Calcium Channel Blocker Overdose Research Articles

Developments in the epidemiology of calcium channel blocker poisoning and implications for management.

The aim of this study was to outline recent developments in calcium channel blocker (CCB) poisoning. The dihydropyridine CCB amlodipine is commonly prescribed in the United States, and amlodipine poisoning is increasing in frequency, presenting new challenges for clinicians because current paradigms of CCB poisoning management arose from literature on non-dihydropyridine agents. Amlodipine is now the most common CCB involved in poisoning. High-dose insulin is a potent inotrope and vasodilator; as such, it should be used cautiously, and typically in conjunction with vasopressors, as it theoretically may worsen vasodilation in amlodipine poisoning. High-dose insulin is best used when some degree of cardiogenic shock is suspected. Venoarterial extracorporeal membrane oxygenation utilization in CCB poisoning appears to be increasing, but high flow rates may be needed to combat amlodipine-induced vasoplegia. Intravenous lipid emulsion cannot be routinely recommended but may have a role in peri-arrest situations. Adjunct treatments such as angiotensin II, methylene blue, and hydroxocobalamin offer theoretical benefit but warrant further study. Amlodipine causes most cases of CCB poisoning and can induce both cardiogenic and distributive shock through multiple mechanisms. Clinicians should tailor treatment to suspected shock etiology, be aware of adjunct treatments for refractory shock, and consult an expert in poisoning.

Levosimendan as an Antidote in Experimental Calcium Channel Blocker Intoxication.

The effects of the calcium sensitizer levosimendan on hemodynamics and survival in guinea pigs intoxicated with the calcium blockers verapamil or diltiazem were evaluated in a randomized controlled study. One hundred four animals were randomized to be intoxicated with either verapamil (2.0 mg/kg) or diltiazem (4.5 mg/kg) and thereafter further randomized into 6 groups which received either saline (control), 3 different regimes of levosimendan, calcium chloride, and levosimendan combined with calcium chloride. The hemodynamics and survival of the animals were followed for 60 minutes after intoxication.The negative inotropic effect of calcium blockers was seen as a decrease by over 70% of the positive derivative of the left ventricular pressure. This was reversed by levosimendan. Moreover, both verapamil and diltiazem-induced marked hypotension (-69% and -63% of the baseline value, respectively) which was also reversed by levosimendan. The combined levosimendan and calcium chloride treatment had a synergistic effect in reversing verapamil or diltiazem-induced deterioration in hemodynamics.Both verapamil and diltiazem intoxications decreased the survival rate of guinea pigs to 13%. Levosimendan addition improved survival dose-dependently up to a survival rate of 75% and 88% in the verapamil and diltiazem groups, respectively. Low dose of levosimendan combined with calcium chloride improved survival in verapamil and diltiazem group to 88% and 100%, respectively.In conclusion, the administration of levosimendan improved hemodynamics and survival in calcium channel blocker intoxicated guinea pigs. The synergistic effect of levosimendan and calcium chloride suggests that this combination could be an effective antidote in calcium channel blocker intoxications.

The use of hyperinsulinemia‐euglycaemia therapy in the treatment of amlodipine overdose in a dog

AbstractA 1‐year‐old, female, spayed, mixed breed dog presented for lethargy, ataxia and possible ingestion of amlodipine. Based on clinical signs, history and clinicopathological findings, a diagnosis of amlodipine toxicosis was made. The patient's clinical signs and bloodwork derangements were refractory to traditional medical management for calcium channel blocker toxicosis, but a significant improvement was made after initiation of hyperinsulinemia‐euglycaemia therapy. The dog survived and made a full recovery. The use of hyperinsulinemia‐euglycaemia therapy for amlodipine toxicosis has not previously been reported in dogs. Hyperinsulinemia‐euglycaemia therapy can be used for treatment of hypotension as well as other clinical signs associated with calcium channel blocker toxicosis. The use of hyperinsulinemia‐euglycaemia therapy should be considered for amlodipine toxicosis in dogs.

