Hyperparathyroidism in Emergency Medicine Clinical Presentation

Updated: Oct 18, 2016
  • Author: Philip N Salen, MD; Chief Editor: Erik D Schraga, MD  more...
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Most patients with PHPT are asymptomatic or minimally symptomatic. At time of diagnosis, PHPT patients' symptoms and signs are subtle and the diagnosis is made fortuitously as part of the work-up of hypercalcemia. [9] 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.

When a patient has symptoms secondary to PHPT induced hypercalcemia, classically, PHPT targets the kidney and the skeleton. [10]  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 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.

As many as 75% of patients who eventually undergo surgical treatment for PHPT present initially with recurrent ureteral colic. Patients with PHPT not only have a greater risk of renal stone disease, but this risk persists for 10 years postparathyroidectomy. [11]

Some PHPT patients suffer from easy fatigability, asthenia, a sense of generalized weakness, or mild cognitive impairment. 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, symptomatic PHPT may abruptly worsen and cause severe hypercalcemic complications such as profound dehydration, delirium, or coma; this is referred to as hypercalcemic parathyroid crisis.

In the modern era, even though most patients present with “asymptomatic” PHPT, careful questioning and examination can often elucidate subtle neurocognitive and psychiatric complaints. [7]



There are no sine qua non physical exam findings that corroborate the diagnosis of hyperparathyroidism without confirmatory laboratory evidence.

  • Central nervous system manifestations of PHPT are neuropsychiatric or neurocognitive. Symptomatic PHPT 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. [9] If hyperparathyroid induced hypercalcemia levels are high enough, which is rare, patients can manifest hypercalcemia-induced delirium.
  • PHPT may have cardiovascular sequelae as well. There is evidence that PHPT is associated with hypertension, left ventricular hypertrophy, vascular calcifications and stiffness, and even myocardial events. [12] Even very mild PHPT, with a mean serum calcium in the range of 10.6 mg/dL, can increase aortic valve calcification area, increase aortic and carotid stiffness, and increase vascular wall thickness, all of which are preclinical predictors of deleterious cardiovascular outcomes. [7]
  • Musculoskeletal system manifestations of hyperparathyroidism typically manifest as skeletal demineralization.
    • Overt bone disease, including subperiosteal bone resorption and osteitis fibrosa cystica, is a serious but rare manifestation of hyperparathyroidism. Osteitis fibrosa cystica, cystic bone lesions ("brown tumors") of bones, and periosteal bone resorption were commonly seen in typical PHPT historically, which rarely manifests now with improved laboratory screening techniques for PHPT and hypercalcemia along with curative therapy. [7]
    • Both men and women with PHPT are more likely to have low bone density, osteopenia/osteoporosis, and increased fracture risk, out of proportion to their relative risk secondary to their age and gender. [12] Surgical correction of PHPT results in reduction in bone turnover and significant improvements in bone mineral density. [13]
    • Other manifestations of hyperparathyroidism are chondrocalcinosis, pseudogout, and easily fatigued musculature, particularly the proximal muscle groups.
  • Gastrointestinal manifestations of hyperparathyroidism are pancreatitis, pancreatic calcification, and peptic ulcer disease.
  • Renal manifestations of PHPT include recurrent calcium nephrolithiasis, nephrocalcinosis, and impaired renal function. [11]


Causes include the following:

  • A single parathyroid adenoma is the underlying pathology of PHPT in 85% of cases.
  • Diffuse hyperplasia of all parathyroid glands occurs in approximately 15% of cases. More than half of multiple parathyroid gland involvement cases are part of multiple endocrine neoplasia syndromes.
  • Parathyroid carcinoma is an uncommon cause of PHPT.
  • Secondary hyperparathyroidism is a frequent complication of chronic renal failure. [14] Secondary hyperparathyroidism occurs when the parathyroid glands are chronically stimulated to release PTH. Hypocalcemia, hyperphosphatemia, and depressed 1.25 vitamin D (calcitriol) levels are the main triggers for the development of secondary hyperparathyroidism in chronic renal failure, malabsorption syndromes, and rickets. [15]
  • Tertiary hyperparathyroidism results when long-standing secondary hyperparathyroidism progresses to autonomous hypersecretion of PTH even after correction of chronic hypocalcemia.
  • External radiation to the head, neck, and chest regions is associated with an increased likelihood of developing parathyroid tumors. Parathyroid adenomas manifesting after radiation exposure are usually hyperfunctioning and often manifest as symptomatic PHPT. [16] Patients with radiation-induced hyperparathyroidism are also more likely to have coexistent nodular goiter and thyroid gland carcinoma than patients with spontaneous hyperparathyroidism. [17]

Physical Examination

In developed countries, most patients with hyperparathyroidism have no specific physical findings. Patients may present with nonspecific symptoms such as fatigue, mild depression, or cognitive impairment. While it is important to exclude neck masses in patients with suspected hyperparathyroidism, parathyroid adenomas and carcinomas are rarely palpable. Band keratopathy, the deposition of calcium phosphate in the exposed regions of the cornea that is detected by a slit-lamp examination, is an exceedingly rare hyperparathyroidism manifestation and only occurs with very high serum calcium and phosphate levels, which is rare in PHPT. [18]

In developing nations where biochemical screening is not widely available, patients can develop and present with more severe physical examination findings because they present with more advanced cases of hyperparathyroidism. Advanced, initial presentation of hyperparathyroidism include: brown tumors of the maxilla, sphenoid, sinus, and occipital bone; nephrocalcinosis, neuropsychiatric disturbances. The brown tumor is an unusual presentation of fibrous osteitis that represents a serious complication of renal osteodystrophy, affecting predominantly the hands, feet, skull, and facial bones. [14]   Neuropsychiatric disturbances vary and can include lethargy, decreased cognitive and social function, depressed mood, psychosis, and coma when there is severe hypercalcemia. [18]




When the diagnosis of hyperparathyroidism is delayed, patients are more likely to present with complications or sequelae of their disease. Recurrent nephrolithiasis with consequent ureteral colic results from hyperparathyroidism induced hypercalciuria. Hyperparathyroid induced osteoporosis increases the risk of fractures compared to the general population. [2]  Brown tumor, a musculoskeletal complication of hyperparathyroidism, is a focal bone lesion caused by increased osteoclastic activity and fibroblast proliferation encountered in primary and, more rarely, in secondary hyperparathyroidism. [14]  Rheumatologic diseases such as gout and pseudogout have been associated with hyperparathyroidism induced alterations in calcium homeostasis. [18]   The risk of pancreatitis is approximately 10 times higher in PHPT patients than in the general population. [2]  Another gastrointestinal manifestation of PHPT is its association with chronic autoimmune atrophic gastritis. PHPT is associated with a higher incidence of arterial hypertension and an increased risk of overall cardiovascular mortality. [2]