Abstract: SA-PO937

Perioperative Acute Systolic Cardiac Dysfunction as Complication of Parathyroidectomy

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports

Authors

  • Owoyemi, Itunu O., University of Virginia, Charlottesville , Virginia, United States
  • Nishio-Lucar, Angie G., University of Virginia HS, Charlottesville, Virginia, United States
  • Swaminathan, Sundararaman, University of Virginia, Charlottesville , Virginia, United States
  • Warburton, Karen M., None, Charlottesvilee, Virginia, United States
  • Vranic, Gayle M., University of Virginia Health System, Charlottesville, Virginia, United States
  • Lobo, Peter I., University of Virginia, Charlottesville , Virginia, United States
  • Doyle, Alden Michael, None, Charlottesvilee, Virginia, United States
Background

Several factors including hypocalcemia have been incriminated in the pathogenesis of abnormal cardiac function in End Stage Kidney Disease (ESKD).

Methods

We report a case of a 57 yo woman with ESKD due to hypertension, failed kidney transplant graft from BK nephropathy 8 years ago referred for management of severely elevated parathyroid hormone levels (PTH). Patient had undergone subtotal parathyroidectomy 5 years prior. Despite intensive therapy with calcitriol and cinacalcet, her PTH levels had remained around 2000 pg/mL. She had stress test done 2 months prior to operation that showed no evidence of inducible myocardial ischemia and preserved ejection fraction. Her evaluation included a sestamibi scan with showed activity within the mediastinum prompting the decision for resection and auto-transplantation. A day prior to surgery, she recieved IV calcitriol during dialysis and was down to her target weight. Cinacalcet was discontinued.
Her surgery was uncomplicated. She received 1 g of IV calcium chloride. She was extubated quickly in the recovery room and initially did well. Over the next hour, she developed acute shortness of breath with hypercapneic respiratory failure. A stat chest X-ray revealed left pleural effusion and mild cardiomegaly, which were new findings compared to chest X-ray done a day before surgery. Pertinent laboratory findings prior to this episode include hemoglobin 10.7mg/dL, ionized calcium 3.9 mg/dL, and phosphorus 7.7 mg/dL. PTH was 190 pg/mL, down from 1399 pg/mL at beginning of surgery, troponin – 0.03 with no EKG changes. An Echocardiogram done showed decreased left ventricular systolic global function and small pericardial effusion adjacent to the right ventricle. A protocol for prevention of hypocalcemia was immediately embarked upon to prevent further episodes of hypocalcemia which resulted in good control of serum calcium and phosphorus levels. Her cardiac dysfunction resolved prior to discharge and she has done well since.

Conclusion

Modifications of myocellular calcium interactions or sensitivity which may alter relaxation and contribute to cardiac dysfunction. Patients with severe hyperparathyroidism are at risk in the early post-operative period and should be monitored closely for hypocalcemia and, less commonly, acute cardiac dysfunction.