Introduction

Acute tetany is a neuromuscular emergency characterised by sudden onset of involuntary muscle contractions, cramps, and spasms, most commonly resulting from severe disturbances in calcium homeostasis. Although tetany may occur in chronic settings, the acute form poses an immediate threat to patient well-being, given its potential to precipitate laryngospasm, seizures, and life-threatening cardiac arrhythmias. Prompt recognition and management of acute tetany are therefore critical to prevent morbidity and mortality. This review synthesises current understanding of the pathophysiology, causes, clinical presentation, diagnostic evaluation, and evidence-based emergency management strategies for acute tetany, with particular emphasis on calcium repletion protocols, correction of accompanying electrolyte abnormalities, and treatment of underlying causes.

Pathophysiology of tetany

The fundamental disturbance in tetany is neuromuscular hyperexcitability, driven primarily by a reduction in extracellular ionised calcium (Ca²⁺). Ionised calcium plays a pivotal role in stabilising the resting membrane potential of neurons by screening negative charges on the exterior of voltage-gated sodium channels. When ionised calcium levels fall below the normal range (1.12–1.30 mmol/L), the threshold for sodium channel activation is lowered, resulting in spontaneous action potentials in peripheral and central neurons and manifesting as muscle cramps and spasms.¹ Beyond hypocalcemia, two additional physiological disturbances commonly co-occur and exacerbate neuromuscular irritability. First, hypomagnesemia impairs parathyroid hormone (PTH) secretion as well as the responsiveness of target organs to PTH, thereby perpetuating or worsening hypocalcemia.² Second, alkalosis—whether respiratory (e.g., hyperventilation) or metabolic (e.g., excessive bicarbonate administration)—promotes increased binding of calcium to albumin, effectively reducing the ionised fraction available to stabilise neuronal membranes.² The interplay of these factors creates a clinical scenario in which even modest declines in total serum calcium may precipitate severe neuromuscular symptoms.

Aetiologies of acute tetany

A wide spectrum of disorders can lead to the dangerous fall in ionised calcium that triggers acute tetany. Hypoparathyroidism—most often arising as a complication of thyroid or parathyroid surgery—remains the leading cause of acute postsurgical hypocalcemia worldwide. Inadvertent removal or devascularization of parathyroid glands during thyroidectomy or neck surgery results in insufficient PTH production, causing rapid declines in serum calcium levels.³ Autoimmune destruction of the parathyroids and congenital absence of parathyroid tissue represent less common, non-surgical aetiologies.

Vitamin D deficiency or resistance constitutes another major contributor to hypocalcemia. Nutritional deficits, malabsorption syndromes (e.g., celiac disease), and chronic kidney disease (CKD) impair intestinal absorption of calcium by reducing either substrate availability (vitamin D₂ or D₃) or the 1α-hydroxylation step in the kidneys that generates active calcitriol (1,25-dihydroxyvitamin D₃). Insufficient calcitriol leads to diminished transcellular calcium transport and subsequent hypocalcemia.⁴ CKD itself amplifies hypocalcemia by promoting phosphate retention and reducing renal 1α-hydroxylase activity. Elevated serum phosphate binds free calcium, further lowering ionised levels. Additionally, CKD impairs excretion of magnesium and other electrolytes, complicating the metabolic milieu.⁵

Acute pancreatitis can induce hypocalcemia through fat necrosis and saponification. Inflammatory pancreatic enzymes release fatty acids that chelate calcium, forming insoluble soaps and depleting available ionised calcium.⁶

Massive blood transfusion is another iatrogenic cause. citrate, used as an anticoagulant in stored blood products, avidly chelates calcium when administered in large volumes, leading to transient but clinically significant hypocalcemia.⁸

Prolonged diuretic use, malnutrition, gastrointestinal losses (e.g., diarrhea, vomiting), and chronic alcoholism predispose to hypomagnesemia, which concurrently reduces PTH secretion and end-organ response, thus compounding hypocalcemia.²

Respiratory alkalosis from hyperventilation and metabolic alkalosis from excessive bicarbonate therapy both shift calcium into protein-bound forms, decreasing the ionised fraction and potentially precipitating tetany.²

