Hypocalcemic tetany associated with simultaneous administration of cimetidine and nifedipine: a case report.

BACKGROUND: Acute hypocalcemia is generally caused by a sudden drop in serum calcium ion and presents with a mild or severe form of tetany. Even though the occurrence of hypocalcemia is well documented with certain drugs such as calcium chelators, bisphosphonates, and cisplatin, it is a very unusual and poorly documented adverse event with cimetidine and nifedipine. Here, we present a case of severe hypocalcemic tetany during simultaneous administration of cimetidine and nifedipine in a hypertensive patient with dyspepsia. CASE PRESENTATION: A 46-year-old known human immunodeficiency virus patient from Ethiopia on antiretroviral therapy over the past 14 years presented to the emergency department with acute exacerbation of dyspepsia and hypertensive urgency. She was given intravenous cimetidine (400 mg) and oral nifedipine (30 mg) simultaneously. One hour after the administration of these two drugs, she developed severe hypocalcemic tetany with carpopedal spasm, involuntary plantar flexion, and muscle spasms. She also had severe retrosternal chest pain and shortness of breath. Her blood pressure was 160/110 mmHg during the attack and she had no skin changes, such as urticaria. She was immediately given 1 g of calcium gluconate intravenously over 30 minutes. The carpopedal spasm progressively decreased during calcium gluconate administration. An hour later, she completely regained voluntary movement of her fingers and feet. The chest pain persisted, but resolved over the next 12 hours. The patient was discharged home after 2 days of observation. This is an unusual adverse effect that needs caution during concomitant administration of these drugs. CONCLUSIONS: Severe hypocalcemic tetany can occur with concomitant administration of cimetidine and nifedipine. Immediate treatment with calcium gluconate quickly reverses this adverse event. Concomitant administration of these drugs should be done with caution or be avoided if possible.

Effects of calcium supplementation to resuscitation fluids in endurance horses: A randomized, blinded, clinical trial.

BACKGROUND: The addition of calcium to resuscitation fluids is a common practice in horses, but studies evaluating the effects of calcium supplementation are limited. In healthy horses, decreases in heart rate and changes in serum electrolyte concentrations have been reported. HYPOTHESIS: Calcium gluconate administration at a rate of 0.4 mg/kg/min to eliminated endurance horses with metabolic problems will affect heart rate, gastrointestinal sounds, and serum electrolyte concentrations. ANIMALS: Endurance horses eliminated from the Tevis Cup 100-mile (160 km) endurance ride for metabolic problems and requiring IV fluid therapy were eligible. METHODS: Sixteen horses were randomly assigned to receive 0.4 mg/kg/min of calcium (23% calcium gluconate solution) over 1 hour diluted in 10 L of a non-calcium containing isotonic crystalloid (CAL group) or 10 L of a non-calcium containing isotonic crystalloid (CON group). Staff members administering the fluids were blinded to treatment group. Blood samples were collected and physical examinations performed before and after treatment. Heart rates were recorded every 15 min during fluid administration. Data were compared using 2-way analysis of variance (ANOVA) with repeated measures for continuous variables and Fisher's exact test for categorical variables. RESULTS: Calcium was associated with lower heart rates 45 min after starting the infusion (P = .002). Gastrointestinal sounds were less likely to improve in the calcium group compared with the control group (P = .005). An increase in plasma phosphorus concentration (P = .03) was associated with calcium administration. CONCLUSIONS: Intravenous calcium supplementation to endurance horses eliminated from competition after development of metabolic problems may decrease heart rate but impairs improvement in gastrointestinal sounds.

Analysis of Factors Contributing to the Occurrence of Systemic Toxicity in Patients with Hydrofluoric Acid Skin Exposure Injury: An Individual Participant Data Meta-Analysis of 125 Clinical Cases from 1979 to 2020.

