A 45-year-old male was admitted to the hospital with a one-day history of abdominal pain and dyspnea. The abdominal pain started the day of admission; however, he noted worsening shortness of breath and a productive cough with clear sputum over the course of several days. He also noted a 20-pound weight loss occurring over a three-month period but denied fevers, chills, or night sweats. Physical exam was notable for tachycardia, distant heart sounds, and decreased breath sounds of the lung bases bilaterally. Vitals at presentation included a temperature of 99.2 F, heart rate of 104, respiratory rate of 20, blood pressure 182/106 mmHg, and an oxygen saturation of 95% of 2 liters via nasal cannula.
Our patient has a past medical history significant for hypertension, chronic anemia, and end stage renal disease, due to focal segmental glomerular nephritis, on hemodialysis three times per week. He has required hemodialysis for approximately four years and unfortunately does not have an arteriovenous fistula due to financial restraints; therefore, his dialysis access is via a left jugular tunneled catheter. He has required multiple tunneled catheters over the past four years.
Initial metabolic panel was within normal limits except for his creatinine of 7.99 mg/dL. Complete blood cell count revealed anemia with a hemoglobin of 10.6 g/dL and hematocrit of 33.7% but otherwise within normal limits. Chest x-ray was remarkable for bilateral pleural effusions and prominence of the cardiopericardial silhouette consistent with pericardial effusion (Figure 1). Given his abdominal pain a CT of the abdomen and pelvis without intravenous contrast was performed showing large right and small left pleural effusions and a large pericardial effusion. Since the CT scan was able to capture a majority of both the pleural and pericardial effusions a dedicated CT scan of the thorax was initially deferred.
Given his dyspnea and pleural effusions our patient underwent a right-sided thoracentesis by interventional radiology with removal of 1.5 liters of cloudy amber-colored fluid. Body fluid studies revealed a total protein of 3.3 g/dL, LDH 110, glucose 106, RBC 45, WBC 993, lymphocyte predominance of 91%, and pH of 7.0. Serum LDH was 247 and serum protein was of 6.6 g/dL. Using Light's Criteria (Table 1) our patient did not meet criteria for exudative effusion; however, results were borderline with a pleural fluid protein/serum protein ratio of 0.5 and pleural fluid LDH/serum LDH ratio of 0.445. Acid fast smear and cultures were obtained and resulted negative. Cytology was negative for malignancy but showed many small mature lymphocytes, mesothelial cells, and a few acute inflammatory cells.
Following thoracentesis, he had significant improvement in dyspnea and oxygen saturation improved to the upper 90s on room air. Regarding the pericardial effusion, a transthoracic echocardiogram was obtained revealing a large circumferential pericardial effusion measuring 1.67 cm anteriorly and 1.29 cm posteriorly. The chambers of the right atrium (RA) and right ventricle (RV) were very small, with complete obliteration of the RV chamber during systole, suggesting high intrapericardial pressure. The IVC was collapsible, measuring 1.67 cm, with a 50% collapse during inspiration. No diastolic collapse of the RV or complete systolic collapse of the RA was noted. Cardiology was consulted and during their physical exam he displayed no jugular venous distention, negative Kusmaul's sign, and no clinical signs of tamponade. An EKG was obtained showing sinus rhythm and no electrical alternans; thus pericardiocentesis was deferred.
Over the next four days he continued his regularly scheduled hemodialysis sessions and showed improvement in the pericardial effusion. Give hemodynamic stability and significant improvement there were no plans for intervention and the decision was made to closely follow with cardiology as an outpatient. However, on the planned day of discharge he developed supraventricular tachycardia and was kept another night for observation and evaluation by electrophysiology. During this time a repeat chest X-ray was performed revealing a reoccurrence of his pleural effusions; therefore, pulmonary medicine was consulted to further investigate.
Previous body fluid studies were reviewed, and, given significantly elevated lymphocytes of 91% and borderline Light's Criteria for exudative effusion, there was initial concern for common etiologies including tuberculosis, sarcoidosis, and malignancy. Our patient immigrated from Mexico to the United States approximately 20 years ago but denied any Tuberculosis exposure or previous diagnosis. He did have a 20-pound weight loss but denied other B like symptoms. We elected to further investigate the thorax for the presences of anatomical abnormalities, so a CT thorax was obtained. CT demonstrated a reaccumulation of the right pleural effusion and persistent moderate to large pericardial effusion (Figure 2) but surprisingly showed stenosis or occlusion of the superior vena cava (Figure 3). This new finding was discussed with radiology that further commented on mediastinal collaterals and evidence of SVC stenosis particularly around the patient's tunneled catheter.
A repeat thoracentesis was performed and 1.6 liters of milky fluid with a pink tinge was removed. Body fluid was remarkable for total protein of 4.6 g/dL, glucose 72, triglycerides 1,056 mg/dL, cholesterol 116 mg/dL, RBC 423,195, WBC 1,760, lymphocytes 86%, and pH 8.0. These findings were consistent with chylothorax likely form newly discovered SVC stenosis.
Other labs to evaluate for autoimmune etiology including rheumatoid factor, c-ANCA, p-ANCA, ANA, and hepatitis screen were also obtained and were unremarkable.
Repeat echocardiogram was performed and worsening pericardial effusion was noted revealing RA collapse and diastolic RV collapse suggestive of cardiac tamponade (Figure 4). Hemodynamically the patient remained stable and a scheduled pericardial drain was placed with aspiration of 775 mL of bloody fluid consistent with chylopericardium.
Given recurrent pleural and pericardial effusions vascular surgery was consulted for SVC stenosis. He underwent angioplasty of the SVC and left brachiocephalic vein using a 12x4 angioplasty balloon and replacement of the tunneled hemodialysis catheter into the left jugular vein. Ultimately, after balloon angioplasty, high triglyceride diet, and draining both the pleural and pericardial effusion his symptoms significantly improved, and he was discharged home. There are plans to establish permanent hemodialysis access by creating an AV fistula in the near future.