Electrolyte Disorders (Calcium, Magnesium, Phosphate) — Written Clinical Reasoning

Model answer — Part A: severe hypercalcaemia with suppressed PTH in myeloma

Frame the problem. This is severe, symptomatic hypercalcaemia of malignancy — corrected calcium 3.4 mmol/L with confusion — complicated by acute kidney injury from the calcium-driven diuresis and vomiting loop. Suppressed PTH confirms a non-parathyroid mechanism; in myeloma the dominant mechanism is lytic bone disease with local osteoclast activation, with calcitriol-mediated hypercalcaemia a recognised minority mechanism [1].

Immediate assessment and management run together. Confirm airway, breathing and circulation; ECG for short QT and arrhythmia; volume status; urine output; and precipitating drugs (thiazides, lithium, calcium, vitamin D). Begin isotonic saline immediately — repletion first, because antiresorptives fail in a depleted kidney — then add calcitonin 4–8 IU/kg for effect within hours, and an antiresorptive for durability. The antiresorptive choice states the renal reasoning: zoledronate 4 mg IV is the trial-proven standard in malignant hypercalcaemia but demands renal caution at this creatinine, so either a cautious renally-adjusted zoledronate approach or denosumab 120 mg SC, which is not renally cleared and is effective including in bisphosphonate-refractory disease [1] [2] [3]. Loop diuretics are explicitly NOT part of acute management — reserve them only for fluid overload after repletion [1].

Mechanism workup in parallel: phosphate, magnesium, 25-OH and 1,25-dihydroxy vitamin D (a high 1,25 level would flag calcitriol-mediated disease and add glucocorticoids), SPEP/free light chains and disease-response markers, and review of his myeloma treatment status — because definitive control of the calcium requires treating the myeloma itself [1].

Ongoing plan: recheck calcium and renal function at least daily until stable (calcitonin tachyphylaxes by 48–72 hours and the antiresorptive takes 2–4 days — anticipate the rebound gap); watch for over-correction into hypocalcaemia, especially with denosumab in renal impairment; mobilise; stop precipitants; and discuss prognosis and treatment intent with haematology, since recurrent hypercalcaemia tracks with uncontrolled disease [1] [3].

Model answer — Part B: acute post-thyroidectomy hypocalcaemia

Recognition. Perioral paraesthesia and cramps 30 hours after total thyroidectomy is acute post-surgical hypoparathyroidism until proven otherwise — the calcium nadir is 24–72 hours, after apparent early stability, which is exactly when this call arrives [4].

Assess severity first: any stridor, hoarse new voice, seizures or carpopedal spasm on examination; Chvostek and Trousseau signs as supporting evidence; ECG for QT prolongation; and a magnesium level, because hypomagnesaemia both mimics and sustains hypocalcaemia by impairing PTH secretion and action [4].

Immediate management for symptomatic hypocalcaemia is intravenous: calcium gluconate 10% 10–20 mL over 10–20 minutes with ECG monitoring — slowly, never pushed — followed by a titrated calcium gluconate infusion with 4–6-hourly calcium checks, because the bolus effect lasts only hours [4] [5]. Replace magnesium concurrently; without it the calcium will not hold [4].

Transition over the following week: start oral calcium carbonate plus calcitriol (active vitamin D — a hypoparathyroid patient cannot upregulate 1-alpha-hydroxylase for plain cholecalciferol), wean the infusion as oral therapy holds the level, and send a PTH to document parathyroid failure. Before discharge: explicit paraesthesia and cramp instructions, early calcium recheck, and arrangement for follow-up — because if hypoparathyroidism persists beyond 6–12 months it is permanent, and chronic management targets the low-normal calcium range with a normal urine calcium to avoid nephrocalcinosis and basal ganglia calcification from overtreatment [4] [5].