The patient is a 38-year-old African American male with a past medical history of schizoaffective and bipolar disorder who presented to the ED with altered mental status and chest pain. The patient had been issued a day / evening pass to leave the psychiatric facility where he currently resides and spent the evening at home with family. Upon returning to the facility, the staff noted the patient “appeared out of it” and somnolent. After the patient reported chest pain, the psychiatric facility called EMS. Per EMS and facility staff, the patient was difficult to arouse and maintained an altered mental status.
In the emergency department, the patient repeatedly fell asleep in the exam room but arose to verbal and physical stimuli. On exam the patient endorsed pleuritic chest pain and “sinus congestion.” The patient also had a productive cough with rust tinged sputum. The patient reported his family members had “shared their sinus congestion medicine with him.” The patient remained somnolent throughout the exam.
Other than a history of psychiatric disorders, the patient is normally otherwise healthy, with no previous surgeries. He denied alcohol, smoking, or any drug abuse. The patient’s daily medications included: benztropine (Cogentin 2 mg oral tablet) and zolpidem (Ambien 10 mg oral tablet).
Due to the patient’s altered mental status, a more thorough history was difficult to obtain.
Vitals: P= 104/min; RR= 16/min T= 36.4 C (97.5 F); BP = 115/70 mmHg; Pulse Ox: 98%
Skin: Warm, dry, no pallor, no needle tracks
Eye: Pupils pinpoint, equal, round, sluggish but reactive to light. Extra ocular movements intact, no nystagmus
ENT: Patent airway. No pharyngeal erythema or exudate.
Neck: Supple, trachea midline, no stridor
Lungs: Right side = clear to auscultation. Left side = left lower lobe significant for diminished breath sounds with noted crackles and dullness to percussion.
Heart: Sinus tachycardia with sinus rhythm, normal S1 & S2, no murmurs.
Abdominal: Normal bowel sounds. Soft. Nontender. Non-distended.
Back: Nontender. Normal range of motion. Normal alignment.
Extremity: Normal range of motion. Normal tone. No swelling. No tenderness.
Neurological: Alert when aroused to verbal and physical stimuli. Disoriented, changing stories multiple times, sleepy, nodding off; no aphasia, no dysarthria.
CBC: WBC = 31K RBC = 3.6 Hgb/Hct = 35/12 PLT = 219K
BUN/Cr: 32/1.7 Glucose = 130
CXR: Left lung opacity, within the lingula, suspicious for pneumonia.
U/A: 0 WBCs 0 RBCs
Urine toxicology screen: Negative for opioids, benzodiazepines, cocaine, PCP, amphetamines, cannabinoids
APAP/ASA levels: nondetectable;
ECG: sinus tachycardia rate 100 beats per minute, no ischemia, no ectopy
Dx: Afrin Overdose
The ED physician noted that the patient was nodding off in the exam room and had pinpoint pupils and a slow respiratory rate. The physician suspected an opioid overdose and administered 1mg of naloxone. There was a noted improvement in the patient’s mental status post naloxone administration consistent with either an opioid overdose or toxicity from an alpha agonist such as oxymetazoline, given the patient’s history of “sinus medication” exposure.
After the patient’s mental status improved, he stated he had spent the evening with family members the previous night. The patient stated that many of those family members had colds and were taking over-the-counter decongestants and utilizing nasal sprays. After repeated questioning, the patient indicated that he had used nasal spray for several hours because he too felt “congested.” While the patient did not recall the brand of the nasal spray, he stated he may have “used two entire bottles.” Subsequently two empty bottles of Afrin were discovered in the patient’s jacket pocket.
Oxymetazoline is a chemical found in readily available, over-the-counter drugs including Afrin, Nasivin, Dristan, Dimetapp, Zicam, Logicin, Vicks Sinex, Mucinex Full Force, Visine LR, Sudafed OM, and Facimin.
