Naphazoline intoxication managed with minimally invasive cardiac output monitoring

• Published in: The American journal of emergency medicine Vol. 77; pp. 233.e5 - 233.e7
• Main Authors: Oishi, Takatoshi, Kashiura, Masahiro, Yasuda, Hideto, Kishihara, Yuki, Tominaga, Keiichiro, Tamura, Hiroyuki, Moriya, Takashi
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-03-2024; Elsevier Limited
• Subjects: Adrenergic receptors; Adult; Antiseptics; Arteries; Blood pressure; Bradycardia; Calcium antagonists; Calcium channels; Cardiac arrhythmia; Cardiac Output; Complications; Cyanosis; Dosage; Emergency medical care; Heart; Humans; Ingestion; Intoxication; Male; Monitoring systems; Naphazoline; Nicardipine; Patients; Phentolamine; Poisoning; Receptors, Adrenergic; Sprays; Suicides & suicide attempts; Toxicology; Vascular resistance; Writing; Toxicology; Nicardipine; Vascular resistance; CI; Naphazoline; LVEF; Poisoning; Phentolamine; PWA; CO; SVRI
• ISSN: 0735-6757; 1532-8171; 1532-8171
• DOI: 10.1016/j.ajem.2023.12.034

Naphazoline, a nonspecific alpha-adrenoceptor stimulant, is a potent vasoconstrictor used in nasal sprays, eye drops, and over-the-counter antiseptics. Naphazoline intoxication increases afterload by constricting the peripheral arteries, which can lead to complications including multiple organ failure. Although phentolamine, a nonselective alpha-adrenoceptor antagonist, and nicardipine, a calcium channel blocker, are used for the treatment of naphazoline intoxication, no established administration protocols currently exist.
We present the case of a 32-year-old male with depression who ingested 150 mL of an antiseptic containing 0.1% naphazoline (equivalent to 150 mg of naphazoline). Five hours after ingestion, the patient was admitted to hospital exhibiting signs of naphazoline intoxication, such as bradycardia (46 beats/min), blood pressure of 166/122 mmHg, and peripheral cyanosis. We used the FloTrac™/EV1000™ system (Edwards Lifesciences, Irvine, CA, USA), a minimally invasive cardiac output monitoring system, to monitor systemic vascular resistance. The systemic vascular resistance index (SVRI) was elevated (4457 dyne.s/cm5/m2; nomal range: 1970–2390 dyne.s/cm5/m2) upon admission and initial treatment with continuous intravenous infusion of phentolamine led to SVRI normalization within 2 h. With the goal of maintaining SVRI normalization, continuous infusion with nicardipine was then started. At 10 h after treatment initiation, the nicardipine dose peaked at 9 mg/h (1.9 μg/kg/min). Treatment was discontinued 8 h later, and the patient was discharged on the fourth day without sequelae.
In conclusion, the use of a minimally invasive cardiac output monitoring system to track vascular resistance can effectively guide the dosing of phentolamine or nicardipine in the treatment of naphazoline intoxication.