Hungry Bone Syndrome Definition, Symptoms, Causes, Treatment

Learn all about hungry bone syndrome definition symptoms, causes and treatment.

Hungry Bone Syndrome should really be called “Bad Doctor Syndrome” because it should almost never happen in patients with primary hyperparathyroidism. “Hungry Bone Syndrome” is almost always due to poor doctor management of calcium requirements after parathyroid surgery.

Primarily the HBS is found in cases where hyperparathyroidism is a problem, and must be removed via parathyroidectomy. This treatment is deemed the most efficient way of dealing with the disease, and therefore is widely accepted. Transient hypocalcaemia or HBS is rarely life threatening, but can develop after this surgery. HBS can be severe and long lived, where according to The Society for Endocrinology BES says a patient will be requiring massive amounts of calcium to prevent symptoms of neuromuscular irritability, tetany.

The syndrome is reported in 25-90% of patients with radiological evidence of hyperparathyroid. Depletion of vitamin D is often associated to PHPT, and restoration of normal levels is to be attained, given the importance of this vitamin for calcium metabolism. Oral supplementation of large amounts of calcium (up to 12 grams per day) is required to treat HBS; intravenous calcium gluconate is administered in the acute presentation, until recovery from symptoms of tetany has been gained and oral administration can maintain adequate levels of serum calcium one disease vs only 0-6% of patients without skeletal involvement. There is insufficient data-based evidence on the best means to treat, minimize or prevent this severe complication of parathyroidectomy.

Treatment of HBS is basically the administration of high amounts of calcium immediately after the onset of postoperative hypocalcaemia. Supplements of active metabolites of vitamin D, as well as magnesium in depleted subjects are complementary in supporting bone remineralization. Oral supplementation may be requested for months after parathyroidectomy. Prevention is poorly documented, but it is reasonable to propose the correction of vitamin D deficit and the use of bisphosphonates aimed to lower PTH levels and bone resorption before parathyroidectomy.

Hungry Bone Syndrome Definition, Symptoms, Causes, Treatment

What is Hungry Bone Syndrome?

Hungry Bone Syndrome is a term that refers to a patient who has such severe symptoms of low blood calcium (hypocalcemia) that they require admission to the hospital for several days (2-10 days) to get IV calcium to make their low-calcium symptoms go away. It is said that their bones are so hungry for calcium that they can’t get enough oral calcium to replenish the bones. The theory is that their bones are so depleted of calcium because of many years of untreated hyperparathyroidism that the patient simply can’t get enough calcium orally and it must be given IV for days. Importantly, Hungry Bone Syndrome occurs almost exclusively in patients with hyperparathyroidism associated with kidney failure and dialysis.

Hungry Bone Syndrome Definition

Hungry bones syndrome is a disorder characterized by significant and persistent hypocalcemia, even though serum parathormone levels may be normal or even augmented. This disorder occurs following an increase of the bone formation to bone resorption ratio, a state which leads to the abundant amount of calcium than that required by the organism.

Hungry Bone Syndrome Symptoms

Severe hypocalcaemia (serum calcium concentration %2.1 mmol/l) is associated with neuromuscular irritability, clinically manifested by carpopedal spasms, perioral paresthesiae, tingling extremities, Chvostek sign and Trousseau sign. Patients can also develop generalised convulsions, which can lead to pathological fractures and ultimately if remaining uncorrected to coma and even death. Congestive heart failure, which is reversible after normalization of serum calcium concentration, has also been reported. Signs of HBS highly depend on the intensity and volume of calcium level drop over time. Clinical symptoms are notices when the level of calcium drops below 1.7 mmol/L. Basic symptoms are neurological and the patient feels numbness in extremities and around .

Muscle spasms are also commonly showing, such as cases when the muscle cramps up on slightly stronger contact this is easily discovered on facial muscles, where the patient’s muscles will cramp up after a gentle slap. An advanced phase can include whole body cramping up in a certain position, which can lead towards laryngospasm and respiratory arrest, which makes HBS an extremely perilous condition. Contraction of the smooth musculature can also cause cramps of organs found in the stomach cavity as well as strong urges for urination. Mental disorders manifest as irritability, , psychosis and dementia. The before mentioned hypocalcaemia can also lead toward heart failure and a disordered function of beta adrenergic.

Hungry Bone Syndrome Causes

Causes for this to happen can be chronic exhaustion of kidneys, hypo parathyroid (reduced excretion of parathyroid hormones), septic shock, lack of vitamin D and many others. Apart from hypocalcaemia, hypophosphatemia and hypomagnesaemia play an important role in developing this condition as these are closely associated with HBS.

Hungry Bone Syndrome Treatment

Hungry bone 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 normalization 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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