Hypercalcemia, the identifiable result of hyperparathyroidism, also leads to the most important clinical complications. The body is able to compensate for slowly increasing calcium levels but eventually becomes overcome with calcium excess and phosphorus deficiency. Since the bones hold the majority of the body’s calcium, extracellular hypercalcemia is a result of demineralization of the bones. The calcium in the bones is replaced by cysts and fibrous tissue, thus leading to severe osteoporosis (reduction of bone mass per volume) and osteopenia (diminished bone tissue). Increased levels of extracellular calcium may be deposited in the soft tissues of the body and the kidney and lead to renal calculi, renal insufficiency, urinary tract infections, and eventually, renal failure. Hypercalcemia can also trigger the increased secretion of gastrin, which leads to peptic ulcer disease. Other GI dysfunctions that may result include cholelithiasis and pancreatitis.
Primary hyperparathyroidism, which leads to the enlargement of at least one of the parathyroid glands, occurs in more than 85% of the cases because of a single benign adenoma (neoplasm of glandular epithelium). Other causes include genetic disorders and endocrine cancers such as pancreatic or pituitary cancers. Patients who have had head or neck radiation are also at increased risk. Secondary hyperparathyroidism occurs when a source for hypocalcemia occurs outside the parathyroid gland, thus stimulating the parathyroid glands to overproduce PTH. These conditions include chronic renal failure, rickets, vitamin D deficiency, and laxative abuse.
Nursing care plan assessment and physical examination
Many patients are asymptomatic. Early symptoms are polyuria (large amounts of urine), anorexia, and constipation, as well as weakness, fatigue, drowsiness, and lethargy. As the hypercalcemia increases, abdominal pain (from peptic ulcer disease), nausea, and vomiting are typical. The patient may report generalized bone pain and may have had recent fractures from what appeared to be little cause.
Little definitive data can be obtained in a physical examination. Hypertension is common, and if the patient is on digitalis, there may be a significantly lowered pulse rate, which signals increased sensitivity to the drug. Muscle atrophy and depressed tendon reflexes are late signs of hypercalcemia. The patient may have marked muscle weakness and atrophy (particularly in the legs) and skeletal deformities. If the central nervous system is affected, there will be changes in mental status, such as confusion, disorientation, and even coma. Palpation of even grossly enlarged parathyroid glands is generally impossible because of their location.
The hypercalcemic patient or the significant others may note memory changes, confusion, irritability, and symptoms of depression or paranoia (or both). The psychological clinical manifestations may range from mild to acute psychosis, or possibly paranoid hallucinations. The patient and significant others may be understandably upset or anxious about the changes in the patient’s behavior.
Nursing care plan primary nursing diagnosis: Activity intolerance related to fatigue, muscle weakness, and bone pain.
Nursing care plan intervention and treatment plan
Surgical removal of the parathyroid glands is the only definitive treatment and is the treatment of choice for primary hyperparathyroidism. Indications for surgery include symptoms resulting from hypercalcemia, nephrolithiasis, reduced bone mass, serum calcium level in excess of 12 mg/dL, age younger than 50 years, and infeasibility of long-term follow-up. If hyperplasia (proliferation of normal cells) of the glands is excessive, all but one-half of one gland is removed because only a small amount of glandular tissue is necessary to maintain appropriate levels of PTH. The individual who has had all four glands removed will quickly become hypoparathyroid and must be treated accordingly. To prevent postoperative deficits of calcium, magnesium, and phosphorus, the patient may need either IV or oral supplements. Bone pain may subside as soon as 3 days after surgery, but renal dysfunction may be irreversible.
Nonsurgical management includes medications to assist in the excretion of calcium by the kidneys. Medical therapy, however, has not been shown to affect the clinical outcome of primary hyperparathyroidism. Postmenopausal women with primary hyperparathyroidism may receive estrogen replacement therapy. The patient may be placed on a low–vitamin D diet that is high in calories, but calcium restrictions are generally not beneficial. To increase calcium excretion, the patient needs a large fluid intake, at least 2 to 3 L per day, and 8 to 10 g of salt per day. Foods high in fiber will assist the patient to have normal bowel function.
Secondary hyperparathyroidism is managed by treating the underlying cause; either vitamin D therapy, prednisone, or aluminum hydroxide may be used, depending on the underlying cause of the disorder.
Generally, increase the patient’s mobility, protect the patient from injury, monitor for possible complications, and provide patient education. Provide comfort measures for bone and joint pain. Increased activity limits further bone demineralization. Moderate weight-bearing activities are more beneficial to the patient than either range-of-motion exercises in bed or chair rest. Patients with hyperparathyroidism may be weak and at risk for falls and trauma. If the patient is hospitalized, maintain safety measures.
If the patient is recovering from a parathyroidectomy, the most life-threatening complication is airway compromise, either from swelling or from acute hypocalcemia. Keep emergency intubation and tracheostomy equipment in a readily available location. Notify the surgeon immediately if the patient develops respiratory distress, stridor, neck swelling, or hoarseness because of laryngeal nerve damage. Maintain the patient in a semi-Fowler position to decrease postoperative edema. If the patient develops tingling in the hands and around the mouth, notify the surgeon and obtain serum calcium levels if prescribed to determine if tetany is beginning.
As with many endocrine disorders, the patient may be frustrated with the clinical manifestations of the disease and require frequent reassurance. Reassure the patient that most of the symptoms will reverse with the return of normal calcium levels. Assist the patient in identifying stressors and methods of coping with the stressors.
Nursing care plan discharge and home health care guidelines
Teach the patient about the disease process and the signs and symptoms of calcium imbalance. Stress that the symptoms require immediate medical attention. Describe any dietary considerations, including a diet low in calcium with limitation and avoidance of milk products. If the patient is on potassium-depleting diuretics, note that a diet high in potassium-rich foods (apricots, fresh vegetables, citrus fruits) is necessary if no potassium supplements are prescribed. In addition, a diet with adequate fiber and fluid will aid normal bowel function. Teach the action, dosage, route, and side effects of all medications. If the patient has a surgical incision, describe incisional care and arrange for a follow-up visit with the surgeon. Instruct the patient on the appropriate activity level. Note that recalcification of the bones will take some time. If the patient maintains mobility, recalcification will be increased. Suggest that the patient avoid bedrest; encourage the patient to space activity throughout the day and use the energy levels as a guide to activity. Remind the patient to avoid contact sports or other activities that place her or him at risk for falls or fractures.