Presence of acute optic disc and optic nerve infarction in a young man is uncommon finding. This is most commonly seen in the setting of vasculitis and infection. Ischemic optic neuropathy has been reported with cocaine use, amlodipine and alcohol use. To our knowledge there is no reported case of ischemic optic neuropathy in the setting of heroin / opioid use. MR imaging findings in the setting of substance use are similar to other etiologies of ischemic optic neuropathy, with high T2/FLAIR signal, diffusion restriction and abnormal gadolinium enhancement. Here we report a case of 23-year-old man with heroin use disorder presenting with optic nerve infarct resulting in acute painless monocular vision loss.

Incorrect dispensing of medications by community pharmacies can lead to accidental poisonings. This may not be considered by emergency medicine physicians in patients describing vague symptoms. We present a case of a paediatric ingestion of amlodipine, resulting from a community pharmacy dispensing error, that was recognized by the child's mother, and consider the liability implications.

Calcium-channel blocker overdose can result in profound vasoplegia and cardiogenic shock, which can quickly spiral into multi-organ failure and death. In this case report, we discuss two separate cases of massive amlodipine overdose with polydrug intoxication (Patient A: amlodipine and quetiapine; Patient B: amlodipine, fluoxetine and zopiclone), both of which were complicated by life-threatening vasoplegic shock refractory to supportive therapy (endotracheal intubation, fluid resuscitation, activated charcoal, vasopressors and inotropes), multimodal antidotes (calcium and hyper-insulinemic euglycemic therapy) and even second-line treatment (methylene blue and therapeutic plasma exchange). Despite exhausting all therapeutic options, resuscitation remained futile with no clinical response elicited until veno-arterial extracorporeal membrane oxygenation (ECMO) salvage therapy was initiated in both cases as a bridge-to-recovery. Albumin dialysis was also commenced to further enhance elimination of amlodipine given its high plasma protein-binding properties. Both patients improved drastically once perfusion to vital organs was maintained by ECMO and eventually survived with good neurological outcomes and preserved cardiac contractility on discharge. This case report supports the growing evidence that although ECMO support represents a potentially life-saving salvage therapy for refractory poisoning-induced shock, escalation to ECMO must be considered and instituted early before irreversible multi-organ failure sets in to ensure good clinical outcomes.

Although the basics of evaluating and treating most unknown ingestants are well known, many overdoses require very specific treatment if the patient is to have any chance of survival.[1] Countless studies have been published supporting Dr. Gideon Koren's 1993 landmark article "Medications Which Can Kill a Toddler with One Tablet or Teaspoonful" in the Journal of Toxicology.[2][3][4][5] while each has its own merits, most focus solely on pediatric overdoses, and relatively few of them provide an exhaustive list or act as a "quick-reference" when dealing with real-time ingestions.  Despite widespread public education, childproof containers, and other safety measures, accidental overdoses continue to occur.  In the United States, poison control centers receive over 2.2 million calls each year, 47% of which concern children less than six years of age.  Most pediatric accidental ingestions involve cosmetics and personal care products, followed by cleaning products, and then analgesics and prescription medications.  Adult overdoses usually are due to the intentional ingestion of analgesics and sedative-hypnotics.  Following are the list of toxic drugs (in decreasing severity/difficulty of treatment) included in this summary:  1. Alpha-2 adrenergic agonists - clonidine, naphazoline, oxymetazoline, tetrahydrozoline. 2. Sulfonylureas - chlorpropamide, glyburide, glipizide, glimepiride. 3. Calcium channel blockers - nifedipine, verapamil, diltiazem, amlodipine, nicardipine. 4. Beta-blockers - metoprolol, labetalol. 5. Tricyclic antidepressants - imipramine, desipramine, amitriptyline, nortriptyline. 6. Opioids - codeine, hydrocodone, methadone, morphine, heroin. 7. Anti-diarrheals - diphenoxylate + atropine, loperamide. 8. Salicylates/Methyl salicylates - wintergreen oil, bismuth subsalicylate, mentholated balms. 9. Antipsychotics - loxapine, thioridazine, chlorpromazine. 10. Antimalarials - chloroquine, hydroxychloroquine, quinine. 11. Antiarrhythmics - quinidine, disopyramide, procainamide, flecainide. 12. Terpenoid (camphor) - analgesic, anti-itch, and cooling gels, ointments, and balms. 13. Non-alkaloid toxic lignan - podophyllin, podofilox. 14. Plant toxin/secondary metabolite - colchicine. 15. Oral acetylcholinesterase inhibitors - rivastigmine, donepezil, galantamine. 16. Methylxanthine - theophylline: 1,3-dimethylxanthine. 17. Partial opioid agonist/synthetics - buprenorphine/fentanyl. 18. Toxic alcohols - methanol, ethylene glycol. 19. Caustics /household products - acidic or alkaline household products, hydrofluoric acid, selenious acid, ammonia fluoride, methacrylic acid (cosmetic glue), naphthalene (mothballs).

