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      Fatal Hypocalcaemia Due to Hungry Bone Syndrome with Secondary Refractory HyperParathyroidism After Parathyroidectomy: A Case Report

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          Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcaemia associated with hypophosphatemia and hypomagnesaemia, and is exacerbated by suppressed parathyroid hormone (PTH) levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism (PHPT) and preoperative high bone turnover. [ 1]

          Case report

          This report concerns a dialysed patient who underwent surgical treatment for secondary refractory hyperparathyroidism. Haemodialysis was carried out pre-operatively, and subsequently, a total parathyroidectomy with auto-transplantation of parathyroid tissue in the sternocleidomastoid muscle (SCM) was performed. Rapid and progressive hypocalcaemia symptoms developed during the second day postoperatively. Acute cardiac symptoms with tachyarrhythmia, haemodynamic instability and finally asystole occurred, which required cardiopulmonary resuscitation (CPR). The ionic calcium level was 2.2 mg/dL being consistent with a diagnosis of HBS. A second cardiac arrest unresponsive to CPR followed an initial period of normal sinus rhythm. Death ensued shortly after. Before death, the ionic calcium was 3.1 mg/dL.


          HBS, after parathyroidectomy in patients with secondary hyperparathyroidism (SHPT), may be severe, prolonged and sometimes fatal. Generally, HBS symptomatology is that of a mild hypocalcaemia. It can, however, include heart rhythm disturbances with haemodynamic alterations requiring intensive care measurements and even cardiopulmonary resuscitation. A close clinical and laboratory post-parathyroidectomy monitoring of dialysed patients is of the utmost importance.

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          Most cited references 19

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          Hungry bone syndrome: still a challenge in the post-operative management of primary hyperparathyroidism: a systematic review of the literature.

          Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcaemia associated with hypophosphataemia and hypomagnesaemia, and is exacerbated by suppressed parathyroid hormone (PTH) levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism (PHPT) and preoperative high bone turnover. It is a relatively uncommon, but serious adverse effect of parathyroidectomy. We conducted a literature search of all available studies reporting a 'hungry bone syndrome' in patients who had a parathyroidectomy for PHPT, to identify patients at risk and address the pitfalls in their management. The severe hypocalcaemia is believed to be due to increased influx of calcium into bone, due to the sudden removal of the effect of high circulating levels of PTH on osteoclastic resorption, leading to a decrease in the activation frequency of new remodelling sites and to a decrease in remodelling space, although there is no good documentation for this. Various risk factors have been suggested for the development of HBS, including older age, weight/volume of the resected parathyroid glands, radiological evidence of bone disease and vitamin D deficiency. The syndrome is reported in 25-90% of patients with radiological evidence of hyperparathyroid bone disease vs only 0-6% of patients without skeletal involvement. There is insufficient data-based evidence on the best means to treat, minimise or prevent this severe complication of parathyroidectomy. Treatment is aimed at replenishing the severe calcium deficit by using high doses of calcium supplemented by high doses of active metabolites of vitamin D. Adequate correction of magnesium deficiency and normalisation of bone turnover are required for resolution of the hypocalcaemia which may last for a number of months after successful surgery. Preoperative treatment with bisphosphonates has been suggested to reduce post-operative hypocalcaemia, but there are to date no prospective studies addressing this issue.
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            Post-parathyroidectomy hypocalcemia: incidence, risk factors, and management.

            The purpose of this study was to evaluate the incidence and severity of hypocalcemia after parathyroidectomy and delineate its risk factors. Data was retrieved from a prospective database. Patients with postoperative hypocalcemia were identified and risk factors were investigated including primary versus renal hyperparathyroidism (HPT), preoperative calcium, parathyroid hormone (PTH) and alkaline phosphatase levels, gland weight, pathology, extent of surgery, and reoperative surgery. Of the 162 patients who underwent parathyroidectomy, 84 (52%) were hypocalcemic postoperatively: 55 (42%) of 132 patients with primary and 29 (97%) of 30 patients with renal HPT (P = 0.0001). Patients with renal HPT had more profound hypocalcemia with a mean +/- SD calcium of 7.34 mg/dL +/- 1.07 versus 7.76 mg/dL +/- 0.59 for patients with primary HPT (P < 0.05). Symptoms were present in 28 (51%) of 55 patients with primary and 13 (45%) of 29 patients with renal HPT. Only three (2%) patients with primary compared to 29 (97%) with renal HPT were treated with intravenous calcium. The average length of stay for hypocalcemic patients was 0.7 days for primary HPT versus 4.7 days for renal HPT (P < 0.0005). Patients with primary HPT who underwent subtotal parathyroidectomy had significantly lower postoperative calcium levels (7.95 mg/dL +/- 0.64) than patients who had a single or double adenoma removed (8.49 mg/dL +/- 0.79) (P = 0.036). No other factor was predictive of postoperative hypocalcemia. Patients with renal HPT develop profound postoperative hypocalcemia requiring intravenous calcium and vitamin D therapy. Hypocalcemia in patients with primary HPT develop less severe hypocalcemia that is amenable to outpatient oral calcium therapy and should be routinely initiated following subtotal parathyroidectomy.
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              Reversible congestive heart failure related to profound hypocalcemia secondary to hypoparathyroidism.

              A 71-year-old man presented with acute pulmonary edema related to new onset of severe left ventricular dysfunction (ejection fraction, 30%). His symptoms did not improve with emergency therapy with diuretics and dobutamine. He was noted to be severely hypocalcemic (5.5 mg/dL) and subsequently showed dramatic improvement in symptoms and ejection fraction (58%) with correction of hypocalcemia with intravenous calcium and calcitriol replacement. Hypocalcemia was related to surgically induced hypoparathyroidism. The patient had been instructed to decrease calcium supplements and to discontinue calcitriol 3 months previously due to hypercalcemia. Additional factors that may have contributed to hypocalcemia included vitamin D deficiency, alendronate therapy for osteoporosis, and chronic kidney disease. We concluded that the patient's congestive heart failure was precipitated by severe hypocalcemia and resolved with correction of hypocalcemia. Hypocalcemia is a rare cause of reversible congestive heart failure that should be in the differential diagnosis in any patient presenting with heart failure and not responding to traditional therapy.

                Author and article information

                J Crit Care Med (Targu Mures)
                J Crit Care Med (Targu Mures)
                The Journal of Critical Care Medicine
                October 2019
                27 November 2019
                : 5
                : 4
                : 140-144
                [1 ]Endocrinology Department, Mures County Emergency Hospital , Targu Mures, Romania
                [2 ]University of Medicine, Pharmacy, Science and Technology of Targu Mures , Targu Mures, Romania
                [3 ]2nd Surgery Department, Mures County Emergency Hospital , Targu Mures, Romania
                [4 ]Hon Fellow, University of Edinburgh , Edinburgh United Kingdom
                Author notes
                [* ] Valentin Daniealopol, Mures County Emergency Hospital, 2 nd Surgery Department, Gheorghe Marinescu street no.50, Targu Mures, 540136, Romania valentin.daniealopol@
                © 2019 Corina Pop Radu, Valentin Daniealopol, Ario Santini, Ruxandra Darie, Daniela Tatiana Sala, published by Sciendo

                This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

                Page count
                Pages: 5
                Case Report


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