The purpose of this study is to analyze the factors contributing to the occurrence of systemic toxicity in patients injured after skin exposure to hydrofluoric acid (HFA) and to present guidelines for active treatment intervention based on this analysis. Data were acquired from EMBASE, PubMed, and Cochrane library for individual participant data (IPD) meta-analysis. Key searching terms included calcium gluconate (CAG), hydrofluoric acid, and case. This research consisted of case studies published between 1979 and 2020. Systemic toxicity was set as the main outcome. Data sets from 50 case studies (N = 125 participants) were analyzed. Multivariate binary logistic regression analyses of IPD found significant association effect of the total body surface area (TBSA) burned, indicating systemic toxicity [Regression coefficient estimate, 0.82; SE, 0.41; Odds ratio, 2.28; [95% confidence interval, 1.03-5.06], and p = 0.0424]. The optimal cutoff point (sensitivity; specificity) of the receiver operating characteristic curve of the total body surface area (TBSA) burned for contributing occurrence of systemic toxicity was 2.38(0.875; 0.959). IPD meta-analysis indicates that existing evidence supports the positive proportional association of the TBSA burned for systemic toxicity. If the TBSA burned (%) in patients exposed to hydrofluoric acid is greater than 2.38, early aggressive treatment intervention, including decontamination and various CAG application, should be recommended as the guideline.

A case report of severe adverse reaction of exenatide: Anaphylactic shock.

BACKGROUND: Anaphylactic shock is the severe state of the allergic reaction, which is rapid in onset and fatal. This is the first study that discusses the anaphylactic shock of exenatide reexposure in the patient who has interrupted exenatide treatment. PATIENT CONCERNS: A 47-year-old man was treated with exenatide owing to high blood glucose and obesity. Then he developed localized urticarial on the face, white lip, hands tremble, nausea, vomit, chest stuffiness, dizziness, accompanying with confusion and dyspnea. His blood glucose was 4.6 millimole per liter (mmol/L) and blood pressure was 85/50 millimeters of mercury (mm Hg). DIAGNOSIS: Exenatide-induced anaphylactic shock was considered. INTERVENTIONS: The emergency electrocardiogram was performed. The patient was treated with dexamethasone sodium phosphate and calcium gluconate, combined with exenatide withdrawal. He also received oral antiallergic agents and intravenous nutrition treatment. OUTCOMES: After antishock treatment, the clinical response gradually alleviated. LESSONS: Although exenatide is not prone to anaphylaxis, it is the synthetic peptide that can induce antibody formation. Exenatide has immunogenicity with the potential to elicit an allergic reaction upon administration. Clinicians should always pay more attention to the anaphylactic shock of exenatide, when prescribing for diabetics.

Effect of Intravenous Calcium Gluconate on Prevention of Post Spinal Hypotension during Spinal Anaesthesia for Caesarean Section: A Randomized Double-Blind Controlled Study.

BACKGROUND: Calcium, a physiological ion, causes vasoconstriction and has a positive ionotropic action on heart. Its use to prevent post-spinal hypotension has been suggested but never formally evaluated for patients undergoing caesarean section. This study investigated the hemodynamic effects of calcium administration in parturients with the primary aim of comparing the incidence of post-spinal hypotension. METHODS: Sixty healthy full-term pregnant patients scheduled for caesarean section were randomly allocated to two equal groups to receive either calcium gluconate or normal Saline bolus over 20min by syringe infusion pump under electrocardiography monitoring immediately after the patient was turned supine following spinal anaesthesia. Blood pressure and heart rate were recorded at baseline, and at regular intervals following spinal. Maternal calcium levels were estimated before and after infusion. Neonatal blood gas analysis and calcium level were analyzed. Total mephentermine requirement was recorded in both groups. RESULTS: The heart rate values remained comparable to baseline value in group calcium gluconate while in group normal Saline, it decreased significantly at 8,12 and 16min. Blood pressure decreased significantly as compared to the baseline value from 4min onwards in both the groups. However, it was comparable in the two groups at all time points(0.622). Nineteen patients(63.33%) required mephentermine infusion in group calcium gluconate as compared to 23 patients(76.6%) in group normal Saline for maintenance of systolic blood pressure.(p=0.791) Umbilical venous pH (p=0.038) and partial pressure of carbon dioxide(p=0.038) were significantly better in group calcium gluconate. CONCLUSIONS: Calcium used for prophylaxis of hypotension in healthy parturients undergoing caesarean section reduced the vasopressor requirements and total mephenteramine dose, but the difference did not attain statistical significance.

Calcium gluconate infusion is not as effective as dopamine agonists in preventing ovarian hyperstimulation syndrome.

