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Amlodipine, a widely used antihypertensive medication, can cause serious complications in overdose, including hypotension, bradycardia, non-cardiogenic pulmonary oedema (NCPO) and death. This report describes a young adult woman who ingested 100 mg of amlodipine in a polypharmacy suicide attempt. Although she initially stabilised, she unexpectedly developed delayed NCPO 3 days post ingestion, requiring intubation and intensive care unit readmission. She recovered fully with supportive care and was discharged in good health. This case highlights the importance of prolonged monitoring and vigilance in managing long-acting calcium channel blocker overdoses, even when the initial clinical response appears satisfactory., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2025. No commercial re-use. See rights and permissions. Published by BMJ Group.)

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.

Introduction: Tarka (trandolapril/verapamil hydrohloride extended-release) is a fixed-dose combination antihypertensive drug formed from verapamil hydrochloride and trandolapril. Toxicologic manifestations of Tarka overdose are altered mental status, bradycardia, hypotension, atrioventricular block (first-degree), hyperglycemia, metabolic acidosis, and shock., Case Presentation: We report a case of Tarka toxicity in a 2-year-old girl who presented with altered mental status, cardiogenic shock, hypotension, bradycardia, severe metabolic acidosis, hyperglycemia, and first-degree atrioventricular block. We started fluid resuscitation, epinephrine, norepinephrine, and insulin. Because of the patient's hyperlactatemia and hypotension despite standard therapies, we initiated intravenous lipid emulsion (ILE) therapy, after which her condition improved promptly., Discussion: Tarka overdose may be life-threatening as it can cause cardiogenic shock. In our patient, the regression of lactate elevation in a short time with ILE therapy and the improvement of her general condition highlight the importance of ILE., Conclusions: ILE is an alternative treatment method for acute lipophilic drug intoxications, such as Tarka., (Copyright© Board of Regents of the University of Wisconsin System and The Medical College of Wisconsin, Inc.)

Intravenous lipid emulsion (ILE) is typically applied as a rescue therapy after the use of conventional treatments for beta blocker (BBs) or calcium channel blocker (CCB) overdoses. We describe the case of a 72-year-old man who presented to our ED after attempting suicide by antihypertensive drug overdose. His blood pressure dropped upon arrival at the ED, and we consequently administered multitherapy including relatively early ILE to prevent prolonged hypotension. He regained stable hemodynamic status on the third day and was later discharged without major sequelae., Competing Interests: Declaration of Competing Interest The authors declare no conflict of interest., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: Despite multiple treatment options, antihypertensive overdose remains a cause of significant morbidity and mortality. Intravenous angiotensin II (AG II) is approved for use in vasodilatory shock. We describe 2 cases of refractory shock from antihypertensive overdose that were successfully treated using AG II., Case Reports: A 24-year-old female presented after an overdose of multiple antihypertensive medications, including an angiotensin converting enzyme inhibitor (ACEI). She developed hypotension that was refractory to norepinephrine, epinephrine, and vasopressin, with a mean arterial pressure (MAP) of 57 mm Hg 9 h after emergency department arrival. Fifteen minutes after starting AG II at 10 ng/kg/min, her heart rate and MAP rose by 7 beats/min and 12 mm Hg, respectively. Her hemodynamic parameters continued to improve thereafter. She developed acute kidney injury, which resolved prior to discharge. The second patient, a 65-year-old male, presented after an overdose of multiple antihypertensive medications, including an ACEI. Despite norepinephrine, epinephrine, and hyperinsulinemia-euglycemia, he remained bradycardic and hypotensive, with a heart rate of 47 beats/min and MAP of 59 mm Hg. Thirty minutes after starting AG II at 10 ng/kg/min, his heart rate was 61 beats/min and MAP was 66 mm Hg. He recovered without apparent sequelae. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Antihypertensive overdose can lead to shock refractory to catecholamine and vasopressin therapy. Our experience suggests that AG II is efficacious in antihypertensive overdose and may be particularly efficacious in instances of ACEI overdose. However, further study is required to confirm the appropriate indication(s)., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Hydralazine is an FDA-approved antihypertensive agent which has been utilized for years either alone or in combination with other medications especially the beta-blockers. Hydralazine works as a direct-acting vasodilator, thereby exerting a decrease in vascular resistance and increase in intravascular volume. When overdosed, hydralazine applies its toxic effects by extending its pharmacological action, which produces hypotension, syncope, tachycardia, and nausea. However, studies and case reports of acute hydralazine toxicity and its effects on electrocardiographic changes are rare, and most of the medical literature have only highlighted its immunological side effects. In this report, we are presenting a case of acute hydralazine overdose in a young woman who ended up in CCU due to remarkably abnormal electrocardiogram and unstable hemodynamics followed by myocardial infarction., (© 2019 The Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.)

