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. 2024 Oct 19;16(10):e71840. doi: 10.7759/cureus.71840

Nutmeg Poisoning With Electrolyte Abnormalities: A Case Report

Ryo Ichibayashi 1,✉, Takanobu Sato 1, Ryogo Ohashi 1, Katsuya Konishi 2
Editors: Alexander Muacevic, John R Adler
PMCID: PMC11571034  PMID: 39559662

Abstract

Nutmeg is a commonly used spice that contains myristicin, a compound with anticholinergic and psychoactive properties. Excessive consumption can lead to toxicity, causing psychiatric and anticholinergic symptoms such as tachycardia, dizziness, dry mouth, tremors, and nausea. Nutmeg poisoning is rare and not widely recognized. This report describes the case of a 33-year-old woman who accidentally ingested a toxic amount of nutmeg while cooking. She presented with symptoms of dry mouth, tremors, dizziness, and anxiety and was subsequently diagnosed with nutmeg poisoning. Blood tests revealed electrolyte abnormalities, while cardiac function and respiratory status were normal. The patient was treated with fluid restriction and symptomatic management, with symptoms resolving within 24 hours. This case highlights the need for greater awareness of nutmeg’s toxic effects and the importance of recognizing its symptoms and providing appropriate treatment. Nutmeg can pose significant health risks if consumed excessively despite its widespread availability. Education and prevention measures are crucial to avoid complications, including electrolyte abnormalities. Healthcare providers should consider nutmeg poisoning in differential diagnoses involving anticholinergic and sympathomimetic symptoms, as early recognition and management are essential to patient recovery.

Keywords: anticholinergic effects, electrolyte abnormalities, hyponatremia, nutmeg intoxication, poisoning

Introduction

Nutmeg is a spice used in household dishes to remove the odor of meat [1,2]. The myristicin in nutmeg has anticholinergic and psychoactive effects and may cause organ damage, such as liver, heart, and kidney damage [1,2]. As a result, excessive nutmeg intake can cause anticholinergic and psychiatric symptoms. Signs and symptoms include tachycardia, dizziness, excitement, anxiety, headache, limb weakness, dry mouth, and nausea [1,3].

There have been cases of people taking nutmeg in excess to achieve hallucinations and euphoria, but severe cases and deaths have also been reported due to taking large amounts [3,4]. There have also been reported cases of people taking excessive amounts of nutmeg in addition to smoking marijuana to achieve a euphoric effect [5]. In general, awareness of the poisoning symptoms of nutmeg is low [3]. In this report, we describe a case of nutmeg poisoning and electrolyte abnormalities caused by accidentally ingesting a large amount of nutmeg in a meal without being aware of its toxicity.

Case presentation

A 33-year-old woman presented with symptoms nutmeg poisoning. She had no medical history or allergies. At around 6 p.m. earlier that day, she had eaten spaghetti with meat sauce; the inner cap of the nutmeg bottle came off during cooking, and two-thirds of the bottle's contents fell into the spaghetti. At around 9 p.m., she began to feel a dry mouth, and at the same time, she began to feel trembling and dizziness. She researched nutmeg online and found that the symptoms matched the nutmeg bottle's symptoms. She realized that she had consumed a toxic amount. As her mouth felt excessively dry, she panicked and drank more than 1 liter of water in 30 minutes. After that, she also experienced headaches, nausea, and discomfort in the epigastric region, and as the symptoms did not improve, she was brought to our hospital by ambulance.

On arrival, she was conscious, with a blood pressure of 131/91 mmHg, respirations of 24/minute, pulse of 105/minute, and saturation of peripheral oxygen (SpO2) of 100%. She complained of gagging and had a gross tremor in her left upper limb. There was no dry skin. The pupil diameter measured with a quantitative pupillometer was 5.8 mm on the right and 5.1 mm on the left, and a light reflex was observed. A chest X-ray and an electrocardiogram were normal. The total weight of the vial of nutmeg was 15 g, which means that the patient had ingested a toxic amount of 5-10 g. We diagnosed her with nutmeg poisoning because we believed her gagging, tachycardia, and dilated pupils were due to the anticholinergic effects of nutmeg. The blood test results at the time of admission are shown in Table 1.