OBJECTIVE: The aim of the study was to compare the effectiveness of calcium gluconate and cabergoline therapy in the prevention of ovarian hyperstimulation syndrome (OHSS). PATIENTS AND METHODS: Eight hundred and forty-five women who underwent GnRH antagonist protocol and at high risk for developing OHSS were divided into two groups, those given cabergoline (n=435) or calcium gluconate (n=410). In cabergoline group, 0.5 mg of cabergoline was administered once daily p.o. starting on the day of ovulation trigger and continued until the following 8 days. In calcium gluconate group, intravenous calcium gluconate was administered daily for four days starting on the day of oocyte pickup (OPU). 10 ml of 10% calcium gluconate solution was dissolved in 200 ml of physiological saline and administered by intravenous route within 40 minutes. Infusion was started within the first 30 minutes following the OPU and continued on the 1st, 2nd and 3rd days after OPU. RESULTS: Mild OHSS was developed in 367 (89%) patients receiving calcium gluconate infusion, while 251 patients (57%) in the cabergoline group developed mild OHSS. The frequency of mild OHSS in the calcium group was significantly higher than the cabergoline group (p<.001). Moderate OHSS was observed in 32 people (7.8%) in the calcium gluconate group, while it was observed in 184 people in the cabergoline group (42.3%). Calcium gluconate infusion significantly reduced the development of moderate OHSS compared to cabergoline therapy (p<.001). Severe OHSS developed in 11 patients (2.7%) in the calcium gluconate group, while severe OHSS did not develop in those given cabergoline (0%, p<.001). Clinical pregnancy, live birth and abortion rates were similar in the two groups. When logistic regression analysis was performed, a significant correlation was found between age, BMI, AMH, the number of antral follicle count, OHSS history, paracentesis, progesterone on the day of hCG, 2 PN zygotes, and HbA1c levels and the development of OHSS. No correlation was found between the use of metformin or cetrotide and the development of OHSS. CONCLUSIONS: Calcium gluconate treatment is not effective in the prevention of OHSS.

Iatrogenic calcinosis cutis in 9-month-old baby boy: a case report.

BACKGROUND: Calcinosis cutis is a rare condition, characterized by an accumulation of calcium salts in the skin and subcutaneous tissue. There are several types of this condition, including dystrophic, metastatic, idiopathic, calciphylaxis, and iatrogenic calcinosis cutis. The type related to our case is iatrogenic calcinosis cutis, and one its possible causes is calcium intravenous infusion. Physicians should be aware of this condition when giving calcium infusion. CASE PRESENTATION: Here we report the case of a 9-month-old Arabic - Saudi baby boy, who presented with abnormal movement for 1 day. Upon further investigation, his abnormal movement was found to be a manifestation of hypocalcemia and vitamin D deficiency. He was treated with intravenous calcium gluconate. Later, he had a treatment-related complication of intravenous calcium at the site of venipuncture causing swelling, which was initially soft but progressed to hard, over the left hand. Eventually, he was diagnosed with a case of iatrogenic calcinosis cutis due to intravenous calcium treatment. CONCLUSION: There are multiple differential diagnoses of calcinosis cutis, as it resembles many other conditions. Careful history-taking, physical examination, and other investigations, such as radiological investigations, will aid in reaching a more accurate diagnosis and, thus, early treatment and intervention. Frequently checking the intravenous line and diluting the intravenous calcium may help reduce the occurrence of iatrogenic calcinosis cutis.

Critical care management of hydrofluoric acid burns with a negative outcome.

Hydrofluoric acid is a highly corrosive acid widely used in various industries. When in contact with skin it causes local and systemic reactions due to the generation of fluoride ions. Severe burns are associated with high mortality rates, approaching 100%. We present a 21-year-old man with 15% full thickness burns, severe metabolic acidosis, hypoxia and electrolyte disturbances. The burns were treated with topical and subcutaneous injections of calcium gluconate, and the patient was given intravenous fluid, calcium chloride, magnesium and insulin-glucose infusions. Continuous renal replacement therapy was initiated due to the severity of the systemic toxicity. Extracorporeal membrane oxygenation was considered as it plays a vital role when conventional therapies fail. Our patient suffered multiple cardiac arrests and cardiopulmonary resuscitation was conducted several times but despite extensive efforts, he did not survive.