Severe amlodipine toxicity: A medical dilemma managed with therapeutic plasma exchange

Amlodipine poisoning is a nightmare for treating clinicians because of the intractable hypotension and bradycardia induced by the drug, which requires a balanced treatment algorithm. We encountered a case of severe Amlodipine toxicity (450 mg) who presented with complaints of nausea, multiple episodes of vomiting, and chest discomfort. On arrival at the EMD, the patient had significant hypotension (80/46 mmHg), bradycardia (40 beats/min), and a fall in oxygen saturation (75 %). He was symptomatically managed with inotropes, IV calcium, IV fluids, and oxygen supplementation. We decided to go forward with Therapeutic Plasma Exchange (TPE) in an attempt to remove the inciting agent. Two sessions of TPE were performed and the patient showed significant improvement post-procedure which led to the discharge of the patient within 10 days of admission. This case report highlights the noteworthiness of TPE in treating significantly high doses of drug poisoning.

Effect of intravenous lipid therapy in critically ill pediatric patients with calcium channel blocker toxicity.

Overdose with calcium-channel blockers (CCBs) still maintain their importance with a high lethality rate after exposure. We report the intravenous lipid emulsion therapy (ILE) therapy in our CCB overdose patients. We retrospectively analyzed the records of 6 patients with CCB intoxication from Batman Training and Research Hospital PICU between March 2021 and September 2022. Patients aged 0-18 years who received ILE treatment for CCB poisoning were included. All six patients ingested CCB with the intention of committing suicide and were followed up in the pediatric intensive care unit (PICU). All patients received ILE therapy due to hemodynamic instability despite intravenous fluid boluses, calcium, glucagon, insulin-dextrose, and vasoactive agents. Vasoactive-Inotropic Score (VIS) decreased after ILE treatment. All patients were transferred from the PICU after recovery. ILE therapy should be kept in mind as a salvage therapy in hemodynamically unstable CCB poisoning cases that do not respond to initial and advanced options.

Successful treatment of severe calcium channel blocker poisoning, new experience with the guidance of invasive hemodynamic monitoring in a 17-year-old girl: a case report

BackgroundCalcium channel blocker poisoning is one of the most lethal cardiac drugs overdoses. Calcium and high-dose insulin infusion are the first-line therapy for symptomatic patients, and Intralipid emulsion infusion is useful for refractory cases.Case presentationIn this report, we describe a 17-year-old Iranian girl who took 250 mg of the drug for a suicidal attempt and presented with refractory hypotension and non-cardiogenic pulmonary edema treated successfully with the guidance of invasive hemodynamic parameters.ConclusionFor complicated cases, in addition to supportive care and adjuvant therapy such as high-dose insulin and Intralipid, it is mandatory to utilize advanced hemodynamic monitoring to treat hypotension in severe calcium channel blocker poisoning to guide the treatment.

Calcium Channel Blocker Overdose.

Emergency medicine residents and medical students on emergency medicine rotation. Calcium channel blocker (CCB) overdoses can be severe with potentially serious adverse outcomes. CCBs work by blocking the calcium channels on smooth and cardiac muscle tissue. At low dose ranges, dihydropyridine CCBs (such as nifedipine, amlodipine, and nicardipine) block the L-type calcium receptors in the peripheral vasculature, whereas non-dihydropyridine CCBs (such as: verapamil and diltiazem) affect the L-type calcium receptors in the myocardium.1 Because of this distinction, dihydropyridine CCB toxicity manifests as arterial vasodilation and non-dihydropyridine CCB toxicity is associated with cardiac manifestations such as bradycardia and negative inotropy.2 It is important to note that in high concentrations (such as in overdoses), CCBs lose specificity for their specific receptors and can show all the manifestations of toxicity such as bradycardia, peripheral vasodilation, and hypotension. Patients can develop both vasoplegic shock from peripheral vasodilation and cardiogenic shock. This is a high acuity low occurrence case with infrequently used but specific treatments, and thus this case provides educational value. At the end of this oral board session, examinees will: (1) demonstrate ability to evaluate a patient with undifferentiated shock with bradycardia and discuss the differential diagnosis, (2) recognize the signs and symptoms of calcium channel blocker overdose, (3) demonstrate ability to manage treatment of a patient with calcium channel overdose. This oral board case followed the standard American Board of Emergency Medicine-style case in a tertiary care hospital with access to all specialists and resources needed. This case was tested using 12 resident volunteers ranging from PGY 1-2 in an ACGME (Accreditation Council for Graduate Medical Education) accredited emergency medicine residency program. Immediate feedback was solicited both from the learners and from the evaluators following the debriefing session. Residents were asked to evaluate the educational value of the case using a 1-5 Likert scale (5 being excellent). Evaluators were asked to score the residents using the ACGME core competencies with a scale of 1-8, 1-4 being unacceptable and 5-8 being acceptable. Seven PGY1 residents and five PGY2 residents, thus twelve residents in total, completed the case. The average score was 5.10/8. Three residents missed zero critical actions. The most common critical action missed was consulting cardiology or cardiothoracic surgery for circulatory support options. Many residents failed to recognize that the patient did not have a perfusing blood pressure at the beginning of the case and did not start CPR. Although most residents recognized the patient's hemodynamic collapse was from a calcium channel blocker overdose, most did not know the treatment for this beyond atropine and intravenous fluids.The learners rated the educational value of the case as 4.9/5. Seven residents reported that the case definitely increased their medical knowledge; five residents reported that it somewhat increased their medical knowledge. All residents rated the case as helpful in preparing to manage this medical condition. The educational content from this case was effective. This is a high acuity low occurrence case that has unique treatments that are not commonly used. This makes this case excellent for practice and discussion. We learned during implementation that this case has a high degree of difficulty compared to other cases, and junior learners will need more prompting. It is also important for the proctor to keep the case moving because there is a lot to cover in the allotted amount of time. Calcium channel blocker overdose, toxicology.

