Abstract Background Severe hypocalcemia is a medical emergency that can precipitate neuromuscular paralysis, arrhythmia, and respiratory failure, with mortality rates approaching 20-30% in critically ill patients. Although mild hypocalcemia is common in hospitalized populations, symptomatic or life-threatening cases occur in fewer than 2% and are rarely the initial clue to renal failure. Calcium is vital for diaphragmatic contractility and cardiac repolarization, and its deficiency can lead to ventilatory collapse. In malnourished individuals with substance use and unrecognized kidney disease, derangements in calcium-phosphate-vitamin D balance may cause catastrophic decompensation. Case Presentation A 63-year-old man with untreated hepatitis C, homelessness, and intravenous heroin/cocaine use presented with diffuse pain, dyspnea, anxiety, and involuntary movements consistent with generalized tetany (e.g., carpopedal spasms and muscle cramps). He was cachectic (BMI 14.7 kg/m²) with a positive Chvostek sign and fasciculations. Labs showed renal failure (Cr 19.8 mg/dL, BUN 210 mg/dL, CrCl 3 mL/min), high anion-gap acidosis (AG 35, HCO3 7.3 mEq/L, pH 7.13), corrected Ca 6.2 mg/dL, K+ 6.6 mEq/L with corrected QTc 499 ms, and phosphate 14.9 mg/dL. Progressive diaphragmatic weakness caused hypoventilation requiring intubation. Urgent hemodialysis was initiated per KDIGO emergency criteria. Endocrinology advised against calcitriol during hyperphosphatemia; calcium-gluconate infusion was started and discontinued after post-dialysis correction. After dialysis, calcium and bicarbonate improved, phosphate decreased, and QT interval normalized. Neuromuscular irritability resolved following correction, allowing discontinuation of the calcium infusion. Ventilatory parameters improved, and the patient was successfully extubated on day five after three hemodialysis sessions. Discussion Profound hypocalcemia impairs diaphragmatic contractility and alters cardiac repolarization, precipitating ventilatory failure and arrhythmia. In ESRD, phosphate retention and decreased 1,25-OH vitamin D synthesis reduce ionized calcium. While IV calcium provides transient relief, dialysis corrects phosphate load and acidosis. This patient’s social vulnerability and lack of medical access likely delayed ESRD recognition, underscoring the need for earlier screening in high-risk populations. Management followed KDIGO and AACE guidelines. Conclusion Hypocalcemia-induced respiratory failure may unmask occult ESRD. Early recognition, prompt renal replacement therapy, and coordination among nephrology, endocrinology, and critical-care teams are lifesaving. In socioeconomically disadvantaged groups, addressing malnutrition and substance use is key to preventing metabolic crises. Recognizing the silent progression of metabolic derangements remains one of the most powerful life-saving skills in critical care. This abstract is funded by: None
Rosa-Rosario et al. (Fri,) studied this question.