Author Affiliations
Abstract
Hypocalcemia, characterized by low levels of ionized calcium, is a potentially life-threatening electrolyte disturbance that can result in neuromuscular symptoms such as tetany, carpopedal spasms, and seizures. This case report presents a 7-year-old previously healthy girl who developed painful bilateral carpopedal spasms following multiple episodes of non-bilious vomiting. Vomiting causes metabolic alkalosis, which subsequently led to a significant drop in ionized calcium levels, inducing hypocalcemia. On presentation, laboratory tests revealed low ionized calcium, though total calcium and other electrolytes were within normal limits. The patient was treated promptly with intravenous calcium gluconate and oral calcium supplementation, leading to a rapid resolution of her symptoms. She was discharged with continued oral calcium and regular follow-up. This case highlights the importance of considering hypocalcemia in pediatric patients presenting with carpopedal spasms, particularly in the context of metabolic disturbances caused by gastrointestinal issues such as vomiting. Early recognition and treatment of hypocalcemia are essential to prevent more severe complications such as seizures or laryngospasm. Clinicians must maintain a high index of suspicion for electrolyte imbalances in similar cases, and management should involve both immediate correction of calcium levels and addressing the underlying cause.
Keywords
Hypocalcemia, Carpopedal spasm, Pediatrics, Metabolic alkalosis, Electrolyte imbalance.
Introduction
Hypocalcemia is an electrolyte disturbance that can present with a spectrum of clinical manifestations, ranging from asymptomatic if mild, to life-threatening seizures, refractory heart failure, or laryngospasm if severe.[1] Tetany was typically realized when the ionized calcium level was lower than 1.1 mmol/L or the corrected total serum calcium level fell below 7.0 mg/dL. Acute hypocalcemia is characterized by neuromuscular irritability resulting in tetany, with symptoms ranging from mild, such as paraesthesia, to severe, such as carpopedal spasms, laryngospasm, and seizures.[2] Excessive vomiting can lead to metabolic alkalosis and subsequent decrease in ionized calcium levels, resulting in tetany and carpopedal spasms.[3,4] We report on a case of a child presenting with carpopedal spasms secondary to hypocalcemia induced by excessive vomiting.
Case Presentation
A 7-year-old previously healthy girl presented to the emergency department with painful spasms and flexion of both hands for a few hours. She had multiple episodes of non-bilious vomiting for one day prior to the onset of spasms. She also had a fever for two days before admission. There was no history of diarrhoea, spasms in other parts of the body, lock jaw, laxative or diuretic use, or difficulty swallowing. On examination, she appeared dehydrated with dry oral mucosa. Vital signs were normal. She had tender bilateral carpopedal spasms. Abdomen was soft and nontender. The neurological exam was otherwise unremarkable.
Case Management
Two intravenous (IV) lines were secured, and she received normal saline boluses at 10 ml/kg. Labs revealed low ionized calcium at 1.00 mmol/L (normal 1.15-1.32), with normal total calcium, magnesium, phosphate, vitamin D, and parathyroid hormone levels. Complete blood count, liver, and renal function were normal. Dengue and malaria were ruled out. She was treated with further intravenous normal saline, calcium gluconate infusion, and oral calcium supplements. Her carpopedal spasms resolved over the next few hours. She was discharged home after 3 days on oral calcium with outpatient follow-up.