Intravenous calcium therapy in calcium channel blocker poisoning - A double-edged sword.

Intravenous calcium therapy in calcium channel blocker poisoning - A double-edged sword.

A Case of Amlodipine Poisoning in Children and Literature Review

A Case of Amlodipine Poisoning in Children and Literature Review

Hemoadsorption Therapy for Calcium Channel Blocker Overdose: A Case Report

BackgroundModern resin hemoadsorption/hemoperfusion for calcium channel blocker overdose is yet to be reported. The characteristics of calcium channel blockers make them unamenable to removal by hemodiafiltration or charcoal hemoperfusion; however, elimination, using styrene bead adsorption in an ex vivo model, has been demonstrated. Its clinical use is described. Case ReportA man in his 20s was admitted with shock into the Intensive Care Unit (ICU) after an overdose of amlodipine and risperidone. Resuscitation and supportive care were administered, but hypotension did not resolve despite the administration of intravenous fluids, infusions of calcium, adrenaline, and hyperinsulinemic-euglycemic therapy. Methylene blue was then administered to maintain the mean arterial pressures. However, the hemodynamic effect did not allow the weaning of the adrenaline. Drug clearance using hemoadsorption/hemoperfusion was attempted using a styrene resin filter (Jafron HA230; Jafron Biomedical Co., Ltd., Guangdong, China). During the two hemoperfusion sessions (6 h duration each, and 18 h apart) the patient had successfully weaned off all supportive measures, with lactate levels returning to normal and was later discharged home. At the end of each session, significant amlodipine concentrations were detected in blood aspirated from both filters, suggesting enhanced clearance. Why Should an Emergency Physician Be Aware of This?Our case illustrates a temporal relationship between resin hemoperfusion therapy, resolution of hemodynamic instability, and shock without proving causation. Significant amlodipine elimination was suggested by high concentrations found in blood from the filter. At the same time, shock resolution after initiation of hemoperfusion occurred in less than one elimination half-life of amlodipine.

Central ECMO cannulation for severe dihydropyridine calcium channel blocker overdose

Calcium channel blocker (CCB) toxicity carries a high mortality and is the sixth most fatal drug class reported to US poison centers. Amlodipine overdose is characterized by a life-threatening arterial vasodilation that compromises organ perfusion. The management of CCB intoxication is focused on maintaining adequate organ perfusion. In cases refractory to medical therapies, hemodynamic support with extracorporeal membrane oxygenation (ECMO) is warranted necessitating higher flows than usual to compensate for the vasodilation and requiring central cannulation. We present a case of a 12-year-old with severe dihydropyridine CCB ingestion, refractory to medical management and successfully treated with central ECMO cannulation. The patient was discharged home with no significant disability. Central ECMO cannulation may be helpful to facilitate adequate flows in vasodilatory shock such as CCB overdose.

