Extracorporeal therapy for amlodipine poisoning.

A young male presented in refractory shock from amlodipine poisoning despite vasopressors, insulin-normoglycemia therapy, calcium gluconate and glucagon. He needed venoarterial ECMO for hemodynamic support and TPE to remove protein-bound amlodipine. The use of extracorporeal membrane oxygenation (ECMO) for cardiotoxic poisoning and Total Plasma Exchange (TPE) in removing drugs has been described in the literature. We report a rare case where both lifesaving extracorporeal therapies were used in a patient with a severe drug overdose. Stabilizing hemodynamics with ECMO combined with TPE for drug removal is a feasible strategy in unstable patients with amlodipine overdose.

Use of veno-venous extracorporeal membrane oxygenation to treat severe combined calcium channel blocker and angiotensin converting enzyme inhibitor overdose.

INTRODUCTION: Calcium channel blockers (CCBs) are a commonly prescribed medication that, at toxic levels, are capable of causing severe refractory hypotension, hypoxic respiratory failure and cardiotoxicity. There is little evidence currently guiding the approach to managing CCB overdose, particularly when combined with other antihypertensive agents. CASE REPORT: We describe the use of veno-venous extracorporeal membrane oxygenation (VV ECMO) in a previously healthy man following combined overdose with amlodipine and lisinopril in a suicide attempt. ECMO was used to provide oxygenation support, allowing for the amlodipine and lisinopril to be metabolized and cleared while also reducing ventilator-induced lung injury (VILI) and avoiding the complications associated with venous-arterial (VA) ECMO, such as differential hypoxemia. CONCLUSION: Limited case reports suggesting the use of ECMO in CCB overdose have employed VA ECMO due to CCB-induced cardiotoxicity. We believe that, if cardiac function has been preserved, VV ECMO should be considered a viable treatment strategy for CCB and ACE-I overdose resulting in refractory hypoxemic respiratory failure.

High dose insulin for beta-blocker and calcium channel-blocker poisoning.

BACKGROUND/OBJECTIVES: High dose insulin (HDI) is a standard therapy for beta-blocker (BB) and calcium channel-blocker (CCB) poisoning, however human case experience is rare. Our poison center routinely recommends HDI for shock from BBs or CCBs started at 1U/kg/h and titrated to 10U/kg/h. The study objective was to describe clinical characteristics and adverse events associated with HDI. METHODS: This was a structured chart review of patients receiving HDI for BB or CCB poisoning with HDI defined as insulin infusion of ≥0.5U/kg/h. RESULTS: In total 199 patients met final inclusion criteria. Median age was 48years (range 14-89); 50% were male. Eighty-eight patients (44%) were poisoned by BBs, 66 (33%) by CCBs, and 45 (23%) by both. Median nadir pulse was 54 beats/min (range 12-121); median nadir systolic blood pressure was 70mmHg (range, 30-167). Forty-one patients (21%) experienced cardiac arrest; 31 (16%) died. Median insulin bolus was 1U/kg (range, 0.5-10). Median starting insulin infusion was 1U/kg/h (range 0.22-10); median peak infusion was 8U/kg/h (range 0.5-18). Hypokalemia occurred in 29% of patients. Hypoglycemia occurred in 31% of patients; 50% (29/50) experienced hypoglycemia when dextrose infusion concentration ≤10%, and 30% (31/105) experienced hypoglycemia when dextrose infusion concentration ≥20%. CONCLUSIONS: HDI, initiated by emergency physicians in consultation with a poison center, was feasible and safe in this large series. Metabolic abnormalities were common, highlighting the need for close monitoring. Hypoglycemia was more common when less concentrated dextrose maintenance infusions were utilized.

Severe beta blocker and calcium channel blocker overdose: Role of high dose insulin.