Background: Pediatric exposure to prazosin is unusual because it is most commonly indicated for the treatment of hypertension. Prazosin's increase in popularity as a treatment for posttraumatic stress disorder makes it important for emergency physicians to be aware of how to manage potential toxic ingestion because of prazosin overdose., Case Report: A 16-year-old, 76-kg female presented after ingesting 110 mg of prazosin, 209.3 g of acetaminophen, and 55 g of naproxen. She was admitted to the pediatric intensive care unit for rapidly deteriorating hypotension (lowest blood pressure 47/19 mm Hg) refractory to aggressive fluid resuscitation and infusions of epinephrine and norepinephrine each at 0.5 mcg/kg/min. Stabilization of blood pressure was eventually achieved, and associated with use of a vasopressin infusion of 0.004 units/kg/min. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Because of the increasing exposure of children to prazosin, clinicians should be aware of the pharmacology behind alpha-1 antagonist overdose and consider treatment options, such as vasopressin, when hypotension is resistant to standard fluid and catecholamine therapy., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Objectives: It has been suggested that ingestion of even small amounts of minoxidil by young children may result in serious adverse effects. The intent of this study was to describe pediatric minoxidil exposures reported to a statewide poison center system., Methods: Cases were minoxidil exposures among patients 5 years or younger reported to Texas poison centers during 2000 to 2014. The distribution by various demographic and clinical factors was determined., Results: Of 125 total cases, 58% were male and 78% aged 1 to 2 years. Ingestion alone was reported in 92% of the exposures. Ninety-eight percent of the exposures were unintentional, and 94% occurred at the patient's own residence. Sixty-two percent of the patients were managed on site. The outcome was not serious (no effect, minor effect, not followed [nontoxic], not followed [minimal effects]) in 88% of the exposures. The most common adverse effect was vomiting, reported in 8% of the exposures. The most common treatments were dilution/irrigation/wash (53%), activated charcoal (18%), food/snack (17%), and intravenous fluids (8%)., Conclusions: Few pediatric minoxidil exposures were reported to Texas poison centers. Of these exposures, most involved ingestion, were unintentional, and involved patients who were male and aged 1 to 2 years. Although it has been suggested that pediatric minoxidil ingestions might result in serious adverse effects, this study suggests that most pediatric minoxidil exposures reported to poison centers are not likely to have serious outcomes and may be managed at home.

Context: There are limited reports of adult clonidine overdose. We aimed to describe the clinical effects and treatment of clonidine overdose in adults., Methods: This was a retrospective review of a prospective cohort of poisoned patients who took clonidine overdoses (>200 μg). Demographic information, clinical effects, treatment, complications (central nervous system and cardiovascular effects) and length of stay (LOS) were extracted from a clinical database or medical records., Results: From 133 admissions for clonidine poisoning (1988-2015), no medical record was available in 14 and 11 took staggered ingestions. Of 108 acute clonidine overdoses (median age 27 years; 14-65 years; 68 females), 40 were clonidine alone ingestions and 68 were clonidine with co-ingestants. Median dose taken was 2100 μg (interquartile range [IQR]: 400-15,000 μg). Median LOS was 21h (IQR: 14-35 h) and there were no deaths. Glasgow coma score [GCS] <15 occurred in 73/108 (68%), and more patients taking co-ingestants (8/68; 12%) had coma (GCS <9) compared to clonidine alone (2/40; 5%). Miosis occurred in 31/108 (29%) cases. Median minimum HR was 48 bpm (IQR: 40-57 bpm), similar between clonidine alone and co-ingestant overdoses. There was a significant association between dose and minimum HR for clonidine alone overdoses (p = 0.02). 82/108 (76%) had bradycardia, median onset 2.5 h post-ingestion (IQR: 1.7-5.5 h) and median duration 20 h (2.5-83 h), similar for clonidine alone and co-ingestant overdoses. There were no arrhythmias. Three patients ingesting 8000-12,000 μg developed early hypertension. Median minimum systolic BP was 96 mmHg (IQR: 90-105 mmHg) and hypotension occurred in 26/108 (24%). 12/108 patients were intubated, but only 2 were clonidine alone cases. Treatments included activated charcoal (24), atropine (8) and naloxone (23). The median total naloxone dose was 2 mg (IQR: 1.2-2.4 mg), but only one patient given naloxone was documented to respond with partial improvement in GCS., Discussion: Clonidine causes persistent but not life-threatening clinical effects. Most patients develop mild central nervous system depression and bradycardia. Naloxone was not associated with improved outcomes.

The objective of the present study was to elucidate the specific features of amlodipine distribution in the organism of the warm-blooded animals (rats) following a single intragastric administration of the poisonous substance at a dose of 686 mg/kg b/w/ (LD50). Amlodipine was isolated from the blood and various organs of the animals by means of acetone extraction and purified on the silica gel column (100/160 mcm) with the elution by an ethanol-hexane (7:3) mixture. The identification and the quantitative measurement of amlodipine were performed with the use of the TLC, GC-M, and UV-spectrophotometry. The study has shown that unmetabolized amlodipine was present in large amounts in the internal organs and blood of the poisoned animals. The principal organs of its accumulation were the stomach, kidneys, and blood.