Malignant prolongation of the QTc interval due to severe vitamin D deficiency: an unusual presentation.

Long QT syndrome with Torsades de Pointes (TdP) is a life-threatening polymorphic ventricular arrhythmia. The corrected QT (QTc) prolongation >500 milliseconds (ms) has been associated with TdP. Hypocalcaemia due to severe vitamin D deficiency is an uncommon cause of acquired long QT. We hereby present a case of a 40-year-old woman with sensorineural deafness and having symptoms of palpitations and presyncope. She had a QTc interval of 556 ms (reference range, QTc 451-470 ms in adult healthy woman) on 24-hour Holter analysis. Genetic analysis for congenital long QT syndrome was negative. She was diagnosed with severe hypocalcaemia secondary to severe vitamin D deficiency. After treatment with intravenous calcium gluconate, followed by oral vitamin D and calcium supplementation, the QTc became normalised and no further episode of palpitations or presyncope occurred. The causes of vitamin D deficiency was due to inadequate exposure to sunlight and a strict vegan diet.

Theophylline toxicity: Successful management of a patient with distributive shock secondary to drug overdose.

Presenting a case of acute theophylline and salbutamol overdose with distributive shock. Twenty one years old lady presented with history of consumption of 3 gram of theophylline and 40 mg of salbutamol. On admission she had altered sensorium with the systolic blood pressure of 60 mmHg, unrecordable diastolic blood pressure and heart rate of 147/min. Investigations revealed severe metabolic acidosis, hypokalemia, hypocalcemia which was managed by intravenous fluids, vasopressors, infusion of injection calcium gluconate and injection potassium chloride. As her hemodynamic status did not improve, she has been initiated on 1.5 mL/kg of lipid emulsion as bolus and then 0.5 mL/kg/h as infusion. Her hemodynamic status improved gradually and she was discharged in 24 h. Lipid emulsion had been used in local anesthetics and many tablet overdoses. In this patient timely administration of lipid emulsion resulted in early recovery of shock.

Síndrome de Fahr por hipoparatiroidismo secundario / Fahr syndrome due to secondary hypoparatiroidism

Objetivo: Describir la obtención del diagnóstico etiológico del síndrome de Fahr en una paciente sin antecedentes familiares de calcificaciones cerebrales.Caso clínico: Se presenta una paciente que ingresó con trastornos psiquiátricos,convulsiones y movimientos involuntarios. Se le realizó una tomografía computarizada de cráneo donde fue evidente gruesas y simétricas calcificaciones en ganglios basales,cerebelo y en sustancia blanca. Se diagnosticó un síndrome de Fahr por hipoparatiroidismo secundario debido a las lesiones observadas, los resultados de las pruebas hormonales y losantecedentes de tiroidectomía de varios años atrás. Fue tratada con gluconato de calcio y fenitoína. Falleció posteriormente por shock cardiogénico.Conclusión: El análisis de las características clínicas, los hallazgos de neuroimagen, las pruebas de laboratorio, los resultados anatomopatológicos y antecedentes quirúrgicos, permitieron el diagnóstico etiológico del síndrome de Fahr en esta paciente(AU)

Objective: To describe the etiological diagnosis process of Fahr syndrome in a patient with no family history of brain calcifications.Clinical case report: We report a female patient who was admitted because of psychiatric disorders, seizures and involuntary movements. A computed tomography scan of the skull was performed, which showed thick and symmetrical calcifications in the basal ganglia, cerebellum, and white matter. Fahr syndrome was diagnosed from secondary hypoparathyroidism because of the injuries observed, the results of hormonal tests, and a history of thyroidectomy from several years. She was treated with calcium gluconate andphenytoin, and subsequently died of cardiogenic shock.Conclusions: The analysis of the clinical characteristics, the neuroimaging findings, the laboratory tests, the pathological results and the surgical history, allowed the etiologicaldiagnosis of Fahr syndrome in this patient(AU)

Application of calcium nebulization for mass exposure to an accidental hydrofluoric acid spill.