Finally, rare genetic disorders affecting the calcium-sensing receptor (e.g., autosomal dominant hypocalcemia) or mutations in the G-protein subunit alpha-11 result in familial hypocalciuric hypercalcemia or hypocalcemia syndromes, respectively, though these are uncommon in the acute setting.⁹

Clinical presentation

Acute tetany typically manifests with a constellation of neuromuscular and systemic signs that develop over minutes to hours. The earliest symptoms often include paresthesias/pins and needles—perioral numbness and tingling in the fingertips and toes. As hypocalcemia worsens, patients develop carpopedal spasms characterised by flexion of the wrist and metacarpophalangeal joints and extension of the fingers (Trousseau’s sign), as well as a positive Chvostek’s sign, in which tapping the facial nerve elicits facial muscle twitching.¹⁰ Severe neuromuscular irritability may progress to laryngospasm, manifesting as stridor, respiratory distress, and hypoxia, and may advance rapidly to complete airway obstruction if not promptly addressed. Seizures can occur as a result of generalised neuronal hyperexcitability. Cardiac manifestations include prolonged QT interval on electrocardiogram (ECG), predisposing to life-threatening arrhythmias such as torsades de pointes and ventricular fibrillation, as well as hypotension and reduced myocardial contractility in severe cases.¹⁰ Given the overlap of these signs with other neuromuscular and metabolic conditions, rapid biochemical confirmation of hypocalcemia—and concurrent review of other electrolytes—is essential.

Diagnostic evaluation

The diagnostic workup for suspected acute tetany must be swift and comprehensive. Measurement of both total and ionised serum calcium is imperative; ionised calcium is the physiologically active fraction and may be normal in the setting of hypoalbuminemia if only total calcium is assessed.¹⁰ Simultaneous evaluation of serum magnesium is crucial, as hypomagnesemia both precipitates and aggravates hypocalcemia by impairing PTH release and renal responsiveness.² Serum phosphate levels help identify CKD-related disturbances or pancreatitis-induced saponification. Assessment of PTH distinguishes hypoparathyroidism (inappropriately low PTH) from secondary hyperparathyroidism in CKD or vitamin D deficiency (elevated or inappropriately normal PTH).³ Measurement of 25-hydroxyvitamin D and, when indicated, 1,25-dihydroxyvitamin D provides insight into vitamin D status and conversion defects.⁴ Arterial blood gas analysis may reveal respiratory or metabolic alkalosis, which worsens ionised calcium binding to albumin.² ECG monitoring should be instituted immediately to detect QT prolongation or arrhythmias, guiding urgency and safety of intravenous calcium administration.¹ Bedside elicitation of Chvostek’s and Trousseau’s signs remains a rapid, low-cost adjunct to laboratory testing in confirming neuromuscular irritability.

Emergency management principles

Effective management of acute tetany prioritises rapid restoration of ionised calcium to alleviate neuromuscular symptoms while concurrently identifying and treating underlying aetiologies. The cornerstone of initial therapy is parenteral calcium administration, with calcium gluconate being preferred for peripheral infusion due to its lower risk of tissue necrosis if extravasation occurs. An initial bolus of 10–20 mL of 10% calcium gluconate (2.2 mmol elemental Ca²⁺/10 mL) diluted in 50–100 mL of 5% dextrose or 0.9% saline is infused over 10–20 minutes under continuous ECG monitoring. Bolus doses may be repeated every 10 minutes, up to three doses, until tetany resolves or ionised calcium rises into the normal range.^1,6 Following stabilisation, a continuous infusion—typically 100 mL of 10% calcium gluconate in 1 L of diluent at 50–100 mL/hour—is administered, with titration guided by serial ionised calcium measurements to maintain mid-normal levels without producing hypercalcemia.⁶ While calcium chloride (13.6 mmol elemental Ca²⁺/10 mL) contains more than three times the elemental calcium of calcium gluconate, it is more irritant to veins and should be reserved for central venous administration if rapid replacement is required and central access is available.