Calcium channel blocker ingestions remain one of the leading causes of death related to cardiovascular medication ingestion in both adults and pediatric patients. We report a case of a 17-year-old, 103 kg female presenting after an intentional polypharmacy ingestion, including 500 to 550 mg of amlodipine. She presented with profound vasoplegia and cardiovascular collapse requiring high-dose inotropes and eventual life support with extracorporeal membrane oxygenation (ECMO). Current available treatments, designed for adults, including lipid emulsion and methylene blue, provided no sustained clinical improvement. This resulted in the initiation of single-pass albumin dialysis (SPAD). We aim to describe the clinical implications, amlodipine toxic dose effects, and clinical challenges associated with large pediatric patients and high-dose medications. We also discuss several challenges encountered related to dosing and concentration of medications, which led to fluid overload. Given the ongoing obesity epidemic, we routinely see pediatric patients of adult size. This will continue to challenge pediatric use of adult dosing and concentrations to avoid excessive fluid administration for high-dose medications, such as insulin and vasoactive agents. To our knowledge, this is the first successful case of using SPAD in conjunction with ECMO for salvage therapy after refractory life-threatening calcium channel blocker toxicity.

We report a case of concurrent ingestion of Clonazepam and Amlodipine in a 25-year-old man, in a second attempt to take his life, which resulted in unconsciousness, hypotension, and hypokalemia. The clinical and/or biochemical presentation varied from the individual pattern when ingested. In the scarcity of consensus recommendations, supportive treatment helped.

A young adult female presented with hypotension and depressed mental status after intentional overdose of Amlodipine. After intubation and institution of lung-protective mechanical ventilation, initial management focused on maintenance of a mean arterial blood pressure over 65 mmHg and included fluid resuscitation (eight liters of crystalloid), Insulin and dextrose, intravenous calcium and, finally, vasopressor support. Her course was complicated by hypoxia due to non-cardiogenic pulmonary edema requiring diuresis. She was extubated soon thereafter but developed severe hypoxia within 72 hours requiring re-intubation. A subsequent bronchoscopy demonstrated diffuse alveolar hemorrhage (DAH). This is the first report of DAH complicating amlodipine overdose.

SummaryWe report the case of a 73-year-old woman who intentionally ingested 400 mg of amlodipine in a suicidal attempt who initially presented with hypotension which persisted despite aggressive therapy with fluid resuscitation, multiple pressor support, high-dose insulin therapy and calcium infusion. Her haemodynamic instability evolved to include bradycardia requiring atropine and transcutaneous pacing. Eventually she required salvage therapy with intravenous lipid emulsion (ILE) therapy . Despite all aggressive therapy, she developed multi-organ failure resulting in death. The literature on high-dose insulin euglycaemic therapy (HIET) and ILE therapy shows mixed results with some showing significant improvement in haemodynamic status. In our case, it had no significant positive impact on the outcome.

Calcium-channel blockers (CCBs) are widely used in people and animals. Overdose can result in cardiovascular collapse and death. Hyperinsulinemia/euglycemia therapy (HIET) and intralipid therapy (ILT) are reported treatment options in people. This is the first report describing HIET and ILT as treatments for amlodipine toxicosis in a cat.

