Case vignette:
30yo male with a past medical history of HIV, HTN, bipolar disorder, and depression who presented to the ED, brought in via EMS for evaluation of an intentional overdose. Patient reportedly called EMS himself and reported taking Benadryl and Ativan. EMS found the patient with an empty bottle of Amlodipine, a 90-day prescription of 5 mg pills filled one week prior. He was also found with bottles of Biktarvy and Gabapentin. Time of ingestion unknown, per chart review he had been discharged from the ED early that morning for SI (~6 hours prior to arrival).
VS: 100/50, HR 128 RR 19 SpO2 95%
Somnolent, dry mucous membranes. PERRL. Tachycardic, normal pulses. No respiratory distress, normal breath sounds. Abdomen soft, non-tender, non-distended. Skin is warm and dry. GCS 8, no rigidity, no clonus.
Next steps:
ABCs: patient started to become more somnolent, c/f not protecting his airway. Plan for intubation, however, patient continued to become more hypotensive. The team worked to improve his BP with boluses of IVF, Norepi, then with addition of Epi, prior to sedation for intubation.
ECG: sinus tachycardia, prolonged QR interval, no acute ST changes
Glucose: 110
Primary concern at this time was Amlodipine overdose due to vasoplegia, requiring two pressors
Continued to manage hemodynamics with patient now intubated and on a ventilator, Norepi and Epi
Contacted poison control and MICU for recommendations
Poison control recommended concentrated doses of vasopressors and calcium gluconate. MICU placed central and arterial lines.
Consult to ECMO team for consideration of VA ECMO
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Yes, it is often used in the treatment course of this disease to determine the type of shock that the patient is experiencing due to calcium channel toxicity.
Non-dihydropyridines (verapamil, diltiazem) have a more profound negative ionotropic effect, causing severe bradycardia. Dihydropyridines (amlodipine, nifedipine) typically cause profound vasodilation but may become cardiotoxic in massive overdoses.
A quick cardiac POCUS can assess the function of the heart and estimate the EF to determine if their hypotension is due to cardiogenic shock or distributive shock.
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It is great at estimating the EF and overall squeeze of the heart. In this specific case, the patient was experience vasoplegia from amlodipine overdose, so there is not evidence of cardiogenic shock.
US shows good squeeze, normal EF, and no signs of fluid overload when looking at the IVC.
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Decontamination with activated charcoal or whole bowel irrigation can be considered if within 1-2 hours of known ingestion time (our patient had unknown time, last known normal was 5+ hours prior)
Hemodynamic interventions, ie airway management, volume resuscitation, vasopressor therapy.
Hyperinsulinemic euglycemia therapy:
1. Also works best in patients with myocardial dysfunction, unlikely to help in patients with predominantly vasodilatory shock. So, this was not recommended per poison control for our patient.
2. Helpful for patients’ with cardiogenic shock d/t calcium channel blocker toxicity because it works to overcome the metabolic starvation that results.
3. Toxicity also causes overall hypoinsulinemia, because CCB act on L-type calcium cannels, blocking and preventing influx of calcium ions. These same channels control insulin release, so hypoinsulinemia results.
4. The exogenous insulin increases glucose and lactate uptake by myocardial cells, improves function without increased oxygen demand. It has also been shown to have positive inotropic effects.
Sources:
https://emcrit.org/ibcc/ccb-2/
https://www.emra.org/emresident/article/poisoned-pump-management-of-calcium-channel-blocker-toxicity
https://litfl.com/high-dose-insulin-euglycaemic-therapy/
https://emergencymedicinecases.com/low-slow-poisoning/
https://www.atsjournals.org/doi/abs/10.1164/ajrccm.2025.211.Abstracts.A3842