A 54-year-old female presented after taking an overdose of an unknown amount of hydrochlorothiazide, doxazocin, atenolol and amlodipine. She was initially refractory to treatment with conventional therapy (intravenous fluids, activated charcoal, glucagon 5 mg followed with glucagon drip, calcium gluconate 10%, and atropine). Furthermore, insulin at 4 U/kg was not effective in improving her hemodynamics. Shortly after high dose insulin was achieved with 10 U/kg, there was dramatic improvement in hemodynamics resulting in three of five vasopressors being weaned off in 8 h. She was subsequently off all vasopressors after six additional hours. The role of high dose insulin has been documented in prior cases, however it is generally recommended after other conventional therapies have failed. However, there are other reports that suggest it as initial therapy. Our patient failed conventional therapies and responded well only with maximum dose of insulin. Physicians should consider high dose insulin early in severe beta blocker or calcium channel blocker overdose for improvement in hemodynamics. This leads to early discontinuation of vasopressors. It is important that emergency physicians be aware of the beneficial effects of high dose insulin when initiated early as opposed to waiting for conventional therapy to fail; as these patients often present first to the emergency department. Early initiation in the emergency department can be beneficial in these patients.

Experts Consensus Recommendations for the Management of Calcium Channel Blocker Poisoning in Adults.

OBJECTIVE: To provide a management approach for adults with calcium channel blocker poisoning. DATA SOURCES, STUDY SELECTION, AND DATA EXTRACTION: Following the Appraisal of Guidelines for Research & Evaluation II instrument, initial voting statements were constructed based on summaries outlining the evidence, risks, and benefits. DATA SYNTHESIS: We recommend 1) for asymptomatic patients, observation and consideration of decontamination following a potentially toxic calcium channel blocker ingestion (1D); 2) as first-line therapies (prioritized based on desired effect), IV calcium (1D), high-dose insulin therapy (1D-2D), and norepinephrine and/or epinephrine (1D). We also suggest dobutamine or epinephrine in the presence of cardiogenic shock (2D) and atropine in the presence of symptomatic bradycardia or conduction disturbance (2D); 3) in patients refractory to the first-line treatments, we suggest incremental doses of high-dose insulin therapy if myocardial dysfunction is present (2D), IV lipid-emulsion therapy (2D), and using a pacemaker in the presence of unstable bradycardia or high-grade arteriovenous block without significant alteration in cardiac inotropism (2D); 4) in patients with refractory shock or who are periarrest, we recommend incremental doses of high-dose insulin (1D) and IV lipid-emulsion therapy (1D) if not already tried. We suggest venoarterial extracorporeal membrane oxygenation, if available, when refractory shock has a significant cardiogenic component (2D), and using pacemaker in the presence of unstable bradycardia or high-grade arteriovenous block in the absence of myocardial dysfunction (2D) if not already tried; 5) in patients with cardiac arrest, we recommend IV calcium in addition to the standard advanced cardiac life-support (1D), lipid-emulsion therapy (1D), and we suggest venoarterial extracorporeal membrane oxygenation if available (2D). CONCLUSION: We offer recommendations for the stepwise management of calcium channel blocker toxicity. For all interventions, the level of evidence was very low.

Terlipressin in refractory shock induced by diltiazem poisoning.

Poisoning caused by calcium-channels blockers (CCB) can cause refractory vasoplegic shock, resulting in multiple-organ failure and death despite maximal therapy including high doses of vasopressors. We report one CCB-induced refractory shock complicated with lactate acidosis despite very high doses of epinephrine and norepinephrine. The hemodynamic status of the patient dramatically improved after intermittent boluses of terlipressin, which corrected the acidosis.

Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies.

