Hyperparathyroidism, which is caused by overproduction of parathyroid hormone by the parathyroid glands, is characterized by bone decalcification and the development of renal calculi (kid-ney stones) containing calcium.
Primary hyperparathyroidism occurs two to four times more often in women than in men and is most common in patients be-tween 60 and 70 years of age. About 100,000 new cases of hyper-parathyroidism are detected each year in the United States. The disease is rare in children younger than 15 years, but the inci-dence increases tenfold between the ages of 15 and 65 years. Half of the patients diagnosed with hyperparathyroidism do not have symptoms.
Secondary hyperparathyroidism, with manifestations similar to those of primary hyperparathyroidism, occurs in patients with chronic renal failure and so-called renal rickets as a result of phos-phorus retention, increased stimulation of the parathyroid glands, and increased parathyroid hormone secretion.
The patient may have no symptoms or may experience signs and symptoms resulting from involvement of several body sys-tems. Apathy, fatigue, muscle weakness, nausea, vomiting, con-stipation, hypertension, and cardiac dysrhythmias may occur; all are attributable to the increased concentration of calcium in the blood. Psychological manifestations may vary from irri-tability and neurosis to psychoses caused by the direct effect of calcium on the brain and nervous system. An increase in cal-cium produces a decrease in the excitation potential of nerve and muscle tissue.
The formation of stones in one or both kidneys, related to the increased urinary excretion of calcium and phosphorus, is one of the important complications of hyperparathyroidism and occurs in 55% of patients with primary hyperparathy-roidism. Renal damage results from the precipitation of calcium phosphate in the renal pelvis and parenchyma, resulting in renal calculi (kidney stones), obstruction, pyelonephritis, and renal failure.
Musculoskeletal symptoms accompanying hyperparathyroidism may result from demineralization of the bones or bone tumors composed of benign giant cells resulting from overgrowth of osteoclasts. The patient may develop skeletal pain and tender-ness, especially of the back and joints; pain on weight bearing; pathologic fractures; deformities; and shortening of body stature. Bone loss attributable to hyperparathyroidism increases the risk for fracture.
The incidence of peptic ulcer and pancreatitis is increased with hyperparathyroidism and may be responsible for many of the gastrointestinal symptoms that occur.
Primary hyperparathyroidism is diagnosed by persistent eleva-tion of serum calcium levels and an elevated level of parathor-mone. Radioimmunoassays for parathormone are sensitive and differentiate primary hyperparathyroidism from other causes of hypercalcemia in more than 90% of patients with elevated serum calcium levels. An elevated serum calcium level alone is a nonspecific finding because serum levels may be altered by diet, medications, and renal and bone changes. Bone changes may be detected on x-ray or bone scans in advanced disease. The double antibody parathyroid hormone test is used to distin-guish between primary hyperparathyroidism and malignancy as a cause of hypercalcemia. Ultrasound, MRI, thallium scan, and fine-needle biopsy have been used to evaluate the function of the parathyroids and to localize parathyroid cysts, adenomas, or hyperplasia.
Acute hypercalcemic crisis can occur with extreme elevation of serum calcium levels. Serum calcium levels higher than 15 mg/dL (3.7 mmol/L) result in neurologic, cardiovascular, and renal symptoms that can be life-threatening. Treatment includes rehy-dration with large volumes of intravenous fluids, diuretic agents to promote renal excretion of excess calcium, and phosphate therapy to correct hypophosphatemia and decrease serum cal-cium levels by promoting calcium deposit in bone and reducing the gastrointestinal absorption of calcium. Cytotoxic agents (mithramycin), calcitonin, and dialysis may be used in emergency situations to decrease serum calcium levels quickly.
A combination of calcitonin and corticosteroids has been ad-ministered in emergencies to reduce the serum calcium level by increasing calcium deposition in bone. Other agents that may be administered to decrease serum calcium levels include bisphos-phonates (eg, etidronate [Didronel], pamidronate).
The patient requires expert assessment and care to minimize complications and reverse the life-threatening hypercalcemia. Medications are administered with care, and attention is given to fluid balance to promote return of normal fluid and electrolyte bal-ance. Supportive measures are necessary for the patient and family.
The insidious onset and chronic nature of hyperparathyroidism and its diverse and commonly vague symptoms may result in de-pression and frustration. The family may have considered the pa-tient’s illness to be psychosomatic. An awareness of the course of the disorder and an understanding approach by the nurse may help the patient and family to deal with their reactions and feel-ings. The recommended treatment of primary hyperparathyroidism is the surgical removal of abnormal parathyroid tissue. In some patients without symptoms and with only mildly elevated serum calcium levels and normal renal function, surgery may be delayed and the patient followed closely for worsening of hypercalcemia, bone deterioration, renal impairment, or the development of kid-ney stones.
Because kidney involvement is possible, patients with hyper-parathyroidism are at risk for renal calculi. Therefore, a fluid in-take of 2,000 mL or more is encouraged to help prevent calculus formation. Cranberry juice is suggested because it may lower the urinary pH. It can be added to juices and ginger ale for variety. The patient is instructed to report other manifestations of renal calculi, such as abdominal pain and hematuria. Thiazide diuret-ics are avoided because they decrease the renal excretion of cal-cium and further elevate serum calcium levels. Because of the risk of hypercalcemic crisis, the patient is instructed to avoid dehy-dration and to seek immediate health care if conditions that com-monly produce dehydration (eg, vomiting, diarrhea) occur.
Mobility of the patient, with walking or use of a rocking chair for those with limited mobility, is encouraged as much as possible because bones subjected to normal stress give up less calcium. Bed rest increases calcium excretion and the risk for renal calculi. Oral phosphates lower the serum calcium level in some patients. Long-term use is not recommended because of the risk for ectopic cal-cium phosphate deposits in soft tissues.
Nutritional needs are met, but the patient is advised to avoid a diet with restricted or excess calcium. If the patient has a coexist-ing peptic ulcer, prescribed antacids and protein feedings are nec-essary. Because anorexia is common, efforts are made to improve the appetite. Prune juice, stool softeners, and physical activity, along with increased fluid intake, help to offset constipation, which is common postoperatively.
The nursing management of the patient undergoing parathy-roidectomy is essentially the same as that of a patient undergoing thyroidectomy. However, the previously described precautions about dehydration, immobility, and diet are particularly impor-tant in the patient awaiting and recovering from parathyroidec-tomy. Although not all parathyroid tissue is removed during surgery in an effort to control the calcium–phosphorus balance, the nurse closely monitors the patient to detect symptoms of tetany (which may be an early postoperative complication). Most patients quickly regain function of the remaining parathyroid tis-sue and experience only mild, transient postoperative hypocal-cemia. In patients with significant bone disease or bone changes, a more prolonged period of hypocalcemia should be anticipated. The nurse reminds the patient and family about the importance of follow-up to ensure return of serum calcium levels to normal (Chart 42-7).
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