Amlodipine is a dihydropyridine calcium channel blocker (CCB) commonly used to treat hypertension. In the United States, approximately 9,500 cases of CCB intoxication due to deliberate or inadvertent overdose were reported to poison centers in 2002. We present a case of a patient who presented with CCB overdose complicated by acute respiratory distress syndrome (ARDS) and recalcitrant shock all of which resolved with methylene blue therapy. We present a case of a 56-year-old African American woman who presented to the emergency department (ED) after intentional ingestion of large amounts of multiple pills likely consisting of cyclobenzaprine, amlodipine, losartan, and ibuprofen following an argument with her boyfriend. Treatment included insulin drip, 10% dextrose, and norepinephrine drip which was titrated up. First insulin drip and 10% dextrose were titrated up; however, vasopressor-resistant hypotension persisted, and the decision was made to administer methylene blue. Over 9,500 cases of CCB toxicity were reported to poison centers in the US in 2002. Although no definitive treatment is outlined, first-line therapy consists of IV calcium, high-dose insulin, and vasopressor support with either norepinephrine or epinephrine. Traditionally, methylene blue is used for methemoglobinemia and in cardiothoracic ICUs for post coronary artery bypass vasoplegia. It acts by selectively inhibiting nitric oxide-activated cyclic guanylate cyclase leading to decreased vasodilation of arteriolar smooth muscles improving vascular tone and systemic vascular resistance. In severe amlodipine overdose, experimental models demonstrate methylene blue improves HR and mean arterial pressure (MAP), improving survival rate. With few adverse side effects (green-tinged discoloration of urine, saliva, tears, and bodily fluids), methylene blue should be explored and implemented in the treatment of CCB overdose with refractory hypotension and ARDS.

Calcium channel blocker poisoning is a rare condition in the pediatric population. Signs and symptoms can be rapidly progressive and lead to cardiovascular collapse and death. Hemodynamic support with inotropics and vasopressors is usually not effective. The insulin/glucose therapy is an effective complement to the initial treatment, which is widely studied and used in different pathologies with hemodynamic compromise. The case of a pediatric patient with a history of highdose ingestion of amlodipine for suicidal purposes, with hemodynamic decompensation refractory to usual inotropic support treatment, is presented. From the insulin/glucose treatment, hemodynamic stability was achieved with a favorable evolution.

Intoxication from calcium channel blockers exhibits almost 50% mortality rates. Amlodipine is a long-acting dihydropyridine and inappropriate dosage poses a great threat for profound vasodilation, hypotension, and refractory vasopressor-resistant shock. A 72-year-old woman with unremarkable medical history presented to the emergency department due to amlodipine overdose after a suicide attempt attributed to COVID-19 pandemic severe anxiety disorder. Vital signs at presentation: heart rate 82 beats/ min, arterial pressure 72/55 mmHg, and oxygen saturation 98%. Resuscitation was initiated with intravenous infusion of normal saline 0,9%, noradrenaline, and calcium chloride, while activated charcoal was orally administrated; however, blood pressure remained at 70/45 mmHg. Abruptly, she experienced acute pulmonary edema and was finally intubated. We commenced high-dose insulin infusion with Dextrose 10% infusion to maintain euglycemic hyperinsulinemia. Hemodynamic improvement occurred after 30 min, systolic blood pressure raised to 95 mmHg, and decongestion was achieved with intravenous furosemide. Insulin effect was dose-dependent and patient's hemodynamic status improved after insulin uptitration. Eight days later, the patient was weaned from the mechanical ventilation and she was successfully discharged after 14 days. High-dose intravenous infusion of insulin up to 10 units/kg per hour appears as an inotropic agent possibly through alterations in myocardial metabolism of fatty acids and augmentation of insulin secretion and uptake. This regimen possibly exhibits additional vasotropic properties. We conclude that euglycemic hyperinsulinemia is a potentially advantageous treatment in CCB toxicity.

We present the case of a 16-year-old female with systemic lupus erythematosus who presented with shock of unclear etiology, refractory to fluid resuscitation and triple vasopressors. She suffered pulseless electrical activity and underwent cannulation onto veno-arterial extracorporeal membrane oxygenation (ECMO). After cannulation, it was discovered she had intentionally overdosed on her home medication, amlodipine, a calcium channel blocker (CCB). She was supported on ECMO, treated with IV calcium and insulin, and was able to be weaned off ECMO after 4 days. She developed oligoanuric acute kidney injury, treated with continuous renal replacement therapy followed by intermittent hemodialysis. At discharge, she was neurologically intact and did not require dialysis. Herein, we review the treatment of CCB overdose, review the literature on the use of ECMO in refractory shock due to cardiovascular medication overdose, and highlight the utility of ECMO in pediatric refractory shock and/or cardiac arrest of unclear etiology.