Management of cardiovascular instability resulting from calcium channel antagonist (CCB) or beta-adrenergic receptor antagonist (BB) poisoning follows similar principles. Significant myocardial depression, bradycardia and hypotension result in both cases. CCBs can also produce vasodilatory shock. Additionally, CCBs, such as verapamil and diltiazem, are commonly ingested in sustained-release formulations. This can also be the case for some BBs. Peak toxicity can be delayed by several hours. Provision of early gastrointestinal decontamination with activated charcoal and whole-bowel irrigation might mitigate this. Treatment of shock requires a multimodal approach to inotropic therapy that can be guided by echocardiographic or invasive haemodynamic assessment of myocardial function. High-dose insulin euglycaemia is commonly recommended as a first-line treatment in these poisonings, to improve myocardial contractility, and should be instituted early when myocardial dysfunction is suspected. Catecholamine infusions are complementary to this therapy for both inotropic and chronotropic support. Catecholamine vasopressors and vasopressin are used in the treatment of vasodilatory shock. Optimizing serum calcium concentration can confer some benefit to improving myocardial function and vascular tone after CCB poisoning. High-dose glucagon infusions have provided moderate chronotropic and inotropic benefits in BB poisoning. Phosphodiesterase inhibitors and levosimendan have positive inotropic effects but also produce peripheral vasodilation, which can limit blood pressure improvement. In cases of severe cardiogenic shock and/or cardiac arrest post-poisoning, extracorporeal cardiac assist devices have resulted in successful recovery. Other treatments used in refractory hypotension include intravenous lipid emulsion for lipophilic CCB and BB poisoning and methylene blue for refractory vasodilatory shock.

Multidrug-related leukocytoclastic vasculitis raising suspicion of sexual homicide-things are not always what they seem.

Ambiguous findings during external examination of a deceased in combination with dubious autopsy findings can raise doubts concerning the manner and cause of death. We report the case of a 35-year-old female deceased who had suffered from a borderline personality and depressive disorder with suicidal ideation. At the death scene, the body showed massive facial swelling accompanied by complete reddening of the skin of the face, with patchy skin abrasions on the forehead and neck, and purple bruise-like discolorations distributed symmetrically over both shoulders, elbows, hands, hips, knees, lower legs, and feet, raising the suspicion of underlying massive external blunt force injury. Police investigators strongly suspected sexual homicide. At autopsy, dissection in layers revealed massive subcutaneous hemorrhages as the cause of the reddish skin discolorations. Toxicological analyses showed fatal levels of lamotrigine with additional proof of zopiclone, zolpidem, diphenhydramine, O-desmethylvenlafaxine, pregabalin, tramadol, and modafinil in venous blood. Histologically, both the macroscopically impressive purple skin changes with underlying bleeding into the subcutaneous tissue and the skin abrasions were due to leukocytoclastic vasculitis, a form of acute hypersensitivity vasculitis that was a reaction to the multiple therapeutic drugs that the woman had taken shortly before death. The manner of death was classified as suicide, and sexual homicide was ruled out.

Efficacy of methylene blue in an experimental model of calcium channel blocker-induced shock.

STUDY OBJECTIVE: Calcium channel blocker poisonings account for a substantial number of reported deaths from cardiovascular drugs. Although supportive care is the mainstay of treatment, experimental therapies such as high-dose insulin-euglycemia and lipid emulsion have been studied in animal models and used in humans. In the most severe cases, even aggressive care is inadequate and deaths occur. In both experimental models and clinical cases of vasodilatory shock, methylene blue improves hemodynamic measures. It acts as a nitric oxide scavenger and inhibits guanylate cyclase that is responsible for the production of cyclic guanosine monophosphate (cGMP). Excessive cGMP production is associated with refractory vasodilatory shock in sepsis and anaphylaxis. The aim of this study is to determine the efficacy of methylene blue in an animal model of amlodipine-induced shock. METHODS: Sprague-Dawley rats were anesthetized, ventilated, and instrumented for continuous blood pressure and pulse rate monitoring. The dose of amlodipine that produced death within 60 minutes was 17 mg/kg per hour (LD50). Rats were divided into 2 groups: amlodipine followed by methylene blue or amlodipine followed by normal saline solution, with 15 rats in each group. Rats received methylene blue at 2 mg/kg during 5 minutes or an equivalent amount of normal saline solution in 3 intervals from the start of the protocol: minutes 5, 30, and 60. The animals were observed for a total of 2 hours after the start of the protocol. Mortality risk and survival time were analyzed with Fisher's exact test and Kaplan-Meier survival analysis with the log rank test. RESULTS: Overall, 1 of 15 rats (7%) in the saline solution-treated group survived to 120 minutes compared with 5 of 15 (33%) in the methylene blue-treated group (difference -26%; 95% confidence interval [CI] -54% to 0.3%). The median survival time for the normal saline solution group was 42 minutes (95% CI 28.1 to 55.9 minutes); for the methylene blue group, 109 minutes (95% CI 93.9 to 124.1 minutes). Pulse rate and mean arterial pressure (MAP) differences between groups were analyzed until 60 minutes. Pulse rate was significantly higher in the methylene blue-treated group beginning 25 minutes after the start of the amlodipine infusion (95% CI 30 to 113 minutes) that was analyzed until 60 minutes. MAP was significantly higher in the methylene blue-treated group starting 25 minutes after the amlodipine infusion (95% CI 2 to 30 minutes) that was analyzed until 60 minutes. CONCLUSION: Methylene blue did not result in a significant difference in mortality risk. There was an increased pulse rate, MAP, and median survival time in the methylene blue group.