Central Extracorporeal Membrane Oxygenation Support Following Calcium Channel Blocker Overdose in Children.

Refractory vasodilatory shock (RVS) following massive calcium channel blocker (CCB) overdose remains a challenging clinical entity. Peripheral venoarterial extracorporeal membrane oxygenation (ECMO) has proven useful in several cases of CCB intoxication, however, its use in the pediatric population poses unique challenges given the generally small size of pediatric peripheral vasculature in comparison to the high flow rates necessary for adequate mechanical circulatory support. As a result of these challenges, our group has adopted a "primary" central ECMO cannulation approach to the treatment of children and adolescents admitted to our center with profound RVS after CCB ingestion. We present four cases within the last year using this approach. All patients were successfully discharged from the hospital with no late morbidity at most recent follow-up. Central ECMO support in cases of massive vasodilatory shock following CCB overdose is safe and effective and should be considered early in the clinical course of these critically ill patients.

Beta-blocker and calcium-channel blocker toxicity: current evidence on evaluation and management.

Beta-blocker and calcium-channel blocker overdoses are associated with severe morbidity and mortality; therefore, it is important to recognize and appropriately treat individuals with toxicity. The most common clinical findings in toxicity are bradycardia and hypotension. In addition to supportive care and cardiac monitoring, specific treatment includes administration of calcium salts, vasopressors, and high-dose insulin euglycaemia treatment. Other advanced treatments (e.g. ECMO) may be indicated depending on the severity of toxicity and specific agents involved.

Insulin concentrations following termination of high-dose insulin euglycemic therapy

Introduction High-dose insulin therapy is used in patients with calcium channel blocker and beta-adrenergic antagonist overdoses. The pharmacokinetics of insulin are scantly reported following high-dose insulin therapy. We present two cases of persistently elevated insulin concentrations following high-dose insulin therapy. Case reports A 50-year-old woman and a 45-year-old man experienced hypotension after overdosing on amlodipine and atenolol. They were treated with high-dose insulin therapy for 54 hours at 2 units/kilogram/hour and 48 hours at 10 units/kilogram/hour, respectively. Following termination, serum insulin elimination was studied. Insulin concentrations remained greater than 1,000 µU/mL (fasting reference 2.6–24.9 µU/mL) for longer than 4 hours (case 1) and 11 hours (case 2) and greater than 300 µU/mL for longer than 8 hours and 21 hours, respectively. Insulin concentrations decreased with apparent first-order elimination half-lives of 13.0 hours and 6.0 hours. Discussion Following high-dose insulin therapy, insulin concentrations remained elevated for longer than expected based on normal pharmacokinetics in therapeutic dosing. Three previous cases reported insulin half-lives of between 2.2 hours and 18.7 hours. The current cases add to the existing data that insulin has a variable but prolonged half-life following high-dose insulin therapy. Conclusions These findings suggest that patients are at prolonged risk of hypoglycemia following cessation of high-dose insulin infusions.

Treatment Modalities in Calcium Channel Blocker Overdose: A Systematic Review.

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), extracorporeal life support (used in three patients with refractory shock or cardiac arrest), injection glucagon, methylene blue, albumin infusion, and terlipressin were associated with a lower mortality rate as well as improvement in hemodynamic parameters. None of the case reports provided any information on end-organ damage on long-term follow-up.

Hydroxycobalamin Administration in the Treatment of Calcium Channel Blocker-Induced Vasoplegia: A Case Report

Calcium channel blocker (CCB)-induced vasoplegia syndrome is an emergent, life-threatening complication that can occur refractory to traditional therapy in the treatment of an acute CCB overdose. We present a case of acute co-ingestion of many prescription medications, including amlodipine and escitalopram. The patient presented with hemodynamic instability that persisted despite conventional therapies. Hydroxycobalamin (HCO) therapy was initiated, resulting in hemodynamic and clinical improvement. We highlight the unique presentation of this case and the potential benefits associated with HCO administration. Key Points: This case demonstrates the potential benefits of HCO administration in CCB-induced vasoplegia syndrome. Given the significant morbidity and mortality associated with CCB toxicity, HCO may provide considerable benefit in patients with hemodynamic instability refractory to standard treatment modalities.

