What are the clinical manifestations of hypocalcemia?

Many people suffer from hypocalcemia. In fact, hypocalcemia means that blood calcium is lower than normal. It is usually caused by a disorder in calcium metabolism. The symptoms of hypocalcemia are generally not particularly obvious, so they are often easily ignored. However, hypocalcemia has a great impact on people. We know that hypocalcemia can not only detect the disease early, but also treat it as soon as possible to minimize the harm of hypocalcemia to the human body. What are the clinical manifestations of hypocalcemia?

Symptoms of Hypocalcemia

Hypocalcemia often has no obvious clinical symptoms. The severity of clinical symptoms is not completely consistent with the degree of hypocalcemia, but is related to the speed and duration of hypocalcemia. A rapid drop in blood calcium, even at a level of 2 mmol/l, can cause clinical symptoms. The clinical manifestations of hypocalcemia are mainly related to increased neuromuscular excitability. 1. Neuromuscular system: Since calcium ions can reduce the excitability of neuromuscular system, the excitability of neuromuscular system increases in hypocalcemia. Muscle spasms may occur, and the early stage of peripheral nervous system numbness of fingers/toes. For mild cases, the facial nerve percussion test (Chvostek sign) or the arm pressure test (Trousseau sign) can be used to induce typical tics. Severe hypocalcemia can cause spasms of the larynx, wrists, feet, bronchi, etc., epileptic seizures and even respiratory arrest. Psychiatric symptoms such as irritability, depression, and cognitive impairment may also occur. 2. Cardiovascular system: mainly arrhythmias such as conduction block. In severe cases, ventricular fibrillation may occur. Heart failure may cause poor response to digitalis. The typical electrocardiogram shows a marked prolongation of the QT interval and ST segment.

Why does renal failure lead to hypocalcemia?

Hypocalcemia is also related to multiple factors such as insufficient calcium intake, active vitamin D deficiency, hyperphosphatemia, and metabolic acidosis. The blood phosphorus concentration is regulated by intestinal absorption and renal excretion. In renal failure, the glomerular filtration rate decreases and urination decreases. The increased blood phosphorus combines with blood calcium to form calcium phosphate deposits, leading to a decrease in blood calcium, thus forming hypocalcemia and hyperphosphatemia. In the early stage of renal failure, blood calcium can still be maintained normal. In the middle and late stages of renal failure, the glomerular filtration rate decreases significantly, the excretion of blood phosphorus decreases, and the blood phosphorus concentration gradually increases. Increased blood phosphorus concentration will combine with blood calcium to form calcium phosphate and deposit in soft tissue, lowering blood calcium and inhibiting the production of calcitriol (vitamin D3) in the proximal tubule, affecting calcium absorption. This results in hypocalcemia. In the early stage of renal failure, blood calcium can still be maintained normal. In the middle and late stages of renal failure, the glomerular filtration rate decreases significantly, the excretion of blood phosphorus decreases, and the blood phosphorus concentration gradually increases. Increased blood phosphorus concentration will combine with blood calcium to form calcium phosphate and deposit in soft tissue, lowering blood calcium and inhibiting the production of calcitriol (vitamin D3) in the proximal tubule, affecting calcium absorption. This results in hypocalcemia.