Mixed antihypertensive drug intoxication poses a significant risk for patient mortality. In tandem to antihypertensives, hypolipidemic medicines (especially statins) are often prescribed. Among their well-known adverse effects belongs rhabdomyolysis. We report a case of fatal multi-drug overdose in a 65-year-old female alcoholic. The patient was unconscious at admission. Empty blister packs indicated the abuse of 250 tablets of urapidil, 42 tablets of verapamil/trandolapril, 50 tablets of moxonidin, 80 tablets of atorvastatin and 80 tablets of diacerein. Standard measures (gastric lavage, activated charcoal, mechanical ventilation, massive doses of vasopressors, volume expansion, diuretics and alkalinization) failed to provide sufficient drug elimination and hemodynamic support and the sufferer deceased on the fourth day. Dramatic elevations of serum myoglobin (34,020 μg/L) and creatine kinase (219 μkat/L) were accompanied by rise in cardiac troponin I and creatinine. Gas chromatography revealed ethanol 1.17 g/kg (blood) and 2.81 g/kg (urine). Thin layer chromatography and gas chromatography of gastric content and urine verified verapamil, moxonidin and urapidil fragment (diacerein method was unavailable). Atorvastatin and trandolapril concentrations (LC-MS(n)) equaled 277.7 μg/L and 57.5 μg/L, resp. (serum) and 8.15 μg/L and 602.3 μg/L, resp. (urine). Histology confirmed precipitates of myoglobin with acute necrosis of proximal renal tubules in association with striated muscle rhabdomyolysis and myocardial dystrophy. Cardiogenic-distributive shock in conjunction with acute renal failure due to the combined self-poisoning with vasoactive agents and atorvastatin were determined to be this decedent's immediate cause of death. The manner of death was assigned to be suicidal., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Case Report: We describe the case of a 58-year-old woman who developed a severe distributive shock following the intentional ingestion of a large overdose of amlodipine (480 mg) combined with valsartan (3680 mg). Extreme vasoplegia remained refractory to maximal standard therapy including fluid resuscitation, intravenous calcium, vasopressors at very high doses, hyperinsulinemia-euglycemia therapy, lipid emulsion, and methylene blue administration. Besides, the patient exhibited hyperglycemia refractory to very high doses of insulin. Due to its theoretical ability to effectively remove protein-bound drugs such as amlodipine from the circulation, albumin dialysis with the molecular adsorbent recirculating system (MARS™) was performed during two consecutive sessions. Blood was drawn for toxicokinetic calculations. Amlodipine elimination half-life during the first MARS™ session was calculated at 7.6 h. In addition, there was a rapid fall in blood glucose, requiring the introduction of a continuous infusion of glucose in order to achieve euglycemia. Moreover, a few hours after the initiation of the MARS™ therapy, the hemodynamic status was not significantly modified but a significant tapering of epinephrine infusion was possible, together with a progressive decrease of blood lactate level. However, the need for vasopressors in decreasing doses was present until day 5 post-ingestion. Eventually, the patient fully recovered and was discharged home 8 days after admission., Discussion: The role of the MARS™ in the treatment of severe poisoning of calcium channel blockers is still to be defined. We were able to demonstrate a relatively short elimination half-life of amlodipine. A decreased insulin resistance and a reduction of epinephrine infusion were also observed.

Background: Intralipid emulsion (ILE) is a nutritional fatty acid supplementation that is emerging as a potential therapy for local anesthetic systemic toxicity and is also being considered as a therapy for other lipophilic medication intoxications. Isolated reports of pulmonary edema or severe lipemia exist as a complication of therapy., Case Report: A 26-year-old hypertensive, male, kidney transplant recipient presented to an outside emergency department (ED) after an intentional overdose of his medications (ie, amlodipine, metoprolol, lisinopril). At presentation, he had hypotension and bradycardia that was unresponsive to treatment with intravenous saline, calcium, glucagon, and vasopressors. After failure of conventional therapy, an initial bolus of ILE (20%) was given with some improvement in his heart rate, and the dose was repeated. A continuous intravenous infusion of ILE therapy was started. The patient deteriorated, with development of both acute respiratory and renal failure. Continuous venovenous hemofiltration (CVVHF) was attempted to remove volume and correct metabolic abnormalities. Lipemic blood was immediately observed in the CVVHF filter. After 15 min, the transmembrane pressures of the filter began to rise in the absence of observed clotting of the blood and the filter then became completely obstructed. An attempt was made to remove the lipid by plasmapheresis to restart CVVHF, but the patient continued to deteriorate despite maximal vasopressor support. The patient's family decided to withdraw care and the patient expired. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Emergency physicians treat patients with toxic ingestions on a regular basis. Being aware of possible complications of experimental antidote therapy, like ILE, can improve the treatment approach and outcomes for these patients., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Purpose: To report systemic symptoms after an overdose of travoprost., Case Report: We report a patient who, instead of artificial tears, inadvertently used travoprost every 15 minutes for 7 hours after LASIK (laser-assisted in situ keratomileusis) surgery. She experienced abrupt, severe abdominal cramps and sudden, severe menstrual bleeding, which subsided quickly upon discontinuation of the drug., Conclusions: Because of the few systemic adverse effects, prostaglandin analogs are widely used for the treatment of glaucoma. Travoprost should be taken once daily; therefore, overdose is extremely uncommon. Systemic prostaglandins have been found to be mediators of uterine activity and are used to induce labor and terminate pregnancies. The high dose of this topical medication, as well as the compromised cornea, makes this case unique. The unusual circumstances observed in this case greatly expand our knowledge regarding the potential adverse effects of travoprost.