Acute limb ischemia induced by arterial vasospasm remains an exceptional situation, favoured by the use of arterial vasoconstrictors. The risk of these substances is largely underestimated in the general population, especially with the co-administration of strong cytochrome inhibitors like human immunodeficiency virus (HIV) protease inhibitors. A 33-year-old woman, who used to take dihydroergotamine for orthostatic hypotension, was prescribed a post-exposure HIV prophylaxis including lopinavir and ritonavir. One day later, she presented an acute bilateral limb ischemia with a sudden pain in both calves, initially while walking and then at rest with bilateral ischemic toes. Angiography confirmed diffuse arterial vasospasm of the lower limb arteries. A first-line therapy with isosorbide dinitrate and amlodipine was ineffective, with rapid clinical worsening. A combination of intra-arterial injections and intra-venous infusions of vasodilators, transluminal balloon angioplasty and bilateral 4-Compartment fasciotomies permitted rapid improvement and finally resulted in both lower limbs rescue. This case and literature review illustrate ergotism due to ergotamine overdose after taking HIV protease inhibitors. It also demonstrates the benefit of an interventional procedure besides medical therapy with vasodilators in severe arterial vasospasm. All along the lower limb arterial tree, transluminal balloon angioplasty restored the blood flow, without vasospasm recurrence. CONCLUSION: In case of ergotism with acute lower limbs ischemia, combining medical vasodilator therapy with interventional procedure can restore the arterial blood flow, thus allowing to save lower limbs.

Plasmapheresis, a procedure used to remove large molecular weight, protein-bound molecules from a patient's blood, has been shown to be useful in some cases of drug overdose. Levothyroxine sodium intoxication may result from the intentional or accidental ingestion of excessive amounts of the hormone, which can trigger a thyroid storm. However, case reports about the extremely large dose of 15,000 µg of thyroxine intoxication are extremely rare, and even combined with calcium channel blockers (CCBs) poisonings. We present a case of an intentional poisoning with high doses of thyroxine, diltiazem and amlodipine successfully treated with plasma exchange. A 40-year-old woman was admitted showing unconsciousness and sustained hypotension with high levels of thyroid hormones (THs). It was discovered that she had secretly ingested at least 15,000 µg of levothyroxine sodium and CCBs with unknown amounts of diltiazem and amlodipine. Following plasmapheresis, the levels of TH declined dramatically after each of the 4 sessions, with hemodynamics gradually stabilizing and mental state improving. The early and timely use of plasmapheresis appears to be a vital therapeutic tool for the management of acute and severe forms of l-thyroxine and CCB intoxication. Its use can prevent thyroid storm and reverse the disturbances in the patient's hemodynamic status.

Amlodipine is a widely prescribed drugs for the management of hypertension. Its toxicity is associated with severe myocardial depression and refractory hypotension. We present a case of a 28-year-old female known case of seizure disorder and depression who got admitted to our hospital with a history of consumption of 80 tablets of 5 mg amlodipine (total 400 mg). Patient presented to our hospital after 23 hours following consumption of the drug. Patient was managed in the intensive care unit (ICU) with mechanical ventilation support and intravenous infusion of noradrenalin, adrenalin, insulin-dextrose, and calcium gluconate. Due to refractory hypotension, venoarterial extracorporeal membrane oxygenation (VA-ECMO) was initiated on the same day. Patient was successfully managed and discharged home on the 8th day. This report highlights a rare case of a massive amlodipine overdose (400 mg) and ECMO as a rescue therapy.

