Improving the Management of Post-Operative Hypocalcaemia in Thyroid Surgery

Patients who have undergone gastric bypass surgery often have malabsorption and may also require very high doses of calcium and vitamin D to correct hypocalcemia. High doses of vitamin D supplementation are commonly linked to nephrolithiasis and nephrocalcinosis. The most common complication following thyroid surgery is hypocalcemia, caused by transient or persistent hypoparathyroidism. This study aimed to investigate the prevalence of hypocalcemia after thyroidectomy and to identify potential risk factors. A typically benign autosomal dominant disorder, familial hypocalciuric hypercalcemia (FHH), can paradoxically produce neonatal hypocalcemia.

TREATMENT OF HYPOCALCEMIA

Additionally, articles published within Cureus should not be deemed a suitable substitute for the advice of a qualified health care professional. Do not disregard or avoid professional medical advice due to content published within Cureus. Hypercalcemia is most commonly caused by enhanced bone resorption; it can also result from enhanced intestinal absorption or decreased renalCa+2 excretion (Table 3). In the small intestine, Ca+2 is absorbed both paracellularly (passive absorption through tight junctions) and transcellularly (active absorption). Paracellular absorption dominates when Ca+2 intake is high, while transcellular absorption dominates when Ca+2 intake is low 1.

Chronic Hypocalcemia

There is variable improvement in peripheral blood T-cell counts as the patients increase in age. A gene involved in the the features of the DiGeorge syndrome or sequence is the transcription factor TBX1 (35,38-40). Transgenic mice haploinsufficient for TBX1 demonstate some components of the DiGeorge syndrome (41). Complete knockout of the gene is lethal in mice and results in a high incidence of cardiac outflow tract abnormalities (42). If there is evidence of persistent hypocalcemia at less than 2.2 mmol/L of any offending drugs, check bloods for full blood count, PTH, urea and electrolytes, liver blood tests, phosphate, vitamin D, and magnesium levels.

Basal ganglia calcifications have been found in 50% of patients with PHP and may produce extrapyramidal movement disorders. Hypocalcemia may develop insidiously and be preceded by increasing levels of serum PTH. Psychiatric problems such as depression, paranoia, psychosis and delusions have been described in the presence of hypocalcemia. Cognitive defects such as mental retardation and memory impairment have been encountered. Dental defects include dental and enamel hypoplasia, blunted tooth root development, and delay of tooth eruption. The outcomes of the study showed that total thyroidectomy is performed more than subtotal thyroidectomy at our center.

What if all Tests are Negative but Symptoms Persist?

The pathophysiology of chronic hypoparathyroidism is related to the lack of PTH’s actions on its target organs, the skeleton and the kidneys, and to its indirect gastrointestinal actions. Without PTH, the skeleton becomes inactive and no longer serves as a useful reservoir for calcium when there synthroid 5mg is need. Without PTH, the kidneys do not conserve filtered calcium and, thus, a relative hypercalciuria ensues. In addition, the renal tubules lose the phosphaturic actions of PTH, thus leading to hyperphosphatemia.

• Patients with hypocalcemia may be asymptomatic or experience symptoms ranging from mild paresthesia and muscle cramps to severe symptoms such as cardiac arrhythmias, seizures, and laryngospasms (6, 7).
• The deficiency of PTH results in a drop in blood calcium levels, as this hormone helps control the balance of calcium in the body.
• Calcium levels are controlled by parathyroid hormone (PTH), which is secreted by the parathyroid glands.
• Casr mutations are considered to be second to post-surgical hypoparathyroidism in frequency as a cause of hypoparathyroidism in the adult.

CN is the corresponding author, who wrote the case report and was involved in the patient’s postoperative treatment. TG wrote and reviewed the case report and was involved in the patient’s treatment as a supervisor of endocrine surgery. JI wrote and reviewed the case report as the chief of surgery, who was involved in the patient’s treatment. RG took part in writing and finalizing the case report and was involved in the patient’s surgery and treatment as a supervisor of endocrine surgery. On the second postoperative day, the patient suddenly suffered from severe paresthesia at the entire body with dyspnea and stridor—and subjectively described a laryngospasm.

The clinical presentation in these patients ranges from asymptomatic to life-threatening hypocalcemia. PTH levels are frankly low to low normal, and hypercalciuria may be present out of proportion to the degree of hypocalcemia. Activating mutations typically are in the amino-terminal extracellular domain of the receptor. Hypercalciuria can be exacerbated resulting in nephrocalcinosis and impairment of renal function if patients are treated with vitamin D or its analogues.

Vitamin D Supplements

The mean calcium levels in patients decreased significantly and 24 hours after the surgery and decreased further at 48 postoperative hours. The incidence of hypocalcemia was significantly more in total thyroidectomy patients. A recent systematic and meta-analysis conducted by Bai et al. 17 35 studies concluded that total thyroidectomy is one of the significant predictors of hypocalcemia after thyroidectomy.

This disorder is more common in full-term infants than in premature infants. One risk factor is hyperphosphatemia due to administration of cow’s milk, which may reflect an inability of the immature kidney to secrete phosphate. Congenital defects of intestinal magnesium absorption or renal tubular absorption can occur resulting in severe hypocalcemia. Patients with PHP also have a constellation of developmental and somatic defects that are referred to as AHO. Short stature, round facies, brachydactyly (Figure), obesity, and subcutaneous calcifications are classic features of AHO (81-84).

Patients with vitamin D-dependent rickets (VDDR) type 1 usually present with rickets, hypocalcemia, hypophosphatemia, elevated alkaline phosphatase, and as a result of their hypocalcemia, secondary hyperparathyroidism. Because type 1 VDDR results from a defect in the renal production of 1-alpha-hydroxylase (15,16), 1,25-(OH)2 vitamin D levels are decreased or undetectable. In contrast, patients with VDDR type 2 have disrupted production or impaired function of the VDR, resulting in end-organ resistance to 1,25-(OH)2 vitamin D.