Clonidine poisoning's clinical feature is well documented in the medical literature, but the minimal toxic dose has not yet been established. The effectiveness of naloxone is also controversial. The authors describe a clonidine overdose in a 9-year-old boy (25 kg) during a growth hormone test: he received tenfold the prescribed clonidine dose (0.23 mg instead of 0.023 mg) with 6.2 mg betaxolol. About 40 min later, he became drowsy and then complained of low blood pressure, bradycardia, and myosis. By maintaining the Trendelenburg position, administering fluids as well as salbutamol and naloxone (three doses of 0.2 mg were required), he recovered and was discharged from the hospital on day 2. The minimal clonidine toxic dose, the clinical picture, and the effectiveness of naloxone administration are discussed in this paper., (Copyright © 2014 Elsevier Masson SAS. All rights reserved.)

Background: Resuscitation without return to spontaneous circulation in patients with suicidal ingestion of cardiotoxic drugs necessitates alternative bridging therapies for drug removal., Objectives: To show the effectiveness of emergency extracorporeal membrane oxygenation (ECMO) and plasmaspheresis in severe polyintoxication., Case Report: A 21-year-old woman developed asystole after suicidal polyintoxication with 1.75 g carvedilol, 300 mg amlodipine, 6 g amitriptyline, 500 mg torsemide, 1.5 g ketoprofen, 28 g nicotinic acid, and 16 g gabapentin. After 3 h of cardiopulmonary resuscitation without return to spontaneous circulation, ECMO was used as a bridging therapy and a temporary pacemaker was inserted. Plasma peak levels were measured for amlodipine (29.3 μg/L), amitriptyline (1456 μg/L), carvedilol (585 μg/L), and gabapentin (126.8 mg/L). To facilitate drug removal, therapeutic plasma exchange was performed. The patient could be weaned from ECMO at day 4 and extubated on day 8 after admission without neurologic sequelae., Conclusion: ECMO and plasma exchange should be considered as a therapeutic option in selected patients under resuscitation without return to spontaneous circulation after severe intoxication., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Overdose with calcium channel blockers is uncommon, but is associated with high mortality. The management includes fluid resuscitation, calcium gluconate, glucagon, vasopressors, and high-dose insulin-euglycemia therapy. We describe a rare case of massive overdose of lercanidipine with shock, refractory to conventional therapies and multi-organ failure. Charcoal hemoperfusion with continuous venovenous hemodiafiltration was then used successfully and the patient showed remarkable recovery.

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., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Objective: Methyldopa, a centrally acting antihypertensive drug, has been in use since the 1960s, but reports of (severe) overdose are rare. We present a case of severe methyldopa overdose with prolonged profound hypotension., Case Summary: A 50-year-old woman developed sinus bradycardia, prolonged profound hypotension, and drowsiness after ingesting over 300 tablets (> 75 g) of methyldopa. At presentation, her blood pressure was 59/27 mmHg, heart rate 49 beats/minute, and Glasgow Coma Scale Score 14. She needed intensive care unit (ICU) care and intravenous infusion of a large amount of fluids and Gelofusine®, injections of ephedrine sulphate, and intravenous infusion of norepinephrine for 41 hours followed by dopamine for 21 hours to maintain her systolic blood pressure at ~ 100 mmHg. She was observed for 3 more days in the general ward before discharge., Conclusion: Severe methyldopa overdose can be complicated by prolonged profound hypotension. The management of these patients should include close monitoring of vital functions and administration of intravenous fluids, colloids, and vasopressor agents.

