In this episode of Hospital Medicine Unplugged, we dive into hungry bone syndrome (HBS)—spot it early, replace hard, monitor relentlessly, and shorten the stay.

We open with the do-firsts: check calcium, phosphate, magnesium, ALP, and PTH q6–12h in the first 48–72 hours post-op; screen symptoms (paresthesias, cramps, tetany) and get an ECG for QTc if calcium is low. In dialysis patients, sync labs with the dialysis schedule.

Call the diagnosis when you see rapid, profound, and prolonged hypocalcemia (often Ca ≤7.5 mg/dL for >4 days) plus hypophosphatemia and hypomagnesemia after a sharp PTH drop (post-parathyroidectomy or thyroidectomy in thyrotoxicosis). Rising ALP over the first 1–2 weeks supports high bone turnover.

Risk-stratify who will crash (any = high risk):
• SHPT on dialysis (most common, most severe)
• Very high pre-op PTH and ALP, long dialysis vintage, renal osteodystrophy, younger age, heavier gland mass
• PHPT with severe hypercalcemia, big adenoma, radiologic bone disease, vitamin D deficiency
• Thyrotoxicosis post-thyroidectomy with low BMD and high ALP
• Consider comorbidity burden and published PTH/ALP-based risk scores to guide prophylaxis

Management—build the replacement backbone:
• IV calcium for symptoms, ECG changes, or severe hypocalcemia → calcium gluconate bolus then infusion, wean to high-dose oral calcium (often 3–6 g elemental/day, more if needed).
• Active vitamin D early: calcitriol or alfacalcidol and add cholecalciferol to replete stores.
• Magnesium matters: replace to mid-normal (hypomagnesemia blunts PTH action).
• Go easy on phosphate: replete only if severe/symptomatic—overcorrection worsens hypocalcemia.
• Dialysis patients: use higher-calcium dialysate, coordinate IV calcium around runs.

If the backbone buckles:
• Escalate calcium infusion rate, split oral doses across the day, and consider thiazide (if euvolemic, non-CKD) to limit calciuria.
• For persistent losses, reassess Mg, vitamin D dosing, and exclude hypoparathyroidism (very low PTH + hyperphosphatemia points away from HBS).

Etiology plays—treat the cause:
• SHPT (CKD): ensure vitamin D analogs and optimize dialysis; manage renal osteodystrophy.
• PHPT: confirm complete resection; replete vitamin D and calcium aggressively.
• Thyrotoxicosis: keep magnesium topped up; anticipate transient high needs even with intact parathyroids.

HBS vs post-op hypoparathyroidism—don’t mix them up:
• HBS = low Ca, low PO₄, low Mg, PTH normal/low-normal, ALP ↑.
• Hypoparathyroidism = low Ca, high PO₄, low PTH, Mg usually normal. Management differs.

Monitoring & tapering that sticks:
• Daily labs (sometimes q6–12h early) for Ca/PO₄/Mg/ALP; space as stable.
• Trend ALP (peaks ~2 weeks) to anticipate duration.
• ECG when Ca is low; watch for QTc.
• Taper calcium and calcitriol slowly to avoid rebound hypercalcemia; set outpatient lab checks.

Prevention & periop moves (esp. high risk):
• Replete vitamin D pre-op when feasible.
• Consider bisphosphonates selectively in PHPT with very high turnover (evidence evolving).
• Have a standing postop protocol for high-risk patients: preprinted orders for labs, IV→PO calcium, calcitriol start, magnesium targets, and dialysis calcium bath adjustments.

Medication pitfalls you don’t want to meet:
• Under-replacing magnesium (keeps calcium low).
• Over-replacing phosphate (drives calcium down).
• Missing QTc prolongation.
• Forgetting renal dosing and drug interactions with vitamin D analogs.

We close with the system moves: a hospital HBS bundle that (1) flags SHPT/PHPT/thyrotoxicosis cases pre-op; (2) auto-starts calcitriol + calcium with Mg targets; (3) embeds q6–12h labs early; (4) differentiates HBS vs hypoparathyroidism with a PTH/PO₄ check; (5) standardizes dialysate Ca for dialysis patients; (6) maps a taper & follow-up plan before discharge.

Bottom line—HBS is commonest after SHPT, fiercer with high turnover, and beatable with early recognition, aggressive but smart replacement, magnesium vigilance, and protocolized care.