You are in: eMedicine Specialties > Emergency Medicine > TOXICOLOGY Toxicity, TerpeneArticle Last Updated: Dec 11, 2007AUTHOR AND EDITOR INFORMATIONSection 1 of 11
  Author: John Said Kashani, DO, Assistant Medical Director of the New Jersey Poison ad Information Education System; Assistant Professor, Department of Preventive Medicine and Community Health, Assistant Professor, Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey John Said Kashani is a member of the following medical societies: American College of Emergency Physicians and American College of Medical Toxicology Coauthor(s): Steven Marcus, MD, Professor, Department of Preventive Medicine and Community Health, Associate Professor, Department of Pediatrics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey; Executive and Medical Director, New Jersey Poison Information and Education System; Consulting Staff, Departments of Pediatrics and Internal Medicine, University Hospital, University of Medicine and Dentistry of New Jersey; Consulting Staff, Department of Pediatrics, Newark Beth Israel Medical Center Editors: Lance W Kreplick, MD, MMM, FAAEM, FACEP, Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; Michael J Burns, MD, Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital Author and Editor Disclosure Synonyms and related keywords: terpene toxicity, terpenes, terpenoids, monoterpenes, isoprene unit, diterpenes, terpene exposure, terpene poisoning, cantharidin, menthol, pinene, camphor, phytol, vitamin A1, paclitaxel, Taxol INTRODUCTIONSection 2 of 11
  BackgroundTerpenes are natural products derived from plants that have medicinal properties and biological activity. Terpenes may be found in cleaning products, rubefacients, aromatherapy, and various topical preparations. Terpenes may exist as hydrocarbons or have oxygen-containing compounds such as ketone or aldehyde groups (terpenoids). The basic structure of terpenes is repeating isoprene units (C5H8)n, and they are grouped according to the number of repeating isoprene units. Monoterpenes contain 2 isoprene units; examples include cantharidin, menthol, pinene, and camphor. Diterpenes contain 4 isoprene units; examples include phytol, vitamin A11, and paclitaxel (Taxol). The best-known compounds in this group are camphor oil and turpentine. The antineoplastic agent paclitaxel is a terpene derived from yew plant bark. An oil derived from the Saliva officinalis tree, thujone, has recently become popular because of its hallucinogenic qualities, and it is quickly becoming a drug of abuse.2 Absinthe, a green liquor containing thujone, has been thought to be responsible for enhancing the creativity of many famous artists including Edouard Manet, Vincent Van Gogh, and Henri de Toulouse-Lautrec. PathophysiologyTerpenes are local irritants and, thus, are capable of causing GI signs and symptoms. CNS manifestations may range from an altered mental status to seizures to coma. Aspiration is a particular concern and can result in fatalities and long-term complications. Absorption begins in the oral cavity and is rapid as evidenced by the early onset of toxicity in significant ingestions. Terpenes are metabolized through cytochrome P450 and are excreted as conjugated metabolites by the kidney. FrequencyUnited StatesAccording to the 2005 Annual Report of the American Association of Poison Control Toxic Exposure Surveillance System, 4851 exposures to disinfectants containing pine oil, 10,502 exposures to camphor, and 633 exposures to turpentine were reported.3 Seven deaths were reported with exposures to pine oil or pine oil–containing products.3 No deaths were reported with exposure to camphor or turpentine.3 Mortality/MorbidityMorbidity and mortality4 associated with exposure to terpenes is largely related to the degree of CNS depression and if aspiration occurs. Despite the toxicity of these agents, morbidity is extremely low. SexMales overrepresent cases associated with terpenes. AgeMost exposures are the result of unintentional exposures in childhood. CLINICALSection 3 of 11
History
Physical
Causes
DIFFERENTIALSSection 4 of 11
Gastroenteritis Pneumonia, Aspiration Pneumonia, Bacterial Pneumonia, Empyema and Abscess Toxicity, Anticholinergic Toxicity, Antihistamine Toxicity, Cyclic Antidepressants Toxicity, Hydrocarbons Toxicity, Isoniazid
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| Drug Name | Lorazepam (Ativan) |
|---|---|
| Description | Useful to treat seizures and induce sedation. Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of GABA, a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Monitor carefully for respiratory depression. |
| Adult Dose | 2 mg IV/IM titrate to effect; some patients may require larger doses |
| Pediatric Dose | 0.05 mg/kg IV/IM |
| Contraindications | Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma |
| Interactions | Effects potentiated by phenothiazines, narcotics, barbiturates, MAOIs, and other antidepressants |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; monitor for respiratory depression |
| Drug Name | Diazepam (Valium) |
|---|---|
| Description | Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Third-line agent for agitation or seizures because of shorter duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation. Individualize dosage cautiously to avoid adverse effects. Monitor carefully for respiratory depression. |
| Adult Dose | 5-10 mg IV q10-15min until symptoms resolve; not to exceed 30 mg |
| Pediatric Dose | 30 days to 5 years: 0.2-0.5 mg IV (slowly) q2-5min until symptoms resolve; not to exceed 5 mg >5 years: 1 mg IV (slowly) q2-5min until symptoms resolve; not to exceed 10 mg |
| Contraindications | Documented hypersensitivity; acute narrow-angle glaucoma |
| Interactions | Effects potentiated by phenothiazines, narcotics, barbiturates, MAOIs, and other antidepressants |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity); monitor for respiratory depression with high or repeated doses |
| Drug Name | Midazolam (Versed) |
|---|---|
| Description | Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access. Monitor carefully for respiratory depression. |
| Adult Dose | 0.01-0.05 mg/kg (usually 0.5-4 mg, up to 10 mg) IV slowly over several min; may repeat q10-15min until adequate response achieved |
| Pediatric Dose | <32 weeks: 0.5 mcg/kg/min IV infusion >32 weeks: 1 mcg/kg/min IV infusion Children: 0.05-0.2 mg/kg IV over 2-3 min, followed by 1-2 mcg/kg/min continuous infusion Status epilepticus (refractory to standard therapy), >2 months and children: 0.15 mg/kg followed by continuous infusion of 1 mcg/kg/min, titrating dose upward q5min until seizures controlled |
| Contraindications | Documented hypersensitivity; preexisting hypotension, narrow-angle glaucoma, and sensitivity to propylene glycol (diluent) |
| Interactions | Sedative effects may be antagonized by theophyllines; narcotics, cimetidine, ethanol, and erythromycin may accentuate sedative effects because of decreased clearance; reduce dose of thiopental by 15% when using together |
| Pregnancy | D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus |
| Precautions | Caution in congestive heart failure, pulmonary disease, renal impairment, hepatic failure, neuromuscular disease, hypotension, and patients >60 y; monitor for respiratory depression with high or repeated doses; consider lower dosages organic brain syndrome and patients who may have inhibition of benzodiazepine metabolism and clearance (eg, using nicotine, taking cimetidine) |
The authors and editors of eMedicine gratefully acknowledge the assistance of Lada Kokan, MD, with the literature review and referencing for this article.
Article Last Updated: Dec 11, 2007