P3: ECMO and Calcium Channel Blocker Overdose: A Systematic Review

Introduction: The increasing indications and prevalence of extracorporeal membrane oxygenation (ECMO) are evident by the exponential increase in ECMO in the last decade. In recent literature, ECMO use has sustained patients who have intentionally or unintentionally overdosed on cardiac medications. Specifically, calcium channel blocker overdose (CCBOD) can lead to significant cardiopulmonary dysfunction and has increased in recent years. Calcium channel blockers (CCB) block L-type voltage gated calcium channels throughout the body, and overdose results in cardiac depression, vasoplegia, and hyperglycemia. Expert consensus and poison control centers both recommend treatment with calcium, high dose insulin, inotropes, and vasopressors. Our systematic review evaluated when to initiate ECMO in the CCBOD population and the mortality rate with ECMO use. Methods: An electronic literature review was conducted to identify all relevant studies for CCB use and ECMO. PRISMA guidelines for systematic review were followed. Rayyan was used as a screening tool for blinding the authors from each other, and abstracts and full texts were reviewed by three independent authors. Inclusion criteria were strictly limited to CCB ingestion without polypharmacy. A data collection tool was devised and data was independently collected by two authors prior to statistical analysis. Data points included demographics, a list of currently recommended medical treatments for CCBOD, ECMO cannulation type, and survival to hospital discharge. Results: After exclusion of duplicates, 314 abstracts were reviewed; of these 25 papers were included from 6 different countries, with the median year of the study publication 2019. From the 25 papers, 26 patients were studied with an average patient age of 32.7 years with 42% male and 58% female. Between male and female there was no significant difference in age, type of CCB taken, or days on ECMO. Average time on ECMO was 4.3 days. Venoarterial and venovenous ECMO use were 92.3% and 7.7%, respectively. Survival to hospital discharge was 84.6%. Prior to ECMO cannulation, patients received up to six medical treatments for CCBOD, with the majority receiving four to five treatments (53.8%). There was no correlation between number of therapies and days on ECMO (r=0.092, P=0.684). Conclusion: Our systematic review demonstrates that ECMO is a newly used and possibly valuable therapy for CCBOD when medical treatment fails. Most patients received aggressive medical therapies and still were unstable enough to require ECMO. Survival to discharge after ECMO for CCBOD is substantially higher than standard VV or VA ECMO uses. While medical management is still the main therapy for CCBOD, our results show that a persistently unstable patient may benefit from prompt evaluation at an ECMO center for treatment.

P4: Successful VA-Extracorporeal Membrane Oxygenation course in a patient with intentional Calcium Channel Blocker overdose without the need for mechanical ventilation

Background: Cardiovascular medication overdose constitutes about 3.5% of all drug overdoses, and carries a mortality of 16%. Calcium channel blockers (CCBs) and beta blockers account for more than 65% of these deaths. Overdose of cardiovascular medications cause impaired cardiac contractility, vasoplegia, and/or rhythm disturbances. We review the current literature and case reports of VA ECMO being utilized to support patients with cardiovascular medication overdose. Methods: We present a case of a 20-year-old female with no medical history presenting with bradycardia and hypotension after ingesting ninety ezetimibe 10mg, seventy-five nebivolol 10mg, and one hundred and eighty amlodipine 5mg, from her mother’s medication, with the intent of self harm. Patient received glucagon, calcium, lipid emulsion, and was being supported on vasopressin, norepinephrine, epienephrine, phenylephrine and dopamine. The patients HR 78 and SBP 68mmHg. Laboratory significant for leukocytosis and elevated lactic acid. On exam, patient was lethargic, without respiratory distress. Echocardiogram revealed EF 55-65% and a large right ventricular mass suspicious for atrial myxoma. Patient was initiated on peripheral Veno-Arterial ECMO using Femoral-Femoral configuration to provide circulatory support as a bridge to allow drug metabolism and clearance. Results: Following 72 hours of VA-ECMO, vasopressors were weaned, with ECMO successfully being discontinued. Throughout the ECMO course, the patient had no respiratory compromise and did not require intubation or mechanical ventilation. Following decannulation, the patient was discharged to follow for an elective resection of the atrial myxoma. Conclusion: ECMO has been reported as a rescue therapy in CCB and Beta blocker overdose when refractory to medical therapy. Conventional medical therapy includes limiting absorption, increasing elimination and hemodynamic support using vasopressor agents, intravenous (IV) calcium infusion, hyperinsulinemia therapy, glucagon infusion, and IV lipid emulsion. This unique case demonstrates the successful utilization of VA ECMO to support patients with cardiovascular medication overdose and illustrates the potential for hemodynamic support without the need for ventilator support. This is the only known report of VA ECMO being utilized for calcium channel overdose while the patient is awake and unventilated throughout their ECMO course.