Background: Lisinopril is an angiotensin converting enzyme inhibitor used for treatment of hypertension, congestive heart failure, and acute myocardial infarction. Reports of clinical experience with pediatric ingestions are minimal., Method: A 13-year retrospective study of lisinopril ingestions in children reported to the California Poison Control System was analyzed and case notes were reviewed. Institutional Review Board approval was obtained and cases were blinded. Inclusion criteria were lisinopril as a single ingestant, age less than 6 years, treatment in a health care facility, case followed to a known outcome., Results: Inclusion criteria were met in 296 cases. Demographics include 51% of male patients and the mean age was 1.97 years (range: 9 months-5 years). Of the 296 patients, 8 patients (2.7%) developed hypotension (ranges: 55-74 mm Hg systolic and 22-48 mm Hg diastolic). The lowest blood pressure of 55/22 mm Hg was recorded in a 22-month old male who ingested an estimated 120-mg lisinopril (13.3 mg/kg). The lowest dose of lisinopril causing hypotension was with an estimated dose of approximately 50 mg or 3.9 mg/kg in a 2-year old. Two hundred and eighty-two patients (95.3%) were treated and released from the emergency department and 14 patients (4.7%) were admitted. The dose ingested was reported in 189 cases and an exact-dose of lisinopril was reported in 61 patients (20.6%); mean amount ingested was 3.0 mg/kg, median amount ingested was 2.1 mg/kg (range: 0.1-10.9 mg/kg, N = 38); and mean total dose was 33.4 mg, median total dose was 20 mg (range: 2.5-160 mg, N = 61). None of the patients with exact-dose lisinopril ingestions developed hypotension, received intravenous fluids, or were admitted., Conclusion: The lowest estimated dose of lisinopril to cause hypotension was 50 mg or 3.9 mg/kg. Although continued evaluation of pediatric lisinopril ingestions is essential to determine more specific thresholds of toxicity, the lack of effect on blood pressure in children with exact-dose ingestions indicate that pediatric lisinopril ingestions (for ages > 9 months) ≤ 4 mg/kg up to 40 mg total may be safely managed at home.

Introduction: The object of the current communication is to discuss the theory and the evidence for the use of L-carnitine in calcium channel blocker and metformin poisonings., Case Report: A 68-year-old male known for hypertension and type II diabetes was admitted to the critical care unit of a community hospital following an overdose of amlodipine and metformin. The patient was intubated, ventilated, and hemodynamically supported with vasopressors. Despite calcium, glucagon, high-dose insulin (HDI), and lipid emulsion for calcium channel blocker and bicarbonate for metabolic acidosis, the patient remained hemodynamically unstable. The patient was considered too unstable to initiate continuous renal replacement therapy; and without access to extracorporeal life support, the administration of L-carnitine was administered as a last resort. One hour after L-carnitine, the norepinephrine requirements started to decrease, the patient began to improve and was subsequently extubated successfully without apparent sequelae in less than 4 days., Discussion: L-Carnitine combined with HDI may have helped with the calcium channel blocker (CCB) poisoning by decreasing insulin resistance, promoting intracellular glucose transport, facilitating the metabolism of free fatty acids, and increasing calcium channel sensitivity. It may have also stimulated oxidative utilization of glucose instead of converting pyruvate into lactate and contributed to decrease lactate production with metformin poisoning.

Background: Antihypertensive medications, including β-blockers, are widely used in patients with chronic kidney disease. Unlike most β-blockers, atenolol is excreted primarily by the kidney, and its clearance by peritoneal dialysis is poor. These pharmacokinetic factors may predispose patients to gradual accumulation of the drug over time., Objectives: To review the management of a diagnostic dilemma, the role of glucagon therapy, and the clinical implications of atenolol clearance., Case Report: A young woman with end-stage renal disease requiring peritoneal dialysis presented with sudden onset of abdominal pain and hemodynamic instability with hypotension and relative bradycardia. The patient reported that she took her regular four antihypertensive agents, including atenolol, with no excess ingestion or recent dose changes. After resuscitation and consideration of a broad differential diagnosis, the most likely cause of the patient's illness was determined to be unintentional atenolol toxicity, with secondary mesenteric ischemia due to a low-flow state that caused her abdominal pain. Glucagon therapy led to rapid correction of the patient's hemodynamic instability and pain., Conclusion: The unique pharmacokinetics of long-term medications must be considered in patients with impaired clearance, such as this patient with end-stage renal disease treated by peritoneal dialysis. Medications may gradually accumulate to supratherapeutic levels, which over time may lead to symptoms of significant toxicity., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Extended-release guanfacine is a centrally acting α2-adrenergic agonist that was recently approved for treatment of attention-deficit/hyperactivity disorder. The following is a case discussion of a 12-year-old boy with attention-deficit/hyperactivity disorder and Tourette syndrome, who presented 18 hours after ingestion of 3 times his usual dose of extended-release guanfacine. On presentation, he was lethargic, bradycardic, and hypertensive with an otherwise nonfocal neurological examination. He remained hypertensive until administration of an intravenous antihypertensive agent (nicardipine) 24 hours after ingestion. After cessation of the calcium-channel blocker, he continued to have intermittent episodes of symptomatic hypotension for the next 2½ days. This extremely protracted course of hypertension followed by prolonged symptomatic hypotension is rare with ingestions of centrally acting α2-adrenergic agonists. As this drug is increasingly prescribed for treatment of a disease with increasing prevalence, it is imperative that emergency physicians become familiar with the varying presentations of its toxicity.

