Purpose Postoperative hypoparathyroidism is the most common complication of total thyroidectomy and is managed with calcium supplementation guided by serial biochemical monitoring. Respiratory alkalosis decreases measured ionised calcium and can induce or exacerbate symptoms of hypocalcaemia. Aggressive calcium replacement can lead to iatrogenic suppression of parathyroid glands, delaying parathyroid recovery and risking hypercalcaemia. Methodology We present the case of a 30-year-old male who presented for resection of medullary thyroid carcinoma, with a background of depression, anxiety, cannabis use disorder and opioid use disorder. Following total thyroidectomy with lateral neck dissection, postoperative hypoparathyroidism was diagnosed. Prolonged hypocalcaemia led to ICU transfer for intensive calcium monitoring and ongoing intravenous supplementation. Operative findings, postoperative biochemical trends, symptom evolution, and treatment decisions were examined to identify factors contributing to persistent symptomatic hypocalcaemia. Results Arterial blood gas results demonstrated recurrent respiratory alkalosis and hypocalcaemia. Respiratory alkalosis was driven by hyperventilation deemed secondary to anxiety and substance withdrawal. On stepdown to the ward, the patient was found to be hypercalcaemic. We posit that the patient’s anxiety and substance withdrawal led to overly aggressive calcium supplementation. Postoperative hypoparathyroidism is a common complication of thyroid surgery and anxiety is extremely common in the perioperative setting. However, anxiety leading to overly aggressive calcium replacement has not yet been discussed in the literature. Conclusion This case demonstrates how postoperative anxiety and substance withdrawal led to an ICU admission, iatrogenic parathyroid suppression and hypercalcaemia. Judicious calcium supplementation aiming for low-normal calcium levels, as well as a robust understanding of the physiology behind hypocalcaemia, is required to successfully manage postoperative hypoparathyroidism.