Causes and mechanism of development
Parathyroid hormone secretion can decrease for several reasons. The most common are iatrogenic factors: the parathyroid glands are accidentally damaged or removed during surgery on the adjacent thyroid gland, or they are affected by radioactive iodine therapy. Autoimmune destruction, where the immune system destroys the gland tissue, is less common.
The pathophysiological chain of hypoparathyroidism is as follows:
- Parathyroid hormone deficiency occurs.
- The production of the active form of vitamin D in the kidneys is impaired.
- Calcium reabsorption in the renal tubules decreases.
- The level of ionized calcium in blood serum drops sharply (hypocalcemia develops).
It is this calcium deficiency that provokes the main clinical consequence of the disease — a pathological increase in neuromuscular excitability, progressing to tetany.
Clinical presentation
The classic manifestation of hypoparathyroidism is convulsive syndrome. The attack usually begins with mild muscle twitching, which rapidly transforms into full tonic or clonic seizures. A crucial feature is that these seizures are extremely painful, yet the patient remains fully conscious.
During an attack, the body assumes characteristic postures due to specific muscle spasms:
- Upper extremities: the hand is flexed into a position known as the "obstetrician's hand".
- Lower extremities: extensor muscle tone predominates, and the foot is in plantar flexion.
- Face: eyelid spasms and involuntary contractions of the facial muscles are observed.
In addition to skeletal muscles, the smooth muscle of internal organs is also involved (visceral manifestations). This can lead to life-threatening conditions such as bronchospasm or laryngospasm, and mimic acute renal or biliary colic.
Diagnostics and functional tests
Increased convulsive readiness (so-called latent tetany) can be suspected using special bedside provocative tests:
- Trousseau's sign: a sphygmomanometer cuff is applied to the patient's arm and inflated to induce temporary ischemia. If the hand adopts the "obstetrician's hand" posture within 2–3 minutes, the test is positive.
- Chvostek's sign: the physician percusses (taps) anterior to the tragus of the ear — the anatomical exit point of the facial nerve. In hypoparathyroidism, this causes a sharp contraction of the facial muscles.
Laboratory and instrumental methods are used to definitively confirm the diagnosis. A biochemical blood test reveals hypocalcemia combined with hyperphosphatemia. A urinalysis naturally shows decreased calcium excretion (hypercalciuria).
An electrocardiogram is also mandatory. The classic ECG sign of hypocalcemia is prolongation of ventricular electrical systole (the Q–T interval). Notably, the shape and size of the T wave remain unchanged.
Management tactics
The treatment approach for hypoparathyroidism depends on the phase of the disease and the presence of acute complications.
As emergency care for tetany, urgent intravenous administration of calcium preparations (calcium chloride or calcium gluconate solutions are used) is required to rapidly relieve seizures and life-threatening laryngeal spasms.
Basic drug therapy outside of an acute attack relies on continuous combined supplementation of vitamin D preparations and calcium salts.
Once blood calcium laboratory values return to normal, dietary therapy is introduced. It plays a supportive role. The patient's diet should be based on foods rich in calcium, primarily various dairy products and vegetables.
Briefly: answers to topical questions
How is Chvostek's sign tested, and what are the three degrees of its clinical severity?
Chvostek's sign is tested by percussing (tapping) with a reflex hammer at the exit point of the facial nerve, located anterior to the tragus of the ear. A positive reaction is the contraction of facial muscles, indicating increased neuromuscular excitability. Clinical diagnostics distinguish grades I–III of Chvostek's sign, although a detailed description of the criteria for each of the three degrees of severity is not available in open sources.
How to distinguish symptoms: Trousseau — Tonometer (compressing the arm), Chvostek — Clap (tapping the face).
Class and exam questions
Why are seizures in hypoparathyroidism so dangerous if the person is conscious?
The danger lies in the involvement of smooth muscle. Laryngeal spasm (laryngospasm) or bronchial spasm can lead to acute respiratory failure and suffocation.
What is the most frequent cause of hypoparathyroidism?
Iatrogenic causes come first. These include inadvertent removal or trauma to the parathyroid glands during thyroid surgery, as well as the consequences of radioactive iodine radiation therapy.
How does the ECG change in parathyroid hormone deficiency?
An isolated prolongation of the Q–T interval is observed, reflecting an increase in ventricular electrical systole duration. The morphology of the T wave remains unchanged.
What else to study on this topic
- Mechanism of vitamin D's effect on renal calcium reabsorption
- Differential diagnosis of clonic and tonic seizures in tetany
- Differences between hypoparathyroidism and pseudohypoparathyroidism
- Algorithm for emergency intravenous administration of calcium salts
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