67 cm anteriorly contrast was performed showing large right and small lef and1.29cmposteriorly.Techambersoftherightatrium pleural efusions and a large pericardial efusion. Since the (RA) and right ventricle (RV) were very small, with complete CT scan was able to capture a majority of both the pleural obliteration of the RV chamber during systole, suggesting and pericardial efusions a dedicated CT scan of the thorax high intrapericardial pressure. Te IVC was collapsible, was initially deferred. measuring 1.67 cm, with a 50% collapse during inspiration. Given his dyspnea and pleural efusions our patient No diastolic collapse of the RV or complete systolic collapse of underwent a right-sided thoracentesis by interventional radi- the RA was noted. Cardiology was consulted and during their ology with removal of 1.5 liters of cloudy amber-colored fuid. physical exam he displayed no jugular venous distention, Body fuid studies revealed a total protein of 3.3 g/dL, LDH negative Kusmaul’s sign, and no clinical signs of tamponade. 110, glucose 106, RBC 45, WBC 993, lymphocyte predomi- An EKG was obtained showing sinus rhythm and no electrical nance of 91%, and pH of 7.0. Serum LDH was 247 and serum alternans; thus pericardiocentesis was deferred. protein was of 6.6 g/dL. Using Light’s Criteria (Table 1) our Over the next four days he continued his regularly patient did not meet criteria for exudative efusion; however, scheduled hemodialysis sessions and showed improvement results were borderline with a pleural fuid protein/serum in the pericardial efusion. Give hemodynamic stability and Case Reports in Pulmonology 3 Figure 2: Demonstrates reaccumulation of pleural and pericardial fuid. Figure 3: Demonstrates the stenotic area in the SVC around the catheter. signifcant improvement there were no plans for intervention a 20-pound weight loss but denied other B like symptoms. and the decision was made to closely follow with cardiology We elected to further investigate the thorax for the presences as an outpatient. However, on the planned day of discharge of anatomical abnormalities, so a CT thorax was obtained. he developed supraventricular tachycardia and was kept CT demonstrated a reaccumulation of the right pleural another night for observation and evaluation by electrophys- efusion and persistent moderate to large pericardial efusion iology. During this time a repeat chest X-ray was performed (Figure 2) but surprisingly showed stenosis or occlusion of revealing a reoccurrence of his pleural efusions; therefore, the superior vena cava (Figure 3). Tis new fnding was pulmonary medicine was consulted to further investigate. discussed with radiology that further commented on medi- Previous body fuid studies were reviewed, and, given sig- astinal collaterals and evidence of SVC stenosis particularly nifcantly elevated lymphocytes of 91% and borderline Light’s around the patient’s tunneled catheter. Criteria for exudative efusion, there was initial concern for A repeat thoracentesis was performed and 1.6 liters common etiologies including tuberculosis, sarcoidosis, and of milky fuid with a pink tinge was removed. Body malignancy. Our patient immigrated from Mexico to the fuid was remarkable for total protein of 4.6 g/dL, glucose United States approximately 20 years ago but denied any 72, triglycerides 1,056 mg/dL, cholesterol 116 mg/dL, RBC Tuberculosis exposure or previous diagnosis. He did have 423,195, WBC 1,760, lymphocytes 86%, and pH 8.0. Tese 4 Case Reports in Pulmonology Figure 4: Echocardiogram prior to pericardial drain placement showing large pericardial efusion. fndings were consistent with chylothorax likely form newly upper extremity edema [5]. While rare the development of discovered SVC stenosis. chylothorax alone carries a mortality of 10% in most major Other labs to evaluate for autoimmune etiology including medical centers [2]. Once central vein obstruction occurs rheumatoid factor, c-ANCA, p-ANCA, ANA, and hepatitis it may quickly become clinically signifcant as the thoracic screen were also obtained
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