Pulmonary hypertension is defined by 25 mmHg pressure at rest, and 35 mmHg pressure at exercise, in the pulmonary arteries. Hypertension either primary or secondary. The exact prevalence of all types of pulmonary hypertension is not yet known. We present a case of a 58-year-old female patient suffering from CREST syndrome, Raynaud's syndrome, esophageal motility impairment, and severe pulmonary hypertension who had previously obtained a specially developed implantable pump, named Lenus Pro(®), to facilitate continuous parenteral treatment of pulmonary arterial hypertension with treprostinil. Treprostinil is a prostanoid derivative with very stable physiochemical properties which allows subcutaneous treatment of pulmonary arterial hypertension in the outpatient. Treprostinil is normally dosed individually in a range of 0.6 to 50 ng/kg/minute. In the underlying case, a dose of more than 100 mg given over 1 minute is equivalent to a 1000 fold overdose. The patient's critical condition required installment of a central venous access, full monitoring, sedation, oxygen nasal tube, fluid balance, and parenteral nutrition. The patient could be hemodynamically stabilized within 24 hours after the overdose. After 6 days of recovery, the patient left the hospital with no remaining health impairment.

Authors report a retrospective study of all cases of indoramin-only poisoning notified to the Paris poison Centre from 1986 to 2010. Fifty five cases of indoramin self-poisoning were included: 40 adults and 15 children. The mean supposed ingested dose was about 701 mg±464 mg. ECG showed a prolonged QTc interval (equal to or greater than 0.50 s) in 30% of patients. The lowest observed dose for prolonged QTc was 625 mg. This series includes two cases of seizures occurring around two hours after ingestion of 900 and 2 250 mg of indoramin. A review of the literature showed cardiac disorders, with a delayed mechanism of action up until 18 hours after ingestion. Therefore, rapid medical resuscitation and prolonged cardiac monitoring for at least 24 hours after ingestion of 625 mg are recommended., (© 2012 Société Française de Pharmacologie et de Thérapeutique.)

Use of cardiac allograft for transplantation from donors after acute poisoning is a matter of debate because of potential toxic organ injuries, especially if death results from massive ingestion of cardiotoxic drugs. We report successful allograft cardiac transplantation from a brain-dead patient after severe flecainide and betaxolol self-poisoning requiring extracorporeal life support. Extracorporeal life support was initiated in the emergency department because of a refractory cardiac arrest caused by the cardiotoxicants' ingestion and continued after the onset of brain death to facilitate organ donation of the heart, liver, and kidneys. Forty-five months later, each organ recipient was alive, with normal graft function., (Copyright © 2010 American College of Emergency Physicians. Published by Mosby, Inc. All rights reserved.)

Introduction: Intralipid therapy has been used successfully as "rescue therapy" in several cases of overdose. We present a case of iatrogenic lipid emulsion overdose because of a dosing error., Case Report: A 71-year-old female overdosed on 27 tablets of 5 mg amlodipine. Although initially stable in the Emergency Department, she became hypotensive, oliguric, and respiratory failure developed despite medical therapy. The primary treating team felt that meaningful recovery was unlikely to occur without rapid improvement in clinical status, and 12.5 h after presentation, intralipid rescue therapy was initiated. A protocol for intralipid specifying a maximum infusion of 400 mL of 20% lipid emulsion was faxed, but the infusion was continued until 2 L of lipid emulsion was infused. There were no detectable adverse hemodynamic effects of the intralipid infusion. After this time, laboratory values were difficult to obtain. Three hours after the infusion, a metabolic panel was obtained from ultracentrifuged blood showing hyponatremia. A white blood cell (WBC) was obtained from a complete blood count (CBC) performed 22 h after the infusion, hemoglobin and hematocrit could not be obtained from this blood. A platelet count was obtained by smear estimate. Hematocrits were obtained from centrifuged blood and appeared elevated. No oxygenation could be obtained on blood gas. The patient's family chose to withdraw care on hospital day 2 and no further laboratory draws were obtained. Amlodipine was 1,500 ng/mL (ref. 3-11 ng/mL)., Discussion: Lipid emulsion overdose caused no detectable acute adverse hemodynamic effects. The following laboratory values were unobtainable immediately after infusion: white blood cell count, hemoglobin, hematocrit, platelet count, and a metabolic panel of serum electrolytes. Ultracentrifugation of blood allowed for detection of a metabolic panel 3 h after the infusion. Centrifuged hematocrits appeared to be higher than expected.

