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| Year : 2014 | Volume
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| Issue : 6 | Page : 1255-1258 |
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| Continuous venovenous hemodiafiltration along with charcoal hemoperfusion for the management of life-threatening lercanidipine and amlodipine overdose |
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Prashant Nasa, Akhilesh Singh, Deven Juneja, Omender Singh, Yash Javeri
Department of Critical Care Medicine, Max Superspeciality Hospital, New Delhi, India
Click here for correspondence address and email
| Date of Web Publication | 10-Nov-2014 |
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 Abstract | | |
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.
How to cite this article:
Nasa P, Singh A, Juneja D, Singh O, Javeri Y. Continuous venovenous hemodiafiltration along with charcoal hemoperfusion for the management of life-threatening lercanidipine and amlodipine overdose. Saudi J Kidney Dis Transpl 2014;25:1255-8 |
How to cite this URL:
Nasa P, Singh A, Juneja D, Singh O, Javeri Y. Continuous venovenous hemodiafiltration along with charcoal hemoperfusion for the management of life-threatening lercanidipine and amlodipine overdose. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2022 Aug 12];25:1255-8. Available from: https://www.sjkdt.org/text.asp?2014/25/6/1255/144262 |
| Introduction | |  |
We describe an uncommon case of massive drug overdose with calcium-channel blockers lercanidipine and amlodipine causing shock, refractory to standard management. The patient recovered completely after continuous venovenous hemodiafiltration (CVVHDF) along with charcoal hemoperfusion.
| Case Report | | |
A 69-year-old gentleman was admitted with an alleged history of consumption of 30 tablets of lercanidipine (10 mg each, total dose 300 mg) and 10 tablets of amlodipine (5 mg each, total dose 50 mg) about 150 minutes earlier. The patient was a known case of systemic hypertension and was on lercanidipine 10 mg 12-hourly, Type II diabetes mellitus, on oral hypoglycemic glimepiride 1 mg 12-hourly and sitagliptin 50 mg 12-hourly, and coronary artery disease (coronary angiography two months earlier revealed 40% blockage in the proximal left anterior descending artery) on ecosprin 150 mg and clopidogrel 75 mg. The patient was anxious, heart rate (HR) was 74/minute, blood pressure (BP) was 92/54 mm Hg, and the remainder of the systemic examination was normal. He was started on fluid boluses and 2 g of intravenous (i.v.) calcium gluconate. His arterial blood gases showed acute respiratory alkalosis and a lactate of 1.3 mmol /L; the electrocardiograph showed a right bundle branch block. Gastric lavage was done with 70 g charcoal followed by polyethylene glycol. He was then shifted to the medical Intensive Care Unit (ICU) for further management.
In the ICU, his HR was 72/minute, BP was 78/40 mm Hg, and the mean arterial pressure (MAP) was 52 mmHg after administering two liters of fluid. The vasopressor dopamine was started and a central venous line (CVP; right internal jugular vein) was secured. Fluid resuscitation was continued along with vasopressors and calcium gluconate infusion at 0.5 g/hour. He was also given 40 units of insulin along with 50% dextrose and another 40 units of insulin was repeated after 30 minutes. His condition continued to deteriorate despite resuscitation, and thus, he was intubated. The patient developed bradycardia followed by asystole, resuscitation was started and a temporary pacemaker was inserted through the CVP line and the patient was revived in around two minutes. He was given 5 mg glucagon followed by infusion of 3 mg/hour. He was anuric, with cold extremities, arterial blood gases (ABG) showed severe metabolic acidosis, and the lactate was 7.5 mmol/L [Figure 1]. He was given sodium bicarbonate bolus 100 mg i.v. and started on 25 mg/hour infusion. An intra-aortic balloon pump (IABP) was inserted through a right femoral arterial access in view of the associated cardiogenic shock along with vasodilatory shock in view of his inability to maintain MAP, despite very high doses of vasopressors. However, despite all these measures, MAP could not be maintained at more than 65 mm Hg, in spite of very high doses of vasopressors (dopamine 40 μg/minute, norepinephrine 50 μg/minute, epinephrine 35 μg/minute, and terlipressin 20 μg/minute). In view of shock refractory to glucagon and vasopressors, a decision of continuous replacement therapy with charcoal hemoperfusion was taken. The patient was started on charcoal hemoperfusion using HA Resin Hemoperfusion Cartridge (Model HA 280, Jafron Biomedical Co. Ltd.) along with CVVHDF, without ultra-filtration, with a 1 U/mL heparinized extra-corporeal circuit for over four hours followed by CVVHDF [Figure 2]. | Figure 2: Continuous venovenous hemodialysis with charcoal hemoperfusion
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The patient's condition started improving, with an increase in MAP around four hours after starting CVVHDF, with the urine output improving to 50 mL/hour after six hours. Another session of charcoal hemoperfusion was given after four hours. The vasopressors were progressively weaned off in the next 30 hours and CVVHDF was stopped in view of adequate urine output with resolution of metabolic acidosis. The glucagon infusion was continued at 5 mg/hour for 48 hours and then stopped. The IABP was removed 62 hours after insertion and the patient was extubated on day-4, shifted to the ward on day-6, and discharged the next day.