In Hospital Outcome of Patients with Acute St-Elevation Myocardial Infarction Requiring Temporary Pacemaker

Background and Aim: Acute myocardial infarction is a serious public health concern around the globe and temporary pacing is required in a variety of myocardial infarction. The present study aimed to determine the in-hospital outcome of acute ST elevation myocardial infarction patients requiring a temporary pacemaker. Patients and Methods: This descriptive cross-sectional study was carried out on 120 acute myocardial infarction patients in the Cardiology Unit of PIMS Hospital, Islamabad from January 2021 to March 2023. Each individual underwent chest X-ray, ECG and serum markers. A detailed physical history including age, gender, smoking history, occupation, ischemic heart disease, diabetes, and hypertension were noted in specific designed proforma. Inclusion Criteria: Acute myocardial infarction patients who had chest pain, elevated serum markers, New onset ST Elevation and complete heart block on ECG and required pace maker during their hospitalization were enrolled. Exclusion Crieteria: Complete Heart block due to CKD or electrolyte imbalance, beta blocker or calcium channel blocker overdose, congenital heart block were excluded from the study. Results: The overall mean age was 52.64±6.8 years. The incidence of smokers, diabetes, and hypertension was 76 (63.3%), 56 (46.7%), and 52 (43.3%) respectively. The mean duration of symptom’s onset during hospital admission was 7.9±3.8 hours. About 48 (40%) patients had implanted temporary pacemaker at presentation, 66 (55%) on first post MI day, and 6 (5%) on 2nd post MI day. The in-hospital mortality was 8.3% (n=10). The incidence of ventricular tachycardia, ventricular fibrillation, and asystole was 28.3% (n=34), 3.3% (n=4) and 1.7% (n=2) respectively. Conclusion: The present study found that complete heart block is associated with a poorer early prognosis in individuals with ST-Elevation MI who require temporary pacemaker. In these individuals, a more intensive therapy strategy targeted at reducing early death is required. Keywords: Acute myocardial infarction, in-hospital outcome, temporary pace maker

Tissue injury secondary to peripheral xenobiotic administration.

A 57-year-old female with a past medical history of depression was brought in by emergency medical services after intentional ingestion of 400 mg warfarin and 200 mg amlodipine 4 hours before presentation. The patient was started on treatment for calcium channel blocker overdose, including intubation for central nervous system depression, activated charcoal, intravenous calcium and glucagon, high-dose insulin with dextrose infusion, and vasopressor support. On day 2 of hospitalization, a rash was found on the left lower extremity (see Figures 1 and 2). Tissue Injury Due to Peripheral Intravenous Calcium Chloride Administration Intravenous calcium is used to treat acute hypocalcemia, severe hyperkalemia, calcium channel blocker overdose, beta-blocker overdose, and hydrofluoric acid exposure.1 Calcium chloride is preferentially administered via a central venous catheter due to its high osmolarity and its propensity to act as a vesicant.1 Calcium gluconate is preferred over calcium chloride for peripheral administration, as it is less likely to cause tissue injury if extravasation occurs. Adverse effects of both formulations include local tissue injury, skin necrosis, calcium-induced vasoconstriction, and late-onset calcifications or calcinosis cutis.1-4 Treatment for local tissue injury includes stopping the infusion and consideration of intradermal hyaluronidase around the site to diminish tissue injury.1, 4 If tissue necrosis develops, wound care, surgical debridement, and skin grafting may be considered.3 Clinicians should familiarize themselves with local tissue injury, which can be minimized by using calcium gluconate as opposed to calcium chloride when peripheral access is present.