Introduction: Beta-adrenoreceptor antagonist (beta-blocker) poisoning is a common overdose which can lead to significant morbidity and mortality.Objective: To evaluate the effects of treatments for beta-adrenoreceptor antagonist poisoning.Methods: Searches were conducted across MEDLINE (1946-26 November 2019, Ovid); Embase (1974-26 November 2019, Ovid); and the Cochrane Central Register of Controlled Trials (CENTRAL, to 26 November 2019) utilising a combination of subject headings and free text. The search strategy identified 15, 553 citations. Two reviewers screened titles and abstracts prior to selecting 141 articles (Kappa on articles included = 0.982, 95% CI 0.980-0.985). Primary outcomes included mortality and improvement in haemodynamic parameters (e.g., heart rate, blood pressure or a composite measure able to quantitate a haemodynamic response).Results: The risk of bias was high for all interventions.Gastric decontamination: Fifteen case reports described the administration of activated charcoal and five detailed the use of gastric lavage. As there was concurrent utilisation of multiple interventions, it was difficult to draw definitive conclusions regarding the relative contribution of these interventions to mortality or survival.Catecholamines, inotropes and vasopressors: The use of catecholamines in treating beta-blocker toxicity was reported in 16 case reports, 3 case series and 2 animal studies. These agents most likely provided a survival benefit and improved haemodynamics.Atropine: Multiple intravenous boluses of atropine were associated with improvement in heart rate and blood pressure in one case report.Calcium: Intravenous calcium was associated with an improvement in haemodynamics in three out of six case reports but in association with multiple other therapies as well as in two animal studies.High-dose insulin euglycaemic therapy: The use of this therapy was associated with mortality benefit in 10 case series. Two case reports showed clear haemodynamic improvement in a timeframe consistent with insulin administration (bolus then continuous infusion). Maintenance dosing ranged from 1 to 10 units/kg/h of insulin. However, it is unclear whether high-dose insulin euglycaemic therapy improved haemodynamic response above catecholamines and other inotropic agents in humans. Hypoglycaemia and hypokalemia were commonly observed adverse effects.Glucagon: Glucagon was associated with minor improvements in haemodynamics through an increase in heart rate in two cases series, nine case reports and five animal studies.Methylthioninium chloride (methylene blue): Four case reports reported an association with improvement in haemodynamics following administration of methylene blue but in the setting of co-ingestion with amlodipine.Intravenous lipid emulsion therapy: There was variable response to intravenous lipid emulsion therapy reported in 10 case series, 5 animal studies and 21 case reports.Lignocaine: There were four case reports showing variable response to lignocaine in arrhythmias secondary to beta-blocker toxicity.Other treatments: Fructose diphosphate, levosimendan and amrinone did not provide a mortality or significant haemodynamic benefit in three animal studies and nine case reports. .Veno-arterial extracorporeal membrane oxygenation: Veno-arterial extracorporeal membrane oxygenation was associated with improved survival in patients with severe cardiogenic shock or cardiac arrest in an observational study and four cases series.Dialysis: The evidence of four case reports suggest haemodialysis may assist in the management of massive overdose of specific water-soluble beta-blockers (e.g., atenolol) by improving elimination; however, a survival or haemodynamic benefit was not established.Pacing: One case series and a single case report showed the utility of temporary overdrive cardiac pacing to prevent arrhythmias in sotalol toxicity.Conclusions: Catecholamines, vasopressors, high-dose insulin euglycaemic therapy and veno-arterial extracorporeal membrane oxygenation were associated with reduced mortality. However, it must be acknowledged that multiple treatments were often given simultaneously. Haemodynamic improvements in blood pressure and cardiac output were seen with the use of catecholamines, vasopressin and high-dose insulin euglycaemic therapy. Evidence for treatment recommendations is almost entirely drawn from very low- to low-quality studies and subject to bias. However, it is reasonable to have a graduated response to cardiovascular instability beginning with intravenous fluids, commencement of a single or a combination of catecholamine inotropes and vasopressors depending upon the type of haemodynamic compromise (bradycardia, left ventricular dysfunction, vasodilation). High-dose insulin euglycaemic therapy can be introduced as an adjunctive inotrope and lastly, more invasive methods such as veno-arterial extracorporeal membrane oxygenation should be considered in cases unresponsive to other therapies.

Context: Amlodipine is the most common calcium channel blocker (CCB) on the Swedish market, and poison center (PC) consultations for amlodipine overdoses are increasing. The clinical picture is dominated by vasodilation with relative preservation of cardiac function. CCBs selectively dilate vessels on the afferent side of the capillary network which, in states of preserved or increased blood flow may lead to edema formation, including non-cardiogenic pulmonary edema (NCPE). This complication has been considered rare in CCB poisoning. In this cohort study of nineteen amlodipine poisonings with high amlodipine blood levels, the incidence and clinical significance of NCPE in severe amlodipine poisoning are explored.Methods: During 2017-2018 the Swedish PC prospectively encouraged the gathering of blood samples in amlodipine poisonings with symptoms requiring treatment with inotropes or vasopressors. Samples were sent by mail to the Forensic Toxicology Division at the Swedish National Board of Forensic Medicine for screening and quantification of relevant toxicants. Patients with blood amlodipine levels >0.25 µg/mL were included in a cohort whose case details were gathered from medical records and PC-case notes with a special focus on signs of NCPE.Results: Nineteen patients met the blood amlodipine inclusion criteria. Four (21%) died and one patient was treated with VA-ECMO. Nine patients developed NCPE defined as a need for positive pressure ventilation (PPV) while having an echocardiographically normal left ventricular function.Conclusion: In this prospective cohort study of consecutive and analytically confirmed significant amlodipine poisonings NCPE was a common finding occurring in 47% of the whole cohort and in 64% of patients who did not go on to develop complete hemodynamic collapse.