PURPOSE: To determine the long-term prevalence and characteristics of acute hydrofluoric acid (HF) exposure in 2223 patients during the first 30 months after a mass-casualty exposure, and to confirm the antidotal effect of nebulized calcium on inhalation burns caused by HF. METHODS: This observational cohort study included patients after an HF spill in the Republic of Korea on September 27, 2012; registered patients were followed until April 2015. We assessed toxic effects, distance from spill, degree of acute poisoning, and the effect of nebulized calcium in HF-exposed individuals. RESULTS: Overall, 2223 patients received emergency management or antidote therapy for 20 days. Seventy-four of 134 patients with dermal toxicity received calcium-lidocaine gel, and 368 individuals with bronchial irritation signs received calcium gluconate via nebulizer nCG. A total 377 ampoules 786 g of calcium gluconate were used in the nCG formulation. Calcium administration did not cause adverse reactions during the observation period. Long-term cohort observation showed that 120 patients (120/2233, 5.4%) returned to medical facilities for management of HF-related symptoms within 1 month; 18 persons (18/1660, 1.1%) returned 1-3 months later with chronic cough and respiratory symptoms; and 3 patients (3/1660, 0.2%) underwent medical treatment due to upper-airway toxic symptoms more than 2 years after HF exposure. CONCLUSION: Respiratory toxicity after mass exposure to an HF spill was successfully treated by calcium nebulizer. Based on our experience, detoxification processes and the amounts of antidote stocked are important when planning for future chemical disasters at the community level.

Intravenous calcium Gluconate alleviates Lead-induced abdominal pain, a randomized clinical trial.

BACKGROUND: In 2016, in a lead poisoning outbreak in Iran, physicians reported thousands of opium users who presented to emergency departments (EDs) with intractable severe abdominal pain which did not respond to any narcotic medication. During the same period of time, we investigated the efficacy of intravenous calcium gluconate in alleviating lead-induced abdominal pain. METHODS: In a single-center, single blinded, randomized controlled trial, a convenient sample of adult opium-addicted patients who presented to an academic ED with abdominal pain and had an initial diagnosis of lead poisoning were included and randomly subjected to two treatment groups receiving conventional treatment (morphine 0.1 mg/kg + normal saline; group 1) and conventional treatment plus 1 g of intravenous calcium gluconate (group 2) to alleviate their abdominal pain. The visual analogue scale (VAS) was determined by each patient (0 to 100 mm) before treatment, and 15, 30, and 60 min after intervention. RESULTS: A total of 50 patients (25 in each group) were enrolled. Blood lead levels, VAS scores before treatment, and mean administered dose of morphine were similar between the two groups. After treatment, mean VAS score dropped to 64.7± 10.4 vs. 67.1± 10.9 at 15 min (P = 0.437), 64.6± 10.9 vs. 58.0 ± 11.2 at 30 min (P = 0.041), and 63.8± 10.7 vs. 53.6± 10.9 at 60 min (P = 0.002) in groups 1 and 2, respectively. CONCLUSION: Intravenous calcium gluconate administration along with morphine can improve abdominal pain in lead poisoning due to the ingestion of lead-contaminated opium. Further interventional studies are recommended to see if response to calcium salts in suspected lead-induced abdominal pain can rule in lead toxicity. TRIAL REGISTRATION: IRCT20171009036661N2. Registered 27 May 2018 - Retrospectively registered.

Hypocalcemic cardiomyopathy: a rare presenting manifestation of hypoparathyroidism.

Hypoparathyroidism patients present with features of hypocalcemia like carpopedal spasm, numbness and paresthesias but hypocalcemic cardiomyopathy leading to congestive heart failure (CHF) is a rare presentation. We present here a case of 55-year-old Asian man who was a known case of dilated cardiomyopathy for 6 months, presented with the chief complaints of shortness of breath on exertion and decreased urine output. On general physical examination, features suggestive of CHF were seen. Chvostek and Trousseau's sign was positive. The patient had a history of cataract surgery of both eyes 15 years ago. Further investigations revealed hypocalcemia. Echo showed severe global hypokinesia of left ventricle with left ventricle ejection fraction 15%. This CHF was refractory to conventional treatment, though, with calcium supplementation, the patient improved symptomatically. On follow-up after 3 months, an improvement was seen in the echocardiographic parameters with ejection fraction improving to 25%.