Unlabelled: Regarding angiotensin-converting enzyme inhibitors (ACEI) poisoning, only few data are available in the last decade literature. In the previous couple of years especially isolated case reports were published., Material and Method: We analyzed retrospectively all the patients with acute ACEI poisoning admitted in Iaşi Internal Medicine and Toxicology Clinic between 2004 and 2009., Results: 17 cases of poisoning were recorded (enalapril-9 cases, captopril-3 cases, perindopril-3 cases, lisinopril-2 cases). All the poisonings were intentional. A favorable outcome was consistently observed, and were recorded no sequelae or death in this study. The main complain was hypotension, required fluid administration, only one case with 500 mg enalaprilum and severe hypotension required injection of vasopressive amines. No abnormal renal function and no angioedema were noted.

An 89-year-old man with a history of hypertension, chronic obstructive pulmonary disease, personality disorder and previous attempts of self-poisoning attempted suicide by swallowing two mouthfuls of tablets (methyldopa 250 mg, theophylline SR 200 mg, indapamide 2.5 mg and paracetamol 500 mg). He had prolonged, severe hypotension, necessitating the use of 3000 ml of Gelofusine and almost 2 days of intravenous norepinephrine infusion. He had marked diuresis for 4.5 days, requiring continuous and bolus infusions of intravenous fluids. He had marked renal potassium loss, requiring vigorous potassium replacement therapy. Multiple-dose activated charcoal was used to enhance theophylline elimination. The plasma paracetamol level was below the treatment line. Methyldopa via its metabolite stimulates postsynaptic alpha-adrenergic receptors in cardiovascular control centres in the brain, causing a reduction in peripheral sympathetic tone and a fall in arterial blood pressure and heart rate. In overdose, it causes hypotension, bradycardia and drowsiness. The natriuretic, kaliuretic and vasodilatory effects of indapamide are exaggerated in overdose, resulting in diuresis, hypokalaemia and hypotension. Theophylline markedly increases the level of circulating catecholamines, which stimulate the vascular beta(2)-adrenergic receptors with decreased peripheral vascular resistance. Peripheral vasodilation and hypotension occur in significant theophylline poisoning. Intracellular shift of potassium results in hypokalaemia. The prescribing physicians should recognise elderly patients at a high risk of self-poisoning and avoid using drugs with a high toxicity in overdose (e.g. theophylline and methyldopa). Restricting access to hazardous drugs (in overdose) would be of paramount importance to reduce the number of severe acute poisoning cases and case-fatalities., (2009 John Wiley & Sons, Ltd.)

We present a rare case of a 13-year-old girl who took an intentional mixed overdose of nicorandil, lisinopril and metoclopramide. This is the first reported case in the literature of nicorandil overdose in the paediatric age group. The chief presenting clinical signs were hypoxia, peripheral hypoperfusion and hypotension with tachycardia unresponsive to aggressive intravenous volume expansion. Subsequent ECG changes suggested evolving myocardial ischaemia and were accompanied by complaints of back pain and worsening shortness of breath. Vasopressor therapy led to an immediate resolution of the ECG changes and improved the hypotension. This was continued for a further 24 h, until haemodynamic stability was achieved.

Purpose: Brimonidine is a third-generation selective alpha-2 adrenergic agonist that lowers intraocular pressure by decreasing aqueous humor production and increasing uveoscleral flow. Its safety profile for children <2 years of age remains unknown., Methods: We describe a case of ingestion of a single drop of brimonidine 0.2% in a newborn, resulting in sedation, cardiorespiratory depression, and hyperglycemia within minutes., Conclusions: This report adds to the existing evidence that brimonidine can have serious adverse side effects and should therefore be used with extreme caution in infants <2 years of age. Additionally,safety procedures like double-checking should also include vitamins or oral supplements to improve medication safety in the neonatal intensive care unit.

This case study reports the effects of a treprostinil accidental overdose in a patient with pulmonary hypertension. Treprostinil is labeled for treatment of pulmonary hypertension with New York Heart Association (NYHA) Class II, III and IV symptoms. It is characterized as a long-acting prostacyclin analog that can be delivered by intravenous or subcutaneous continuous infusions. This pediatric case report describes a massive overdose without significant side effects, thus suggesting a beneficial therapeutic index in pediatric patients.

The effect of charcoal haemoperfusion on the pharmacokinetics of diltiazem is described in a patient with severe clinical toxicity following acute overdose. The patient presented within 3 h following acute ingestion of multiple medications including sustained-release diltiazem. Routine resuscitation and supportive care were administered, but hypotension did not resolve despite intravenous fluids and infusions of calcium, adrenaline, noradrenaline and vasopressin. Multiple-doses of activated charcoal, haemodialysis and charcoal haemoperfusion were prescribed to expedite the elimination of diltiazem. The maximum diltiazem concentration (577 microg.l(-1)) was recorded 7 h post ingestion which was followed by an erratic and prolonged elimination phase. The maximum clearance of diltiazem due to haemoperfusion was calculated to be 19.4 and 15.1 ml.min(-1) at different times, equating to removal of approximately 1.5 mg diltiazem during 4 h of haemoperfusion. Haemoperfusion did not appear to remove sufficient diltiazem to recommend its routine use in the treatment of patients with acute diltiazem overdose.

