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Abstract: TH-PO341

Navigating Hyponatremia in a Patient with Superior Vena Cava Obstruction from Retained Pacer Wires and Portal Hypertension

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Kavalam, George J., Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Foo, Rucci Marcus C., Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Chitrakar, Solab, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Bergmann, Matthias, Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
  • Nasser, Samer S., Beth Israel Deaconess Medical Center, Boston, Massachusetts, United States
Introduction

Managing hyponatremia proves challenging when multifactorial, involving hypervolemia and continuous total body sodium losses. A 54-year-old male with biopsy-proven nodular regenerative hyperplasia, grade 2 liver fibrosis with portal hypertension, and complete heart block (CHB) attributed to Lyme disease, requiring a pacemaker. Subsequent recovery prompted the removal of the device, resulting in retained pacer wires that precipitated superior vena cava (SVC) obstruction years later. Deemed too risky for extraction, the patient developed recurrent pleural effusions, necessitating management with a Pleur-X catheter. Within two weeks, severe hyponatremia (serum sodium 121 mEq/L) ensued, leading to a prolonged and complex hospitalization.

Case Description

Initially diagnosed with hypovolemic hyponatremia due to sodium losses from frequent pleural fluid drainage, the patient’s sodium levels improved with isotonic fluid replacement. However, he developed hypervolemia and respiratory compromise. Despite treatment with fluid restriction, urea packets, salt tablets, intravenous diuretics, and Tolvaptan, limited success was achieved, with progressive renal failure further complicating the clinical picture. SVC recanalization and stent placement were performed; however, hyponatremia persisted, necessitating continuous renal replacement therapy (CRRT) for volume removal. His course was further complicated by SVC stent migration, precipitating cardiogenic shock requiring extracorporeal membrane oxygenation (ECMO). Subsequently, epicardial lead extraction and SVC reconstruction were performed, restoring kidney function and normalizing sodium levels.

Discussion

This case underscores the complexities of managing hyponatremia caused by volume overload and total body sodium depletion. Managing volume status and electrolyte balance required a multidisciplinary approach involving hepatologists, cardiologists, and nephrologists. The successful preoperative use of CRRT to optimize volume status and electrolytes, followed by complex surgical interventions to treat the underlying problem, highlights the potential of advanced therapeutic modalities when conventional treatments fail. Tailored, collaborative care significantly improves outcomes in complex medical conditions like treatment-resistant hyponatremia.