Discussion
This case illustrates a presentation of hypocalcemia manifesting as carpopedal spasms in a child secondary to excessive vomiting. The differential diagnosis for carpopedal spasms in children includes hypocalcemia, hypomagnesemia, alkalosis, hypoparathyroidism, and vitamin D deficiency.[5] Hypocalcemia due to excessive vomiting is caused by metabolic alkalosis. Hydrogen ions dissociate from albumin during alkalosis, allowing more calcium to bind to albumin, thereby decreasing ionized calcium levels.[3] Hypomagnesemia and hypokalemia can also occur due to gastric losses and can worsen symptoms of hypocalcemia.[4]
Acute hypocalcemia leads to increased neuromuscular excitability, resulting in tetany. Symptoms can range from mild paresthesias and muscle cramps to severe carpopedal spasms, laryngospasm, seizures, and QT prolongation.[1,2] Parenteral calcium is the mainstay of treatment for symptomatic hypocalcemia, with goals to control symptoms, prevent complications, and correct the underlying cause.[6]
Careful history and physical exams are essential to determine the etiology of hypocalcemia. Initial workup includes total and ionized calcium, magnesium, phosphate, vitamin D, and parathyroid hormone levels. Treatment involves IV calcium gluconate, oral calcium supplements, and correction of any electrolyte abnormalities.[7] Prognosis is generally good if recognized and treated promptly.
Conclusion
This case underscores the importance of considering hypocalcemia in a child presenting with carpopedal spasms, even in the absence of other electrolyte abnormalities. Metabolic alkalosis secondary to excessive vomiting can cause decreased ionized calcium and tetany. Initial management involves IV calcium gluconate, oral calcium supplements, and correction of underlying electrolyte disturbances. Serum calcium levels and ECG should be closely monitored.
References
- Cooper MS, Gittoes NJL. Diagnosis and management of hypocalcaemia. BMJ. 2008;336(7656):1298-302. doi:10.1136/bmj.39582.589433.BE PubMed | Crossref | Google Scholar
- Schafer AL, Shoback DM. Hypocalcemia: Diagnosis and Treatment. In: Feingold KR, Anawalt B, Blackman MR, et al., eds. Endotext. South Dartmouth (MA): MDText.com, Inc.; January 3, 2016. Hypocalcemia: Diagnosis and Treatment
- Ghumman GM, Haider M, Raffay EA, Cheema HA, Yousaf A. Hypercalcemia-induced hypokalemic metabolic alkalosis with hypophosphatemia in a multiple myeloma patient: lessons for the clinical nephrologist. J Nephrol. 2023;36(2):315-317. doi:10.1007/s40620-022-01467-x PubMed | Crossref | Google Scholar
- Johnson MM, Patel S, Williams J. Don’t Take It ‘Lytely’: A Case of Acute Tetany. Cureus. 2019;11(10):e5845. doi:10.7759/cureus.5845 PubMed | Crossref | Google Scholar
- Nardone R, Brigo F, Trinka E. Acute symptomatic seizures caused by electrolyte disturbances. J Clin Neurol. 2016;12(1):21-33. doi:10.3988/jcn.2016.12.1.21 PubMed | Crossref | Google Scholar
- Fong J, Khan A. Hypocalcemia: updates in diagnosis and management for primary care. Can Fam Physician. 2012;58(2):158-162. Hypocalcemia: updates in diagnosis and management for primary care
- Kelly A, Levine MA. Hypocalcemia in the critically ill patient. J Intensive Care Med. 2013;28(3):166-77. doi:10.1177/0885066611411543 PubMed | Crossref | Google Scholar
Acknowledgments
Not reported
Funding
Not reported
Author Information
Seelam Keerthi Reddy
Department of Pediatrics
RVM Institute of Medical Sciences and Research Centre, Hyderabad, India
Email: skeerthireddy10@gmail.com
Author Contribution
The author contributed to the conceptualization, investigation, and data curation by acquiring and critically reviewing the selected articles, and was involved in the writing – original draft preparation and writing – review & editing to refine the manuscript.
Informed Consent
Informed consent was obtained from the patient’s guardians for publication of this case report.
Conflict of Interest Statement
The authors declare no conflict of interest.
Guarantor
None
DOI
Cite this Article
Seelam KR. Emesis, Electrolytes, and Extremities: A Case of Hypocalcemic Carpopedal Spasm. medtigo J Med. 2024;2(4):e30622444. doi:10.63096/medtigo30622444 Crossref

