Acute Limb Ischemia after Intake of the Phenylethylamine Derivate NBOMe.
Patricia P Wadowski, Georgiana-Aura Giurgea, Oliver Schlager, Anton Luf, Thomas Gremmel, Eva-Luise Hobl, Sylvia Unterhumer, Henriette Löffler-stastka, Renate Koppensteiner
International Journal of Environmental Research and Public Health December 12, 2019 DOI: 10.3390/ijerph16245071 (opens in new tab) via PubMed
Summary
AI-generated from the abstractA 30-year-old man with schizophrenia and a history of drug abuse was hospitalized with acute ischemia of his left arm—pallor, pulselessness, paresthesia, and motor deficit—after sublingual intake of a substance bought as 25I-NBOMe. Imaging showed reduced artery diameters and pathological flow profiles, suggesting vasospasm, distal thrombosis, or embolization. Intravenous alprostadil and anticoagulation led to symptom improvement within a day; five days of treatment restored normal perfusion. Drug analysis revealed 25I-NBOMe, 25C-NBOMe, 25H-NBOMe, and traces of pentylon. NBOMe ingestion carries a risk of severe, limb-threatening peripheral vasospasms.
Study at a glance
| Characteristics | Case report Peer reviewed |
|---|---|
| Sample size | 1 |
| Population | 30-year-old man with schizophrenia and drug abuse history |
| Interventions | low molecular weight heparin calcium-channel blockers |
| Duration | 5-day treatment |
| Keywords | Limb ischemia Phenylethylamine derivates Upper limb pain Vasospasm |
| Key finding | NBOMe ingestion can cause peripheral vasospasms leading to severe limb-threatening ischemia. |
Abstract
Objective: N-(2-methoxy) benzyl-phenethylamine (NBOMe) derivatives have a high affinity to the serotonin receptor 2A and emerged as new psychedelic agents. We report the case of a 30-year-old man admitted to the hospital because of acute ischemia of the left arm with clinical symptoms of pallor, pulselessness, paresthesia, and a motoric deficit. The patient had a history of schizophrenia and drug abuse and disclosed during the hospital stay the sublingual intake of a substance bought as 25I-NBOMe the night before the ischemic event. Methods: Routine clinical diagnostics including among others color-coded duplex sonography and computed tomography angiography (CTA) were performed. The remainder of the drugs was analyzed using high performance liquid chromatography. Results: Initial color-coded duplex sonography of the upper left limb showed pathological flow profiles of the axillary, brachial, ulnar, and radial artery with a reduced diameter of the ulnar (0.9 mm) and radial (1.1 mm) artery. In consequence, peripheral vasospasm, distal arterial thrombosis, or arterial embolization was anticipated. As therapeutic measures, the patient immediately received intravenous systemic vasodilators (alprostadil) and therapeutic anticoagulation with low molecular weight heparin. Instant symptom improvement was observed within the first day after therapy initiation. The subsequently performed CTA of the heart and left arm showed no signs of thrombotic material. Treatment was continued for five days and the patient was released thereafter having completely normalized perfusion in his left arm. Outpatient treatment was continued with calcium-channel blockers, as the patient had also displayed arterial hypertension. Drug analysis retrieved a composition of the isomers 25I-NBOMe, 25C-NBOMe, and 25H-NBOMe as well as traces of pentylon. Conclusion: NBOMe ingestion implicates the risk of peripheral vasospasms with severe, limb-threatening ischemia.