[A CASE OF SEVERE AMLODIPINE POISONING].

The article is devoted to the actual problem--poisoning by calcium channel blockers. The case of the departure of the patient amlodipine, clinical picture, treatment and its effectiveness. In the discussion described pharmacological characteristics of the group of calcium channel blockers, mechanisms of development syndromes developing in this type of shipment and pathogenetic approach to therapy.

Intravenous lipid emulsion for the treatment of drug toxicity.

Intravenous lipid emulsion (ILE) has emerged as a powerful antidote for the treatment of drug toxicity in the past decade. Initial efficacy of ILE was shown in the setting of local anesthetic systemic toxicity (LAST), but recent case reports suggest its consideration in a variety of other drug toxicities. In this review, we will summarize the experimental evidence as well as the clinical experience in using ILE as an antidote. Specifically, we will look at the evidence for using ILE in LAST as well as toxicity due to beta-blockers, calcium-channel blockers, and tricyclic antidepressants. We will also review the current dosing recommendations as well as potential side effects of ILE as an antidote.

Toxicity of antihypertensives in unintentional poisoning of young children.

BACKGROUND: Knowledge is limited about the toxicity of unintentional exposure to antihypertensives in young children (0-6 years of age). OBJECTIVE: Our aim was to research symptoms and poisoning severity in unintentional poisonings in this group of age and determine adequate poisoning management. METHODS: We performed a 10-year retrospective, explorative analysis of the Mainz Poison Center/Germany database with regard to circumstances of poison exposure, dosage, symptoms, and treatment. To be able to relate drug exposure with reported symptoms, analyses were restricted to single drug exposures. Written follow-up information was obtained in about 50% of all cases. RESULTS: A total of 1489 cases were analyzed, of which 957 were single drug exposures with 421 exposures to beta-blocking agents, 364 to inhibitors of the renin-angiotensin system, 122 to calcium channel blockers, and 50 to antiadrenergic drugs. No severe (Poisoning Severity Score [PSS]=3) or fatal poisonings (PSS=4) were reported and, with the exception of atenolol, propranolol, irbesartan, isradipin, clonidine, and moxonidine, no poisonings with a PSS>1. We did not find a significant relationship between dosage, release formulation and symptoms, or PSS. All patients fully recovered without specific treatment. CONCLUSIONS: In young children with unintentional, single drug exposure to the most popular antihypertensive medication (i.e., metoprolol, bisoprolol, ramipril, enalapril, lisinopril, captopril, candesartan, valsartan, amlodipine, and verapamil), only mild symptoms occurred, and hospital evaluation is not a must. However, children with recent exposure to clonidine or moxonidine should be evaluated at a hospital due to an increased likelihood of poisonings of at least moderate severity.

High-dose insulin and intravenous lipid emulsion therapy for cardiogenic shock induced by intentional calcium-channel blocker and Beta-blocker overdose: a case series.