Table 1. Laboratory results during her admission.

CRP: C-reactive protein, TP: total protein, Alb: albumin, AST: aspartate aminotransferase, ALT: alanine aminotransferase, LDH: lactate dehydrogenase, γ-GTP: γ-glutamyl transpeptidase, BUN: blood urea nitrogen,  eGFR: estimated glomerular filtration, WBC: white blood cell, Hb: hemoglobin, Ht: hematocrit, Plt: platelet, SG: specific gravity

Test Day 1 Result Day 2 Result Day 3 Result Reference range
CRP 0.02 - - <0.3 mg/dL
TP 7.3 - - 6.7-8.3 g/dL
Alb 4.5 - - 3.8-5.2 g/dL
AST 19 19 15 10-40 IU/L
ALT 13 11 11 5-45 IU/L
LDH 168 - - 124-222 U/L
γ-GTP 33 46 47 <30 IU/L
BUN 12.9 7.8 12.1 8.0-20.0 mg/dL
Creatinine 0.59 0.52 0.74 0.47-0.79 mg/dL
eGFR 94 107 73 >60 mL/min/1.73m2
Sodium 128 128 138 137-147 mEq/L
Potassium 3.1 4.3 4.3 3.5-5.0 mEq/L
Chloride 96 98 107 98-108 mEq/L
Glucose 127 - - 70-109 mg/dL
HbA1c 5.4 - - 4.7~6.2%
WBC 7720 11060 4710 3300-9000/μL
Hb 12.7 13.0 13.8 13.5-17.5 g/dL
Ht 44.9 37.2 40.2 39.7-52.4%
Plt 36.5 20.3 19.4 14-34104/μL
Urinalysis - - - -
pH 7.5 7.5 5.5 5.0~8.0
SG 1.013 1.003 1.011 1.010~1.025

Other than hyponatremia and hypokalemia, no other notable findings were noted. Cardiac ultrasound showed no abnormalities in cardiac function, and no respiratory changes were observed in the diameter of the inferior vena cava, so it was determined that there was no dehydration. However, the low urine specific gravity and the large amount of water consumed in a short period suggested water intoxication. After admission to the general ward, intravenous fluids were restricted to 500 mL/24 hours (Ringer's solution). The patient was monitored, and seven hours after ingesting nutmeg, tremors, restlessness, and anxiety disappeared. Twelve hours later, blood pressure improved to 103/66 mmHg and pulse rate to 78/min, normal. The dry mouth improved within 24 hours after ingestion, but epigastric discomfort persisted. On hospital day 2, electrolyte abnormalities improved, and symptoms resolved, so the patient was discharged. One week after discharge, mydriasis and electrolyte abnormalities were not noted. As a result, we have stopped following up on the patient.

Discussion

Nutmeg poisoning can occur with ingestion of 5 g or more, leading to mental symptoms such as anxiety, hallucinations, and restlessness due to myristicin and other compounds in nutmeg [1,3,6,7]. Anticholinergic effects like dry mouth, tremors, tachycardia, and decreased vision may also appear, sometimes necessitating ambulance transport. Symptoms typically begin three hours post ingestion and subside within 48 hours [3,6]. These symptoms are not commonly found in general poisoning textbooks, prompting initial information gathering from the Internet. Despite abundant online details, awareness of nutmeg poisoning is low [3], emphasizing the importance of a patient’s medical history for accurate diagnosis.

In the reported case, the patient exhibited mydriasis with a light reflex, attributed to nutmeg's anticholinergic effects. Myristicin, contained in nutmeg, has anticholinergic effects [2]. Generally, anticholinergic poisoning results in mydriasis with loss of pupil reflex, while sympathomimetic drugs cause pupil dilation with pupil reflex. This contradiction indicates the insufficient elucidation of the pharmacological action of nutmeg [3]. The patient did not exhibit sweating or dry skin but complained of dry mouth. Rapid excess fluid intake was thought to be the cause of hyponatremia [8]. In this way, the anticholinergic dry mouth can lead to excessive water consumption, causing electrolyte abnormalities. In severe cases, it can also cause water intoxication. Metabolites of myristicin and elemicin in nutmeg are amphetamine derivatives, which have neurostimulant effects causing excitement and coma [9]. In the worst case, hyponatremia can worsen these neurological symptoms. Even if there is a dry mouth, excessive fluid therapy is unnecessary. Appropriate fluid therapy and symptomatic treatment are important.