Oxymetazoline is an alpha 1 receptor agonist, and partially agonizes alpha 2 receptors. It has shown subtype selectivity. The result of oxymetazoline used under proper dosage is vasoconstriction due to the alpha 1 receptors commonly expressed in vascular beds. Under local application (typically via nasal spray) endothelial postsynaptic alpha 2 receptors experience vasoconstriction, resulting in increased mucosal blood flow and relief of nasal congestion.
Stimulation of alpha adrenergic receptors causes decreased cardiac output as well as decreased cardiovascular sympathetic activity. An overriding hypotensive effect of oxymetazoline acts to depress central nervous system functioning. Oxymetazoline’s interaction with the central nervous system results in decreased sympathetic outflow.
Oxymetazoline overdose results in central nervous system depression, bradycardia, hypotension, respiratory depression, miosis, hypotonia, and decreased cardiac output which may mimic opioid toxicity.
Oxymetazoline is similar to clonidine in that both are alpha agonists: both have effects on the alpha 2 and alpha 1 receptors. Clonidine is an imidazole derivative which was first used as a nasal decongestant.
Oxymetazoline and other decongestants containing tetrahydrozoline, also an imidazole derivative, can result in symptoms similar to clonidine poisoning when ingested.
As with therapeutic doses of clonidine, large doses of oxymetazoline act primarily as a presynaptic CNS alpha2-agonist, stimulating receptors in the nucleus tractus solitarii of the medulla oblongata. This results in inhibition of sympathetic outflow, which results primarily in a reduction of sympathetically mediated vasoconstriction, cardiac inotropy, and chronotropy. These processes give the desired effects of clonidine at therapeutic doses; however, when super therapeutic doses of clonidine or oxymetazoline are ingested, the effects can resemble an opioid overdose with miosis, bradycardia, respiratory depression, and coma. It requires large quantities of oxymetazoline to cause these CNS effects while clonidine will produce similar effects at baseline doses, thus making an overdose more common with clonidine than with oxymetazoline.
Oxymetazoline overdose is challenging to diagnose because the symptoms of the overdose make it difficult to obtain an accurate patient history; due to the stimulation of alpha adrenergic receptors, cardiac output is decreased, resulting in hypotension. Decreased sympathetic cardiac activity combined with decreased output leads to depressed central nervous system activity, resulting in an altered mental status. Patients may appear sleepy, drowsy, or even comatose.
Although in this case, it was challenging to separate the symptoms caused by the patient’s apparent pneumonia from the symptoms resulting from a large ingestion of oxymetazoline, it was clear that his symptoms did not stem from pneumonia alone. The also patient denied ingestion or overdose of his medications benztropine or zolpidem or any other sinus/cold medications containing dextromethorphan. His somnolence and ability to be roused with loud questioning and sternal rubs resembled the effects of a clonidine overdose. As with clonidine overdose, a patient’s mental status may improve after the administration of naloxone. Although, generally not as abrupt as one would typically see in a true opiate overdose.
There is no targeted antidote for oxymetazoline overdose. In toxic doses of oxymetazoline, clonidine-like toxicitiy can be seen. Guidelines for treating clonidine overdoses are more readily available than guidelines concerning oxymetazoline toxicity. The American Academy of Pediatrics recommends a dose of naloxone of 0.1 mg/kg for infants and children up to age 5 years or weighing 20 kg. Children older than 5 years or weighing more than 20 kg may be given 2 mg of naloxone. Adults with isolated clonidine toxicity may be given 1 mg doses of naloxone, titrated to effect. The use of naloxone can cause hypotensive and hypertensive responses.
The patient’s mental status improved after receiving naloxone in the emergency department. His mental status returned to baseline over the remainder of his stay in the ED. He was admitted to the hospital for further observation, and treatment for pneumonia with ciprofloxacin 400 mg IVPB and Zosyn 3.375 mg, IVPB.
The patient had an uneventful course in the hospital and was discharged after one day. He returned to the psychiatric facility on oral antibiotics for pneumonia. He also received education materials regarding safe usage of nasal decongestants. He did not have any further sequelae from the ingested Afrin throughout his hospital course.
The authors wish to thank Trammell Cox for his assistance with this case report.
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