BACKGROUND: Recently, high-dose insulin (HDI) and intravenous lipid emulsion (ILE) have emerged as treatment options for severe toxicity from calcium-channel blocker (CCB) and beta blocker (BB). OBJECTIVE: Our aim was to describe the use and effectiveness of HDI and ILE for the treatment of CCB and BB overdose. CASE REPORTS: We describe 2 patients presenting to the emergency department after intentional ingestions of CCBs and BBs. A 35-year-old man presented in pulseless electrical activity after ingesting amlodopine, verapamil, and metoprolol. A 59-year-old man presented with cardiogenic shock (CS) after ingesting amlodopine, simvastatin, lisinopril, and metformin. Both patients were initially treated with glucagon, calcium, and vasopressors. Shortly after arrival, HDI (1 unit/kg × 1; 1 unit/kg/h infusion) and ILE 20% (1.5 mL/kg × 1; 0.25 mL/kg/min × 60 min) were initiated. This led to hemodynamic improvement and resolution of shock. At the time of hospital discharge, both patients had achieved full neurologic recovery. CONCLUSIONS: HDI effectively reverses CS induced by CCBs and BBs due to its inotropic effects, uptake of glucose into cardiac muscle, and peripheral vasodilatation. ILE is theorized to sequester agents dependent on lipid solubility from the plasma, preventing further toxicity. To our knowledge, these are the first two successful cases reported using the combination of HDI and ILE for reversing CS induced by intentional ingestions of CCBs and BBs.

Management of calcium channel blocker overdose.

The management of patients who have overdosed with calcium channel blockers (CCBs), which are commonly prescribed for hypertension, arrhythmia and angina, can be difficult but early initiation of the correct treatment increases the likelihood of good outcomes. This article refers to a case study to illustrate the unpredictable nature of overdose with CCBs and describes the treatment needed to reverse their effects.

Calcium Channel Blocker Overdose: What Role Does Extracorporeal Membrane Oxygenation Have in Support? A Systematic Review of the Literature.

Extracorporeal membrane oxygenation (ECMO) has had increasing prevalence and indications in the last decade. Calcium channel blocker overdose (CCBOD) can lead to significant cardiopulmonary dysfunction and has also increased in recent years. CCBOD results in cardiac depression, vasoplegia, and hyperglycemia. Expert consensus recommends 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 associated with use. Electronic literature review identified all relevant studies for CCBOD and ECMO. PRISMA guidelines for systematic review were followed. Three independent authors reviewed abstracts and full texts, and only CCB ingestion without polypharmacy was included. Two authors independently collected data, which included demographics, current medical treatments, ECMO type, and survival. From 314 abstracts, 25 papers were included with a median publication year of 2019. Twenty-six patients were included with an average age of 32.7 years and 42%/58% male/female. Average time on ECMO 4.3 days. VA and VV ECMO use were 92.3% and 7.7%, respectively, and 84.6% of patients survived to hospital discharge. Before ECMO, most patients received 4-5 medical treatments (53.8%). Our systematic review demonstrates ECMO is a newly used, yet valuable therapy for CCBOD when medical treatment fails. Survival to discharge after ECMO for CCBOD is substantially higher than standard VV or VA ECMO. Medical management is still the mainstay therapy for CCBOD, but we show that a persistently unstable patient may benefit from prompt evaluation at an ECMO center for treatment.

Effective Management of Severe Amlodipine/Atenolol Overdose with Intravenous Calcium, Hyperinsulinemic Euglycemia Therapy, and Continuous Veno-Venous Hemodialysis: A Case Report.

