DRG Category: 644
Mean LOS: 4.3 days
Description: Medical: Endocrine Disorders With Complication or Comorbidity
The parathyroid glands—four small endocrine glands located on the posterior surface of the thyroid gland—produce the parathyroid hormone (PTH), which regulates calcium and phosphorus balance by affecting gastrointestinal (GI) absorption of calcium, bone resorption (removal of bone tissue by absorption) of calcium, and renal regulation of both calcium and phosphorus. Calcium and phosphorus have a reciprocal relationship in the body; high levels of calcium lead to low levels of phosphorus. Hypoparathyroidism is a rare clinical syndrome and is associated with a deficiency or absence of PTH or a decreased peripheral action of PTH.
Although both hypocalcemia and hyperphosphatemia result from hypoparathyroidism, hypocalcemia accounts for the majority of clinical manifestations. The human body is able to compensate for low or moderate hypocalcemia. The seriousness of the disease is variable with the degree of hypocalcemia and the speed with which it develops. Acute hypoparathyroidism follows swiftly after trauma or removal of the parathyroid glands. The acute form, as with most hormone deficiencies, can result in life-threatening complications such as tetany, hypocalcemic seizures, cardiac dysrhythmias, and respiratory obstruction caused by laryngospasm. Autoimmune hypoparathyroidism develops more slowly. Most clinical manifestations are reversible with treatment; those caused by calcification deposits associated with chronic hypoparathyroidism (such as cataracts, malformed teeth) and parkinsonian symptoms are not reversible.
Hypoparathyroidism can be classified as idiopathic, acquired, or reversible. Idiopathic hypoparathyroidism has an unknown cause with an unspecified origin. Acquired hypoparathyroidism is irreversible and is most commonly caused by damage to or removal of the parathyroid gland therapeutically (parathyroidectomy) to treat hyperparathyroidism. Some patients receive an autotransplantation of a segment of a parathyroid gland in the forearm or neck to prevent hypoparathyroidism after a parathyroidectomy. Acquired hypoparathyroidism may also occur as an iatrogenic complication during thyroid or other neck surgery in about 1% to 3% of all patients postoperatively, but with repeated neck explorations, the incidence increases to 10%.
Reversible hypoparathyroidism occurs in children before age 16 years as a result of a rare autoimmune disease. It has also been known to occur as a rare side effect of 131I treatment for Graves disease or with metastases of malignant tumors. Other causes of reversible hypoparathyroidism include hypomagnesemia (which impairs PTH synthesis) and delayed maturation of the parathyroid glands.
Hypoparathyroidism is characterized by hypocalcemia and hyperphosphatemia. Many genetic disorders are associated with hypoparathyroidism and have varied patterns of inheritance (autosomal recessive, autosomal dominant, and X-linked recessive). Some examples include DiGeorge syndrome (TBX1 or NEBL), Charge syndrome (CHD7 or SEMA3E), and Kenny-Caffey syndrome (TBCE). Other genes associated with hypoparathyroidism are CASR, GNA11, and PTH, which are involved in parathyroid development.
The disease may occur at any age. In several epidemiological studies in the United States and Europe, 75% of the people with hypoparathyroidism were female and 25% were male. No specific life span considerations exist, although most people living with hypoparathyroidism are over the age of 45 years.
Ethnicity, race, and sexual/gender minority status have no known effect on the risk for hypoparathyroidism.
Hypoparathyroidism occurs around the world but is relatively rare, and no global prevalence statistics are available.
PLANNING AND IMPLEMENTATION
Collaborative
The treatment is to increase the ingestion and absorption of calcium. When the patient is acutely hypocalcemic, generally calcium chloride or gluconate is rapidly administered intravenously. Give oral calcium supplements with meals but not with foods that interfere with calcium absorption, such as chocolate. Vitamin D supplements are usually given to increase the absorption of calcium. The individual with hypoparathyroidism needs a diet that is rich in calcium, low in phosphorus, and includes a high fluid and fiber content.
During the acute phase of hypocalcemia, monitor the ECG patterns for conduction block, the patient's respiratory status for dyspnea and stridor, and the central nervous system for seizure activity. Alkalosis worsens the symptoms of hypocalcemia because more free calcium binds with proteins when the blood pH increases. Strategies that increase carbon dioxide retention, such as breathing into a paper bag or sedating the patient, can control muscle spasm and other symptoms of tetany until the calcium level is corrected.
| Medication or Drug Class | Dosage | Description | Rationale |
|---|
| Calcium supplements | Varies by drug | Electrolyte supplement; emergency supplementation: Calcium gluconate 2 g IV over 10 min followed by an infusion of 6 g in 500 mL D5W over 4–6 hr; oral calcium gluconate, calcium lactate, or calcium chloride; asymptomatic hypocalcemia can be alleviated with oral calcium citrate, acetate, or carbonate | Correct deficiency: IV calcium is given cautiously to patients who are receiving epinephrine or digitalis; note that calcium can be irritating to veins when given by the IV route |
| Vitamin D | Ergocalciferol (Calciferol, Drisdol) 50,000–100,000 units/day PO/IM | Vitamin supplement | Stimulates absorption of calcium and phosphate from small intestine; promotes release of calcium from bone |
| Human parathyroid hormone, recombinant | Individualized dosage, 25–100 mcg/dose SC | Parathyroid hormone analog | Raises serum calcium by increasing renal tubular reabsorption, increasing calcium absorption, and increasing bone turnover |
Independent
The primary nursing goals are to maintain a patent airway and prevent hypocalcemia in the high-risk population: patients with recent neck surgery. In addition to a careful, ongoing assessment for the symptoms of hypocalcemia, the patient should have a calm environment. Tell the patient to notify you immediately if experiencing difficulty swallowing or tightness in the throat. Listen to the patient's speech for hoarseness. To prepare for emergency airway obstruction from tetany, have intubation or tracheostomy equipment available, as well as IV calcium supplements.
Once the acute phase is over and the patient has been switched to oral medications and foods, begin patient teaching about a diet high in calcium and medications. The neuromuscular irritability and weakness place the patient at increased risk for falls. Evaluate the patient's ability to ambulate, and remove any obstructions in the patient's room. Assist the patient to identify both stressors and coping mechanisms to deal with the stressors. In particular, the patient needs to learn to avoid stressors such as fatigue and infection. Encourage the patient to ventilate feelings of anger or fear.
Evidence-Based Practice and Health Policy
Sardella, A., Bellone, F., Morabito, N., Minisola, S., Basile, G., Corica, F., & Catalano, A. (2021). The association between hypoparathyroidism and cognitive impairment: A systematic review. Journal of Endocrinological Investigation, 44, 905–919.
- The authors noted that hypocalcemia and low parathyroid hormone levels may induce central nervous system disturbances. Evidence of cognitive impairment is possibly underestimated. The authors performed a systematic review of the available literature using online databases to summarize the evidence of cognitive impairment in patients with idiopathic and secondary hypoparathyroidism.
- The authors found only 16 case report studies and one cross-sectional controlled study. Five case reports discussed the occurrence of cognitive impairment. The case-controlled study found a significant presence of reduced control over inhibitions, visual-spatial impairment, and slowed psychomotor ability among patients with hypoparathyroidism compared to controls. They concluded that neurological and psychological dysfunctions occur consistently in hypoparathyroid patients.