Naloxone-Induced Non-Cardiogenic Pulmonary Edema: A Case Report

Jiwa, Nasheena; Sheth, Himesh; Silverman, Richard B.

doi:10.1007/s40800-018-0088-x

Cited by 19 publications

(6 citation statements)

References 14 publications

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“…This reduced sensitivity to naloxone could be because of non-MOR-related effects of fentanyl and may explain why deaths from F/FAs continue to increase (Baumann et al, 2018). In fact, naloxone in higher doses causes noncardiogenic pulmonary edema (Jiwa et al, 2018), exacerbating respiratory failure and non-MOR-mediated symptoms of opioid overdose. Rapidity of injection and dose of fentanyl are the key determinants of the incidence, severity, and duration of FIRE (Grell et al, 1970).…”

Section: Fentanylmentioning

confidence: 99%

Fentanyl but not Morphine Interacts with Nonopioid Recombinant Human Neurotransmitter Receptors and Transporters

Torralva

Eshleman

Swanson

et al. 2020

J Pharmacol Exp Ther

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Synthetic opioids, including fentanyl and its analogs, have therapeutic efficacy in analgesia and anesthesia. However, their illicit use in the United States has increased and contributed to the number one cause of death for adults 18-50 years old. Fentanyl and the heroin metabolite morphine induce respiratory depression that can be treated with the m opioid receptor (MOR) antagonist naloxone. With higher or more rapid dosing, fentanyl, more than morphine, causes chest wall rigidity and can also induce rapid onset laryngospasm. Because non-MORs could mediate differing clinical manifestations, we examined the interactions of fentanyl and morphine at recombinant human neurotransmitter transporters, G protein-coupled receptors, and the N-methyl-Daspartate glutamate receptor. Both drugs were agonists at MOR, k, and d opioid receptors. Morphine had little or no affinity at other human receptors and transporters (K i or IC 50 value .100 mM). However, fentanyl had K i values of 1407 and 1100 nM at a 1A and a 1B adrenoceptor subtypes, respectively, and K i values of 1049 and 1670 nM at dopamine D4.4 and D1 receptor subtypes, respectively; it also blocked [ 3 H]neurotransmitter uptake by the vesicular monoamine transporter 2 (IC 50 = 911 nM). Pharmacokinetic models indicate that these Ki and IC 50 values are pharmacologically relevant. Fentanyl had little affinity for other receptors or transporters. Thus, noradrenergic disposition at specific receptor subtypes in relevant organs may play a role in respiratory and cardiothoracic effects of fentanyl. Data suggest that less selective fentanyl receptor pharmacology could play a role in the different clinical effects of morphine compared with fentanyl, including fentanyl-induced deaths after illicit use. SIGNIFICANCE STATEMENTThe synthetic opioid fentanyl induces different clinical effects, including rapid onset muscular rigidity, vocal cord closure, and rapid death, than the heroin metabolite morphine. Our data indicate for the first time that the two drugs have very different effects at recombinant human neurotransmitter receptors and transporters that might explain those clinical differences.

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Section: Fentanylmentioning

confidence: 99%

Fentanyl but not Morphine Interacts with Nonopioid Recombinant Human Neurotransmitter Receptors and Transporters

Torralva

Eshleman

Swanson

et al. 2020

J Pharmacol Exp Ther

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“…Naloxone is an opioid receptor antagonist, and is an effective drug for VE [16]. However, long-term and highdose administration of naloxone may cause arrhythmia, cardiogenic pulmonary edema and even myocardial infarction [17]. Many scholars believe that clinically, a combination of acyclovir and naloxone can effectively relieve the inflammatory response and brain injury caused by VE, and can protect neuronal cells; the combination has a small risk of sequelae, and is conducive to the outcome of the disease [18].…”

Section: Introductionmentioning

confidence: 99%

Acyclovir Combined with Naloxone in the Treatment of Viral Encephalitis: A Meta-Analysis

Wang

Zhao

Zhang

2022

Journal of Healthcare Engineering

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Background. The aim of this study was to systematically evaluate the efficacy and prognosis of acyclovir combined with naloxone in the treatment of patients with viral encephalitis (VE). Methods. PubMed, Web of Science, Embase, CNKI, and WanFang Data were searched for relevant literature published between 2000 and 2021. Meta-analysis was performed using Stata16.0 software. The treatment group was treated with acyclovir combined with naloxone, and the control group was treated with acyclovir alone. Results. A total of 12 studies with 986 participants were included. Compared with the control group, the treatment group could not only significantly improve the treatment response rate (OR = 5.53, 95% CI: 3.50, 8.74; P ≤ 0.001), but also reduce the incidence of adverse reactions (OR = 0.25, 95% CI: 0.17, 0.38; P ≤ 0.001). In addition, the combined treatment significantly inhibited the levels of inflammatory factors and neuron-specific enolase (NSE) in VE patients. The time for cerebrospinal fluid to return to normal (SMD = −2.73, 95% CI: −2.96, −2.51; P ≤ 0.001), as well as the disappearance time of meningeal irritation (SMD = −3.58, 95% CI: −4.96, −2.20; P ≤ 0.001), headache (SMD = −3.87, 95% CI: −5.84, −1.91; P ≤ 0.001), convulsion (SMD = −3.65, 95% CI: −4.56, −2.75; P < 0.001), tic (SMD = −4.083, 95% CI: −5.18, −2.98; P ≤ 0.001) and disturbance of consciousness (SMD = −4.96, 95% CI: −6.28, −3.63; P ≤ 0.001) in the treatment group were significantly shorter than those in the control group. Conclusion. A combination of acyclovir and naloxone can reduce the inflammatory response and shorter the time to symptom relief and disappearance, which is worthy of clinical promotion.

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“…Some case reports have shown furosemide to be an effective treatment for naloxone‐associated pulmonary edema with resultant quick progression to extubation in most adult patients but has not been formally studied 13 . Our patient was also able to wean down quickly on respiratory support without the use of furosemide.…”

Section: Discussionmentioning

confidence: 78%

Naloxone‐associated pulmonary edema in a 3‐year‐old with opioid overdose

2022

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Background Annually, close to 5000 children under age 6 years are treated in emergency departments or admitted for care due to opioid exposures. Naloxone is effectively used to treat opioid overdose in both children and adults. Non‐cardiogenic pulmonary edema is a rare but serious adverse effect of naloxone administration that has been reported in adults. Case Report We present the case of a 3‐year‐old male with suspected opioid overdose who developed acute hypoxia due to pulmonary edema after administration of naloxone following a likely prolonged downtime. Why Should an Emergency Physician Be Aware of This? The copious fluid in the airway made for difficult intubation at a pediatric tertiary care center. Given the incidence of opioid exposures in children, clinicians should be aware of this rare, but dangerous adverse effect of naloxone and consider airway precautions and pediatric critical care availability early in the presentation.

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Naloxone-Induced Non-Cardiogenic Pulmonary Edema: A Case Report

Cited by 19 publications

References 14 publications

Fentanyl but not Morphine Interacts with Nonopioid Recombinant Human Neurotransmitter Receptors and Transporters

Fentanyl but not Morphine Interacts with Nonopioid Recombinant Human Neurotransmitter Receptors and Transporters

Acyclovir Combined with Naloxone in the Treatment of Viral Encephalitis: A Meta-Analysis

Naloxone‐associated pulmonary edema in a 3‐year‐old with opioid overdose

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