BACKGROUND Amlodipine, a calcium channel blocker, and atenolol, a beta blocker, are commonly used as a fixed drug combination (FDC) to treat hypertension. Intentional or non-intentional overdose of amlodipine-atenolol results in hypotension and myocardial depression with a high risk of mortality. This report describes a 64-year-old man with an overdose of amlodipine-atenolol, presenting as an emergency with hypotension, bradycardia, and severe metabolic acidosis. He was successfully treated with intravenous calcium chloride infusion, hyperinsulinemia euglycemia therapy (HIE), and continuous veno-venous hemodialysis (CVVHD). CASE REPORT A 64-year-old man was diagnosed with essential hypertension 1 week prior to the admission. He had been prescribed 1 FDC tablet of amlodipine and atenolol (5+50 mg) per day; however, he took 1 table of the FDC per day for 3 days and then took 3-4 tablets each day during the next 4 days. He was brought to the hospital with hypotension, bradycardia, and severe metabolic acidosis and was diagnosed with amlodipine-atenolol overdose. He was treated with intravenous calcium chloride infusion, HIE, and CVVHD. His hemodynamics started to improve after administering these therapies for 6 h. Inotropes were gradually tapered off and stopped. He was extubated on day 5 and recovered completely. CONCLUSIONS This report shows the serious effects amlodipine-atenolol overdose and the challenges of emergency patient management. An overdose of FDC of amlodipine and atenolol can cause cardiovascular collapse and severe metabolic acidosis. Timely and aggressive management with intravenous calcium infusion, HIE, and CVVHD is essential.

Acute High-Output Heart Failure with Pulmonary Hypertension and Severe Liver Injury Caused by Amlodipine Poisoning: A Case Report.

Acute high-output heart failure (HOHF) with pulmonary hypertension and liver injury caused by amlodipine poisoning is very rare. We report a 52-year-old woman who suffered from severe shock after an overdose of amlodipine. Hemodynamic monitoring showed that while her left ventricular systolic function and cardiac output were elevated, her systemic vascular resistance decreased significantly. At the same time, the size of her right heart, her central venous pressure, and the oxygen saturation of her central venous circulation all increased abnormally. The patient's circulatory function and right ventricular dysfunction gradually improved after large doses of vasopressors and detoxification measures. However, her bilirubin and transaminase levels increased significantly on hospital day 6, with a CT scan showing patchy, low-density areas in her liver along with ascites. After liver protective treatment and plasma exchange, the patient's liver function gradually recovered. A CT scan 4 months later showed all her liver abnormalities, including ascites, had resolved. The common etiologies of HOHF were excluded in this case, and significantly reduced systemic vascular resistance caused by amlodipine overdose was thought to be the primary pathophysiological basis of HOHF. The significant increase in venous return and pulmonary blood flow is considered to be the main mechanism of right ventricular dysfunction and pulmonary hypertension. Hypoxic hepatitis caused by a combination of hepatic congestion and distributive shock may be the most important factors causing liver injury in this patient. Whether amlodipine has other mechanisms leading to HOHF and pulmonary hypertension needs to be further studied. Considering the significant increase of right heart preload, aggressive fluid resuscitation should be done very cautiously in patients with HOHF and shock secondary to amlodipine overdose.

Critical care management of verapamil and diltiazem overdose with a focus on vasopressors: a 25-year experience at a single center.

