Calcium gluconate
Sources réglementaires consultées
Indications approuvées
- Traitement de l'hypocalcémie aiguë, notamment de la tétanie hypocalcémique.
- Supplémentation calcique dans le cadre de la nutrition parentérale.
Contre-indications
Absolues
- Hypersensibilité au gluconate de calcium ou à l'un des excipients.
- Hypercalcémie.
- Hypercalciurie.
- Intoxication par des glucosides cardiotoniques.
- Traitement par des glucosides cardiotoniques. Le calcium intraveineux ne peut être envisagé qu'à titre exceptionnel en cas d'hypocalcémie sévère menaçant le pronostic vital, sans solution plus sûre et lorsque le calcium oral est impossible.
- Utilisation concomitante de ceftriaxone et de produits intraveineux contenant du calcium chez les nouveau-nés âgés de 28 jours ou moins.
Mises en garde cliniques
- Mise en garde majeure · Administrer lentement sous surveillance de la fréquence cardiaque ou de l'ECG. Une administration intraveineuse trop rapide peut provoquer une bradycardie, une vasodilatation, une hypotension, une arythmie ou un collapsus circulatoire. — https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
- Mise en garde majeure · Éviter l'extravasation et l'injection intramusculaire superficielle, qui peuvent provoquer une calcinose cutanée, des abcès, une induration, une desquamation cutanée et une nécrose tissulaire. — https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
- Mise en garde majeure · Si un traitement vital impose l'administration de calcium intraveineux pendant un traitement par glucosides cardiotoniques, assurer une surveillance cardiaque adéquate et disposer d'un traitement d'urgence des arythmies sévères. — https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
Interactions médicamenteuses
- ModéréeAdrénalineC01CA24
Mécanisme: L'administration concomitante peut réduire les effets bêta-adrénergiques de l'adrénaline après une chirurgie cardiaque.
Recommandation: Évaluer la réponse cardiovasculaire clinique pendant l'administration concomitante.
https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
- ModéréeMagnésium
Mécanisme: Le calcium et le magnésium antagonisent mutuellement leurs effets.
Recommandation: Surveiller la réponse clinique et les électrolytes pendant l'administration concomitante.
https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
- ModéréeInhibiteurs calciques
Mécanisme: Le calcium peut antagoniser l'effet des inhibiteurs calciques.
Recommandation: Surveiller la réponse cardiovasculaire.
https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
- ModéréeDiurétiques thiazidiquesC03AA
Mécanisme: Ils réduisent l'excrétion rénale du calcium et peuvent provoquer une hypercalcémie.
Recommandation: Surveiller la calcémie et éviter une charge calcique excessive.
https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
- SévèreCeftriaxone intraveineuseJ01DD04
Mécanisme: Elle peut former des précipités de ceftriaxone-calcium ; des réactions mortelles ont été rapportées chez les prématurés et les nouveau-nés.
Recommandation: Contre-indiqué chez les nouveau-nés âgés de 28 jours ou moins. Chez les patients plus âgés, ne pas mélanger ni administrer simultanément ; pour une administration séquentielle, utiliser des lignes ou sites différents ou rincer la ligne avec une solution saline.
https://cima.aemps.es/cima/dochtml/ft/69465/FT_69465.html
Effets indésirables
Rares mais graves
Nécrose tissulaire et calcinose cutanée après extravasation ou administration incorrecte · Hypotension · Bradycardie · Arythmie cardiaque · Collapsus circulatoire potentiellement mortel · Précipitation grave ou mortelle de ceftriaxone-calcium chez le nouveau-né
Grossesse et allaitement
Le résumé des caractéristiques ne formule aucune recommandation spécifique pendant la grossesse. Le calcium est excrété dans le lait maternel ; pendant l'allaitement, décider d'interrompre l'allaitement ou le traitement selon le bénéfice pour l'enfant et pour la mère.
Bibliographie récente (PubMed)
Zollinger-Ellison syndrome (ZES) is a distinct syndrome characterized by hyperchlorhydria-induced peptic ulcer disease and chronic diarrhea. It is the result of a gastrin-excess state caused by a duodenal or pancreatic neuroendocrine tumor referred to as gastrinoma. This gastrin-secreting neuroendocrine tumor is usually sporadic in nature, or part of multiple endocrine neoplasia type 1 syndrome. The high rate of malignancy associated with gastrinomas substantiates the need for early diagnosis. In order to diagnose ZES with laboratory tests, patients under antacid medication are required to stay off proton pump inhibitors for at least one week and H2 receptor antagonists for 48 h. Fasting serum gastrin level measurement serves as an initial and fundamental diagnostic test, boasting a sensitivity of 99%. Gastrinoma patients will present with a gastrin level greater than 100 pg/mL, while a serum gastrin level higher than 1000 pg/mL, in the presence of gastric pH <2, is considered diagnostic. Since more common causes of hypergastrinemia exist in the setting of hypochlorhydria, ruling those out should precede ZES consideration. Such causes include atrophic gastritis, Helicobacter pylori (H. pylori)-associated pangastritis, renal failure, vagotomy, gastric outlet obstruction and retained antrum syndrome. The secretin stimulation test and the calcium gluconate injection test represent classic adjuvant diagnostic techniques, while alternative approaches are currently being introduced and evaluated. Specifically, the secretin stimulation test aids in differentiating ZES cases from other hypergastrinemic states. Its principle is based on secretin stimulation of gastrinoma cells to secrete gastrin, while inhibiting normal G cells. The rapid intravenous infusion of 4 μg/kg secretin over 1 min is followed by gastrin level evaluation at specific intervals post-infusion. Localization of the primary tumor and its metastases is the next diagnostic step when gastrinoma-associated ZES
Hyperkalemia has been defined as a condition where a serum potassium level is >5.5 mmol/l. It is associated with fatal dysrhythmias and muscular dysfunction. Certain medical conditions, such as chronic kidney disease (CKD), diabetes mellitus, and others, can lead to hyperkalemia. Many of the signs of hyperkalemia are nonspecific. A history and physical examination can be beneficial in the diagnosis of the condition. In this regard, certain characteristic electrocardiogram findings are associated with hyperkalemia along with laboratory potassium levels. In acute and potentially lethal conditions, hyperkalemia treatments include glucose and insulin, bicarbonate, calcium gluconate, beta-2 agonists, hyperventilation, and dialysis. There are several drugs, both old and new, that can additionally aid in the reduction of serum potassium levels. The present investigation evaluated some of these different drugs, including sodium polystyrene sulfonate (SPS), sodium zirconium cyclosilicate (SZC), and patiromer. These drugs each have increased selectivity for potassium and work primarily in the gastrointestinal (GI) tract. Each of these medications has unique benefits and contraindications. Clinicians must be aware of these medications when managing patients with hyperkalemia.
