Role of Hemodiafiltration in Calcium Channel Blocker (CCB) Overdose

Introduction: Overdose of CCBs, a common medication used to treat hypertension, is associated with high mortality rates. Amlodipine, a dihydropyridine class of CCB, is a highly protein-bound medication. Current management of CCB overdose includes intravenous fluid, vasopressor, lipid emulsion, and methylene blue. However, overdose often leads to metabolic acidosis and multiorgan failures, prompting other therapies such as continuous veno-venous hemodiafiltration (CVVH) or extracorporeal membrane oxygenation support (ECMO). We report a case of amlodipine overdose resulting in refractory shock and acidosis, in which CVVH and ECMO were successful. Case Description: A 34-year-old male was admitted due to unresponsiveness. His wife reported an empty bottle of amlodipine next to him. Upon arrival, his oxygen saturation was 70%. Blood pressure (BP) was 70/30 mmHg. Due to severe hypotension, he was started on norepinephrine and vasopressin, with phenylephrine and epinephrine soon being added. Poison control recommended starting methylene blue to reverse amlodipine’s vasodilator effect. Lipid emulsion was initiated to sequester amlodipine, with the mean arterial pressure (MAP) improving from 45 to 62. He also developed acute kidney injury (AKI) with creatinine of 3.57 mg/dL and blood urea nitrogen (BUN) of 30 mg/dL. Arterial blood gas (ABG) showed pH 7.10 and pCO2 59.3 mmHg. Anion gap was 21 mmol/L and lactic acid was 9.9 mmol/L. CVVH was started, maintaining his MAP in the 70s and systolic BP in the 110s. His urine output was around 100-150 cc/hour. However, his acidosis remained refractory (last ABG showed pH of 7.22 and pCO2 of 61.9 mmHg), so he was transferred to another facility for ECMO. At the time of this writing, the patient has fully recovered. Discussion: Hemodialysis is ineffective for eliminating protein-bound medication like amlodipine. Previous literature has suggested the use of albumin as a dialyzer to enhance clearance, although in our case, traditional CVVH was preferred due to other indications such as severe metabolic acidosis, oliguria, and AKI. Our patient’s condition improved significantly following CVVH and ECMO, possibly due to restored kidney function and pH correction, thereby facilitating amlodipine clearance and enhancing responses to other treatments. Further research is warranted to explore the effectiveness of albumin over traditional CVVH in clearing overdose of protein-bound medications.

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Journal
Journal of the American Society of Nephrology
Published
2024-10-01
DOI
https://doi.org/10.1681/asn.20245683y82c
Citations
1
Primary Topic
Poisoning and overdose treatments
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article
Field-Weighted Citation Impact
0.69
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article

Role of Hemodiafiltration in Calcium Channel Blocker (CCB) Overdose

Steven Pham
1 citations
Journal of the American Society of Nephrology
Poisoning and overdose treatments
0.69
article

Role of Hemodiafiltration in Calcium Channel Blocker (CCB) Overdose

Steven Pham
article en
1 citations

Abstract

Introduction: Overdose of CCBs, a common medication used to treat hypertension, is associated with high mortality rates. Amlodipine, a dihydropyridine class of CCB, is a highly protein-bound medication. Current management of CCB overdose includes intravenous fluid, vasopressor, lipid emulsion, and methylene blue. However, overdose often leads to metabolic acidosis and multiorgan failures, prompting other therapies such as continuous veno-venous hemodiafiltration (CVVH) or extracorporeal membrane oxygenation support (ECMO). We report a case of amlodipine overdose resulting in refractory shock and acidosis, in which CVVH and ECMO were successful. Case Description: A 34-year-old male was admitted due to unresponsiveness. His wife reported an empty bottle of amlodipine next to him. Upon arrival, his oxygen saturation was 70%. Blood pressure (BP) was 70/30 mmHg. Due to severe hypotension, he was started on norepinephrine and vasopressin, with phenylephrine and epinephrine soon being added. Poison control recommended starting methylene blue to reverse amlodipine’s vasodilator effect. Lipid emulsion was initiated to sequester amlodipine, with the mean arterial pressure (MAP) improving from 45 to 62. He also developed acute kidney injury (AKI) with creatinine of 3.57 mg/dL and blood urea nitrogen (BUN) of 30 mg/dL. Arterial blood gas (ABG) showed pH 7.10 and pCO2 59.3 mmHg. Anion gap was 21 mmol/L and lactic acid was 9.9 mmol/L. CVVH was started, maintaining his MAP in the 70s and systolic BP in the 110s. His urine output was around 100-150 cc/hour. However, his acidosis remained refractory (last ABG showed pH of 7.22 and pCO2 of 61.9 mmHg), so he was transferred to another facility for ECMO. At the time of this writing, the patient has fully recovered. Discussion: Hemodialysis is ineffective for eliminating protein-bound medication like amlodipine. Previous literature has suggested the use of albumin as a dialyzer to enhance clearance, although in our case, traditional CVVH was preferred due to other indications such as severe metabolic acidosis, oliguria, and AKI. Our patient’s condition improved significantly following CVVH and ECMO, possibly due to restored kidney function and pH correction, thereby facilitating amlodipine clearance and enhancing responses to other treatments. Further research is warranted to explore the effectiveness of albumin over traditional CVVH in clearing overdose of protein-bound medications.

Journal of the American Society of NephrologyVol. 35(10S)
Harding University Main Campus (US)
Openalex Percentile: Top 25%
Poisoning and overdose treatments
0.69
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