Refractory Hypotension and Delayed Respiratory Failure in Amlodipine Toxicity: A Multimodal Management Approach

Pulmonary oedema is a rare but possible paradoxical complication following the withdrawal of high-dose insulin euglycemic therapy (HIET). In the context of calcium channel blocker (CCB) toxicity, other potential confounding factors that could account for delayed pulmonary oedema include inadvertent fluid overload from management of hypotension caused by CCB toxicity, delayed toxicodynamic effects on the pulmonary vasculature and the heart, or a previously unknown underlying cardiac dysfunction. We report a case involving a woman in her early 50s who developed a symptomatic pulmonary oedema following the discontinuation of HIET used in the management of refractory hypotension complicating a massive amlodipine intoxication. This unexpected deterioration occurred despite improved haemodynamics following HIET used in the management of amlodipine toxicity. We have reviewed this case in relation to the existing literature on delayed or paradoxical pulmonary oedema complicating CCB toxicity, to the benefit of clinical personnel managing future similar cases.

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Journal
Cureus
Published
2025-12-04
DOI
https://doi.org/10.7759/cureus.98430
Primary Topic
Poisoning and overdose treatments
Type
article
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article

Refractory Hypotension and Delayed Respiratory Failure in Amlodipine Toxicity: A Multimodal Management Approach

Rabiu Momoh, Muhammad Misbah ul Haq, Chima Iloanugo
Cureus
Poisoning and overdose treatments
article

Refractory Hypotension and Delayed Respiratory Failure in Amlodipine Toxicity: A Multimodal Management Approach

Rabiu Momoh, Muhammad Misbah ul Haq, Chima Iloanugo
article en

Abstract

Pulmonary oedema is a rare but possible paradoxical complication following the withdrawal of high-dose insulin euglycemic therapy (HIET). In the context of calcium channel blocker (CCB) toxicity, other potential confounding factors that could account for delayed pulmonary oedema include inadvertent fluid overload from management of hypotension caused by CCB toxicity, delayed toxicodynamic effects on the pulmonary vasculature and the heart, or a previously unknown underlying cardiac dysfunction. We report a case involving a woman in her early 50s who developed a symptomatic pulmonary oedema following the discontinuation of HIET used in the management of refractory hypotension complicating a massive amlodipine intoxication. This unexpected deterioration occurred despite improved haemodynamics following HIET used in the management of amlodipine toxicity. We have reviewed this case in relation to the existing literature on delayed or paradoxical pulmonary oedema complicating CCB toxicity, to the benefit of clinical personnel managing future similar cases.

CureusVol. 17(12)
Maidstone and Tunbridge Wells NHS Trust (GB), Medway Maritime Hospital (GB)
Openalex Percentile: Top 46%
Poisoning and overdose treatments
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