Hydrofluoric acid (HF), the inorganic acid of elemental fluorine, is a highly dangerous substance and death can result from a very small exposure. In addition to local toxicity, HF can trigger fatal systemic reactions by its high affinity for calcium and magnesium. The authors report the autopsy case of a male worker who was exposed to 50% HF while repairing the leakage from an HF tank valve in a semi-conductor washing factory. His colleagues found blisters on his neck after 6 h of work and he was sent to the hospital. However, he expired from cardiac arrest despite an immediate calcium gluconate injection. At autopsy, burns with eschar covering less than 5% of the total body surface were identified on the neck and around both ears, and microscopic examination of the affected skin revealed extensive necrosis of the epidermis and dermis with pustule formation. In chemical analysis, no fluoride ions were detected in blood, vitreous humor, urine, pleural fluid, bile, or skin tissue from the neck. Considering the chemical burns on the neck and the circumstantial information, the cause of death was determined to be HF poisoning. This article presents the clinical manifestations of local and systemic toxicity after the accidental exposure to a high concentration of HF, with histologic demonstrations of chemical burns.
Calcium channel blocker poisoning is one of the most common poisonings encountered which presents with life-threatening complications. However, there is no unified approach for treating these patients in the existing literature. This study aimed to assess the effects of different treatment modalities used in calcium channel blocker poisoning, as reported by previous studies. The primary outcomes studied were mortality and hemodynamic parameters after treatment. The secondary outcomes were the length of hospital stay, length of intensive care unit stay, duration of vasopressor use, functional outcomes, and serum calcium channel blocker concentrations. A thorough literature search was performed through Ovid, PubMed, Cochrane Library, and Google Scholar from January 2014 to December 31, 2022, to identify all studies analyzing the effects of the treatment of calcium channel blocker poisoning on the desired outcomes. Two reviewers reviewed 607 published articles from January 2014 to December 2022 to identify studies analyzing the effects of the treatment of calcium channel blocker poisoning on desired outcomes. In this review, 18 case reports, one case series, and one cohort study were included. Most patients were treated with an injection of calcium gluconate or calcium chloride. The use of calcium along with dopamine and norepinephrine was found to have lower mortality rates. A few patients were also treated with injection atropine for bradycardia. High-dose insulin therapy was used in 14 patients, of whom two did not survive. In the cohort study, 66 calcium channel blocker toxicity patients were included. These patients were treated with high-dose insulin therapy. A total of 11 patients with calcium channel blocker toxicity succumbed. Although it was found to be associated with improved hemodynamic parameters and lower mortality, side effects such as hypokalemia and hypoglycemia were noted. Intravenous lipid emulsion therapy (administered to eight patients), extracorp
Ototoxicity is a known side effect of cisplatin chemotherapy. The efficacy of various medications used to prevent or reduce ototoxicity in adults receiving cisplatin has not been thoroughly described in the literature. CINAHL, Cochrane Library, PubMed, and SCOPUS. Literature was searched between 1990 and 2024. Studies evaluating interventions to prevent hearing loss in adults receiving cisplatin were included. Audiometric data including pure tone threshold, pure tone average, and incidence of hearing loss were extracted from included studies. Eight studies (N = 431 total patients) pertaining to cisplatin-induced hearing loss in adults were included. Of these studies, six were randomized control trials (N = 372 patients) and two were prospective cohort studies (N = 59 patients). The cytoprotective treatments included diethyldithiocarbamate (intravenously), dexamethasone (intratympanic), N -acetylcysteine (intratympanic), sodium thiosulfate (intravenously), calcium gluconate (intravenously), and aspirin (PO). The treatment group had an incidence in overall hearing loss of 63.3% compared to the 66.2% incidence in the control group ([95% CI, -6.2 to 11.9] p = 0.53). Patients treated with dexamethasone had lower degrees of hearing loss compared to those treated with N -acetylcysteine. However, neither of these interventions were superior to the control group. These results show no difference in reducing the incidence nor severity of hearing loss between the treatment and control groups. Standardization of evaluated frequencies and ototoxicity grading scales will improve investigators' ability to compare various treatments. Unfortunately, the power of this study is limited by the sample size.