Symptoms of hypocalcemic convulsions

Hypocalcemic convulsions are a common symptom of hypocalcemia, mainly because the antagonistic ability of extracellular calcium ions to sodium ions decreases, which causes increased cell excitability, leading to such symptoms. In addition to causing convulsions, patients are also prone to numbness of the limbs and smooth muscle spasms. In more severe cases, it can also cause tracheospasm, leading to tachycardia, etc.

Symptoms of hypocalcemic convulsions

Mild symptoms include numbness and tingling in the lips and limbs, which can be induced by facial nerve percussion test or arm cuff pressure test. Severe symptoms include spasm of skeletal muscles and smooth muscles throughout the body, with manifestations such as bronchial spasm, abdominal organ colic, tachycardia and other crises, which should be differentiated from grand mal epileptic seizures.

Pathogenesis

The excitability of a cell depends on the difference between its resting potential and threshold potential. A decrease in the calcium ion concentration in the blood will cause the threshold potential to approach the resting potential. This is because the ion concentrations inside and outside the cell differ greatly, and the absolute values ​​of both are very small. Therefore, when the external calcium ions decrease within a certain range (but have not yet affected the excitation-contraction coupling), their antagonistic effect on the movement of sodium ions into the cell is reduced.

Thereby, stimulation of the same intensity can open more sodium ion channels, which means that stimulation of lower intensity can induce the unit membrane to reach the starting point of positive feedback, that is, the threshold potential, where sufficient sodium ion channels are opened and sufficient potassium ion channels are closed. The final result is that the threshold potential approaches the resting potential, that is, the irritability of the cell is enhanced, resulting in the constant stimulation of the muscle nerves, which is originally insufficient to induce action potential under normal circumstances, and causes continuous excitement of the muscle nerves.

Causes

Vitamin D3 deficiency, parathyroid hormone (PTH) deficiency, tissue insensitivity to PTH due to genetic factors, acute pancreatitis, senile acidosis and other factors are calcium ion binding, magnesium ion deficiency, excessive infusion of sodium citrate, or liver and kidney abnormalities.