Fatal Hypocalcemia Due to Hungry Bone Syndrome after Total Parathyroidectomy
Journal Title: Journal of Endocrinology and Diabetes - Year 2017, Vol 4, Issue 2
Abstract
Introduction:Mild and transient post-parathyroidectomy hypocalcemia is common and usually resolves within a week in most patients. In some cases, however, postoperative hypocalcemia is more severe and prolonged, despite normal or even elevated levels of parathyroid hormone (PTH). This phenomenon, called hungry bone syndrome, occurs in patients who have developed bone disease preoperatively due to a chronic increase in bone resorption induced by high levels of PTH. The underlying hyperparathyroidism can either be primary or secondary due to end-stage renal disease. Hypocalcemia may cause myocardial dysfunction with or without hypotension. Herein, we present a woman with hungry bone syndrome and hypocalcemia who progressed to cardiopulmonary arrest. Case Report:A 52-year-old woman with a past medical history of end stage renal disease on hemodialysis, calciphylaxis, total parathyroidectomy with auto transplantation 4 years ago and parathyroidectomy (of remnant tissue) 2 weeks prior to presentation, presented with generalized weakness for 4 days and emesis for one day, associated with constipation. She had been receiving oral calcium 1000 mg four times a day along with 800 units of 1,25- dihydroxyvitamin D at home after completing her postoperative recovery at the hospital. On admission, she was hypotensive with aortic systolic murmur and sluggish bowel sounds. Chvostek sign was negative. EKG revealed sinus tachycardia and QTc prolongation. Initial lab work was significant for elevated creatinine, elevated serum phosphorus and severe hypocalcemia (total calcium < 4.0 mg/dL and an ionized 2.1 mg/dL). The patient was dialysed with a high calcium bath. We refrained from giving IV calcium initially due to the risk of precipitating calciphylaxis. Post dialysis the calcium was 5.0 mg/dL. The patient developed supraventricular tachycardia that was not responsive to adenosine and became hypotensive. She received norepinephrine for hemodynamic support and IV calcium was started. Four hours later, she developed asystole. CPR was performed for 8 minutes with return of spontaneous circulation. However, she had three more cardiac arrests in the next 24 hours. Due to the grim prognosis, code status was changed to “Do Not Resuscitate”. Approximately 18 hours after the first code the patient had another asystole and passed away. Discussion:Postparathyroidectomy hypocalcemia results from acute reversal of the effect of PTH on the bone. Sudden withdrawal of PTH in such patients causes an imbalance between bone formation and resumption affecting calcium fluxes, causing a marked increase in bone uptake of calcium, phosphate, and magnesium. Consequently the clinical features of hungry bone syndrome are due to hypocalcemia, hypophosphatemia, hypomagnesemia, and hyperkalemia. The serum calcium typically reaches a nadir two to four days postoperatively. Overt heart failure has been described in patients with myocardial dysfunction and typically resolves after normalization ofthe serum calcium. Careful monitoring of serum calcium is required to prevent and treat symptomatic hypocalcemia, which can be potentially catastrophic. In our case, she presented out of the critical symptomatic window with vague symptoms suggestive of hypocalcemia. Genetic analysis for the second sibling confirmed a novel mutation in the (SCNN1A) subunit gene of the (enac), Conclusion:Hungry bone syndrome is a serious complication that can develop after parathyroidectomy. These patients should be closely monitored for serum ionized or total calcium levels with frequent outpatient labs. Hungry bone syndrome can present few weeks after the operation.
Authors and Affiliations
Mazen O. Al-Qadi, Ameya Hodarkar, Nicole Yang, Mervat Saleh, Ahmad Abdin, Rachel Trippett
Keywords
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- EP ID EP333749
- DOI 10.15226/2374-6890/4/2/00174
- Views 124
- Downloads 0
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