Hypoparathyroidism
Hypoparathyroidism: Excerpt from Professional Guide to Diseases (Eighth Edition)
Hypoparathyroidism is a deficiency of parathyroid hormone (PTH) caused by disease, injury (usually surgical), or congenital malfunction of the parathyroid glands. Because the parathyroid glands primarily regulate calcium balance, hypoparathyroidism causes hypocalcemia, producing neuromuscular symptoms ranging from paresthesia to tetany. The clinical effects of hypoparathyroidism are usually correctable with replacement therapy. However, some complications of this disorder, such as cataracts and basal ganglion calcifications, are irreversible.
Causes and incidence
Hypoparathyroidism may be acute or chronic and is classified as idiopathic or acquired. The acquired form may also be reversible. Idiopathic hypoparathyroidism may result from an autoimmune genetic disorder or the congenital absence of the parathyroid glands. Acquired hypoparathyroidism commonly results from accidental removal of or injury to one or more parathyroid glands during thyroidectomy or other neck surgery; rarely it results from massive thyroid irradiation. It may also result from ischemic infarction of the parathyroids during surgery or from hemochromatosis, sarcoidosis, amyloidosis, tuberculosis, neoplasms, or trauma. An acquired, reversible hypoparathyroidism may result from hypomagnesemia-induced impairment of hormone synthesis, from suppression of normal gland function due to hypercalcemia, or from delayed maturation of parathyroid function. (See What happens in acute hypoparathyroidism.)
PTH isn’t regulated by the pituitary or hypothalamus. It normally maintains blood calcium levels by increasing bone resorption and GI absorption of calcium. It also maintains an inverse relationship between serum calcium and phosphate levels by inhibiting phosphate reabsorption in the renal tubules. Abnormal PTH production disrupts this balance. The incidence is 4 out of 100,000 people. Incidence of the idiopathic and reversible forms is highest in children; that of the irreversible acquired form, in older patients who have undergone surgery for hyperthyroidism or other head and neck conditions.
Signs and symptoms
Although mild hypoparathyroidism may be asymptomatic, it usually produces hypocalcemia and high serum phosphate levels that affect the central nervous system (CNS) as well as other body systems. Chronic hypoparathyroidism typically causes neuromuscular irritability, increased deep tendon reflexes, Chvostek’s sign (hyperirritability of the facial nerve, producing a characteristic spasm when it’s tapped), dysphagia, organic mental syndrome, psychosis, mental deficiency in children, and tetany.
Acute (overt) tetany begins with a tingling in the fingertips, around the mouth and, occasionally, in the feet. This tingling spreads and becomes more severe, producing muscle tension and spasms and consequent adduction of the thumbs, wrists, and elbows. Pain varies with the degree of muscle tension but seldom affects the face, legs, and feet. Chronic tetany is usually unilateral and less severe; it may cause difficulty in walking and a tendency to fall. Both forms of tetany can lead to laryngospasm, stridor and, eventually, cyanosis. They may also cause seizures. These CNS abnormalities tend to be exaggerated during hyperventilation, pregnancy, infection, withdrawal of thyroid hormone, therapy with diuretics, and before menstruation.
Other clinical effects include abdominal pain; dry, lusterless hair; spontaneous hair loss; brittle fingernails that develop ridges or fall out; dry, scaly skin; cataracts; and weakened tooth enamel, which causes teeth to stain, crack, and decay easily. Hypocalcemia may induce cardiac arrhythmias and may eventually lead to heart failure.
Diagnosis
Confirming diagnosis The following test results confirm the diagnosis of hypoparathyroidism:
❑ Radioimmunoassay for PTH: decreased PTH concentration
❑ Serum calcium: decreased
❑ Serum phosphorus: increased
❑ Electrocardiogram (ECG): prolonged QT and ST intervals due to hypocalcemia.
Inflating a blood pressure cuff on the upper arm to between diastolic and systolic blood pressure and maintaining this inflation for 3 minutes elicits Trousseau’s sign (carpal spasm), thereby provoking clinical evidence of hypoparathyroidism.
Treatment
Because calcium absorption from the small intestine requires the presence of vitamin D, treatment includes vitamin D and calcium supplements. Therapy is usually lifelong, except for the reversible form of the disease. If the patient can’t tolerate the pure form of vitamin D, alternatives include dihydrotachysterol, if hepatic and renal function is adequate, and calcitriol, if it’s severely compromised. In patients with preexisting hypomagnesemia, this condition must be corrected to treat the resulting hypocalcemia. A high-calcium, low-phosphorous diet is recommended.
Acute life-threatening tetany requires immediate I.V. administration of calcium to raise serum calcium levels. The patient who’s awake and able to cooperate can help raise serum calcium levels by breathing into a paper bag and then inhaling his own carbon dioxide; this produces hypoventilation and mild respiratory acidosis. Sedatives and anticonvulsants may control spasms until calcium levels rise. Chronic tetany requires maintenance therapy with oral calcium and vitamin D supplements.
Special considerations
While awaiting diagnosis of hypoparathyroidism in a patient with a history of tetany, maintain a patent I.V. line and keep I.V. calcium available. Because the patient is vulnerable to seizures, maintain seizure precautions. Also, keep a tracheotomy tray and endotracheal tube at the bedside because laryngospasm may result from hypocalcemia.
❑ Instruct the patient to follow a high-calcium, low-phosphorus diet.
❑ When caring for the patient with chronic disease, particularly a child, stay alert for minor muscle twitching and for signs of laryngospasm because these effects may signal the onset of tetany.
❑ For the patient on drug therapy, emphasize the importance of checking serum calcium levels at least three times a year. Instruct the patient to watch for signs of hypercalcemia and to keep medications away from light and heat.
❑ Dental changes, cataracts, and brain calcifications are permanent. These can be prevented with early detection and periodic calcium determinations.
Alert Because the patient with chronic disease has prolonged QT intervals on ECG, watch for heart block and signs of decreasing cardiac output. Because calcium potentiates the effect of cardiac glycosides, closely monitor the patient receiving both a cardiac glycoside and calcium. Stay alert for signs of digoxin toxicity, such as arrhythmias, nausea, fatigue, vision changes.
❑ Instruct the patient with scaly skin to use creams to soften his skin. Also, tell him to keep his nails trimmed to prevent them from splitting.
❑ Hyperventilation or recent blood transfusions may worsen tetany. (Anticoagulant in stored blood binds calcium.)
❑ For the patient with tetany, administer 10% calcium gluconate by slow I.V. infusion (1 ml/minute), and maintain a patent airway. The patient may also require intubation and sedation. Monitor vital signs often after administration sedation to make certain that blood pressure and heart rate return to normal.
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Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
» Next page: Chvostek's sign (Professional Guide to Signs & Symptoms (Fifth Edition))
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