Hypocalcaemia after an Occult Calcium Channel Blocker Overdose: A Case Report and Literature Review

Abstract

Hypocalcaemia is a rare complication of calcium channel blocker overdose, having been reported only once previously (J Toxicol Clin Toxicol, 1992, 30, 309). In this article, we report a case of a 37-year-old woman who developed hypocalcaemia after a verapamil overdose, review the literature and propose a mechanism for this rare finding.Calcium channel blockers (CCBs) are responsible for a large number of drug-related fatalities. The 2011 Annual report of the American Association of Poison Control Centers' National Poison Data System showed that CCBs accounted for 61% (78 cases) of all the deaths from cardiovascular medications [1]. Significant toxicity is reported more often with non-dihydropyridines (e.g. diltiazem and verapamil) than with dihydropyridines (e.g. amlodipine) [2]. Classically, patients with CCB overdose present with hypotension and bradycardia. Other findings can include altered mental status, hyperglycaemia, metabolic acidosis, pulmonary oedema and ischaemia to any organ system [3]. While dihydropyridines such as amlodipine mainly affect peripheral vasculature, in overdose, all selectivity is lost. Significant dihydropyridine overdose can lead to significant hypotension and death [4]. Hypocalcaemia is thought to be a rare complication of CCB overdose. Here, we report a case of CCB overdose followed by a precipitous drop in serum calcium from 9.3 mg/dl to 5.5 mg/dl. Case ReportA 37-year-old woman presented to the Emergency Department with a chief complaint of chest pain 12 hr after ingesting five tablets of unknown dose of verapamil. The patient had a history of migraine headaches treated with verapamil and a suicide attempt with nortriptyline 6 months earlier. The patient withheld her ingestion of verapamil from the treatment team as she was afraid that her husband would think this was a second suicide attempt and leave her.One hour after ingestion, the patient felt dizzy and nauseous. She then developed chest pain described as being 'punched in her chest'. The pain radiated to her neck and her arm and prompted her presentation to the emergency department.On presentation, her temperature was 37.2°C, blood pressure was 90/54 mmHg, heart rate was 100 beats/min. and oxygen saturation was 96% on room air. When vital signs were rechecked 150 min. later, the blood pressure was 69/52 and her heart rate was 51 beats/min. Physical examination revealed a somnolent obese female with dry oral mucosa, reactive pupils and warm extremities. Her ECG revealed junctional bradycardia ( fig. 1) with heart rate of 58 but no evidence of acute ischaemia. Her initial serum electrolytes were notable for a creatinine of 1.24 mg/dl (previously 1.0 mg/dl) and a calcium of 9.3 mg/dl (8.6-10.5 mg/dL). Her complete blood count was remarkable for a white blood cell count of 21.1 with 82.3% neutrophils. Arterial blood gas examination revealed a mild metabolic acidosis (pH: 7.30, PaCO 2 : 37 mmHg, PaO 2 : 60 mmHg, serum HCO 3 À: 21). Troponin was <0.01 ng/ml, and lactic acid was mildly elevated at 2.3 mEq/L (0.3-2.2 mE...

Combinatorial analysis of phenotypic and clinical risk factors associated with hospitalized COVID-19 patients

“…In Cohort 2 the PrecisionLife platform identified 18 disease signatures in 80 hospitalized patients with serum calcium values lower than 9.26 mg/dl ( Supplementary Figure 7 ). Out of these, only four signatures were co-associated with the use of the dihydropyridines (calcium channel blockers) and proton-pump inhibitors which may have an effect on calcium homeostasis 28,29 . The hypocalcemia disease signatures were associated with COVID-19 symptoms such as pneumonia and respiratory failure, and comorbidities including diabetes, hypertension and anemia.…”

Combinatorial Analysis of Phenotypic and Clinical Risk Factors Associated With Hospitalized COVID-19 Patients

“…In Cohort 2 the PrecisionLife platform identified 18 disease signatures in 80 hospitalized patients with serum calcium values lower than 9.26 mg/dl ( Supplementary Figure 7 ). Out of these, only four signatures were co-associated with the use of the dihydropyridines (calcium channel blockers) and proton-pump inhibitors which may have an effect on calcium homeostasis ( 27 , 28 ). The hypocalcemia disease signatures were associated with COVID-19 symptoms such as pneumonia and respiratory failure, and comorbidities including diabetes, hypertension, and anemia.…”

Severe Polyantihypertensive Drug Poisoning: Unresponsive to Conventional Therapies Treated by Plasmapheresis

“…3,4 A single-center retrospective reported that 19% of the patients receiving the drug developed acute kidney injury (AKI). 5 However, the cause of AKI was not clarified in the study results. Wanchoo et al 6 reported a case of acute interstitial nephritis (AIN) secondary to the drug in 2016.…”

“…To the Editor: Overdose of antihypertensive drugs may cause hypotension, shock, dysrhythmias, electrolyte disturbances, metabolic disorders, seizures, agranulocytosis, hepatic damage, renal damage, noncardiogenic pulmonary edema, angioneurotic edema, and death. [1][2][3][4][5][6] According to the data from the American Association of Poison Control Centers' 2017 annual report, a total of 108,614 cases of poisoning were reported with cardiovascular drugs. b-Blockers and calcium channel blockers are accused of more than half of mortality due to antihypertensive agents.…”

“…They may lead to severe electrolyte disturbances by affecting cellular ion transfer. [1][2][3][4][5][6] Crystalloids, glucagon, inotropes, hyperinsulinemiaeuglycemia therapy, and intralipid emulsions and, when conduction abnormalities occur, atropine and external PACE are used in patients as medical treatment modalities for poisoning with b-blockers and calcium channel blockers. [11][12][13][14][15][16][17] Crystalloids and inotropes are the medical treatments for poisoning with angiotensin-converting enzyme inhibitors and diuretics.…”