Hyperparathyroidism in Emergency Medicine Clinical Presentation

Most patients with primary hyperparathyroidism are asymptomatic or minimally symptomatic. At present in the United States, more than 80% of patients with primary hyperparathyroidism present with a myriad of nonclassical, subclinical signs and symptoms of this disease.^[7] Because manifestations of hyperparathyroidism are subtle, the disease may run an occult course for years prior to detection. Symptomatic hyperparathyroidism is characterized by vague, nonspecific symptoms including generalized weakness, fatigue, poor concentration, and depression.

A helpful mnemonic, "painful bones, renal stones, abdominal groans, and psychic moans," can be used to recall the typical symptoms of hypercalcemia. Painful bones are the result of abnormal bone remodeling due to overproduction of parathyroid hormone (PTH). Nephrolithiasis occurs secondary to hyperparathyroid disease–induced hypercalcemia and resultant hypercalciuria. Abdominal groans refers to hypercalcemia-induced ileus. Psychic moans or depression may occur in the presence of persistently elevated serum calcium levels.

• The most frequent complication of primary hyperparathyroidism is nephrolithiasis, which occurs in about 20% of patients.^[5] Renal effects of the disease also include decreased glomerular filtration rate. Hypercalciuria (>300 mg daily calcium excretion) is observed in a significant subset of patients (30%). As many as 75% of patients who undergo surgical treatment for primary hyperparathyroidism present with nephrolithiasis. Patients with primary hyperparathyroidism not only have a greater risk of renal stone disease, but this risk persists for 10 years after surgery.^[8]
• Some patients suffer from easy fatigability, a sense of generalized weakness, or mild cognitive impairment.
• Overt bone disease, including subperiosteal bone resorption and osteitis fibrosa cystica, is a serious but rare manifestation of hyperparathyroidism. Proximal muscle weakness may occur, typically affecting the lower limbs more than the upper limbs. Chondrocalcinosis and pseudogout are other potential complications of hyperparathyroidism.
• Rarely, hyperparathyroidism may abruptly worsen and may cause severe hypercalcemic complications such as profound dehydration, altered mental status, or coma. This is referred to as hypercalcemic parathyroid crisis.

No highly specific physical findings are present in hyperparathyroidism.

• Central nervous system

  • Neuropsychiatric illness: Patients frequently display clinical signs of mental depression, poor general health, low energy levels, decreased ability to complete daily tasks at home or at work, decreased social interaction, and pain, particularly in the legs.^[7]
  • Altered mental status
• Cardiovascular system: A growing body of evidence has demonstrated an increased incidence of hypertension, left ventricular hypertrophy, vascular calcification and stiffness, and deleterious myocardial events from primary hyperparathyroidism.^[9]
• Musculoskeletal system

  • Considerable evidence suggests that both men and women with primary hyperparathyroidism are more likely to have low bone density, osteopenia/osteoporosis, and increased fracture risk in comparison to controls without hyperparathyroidism.^[9]
  • Cystic bone lesions
  • Vertebral collapse
  • Chondrocalcinosis and pseudogout
  • Easily fatigued muscle (particularly proximal muscle groups)
  • Many patients with primary hyperparathyroidism will have low bone mineral density and increased fracture risk in part due to their age and gender and in part due to their hyperparathyroidism. It is clear that surgical correction of primary hyperparathyroidism is followed by reduction in bone turnover and significant improvements in bone mineral density.^[10]
• GI system

  • Pancreatitis and pancreatic calcification
  • Peptic ulcer disease
• Renal system: The renal manifestations of primary hyperparathyroidism include recurrent calcium nephrolithiasis, nephrocalcinosis, and impaired renal function.^[8]

• A single parathyroid adenoma is the underlying pathology in 85% of cases.
• Diffuse hyperplasia of all parathyroid glands occurs in approximately 15% of cases. More than half of these are part of a familial syndrome.
• Parathyroid carcinoma is a very rare cause of primary hyperparathyroidism.
• Secondary hyperparathyroidism occurs when the parathyroid glands are chronically stimulated to release PTH.

  • Chronic renal failure- Hypocalcemia, hyperphosphatemia, and low 1.25 vitamin D (calcitriol) levels are the main triggers for the development of secondary hyperparathyroidism in this setting.^[11]
  • Malabsorption syndromes
  • Rickets
• Long-standing secondary hyperparathyroidism may progress into autonomous hypersecretion of PTH even after correction of chronic hypocalcemia; it is termed tertiary hyperparathyroidism.
• External radiation to the head, neck, and chest regions is associated with an increased likelihood of developing benign parathyroid tumors. Parathyroid adenomas reported after radiation exposure are usually hyperfunctioning and are usually detected upon manifestations of primary hyperparathyroidism.^[12] Patients with radiation-induced hyperparathyroidism are also more likely to have coexistent nodular goiter and thyroid gland carcinoma than patients with spontaneous hyperparathyroidism.^[13]