Introduction: Compared to other calcium channel blockers (CCBs), overdose with dihydropyridine CCBs are considered relatively benign due to their vascular selectivity. Although not a sustained-release preparation, amlodipine's prolonged duration of effect is concerning following overdose. In addition, angiotensin II receptor blocker blunting of vasoconstrictive and sympathetic compensatory responses could exacerbate calcium channel blocker toxicity. We describe severe toxicity associated with an overdose of amlodipine and valsartan., Case Report: A 75-year-old woman presented to the ED 45 minutes after a witnessed suicidal ingestion of a "handful" of amlodipine and valsartan tablets. Hypotension, which appeared two hours after ingestion, was refractory to crystalloids and colloids, calcium gluconate, epinephrine, norepinephrine, phenylephrine, and vasopressin infusions. High-dose insulin euglycemia (HIE) therapy, and treatment with glucagon and naloxone were successful in improving her hemodynamic status. In this combined overdose, right heart catheterization demonstrated both negative inotropic effects and decreased systemic vascular resistance., Conclusion: Co-ingestion of amlodipine with valsartan produced profound toxicity. Early institution of HIE therapy may be beneficial to reverse these effects.

Introduction: Little data exist on potentially adverse valsartan ingestions reported to poison control centers., Methods: Using adult ingestions of valsartan reported to Texas poison control centers during 2000-2005, I determined the proportion of cases involving serious outcomes for selected variables and evaluated for statistical significance by calculating the rate ratio (RR) and 95% confidence interval (CI)., Results: Thirteen (7%) of 185 total cases involved serious outcomes. Serious outcomes were significantly more likely to occur with a maximum dose 320 mg (RR 9.06, CI 1.30-100.14) or 4 tablets (RR 9.00, CI 2.07-39.11) or where the circumstances of the exposures involved self-harm or malicious intent (RR 17.28, CI 4.98-67.13)., Conclusions: The severity of the medical outcome associated with adult valsartan ingestions depended on the dose and the circumstances of the ingestion. Such information is useful for creating triage guidelines for the management of adult valsartan ingestions.

There is limited information on potentially adverse lisinopril ingestions reported to poison control centers. Using adult lisinopril ingestions reported to Texas poison control centers during 1998-2005, the proportion of cases involving serious outcomes was determined for selected variables and evaluated for statistical significance by calculating the rate ratio (RR) and 95% confidence interval (CI). Of 468 cases identified, 43 (9%) involved serious outcomes. The severity of the outcome associated with adult lisinopril ingestions depended on the dose and the circumstances of the ingestion. Thus, serious outcomes were significantly more likely to occur with a maximum dose >80 mg (RR 5.69, CI 2.43-13.33) or, if the dose was unknown, > or =3 tablets (RR 9.57, CI 2.39-54.97), where the circumstances of the exposures involved self-harm or malicious intent (RR 6.96, CI 3.65-13.31), or the patient was already at or en route to a health care facility when the poison control center was contacted (RR 7.33, CI 3.09-17.85) or referred to a health care facility by the poison control center (RR 23.76, CI 10.62-55.67). The management of patients with severe outcomes was more likely to involve health care facilities. Such information is useful for creating of triage guidelines for the management of adult lisinopril ingestions.

The objective of this study is to define the etiological and demographical characteristics of the patients applying to the emergency department in Faculty of Medicine, Cukurova University because of poisoning. This retrospective study was carried out by examining the records of 491 people who applied to the main emergency department in Faculty of Medicine, Cukurova University, with the complaint of poisoning between January 1, 2004 and December 31, 2004. It was determined that the reason why 491 of 20 817 persons (2.4%) applied during this term was because of poisoning: 159 (32.4%) of such patients were male and 332 of them (67.6%) were female. It was found that the average age of men was 27.1 +/- 10.5 years and that of women was 24.4 +/- 9.5 years (P = 0.005); 427 of poisoning cases (87.0%) happened intentionally as suicide attempts and 64 of them (13.0%) were accidental. The rate of suicide-purposed poisoning was higher in women and the rate of unintentional poisoning was higher in men (P +/- 0.001). The drugs were accountable for 71.1% of all poisoning cases and the pesticides were accountable for 18.9% of such cases. Poisonings increase during summers. The mortality rate in poisonings was found as 0.8%. The drugs and pesticides in Ckurova region constitute 90.0% of all poisoning cases. The mortality rate in poisoning will be decreased by training the physicians employed in the emergency department about poisoning by drugs and pesticides.

We report the case of a 46-yr-old male who developed severe lactic acidosis, cardiorespiratory arrest, and rhabdomyolysis following an overdose of metformin and ramipril. The lactic acidosis was successfully treated with early high-volume continuous veno-venous haemofiltration. Rhabdomyolysis and lower limb compartment syndrome developed later. The patient otherwise made a good recovery. We discuss the management of severe lactic acidosis secondary to metformin overdose and the association with rhabdomyolysis.