| Discussion | | |
Lercanidipine is a 1,4-Dihydropyridine calcium-channel blocker recommended for control of hypertension in adults. [1] , [2] Its main effect includes inhibition of the influx of calcium ions through the slow channels (L-type) causing vasodilatation because it has greater selectivity for vascular smooth muscle than for cardiac smooth muscle. It is fully absorbed from the gastrointestinal tract, peak plasma levels occur in 1.5-3 hours and the drug is extensively distributed in the tissues and organs. The drug is highly lipophilic and >98% of it is protein-bound. [1],2] It undergoes extensive hepatic metabolism to inactive metabolites, with a mean elimination half-life of 8-10 hours. [1] Amlodipine has peak plasma concentrations of 6-12 hours, with a protein-binding of 97.5% and elimination half-life of 35-50 hours. [1] , [3]
Calcium channel blockers are an uncommon cause of drug overdose; however, when it occurs, it is associated with high mortality. Lercanidipine overdose is very rare, with a search on Pubmed till August 2011 using the words 'lercanidipine,' 'overdose,' and 'poisoning,' revealing only one result. The management of overdose with calcium channel blockers includes bowel decontamination (charcoal and/ or polyethylene glycol), intravenous fluid resus citation, glucagon and/or calcium infusions, and vasopressor therapy. [4] Other measures that can be tried, include, high-dose insulin-euglycemia therapy, sodium bicarbonate therapy to treat academia, and a temporary pacemaker for symptomatic bradycardia. [4]
However, in patients with overdose of calcium channel blockers and shock refractory to the above-mentioned standard therapies, anecdotal therapies have been tried with some efficacy. These include CVVHDF with or without charcoal hemoperfusion, [6],[7] IABP, [8] and cardiopulmonary bypass. [9] Theoretically, hemodialysis is ineffective for the removal of drugs that are highly protein-bound. [4] Calcium channel blockers are lipophilic and highly protein-bound; [2] however, the successful use of charcoal hemoperfusion in diltiazem overdose encouraged us to try charcoal hemoperfusion along with CVVHDF in our case. [7]
Our patient whose shock was refractory to other standard therapies was progressively deteriorating and CVVHDF along with charcoal hemoperfusion was used as the last resort. The patient showed remarkable recovery along with a good neurological outcome, even after an episode of cardiac arrest, after using supraphysiological doses of vasopressors to maintain MAP and organ perfusion.
The limitation of our case was the absence of drug levels of lercanidipine or amlodipine, and hence, the effect of charcoal hemoperfusion on the serum concentration of these drugs. However, our case demonstrates that the management of a massive calcium channel blocker overdose requires the combined use of multiple agents with the goal being to improve organ perfusion. Moreover, extracorporeal therapies such as charcoal hemoperfusion can be considered in patients with shock refractory to standard measures.
Conflict of interest: None
| References | | |
| 1. | Bang LM, Chapman TM, Goa KL. Lercanidipine: A review of its efficacy in the management of hypertension. Drugs 2003;63:2449-72.  |
| 2. | Buckley N, Dawson A, Whyte I. Calcium Channel Channel Blockers. Medicine 2007;35:599-602. |
| 3. | Abernethy DR. The pharmacokinetic profile of amlodipine. Am Heart J 1989;118:1100-3. |
| 4. | Kerns II W. Management of -Adrenergic and Calcium Channel Antagonist Toxicity. Emerg Med Clin N Am 2007;25:309-31. |
| 5. | Hadjipavlou G, Hafeez A, Messer B, Hughes T. Management of lercanidipine overdose with hyperinsulinaemic euglycaemia therapy: Case report. Scand J Trauma Resusc Emerg Med 2011;19:8. |
| 6. | Pfaender M, Casetti PG, Azzolini M, Baldi ML, Valli A. Successful treatment of a massive atenolol and nifedipine overdose with CVVHDF. Minerva Anestesiol 2008;74:97-100. |
| 7. | Amorim S, Dias P, Rocha G, Gama G, de Campos M, Pires S. Poisoning with calcium channel blockers--a case report and review of the literature. Rev Port Cardiol 2001;20:1249-57. |
| 8. | Frierson J, Bailly D, Shultz T, Sund S, Dimas A. Refractory cardiogenic shock and complete heart block after unsuspected verapamil-SR and atenolol overdose. Clin Cardiol 1991;14: 933-5. |
| 9. | Kolcz J, Pietrzyk J, Januszewska K, Procelewska M, Mroczek T, Malec E. Extracorporeal life support in severe propranolol and verapamil intoxication. J Intensive Care Med 2007;22: 381-5. |
Correspondence Address:
Dr. Prashant Nasa
Department of Critical Care Medicine, Max Superspeciality Hospital, New Delhi
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1319-2442.144262
[Figure 1], [Figure 2] |
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| This article has been cited by | | 1 |
Extracorporeal treatment for calcium channel blocker poisoning: systematic review and recommendations from the EXTRIP workgroup |
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| Anselm Wong, Robert S. Hoffman, Steven J. Walsh, Darren M. Roberts, Sophie Gosselin, Timothy E. Bunchman, Sofia Kebede, Valery Lavergne, Marc Ghannoum | | Clinical Toxicology. 2021; 59(5): 361 | | [Pubmed] | [DOI] | |
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