Introduction:
Calcium plays a vital role in platelet adhesion and coagulation. It is also important for the contraction of the heart and the smooth muscle. Clotting factors I, VII, IX, and X, protein C, and protein S require calcium to activate in damaged endothelium. Calcium also plays an essential role in stabilizing fibrinogen and platelets in developing a thrombus. The normal plasma ionized calcium concentration is maintained within 1.15-1.33 mmol/L. Anything less than this is considered hypocalcemia.
What Is Hypocalcemia?
The condition is called hypocalcemia when the serum calcium concentration becomes less than 8.8 mg/dl, or the plasma ionized calcium concentration falls below 1.17 mmol/L. Hypocalcemia can be acquired or hereditary. The acquired causes include hypoparathyroidism, liver diseases, kidney diseases, COVID-19, diet, medication, and surgery. The condition can be clinically presented differently, ranging from asymptomatic to life-threatening.
What Are the Symptoms of Hypocalcemia?
Hypocalcemia is usually asymptomatic. The underlying conditions diagnose Hypocalcemia caused by hypoparathyroidism. They can include short stature, round face, intellectual disability, calcification of the basal ganglia in pseudo hypo parathyroid, and vitiligo in autoimmune hypoparathyroidism.
Neurological Manifestations:
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Muscle cramps in the legs and back are common signs of hypocalcemia.
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Insidious hypocalcemia may cause mild encephalopathy (a decrease in the blood flow to the brain). The condition can be suspected when the patient shows dementia (memory loss), depression, or psychosis. (a mental state where the person shows disconnection from reality).
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Papilledema (swelling of the eye optic disc due to increased intracranial pressure) can be seen occasionally.
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When the serum level goes below 7 mg/dl, there can be hyperreflexia (an increased muscle reflex response), tetany, laryngospasm, or seizures.
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Tetany: This is a manifestation seen in severe cases of hypocalcemia. It shows sensory symptoms like paresthesia (numbness or tingling sensation) of the lips, tongue, fingers, or feet. Carpopedal spasms (or frequent contractions in the muscles of the hands and legs) can be prolonged and painful. There can be generalized aching in the muscles. Spasms in the facial musculature can be seen.
Other manifestations:
Dry and scaly skin, brittle nails, and coarse hair can be other manifestations of hypocalcemia. Patients with hypocalcemia are found to have occasional bouts of candidal infections. Long-standing cases of hypocalcemia might show cataracts (a cloudy area in the eye's lens). However, this does not resolve with the serum calcium levels becoming normal.
What Is Chvostek Sign?
An involuntary twitching of the muscles of the face by tapping gently on the facial nerve in front of the external auditory meatus is called Chvostek Sign. It is seen in less than ten percent of the healthy population and most cases of acute hypocalcemia. However, this sign is absent in chronic cases of hypocalcemia.
What Is Trousseau Sign?
The precipitation of the carpal spasm (a condition where the muscles of the hand contract involuntarily) by reducing the blood flow to the hand, usually using a tourniquet in the forearm for three minutes, is called Trousseau Sign. This condition is seen in alkalosis, hypomagnesemia, hypokalemia, and hyperkalemia. Studies show that about six percent of people with no evident electrolyte imbalance may also show this sign.
How Is Hypocalcemia Managed?
The treatment of hypocalcemia usually includes the following;
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IV calcium gluconate for tetany.
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Oral calcium for postoperative hypoparathyroidism.
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Oral calcium and vitamin D for chronic hypocalcemia.
For tetany, calcium gluconate 10 mL of 10% solution IV is given over ten minutes. The response can be soon but will only last for a while. Hence, a continuous infusion with 20 to 30 mL of 10% calcium gluconate in 1 L of 5% dextrose in water (D/W) over the next 12 to 24 hours might be helpful. In patients receiving digoxin, an infusion of calcium can be dangerous. Hence it should be administered slowly, monitoring the echocardiogram (ECG).
How Does Hypocalcemia Occur in a Massive Blood Transfusion?
Hypocalcemia in a massive blood transfusion is an inadvertent iatrogenic process. It is usually considered due to citrate, which acts as an anticoagulant. There is approximately about 3 gm citrate in each unit of packed red cells used in blood transfusion. This amount of citrate is usually cleared from the blood by the liver within five minutes. However, in sick people, in whom multiple units of blood are transfused, the elimination by the liver might be compromised. In addition, the amount of citrate reaching the body is more. These two factors determine the amount of citrate accumulating in the body during a massive transfusion. The citrated binds to the ionized calcium n the circulation, reducing the plasma ionized calcium concentration. The bound calcium, in turn, remains inactive.
What Are the Effects of Hypocalcemia During a Massive Blood Transfusion?
Hypocalcemia can cause a high mortality rate or increase mortality risk in critically ill patients. It can be due to cardiac dysrhythmias (irregular heartbeat), abnormal or low systemic vascular resistance (vasoplegia), and impaired coagulation. When a hemorrhagic shock is considered in a hypocalcemic patient, the mortality risk increases significantly.
How Is Hypocalcemia During a Massive Blood Transfusion Managed?
Studies show that calcium replacement might not improve calcium levels or reduce mortality. Protocols for calcium replacement may vary from one literature to the other. The role of replacement can be uncertain. Studies show that adding calcium supplements during the transfusion can reduce the risk of hypocalcemia. A study by Cote et al. evaluated burn patients in the pediatric age group that required fresh frozen plasma (FFP) infusion. He concluded that simultaneous calcium replacement was potentially indicated to avoid fluctuations in ionized calcium, which can be dangerous. Another study by Krishnan et al. checked calcium and magnesium supplementation during plasmapheresis (exchange of blood plasma components) and FFP transfusion in children with glomerulonephritis. The group which received the supplementation showed higher values of total ionized calcium and decreased symptoms of tetany.
Conclusion
Studies have shown that hypocalcemia is almost inevitable from massive blood transfusions in trauma patients. Hence, monitoring the plasma concentration of calcium is essential during massive blood transfusions. As the number of units of blood transfused increases, the risk of hypocalcemia also increases.
