Hypoparathyroidism
Hypoparathyroidism: Excerpt from Handbook of Diseases
A deficiency of parathyroid hormone (PTH), hypoparathyroidism is caused by disease, injury, surgical removal, 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. Some complications of long-term hypocalcemia, such as cataracts and basal ganglion calcifications, are irreversible.
Causes
Hypoparathyroidism may be acute or chronic and is classified as idiopathic or acquired:
❑ 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 the parathyroid glands during thyroidectomy or other neck surgery or, rarely, from massive neck irradiation. It may also result from ischemic infarction of the parathyroid glands during surgery or from hemochromatosis, sarcoidosis, amyloidosis, tuberculosis, neoplasms, or trauma.
❑ Acquired, reversible hypoparathyroidism may result from hypomagnesemia-induced impairment of hormone synthesis and release, from suppression of normal gland function due to hypercalcemia, or from delayed maturation of parathyroid function.
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. Incidence of the idiopathic and reversible forms is highest in children; incidence of the irreversible acquired form is highest 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
In the chronic form, 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 brain syndrome, psychosis, mental deficiency in children, and tetany.
Chronic tetany resulting from chronic hypoparathyroidism may cause difficulty in walking and a tendency to fall. It can lead to laryngospasm, stridor and, eventually, cyanosis and seizures.
Acute hypoparathyroidism
More severe than chronic hypoparathyroidism, acute hypoparathyroidism produces more acute symptoms such as tetany, which 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.
Like chronic tetany from chronic hypoparathyroidism, acute tetany in acute hypoparathyroidism may cause laryngospasm, stridor, cyanosis, and seizures. These CNS abnormalities tend to be exaggerated during hyperventilation, pregnancy, infection, withdrawal of thyroid hormone, and administration of 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 eventually lead to heart failure.
Diagnosis
The following test results confirm the diagnosis of hypoparathyroidism:
❑ radioimmunoassay for PTH — decreased PTH concentration
❑ serum calcium — decreased level
❑ serum phosphorus — increased level
❑ electrocardiography (ECG) — prolonged QT and ST intervals due to hypocalcemia.
The following test helps provoke clinical evidence of hypoparathyroidism:
❑ 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).
Treatment
Because calcium absorption from the small intestine requires the presence of vitamin D, treatment includes vitamin D and calcium supplements. Such therapy is usually lifelong, except for the reversible form of the disease.
If the patient can’t tolerate vitamin D because of hepatic or renal problems, calcitriol may be used.
Acute, life-threatening tetany requires immediate I.V. administration of 10% calcium gluconate 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 the diagnosis of hypoparathyroidism in a patient with a history of tetany, maintain a patent I.V. line and keep I.V. calcium gluconate available. Because the patient is vulnerable to seizures, maintain seizure precautions.
❑ Keep a tracheotomy tray and endotracheal tube at bedside because laryngo-spasm may result from hypocalcemia.
❑ For the patient with tetany, administer 10% calcium gluconate slow I.V. (1 mg/minute) and maintain a patent airway. Such a patient may also require intubation, and sedation with I.V. diazepam.
❑ Monitor vital signs often after administration of I.V. diazepam to make sure blood pressure and heart rate return to normal.
❑ When caring for the patient with chronic hypoparathyroidism, particularly a child, stay alert for minor muscle twitching (especially in the hands) and for signs of laryngospasm (respiratory stridor or dysphagia) because these effects may signal onset of tetany.
❑ Because the patient with chronic disease has prolonged QT intervals on an ECG, watch for heart block and signs of decreasing cardiac output.
❑ Closely monitor the patient receiving both cardiac glycosides and calcium gluconate because calcium potentiates the effect of cardiac glycosides. Stay alert for signs of digoxin toxicity (arrhythmias, nausea, fatigue and vision changes).
❑ Do careful patient teaching. (See Discharge instructions in hypoparathyroidism.)
Pictures
Book Source Details
- Book Title: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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