Nutmeg poisoning presents a mix of anticholinergic and sympathomimetic effects, leading to sympathetic nervous system activation. There is no specific cure, but treatment involves body temperature control, rest, and mental health support unless the case is severe. Understanding nutmeg's effects and appropriate first aid for poisoning is vital. Patient education should discourage excessive water drinking and stress the importance of seeking medical attention to prevent complications like electrolyte abnormalities and water intoxication. Regarding pupillary findings, the presence or absence of light reflex may depend on which effect is more dominant. Differential diagnoses for symptoms like mydriasis, elevated blood pressure, tachycardia, and psychiatric symptoms include anticholinergic poisoning, sympathomimetic poisoning, and serotonin syndrome. Awareness of nutmeg poisoning’s dual effects can aid physicians in considering it as a differential diagnosis based on pupillary findings.

Conclusions

Although nutmeg is readily available in homes, knowledge about its toxic risk and pharmacological effects must be improved. Diagnosis and treatment must rely on the medical history and clinical symptoms, and patients may present with electrolyte abnormalities. Prevention and education about nutmeg poisoning and its treatment are important to prevent unnecessary complications.

Disclosures

Human subjects: Consent was obtained or waived by all participants in this study.

Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following:

Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work.

Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work.

Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Author Contributions

Concept and design:  Ryo Ichibayashi

Acquisition, analysis, or interpretation of data:  Ryo Ichibayashi, Takanobu Sato, Ryogo Ohashi, Katsuya Konishi

Drafting of the manuscript:  Ryo Ichibayashi

Critical review of the manuscript for important intellectual content:  Ryo Ichibayashi, Takanobu Sato, Ryogo Ohashi, Katsuya Konishi

Supervision:  Ryo Ichibayashi

References

  • 1.A proteomics study on the mechanism of nutmeg-induced hepatotoxicity. Xia W, Cao Z, Zhang X, Gao L. Molecules. 2021;26:1748. doi: 10.3390/molecules26061748. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 2.Anti-inflammatory effect of myristicin on RAW 264.7 macrophages stimulated with polyinosinic-polycytidylic acid. Lee JY, Park W. Molecules. 2011;16:7132–7142. doi: 10.3390/molecules16087132. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Unintentional nutmeg autointoxication. Roeters van Lennep JE, Schuit SC, van Bruchem-Visser RL, Özcan B. https://www.njmonline.nl/getpdf.php?id=1536. Neth J Med. 2015;73:46–48. [PubMed] [Google Scholar]
  • 4.Nutmeg poisonings: a retrospective review of 10 years experience from the Illinois Poison Center, 2001-2011. Ehrenpreis JE, DesLauriers C, Lank P, Armstrong PK, Leikin JB. J Med Toxicol. 2014;10:148–151. doi: 10.1007/s13181-013-0379-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Toxicology of nutmeg abuse. Sangalli BC, Chiang W. J Toxicol Clin Toxicol. 2000;38:671–678. doi: 10.1081/clt-100102020. [DOI] [PubMed] [Google Scholar]
  • 6.Nutmeg intoxication: a case report. Casale MJ, MacDonald LL, Mitra A. Cureus. 2023;15:0. doi: 10.7759/cureus.46286. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 7.Toxicological evaluation of myristicin. Hallström H, Thuvander A. https://pubmed.ncbi.nlm.nih.gov/9496377/ Nat Toxins. 1997;5:186–192. doi: 10.1002/nt.3. [DOI] [PubMed] [Google Scholar]
  • 8."Bowel prep hyponatremia" - a state of acute water intoxication facilitated by low dietary solute intake: case report and literature review. Windpessl M, Schwarz C, Wallner M. BMC Nephrol. 2017;18:54. doi: 10.1186/s12882-017-0464-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.3-methoxy-4,5-methylenedioxy amphetamine, a new psychotomimetic agent. Shulgin AT. Nature. 1964;201:1120–1121. doi: 10.1038/2011120a0. [DOI] [PubMed] [Google Scholar]

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