STUDY OBJECTIVE: Verapamil or diltiazem overdose can cause severe morbidity and death, and there exist limited human data describing management and outcome of a large number of such patients. This article describes the management and outcome of patients with nondihydropyridine calcium-channel blocker overdose, with an emphasis on vasopressor dosing, at a single center. METHODS: This study is a retrospective chart review of patients older than 14 years and admitted to the inpatient toxicology service of a single tertiary care medical center for treatment of verapamil or diltiazem overdose from 1987 through 2012, and who had the presence of either drug confirmed by urine drug screening. Patients were identified by review of patient encounter logs. Data abstracted from medical records included demographics, laboratory results, drugs used to support blood pressure, complications, and outcomes. A second group included patients with a reported calcium channel blocker ingestion but for whom results of the urine drug testing were no longer available. In an effort to assess selection bias, this group was included to determine whether patients who were excluded from the primary group only because of unavailability of urine drug screen results had different outcomes. RESULTS: During the study period, 48 patients met inclusion criteria. The median age was 45 years, with a range of 15 to 76 years, and 52% were male patients. Verapamil accounted for 24 of 48 (50%) ingestions. Vasopressors were administered to 33 of 48 (69%) patients. Maximal vasopressor infusion doses were epinephrine 150 µg/minute, dopamine 100 µg/kg per minute, dobutamine 245 µg/kg per minute, isoproterenol 60 µg/minute, phenylephrine 250 µg/minute, and norepinephrine 100 µg/minute. The use of multiple vasopressors was common. Hyperinsulinemic euglycemia was used in 3 patients who also received multiple vasopressors. Eight probable or possible ischemic complications were noted in 5 of 48 (10%) patients. Gastrointestinal bleeding occurred in 3 of 48 (6%) patients; a brain magnetic resonance imaging in 1 patient suggested mild ischemia, without clinical evidence of infarction; 1 patient had ischemic bowel; and 3 patients developed renal failure from acute tubular necrosis, which resolved in each case. Six of the 8 ischemic complications were evident before use of vasopressor therapy. Three patients sustained inhospital cardiac arrest before admission and were successfully resuscitated. Each of these arrests occurred before instituting vasopressor infusions. One patient experienced a late cardiac arrest from primary respiratory arrest from administration of sedatives, and multiple organ system failure followed resuscitation, with death occurring during manipulation of a pulmonary artery catheter. The remaining 47 patients recovered. There were 12 patients in the group of additional poisoned patients for whom results of urine drug screening were unavailable. Four patients were treated with vasopressors, 2 experienced acute tubular necrosis that was present before vasopressor use, and all recovered. CONCLUSION: In our series of patients admitted with verapamil or diltiazem overdose, hypotension was common and managed with the use of multiple vasopressors and without hyperinsulinemic euglycemia in all but 3 cases. Despite high doses of vasopressors, ischemic complications were the exception and were usually present before use of vasopressors. Death occurred in a single patient whose death was not attributed directly to calcium-channel blocker toxicity. Vasopressor use after verapamil or diltiazem overdose was associated with good clinical outcomes without permanent sequelae.

Hyperinsulin therapy for calcium channel antagonist poisoning: a seven-year retrospective study.

The use of hyperinsulin therapy (HIT) in severe calcium channel antagonist (CCA) poisoning has become a more common therapy within the last decade. The objective of this study is to report 7 years of experience recommending HIT. This was a retrospective chart review utilizing our regional poison center (RPC) data from January 1, 2002, through December 31, 2008. All cases of CCA poisoning receiving HIT were searched. Endpoints included the number of CCA cases utilizing HIT, insulin dose, time of initiation of HIT, patient outcome, adverse events, age, glucose concentration, and lowest systolic blood pressure recorded. Forty-six cases of CCA poisoning were managed with HIT over 7 years. All the patients received standard antidotal therapy (= intravenous fluids, calcium salts, glucagon, and pressors). HIT administration followed our RPC recommendation 23 times (50%), and no hypoglycemic events occurred. Means (age, highest glucose measured, and lowest systolic blood pressure measured) were 51 years, 282 mg/dL, and 74 mm Hg, respectively. Our RPC recommendations for HIT were followed 50% of the time over the last 7 years. In light of the lack of hypoglycemia associated with HIT in our study population, we recommend HIT as an early and safe antidote in significant CCA poisoning.

Lipid emulsion therapy in cardiodepressive syndrome after diltiazem overdose--case report.

We present a case of diltiazem overdose in which the patient ingested 5.6 g in an apparent suicide attempt. She was admitted in the emergency department 2 hours postingestion with cardiodepressive syndrome. She was treated with gastric lavage, activated charcoal, intravenous fluids, calcium, and epinephrine, without improvement in vital signs. We gave her an infusion of 20% intralipid, leading to a favorable evolution. The patient was stable hemodynamically and metabolic in the following 24 hours. She was alert and oriented and was extubated in the second day. She was discharged after 4 days in a good state and without any neurologic deficits.