Concurrent magnesium repletion is critical in cases of hypomagnesemia, given its role in PTH secretion and calcium handling. Intravenous magnesium sulfate—2 g (8 mmol) over 10–20 minutes—should be administered, with repeat dosing up to a total of 4–6 g based on serum magnesium levels and patient response, while monitoring for hypotension induced by rapid infusion.² Correction of vitamin D deficiency or resistance involves administration of active vitamin D metabolites, such as calcitriol (0.25–0.5 µg orally daily), adjusting dose according to calcium response to avoid overshoot hypercalcemia; in cases of nutritional deficiency, high-dose cholecalciferol (50,000 IU weekly) may be used.⁴

Identifying and treating the precipitating cause is equally important. Postsurgical hypoparathyroidism may require recombinant human PTH (1–84) for refractory hypocalcemia. CKD-related hypocalcemia necessitates phosphate binders, optimisation of dialysis parameters, and vitamin D analogues. In acute pancreatitis, aggressive supportive care and debridement of necrotic tissue reduce saponification. When massive transfusion triggers hypocalcemia, slowing infusion rates and preemptive calcium supplementation in massive transfusion protocols are recommended. Addressing respiratory or metabolic alkalosis by normalising ventilation patterns or adjusting bicarbonate therapy helps restore ionised calcium.

Supportive measures include immediate airway preparedness for laryngospasm—supplemental oxygen, readiness for endotracheal intubation, or cricothyrotomy if necessary—and administration of benzodiazepines for seizures unresponsive to calcium correction. Continuous ECG and hemodynamic monitoring during calcium and magnesium infusions ensure detection of arrhythmias or hemodynamic compromise.

Special populations

Certain patient groups require tailored management. In pregnancy, maternal hypocalcemia poses risks to both mother and fetus; calcium gluconate is safe in pregnancy, but infusion rates should be carefully controlled with frequent maternal and fetal monitoring. Elderly patients and those with renal impairment necessitate slower infusion rates and vigilant electrolyte monitoring to prevent hypercalcemia or volume overload. Neonates and infants, who possess a higher surface-to-volume ratio and increased cardiac sensitivity, benefit from lower-volume preparations (10% calcium gluconate at 10 mg/kg) administered over extended periods (20–30 minutes) to mitigate the risk of cardiac arrhythmias and calcium overload.

Monitoring and follow-up

After initial stabilisation, serum electrolytes—ionised calcium, magnesium, and phosphate—should be reassessed every 4–6 hours until levels stabilise, then daily as appropriate. Renal function and acid-base status require ongoing evaluation to tailor fluid and electrolyte management. Continuous cardiac telemetry should persist during parenteral replacement and for a period thereafter to detect delayed arrhythmias. Once steady ionised calcium levels are achieved, transition to oral therapy with calcium carbonate or citrate (1–2 g elemental calcium daily, divided doses) plus vitamin D analogues aids long-term maintenance. Outpatient follow-up with endocrinology or nephrology ensures monitoring for chronic hypocalcemia and adjustment of maintenance regimens.

Complications and prognosis

Timely and appropriate management of acute tetany generally leads to rapid resolution of neuromuscular symptoms and favorable outcomes. However, overly aggressive calcium infusion risks hypercalcemia, which can present as polyuria, polydipsia, nausea, vomiting, and cardiac arrhythmias; thus, infusion rates must be carefully titrated. Extravasation of calcium chloride can cause severe local necrosis, reinforcing the peripheral preference for calcium gluconate. Failure to address underlying disorders—such as persistent hypoparathyroidism—may predispose patients to recurrent tetany and long-term complications including bone demineralization and calcifications in soft tissues. Reported mortality is low when management is prompt, but delays in recognition or treatment significantly increase the risk of respiratory failure and fatal cardiac events.¹

Conclusion

Acute tetany is a critical endocrine and emergency medicine challenge, with hypocalcemia at its core often compounded by hypomagnesemia and alkalosis. Management hinges on rapid restoration of ionised calcium—preferably via calcium gluconate—concurrent correction of magnesium deficiency, precise treatment of underlying causes, and continuous monitoring to avert iatrogenic complications. Multidisciplinary coordination among emergency physicians, endocrinologists, nephrologists, and critical care teams optimises patient safety and clinical outcomes. Ongoing research into optimal calcium repletion strategies, novel PTH analogues, and prophylactic protocols in high-risk populations promises to further refine and enhance the management of this potentially life-threatening condition.