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Plant Poisoning, Alkaloids - Quinolizidine and Isoquinoline
Updated: Apr 13, 2009
Introduction
Background
Alkaloids are alkali-like compounds that form salts with acids and contain nitrogen, generally in heterocyclic and/or ring structures. Found in a wide variety of plants, animals, and fungi, many alkaloids have medicinal and toxic properties.
Quinolizidine and isoquinoline alkaloids are a widely distributed, heterogeneous group of alkaloids with members of each group having known toxicity to humans and domestic animals.
Plants containing quinolizidine alkaloids with known toxicity include the following:
- Baptisia species (false indigo)
- Cytisus species (scotch broom)
- Laburnum species (goldenchain, laburnum)
- Lupinus species (lupine, bluebonnet)
- Sophora species (mescal bean, frijolito)
Plants containing isoquinoline alkaloids with known toxicity include the following:
- Argemone species (prickly poppy)
- Chelidonium species (celandine poppy)
- Corydalis species (fitweed)
- Dicentra species (dutchman's breeches)
- Papaver species (poppy)
- Sanguinaria species (bloodroot)
Cytisine, a tricyclic quinolizidine alkaloid found in Baptisia, Cytisus, Laburnum, and Sophora species, has nicotinelike effects on the gastrointestinal (GI) tract and the central nervous system (CNS). These plants may be smoked recreationally for their stimulant effects and mild hallucinogenic properties. Mescal bean may have been used by Native American peoples for ceremonial and medicinal purposes. Sophora root is used in traditional Chinese medicine where it is known as "Ku Shen" and is used to treat dysentery, scabies, itchy rashes including eczema, skin lesions, jaundice, edema, urinary dysfunction, and vaginal discharge.
Lupinus species contain sparteine, a tetracyclic quinolizidine alkaloid, and lupinine, a bicyclic quinolizidine alkaloid. Lupinus species are broadly divided into bitter lupins that contain high levels of alkaloids in their seeds, and sweet lupins that contain lower levels of alkaloids and are cultivated for human consumption. Sweet lupins do contain sparteine and lupinine and must be soaked in water to prevent toxicity following ingestion. These two alkaloids are also found in other genera.
The toxic isoquinoline alkaloids include papaverine, sanguinarine, dihydrosanguinarine, protoverine, berberine, coptisine, protopine, and chelidonine. They act as GI tract irritants, CNS stimulants, and have varying degrees of neurologic effects, ranging from relaxation and euphoria to seizures. They are also vasodilatory. Prickly poppy is smoked as a euphoriant.
Papaverine, found in prickly poppy and bloodroot, has been used medically as a smooth muscle relaxant. Prickly poppy extracts act as capillary dilators and have been implicated in epidemic glaucoma in India.
Sanguinaria species (bloodroot) extract was Food and Drug Administration (FDA) approved and used commercially as a dental plaque inhibitor; however, it is no longer added to commercially available toothpaste and mouthwash due to concerns that chronic use may cause oral leukoplakia. Sanguinaria extract may still be purchased over the Internet, where it is marketed as a mouthwash for dental decay, as an escharotic for skin lesions including cancer, and as a tea for a variety of indications. It is not FDA approved for these uses.
Celandine extracts are used in the herbal treatment of gastrointestinal disorders, including dyspepsia, gallstone disease, and irritable bowel syndrome. Celandine extracts have been shown to increase the flow of bile acids and decrease right upper quadrant pain due to biliary dyskinesia. Celandine extract also has stimulatory effects on smooth muscle contraction in the stomach and spasmolytic effects in the small intestine, which may explain its beneficial effects in dyspepsia and irritable bowel syndrome.
Argemone oil poisoning is relatively common in India, where it is known as epidemic dropsy and is a result of argemone oil being added as an adulterant to mustard oil. In 1998, an epidemic of argemone oil poisoning in New Delhi led to 3000 victims and 60 deaths.1 Argemone oil poisoning has also been reported after transcutaneous absorption from adulteration of mustard oil used in massages.
Pathophysiology
Cytisine is similar in action to nicotine. GI irritation is common, and toxic ingestions almost invariably result in emesis. Onset of symptoms is rapid. GI upset and vomiting start 45 minutes to 4 hours after ingestion. CNS effects include drowsiness, weakness, loss of coordination, muscle fasciculations, seizures, coma, and mydriasis. Some anticholinergic effects, such as urinary retention, may manifest. Respiratory failure, as in nicotine poisoning, is observed in patients with severe cases.
Cutaneous exposure to celandine and bloodroot extracts may cause a contact dermatitis, and ingestion of celandine extract is known to be hepatotoxic with numerous cases of acute cholestatic hepatitis reported in the literature. Rarely, necrotizing hepatitis has been reported. Celandine extract has also been implicated in a case of hemolytic anemia.2
Corydalis species (fitweed) ingestion has demonstrated delayed hepatotoxicity.
Argemone oil has been reported to cause oxidative stress by reducing levels of glutathione reductase and glucose-6-phosphate reductase in erythrocytes and glutathione, alpha-tocopherol, and glutathione-S-transferase in erythrocytes and liver.3 Sanguinarine and related isoquinoline alkaloids are the active toxins in argemone oil responsible for its adverse effects. Others postulate that sanguinarine toxicity is additionally mediated by inhibition of Na+ K+ ATPase, inhibition of DNA polymerase, inhibition of the cytochrome P-450 system, and accumulation of pyruvate due to increased rates of glycogenolysis.
Bloodroot extract, which contains the alkaloid sanguinarine, is a strong escharotic that causes cell cycle blockade and apoptosis, especially in cancerous cells.
Both argemone oil and isolated sanguinarine alkaloid have also been reported to be genotoxic in humans, and argemone oil consumption is linked with an elevated incidence of gallbladder carcinoma in India.
Sparteine has been reported to have cardiac, ganglioplegic, and oxytocic effects, while lupinine is anticholinergic. Both have been reported to cause sedation.
Ingestion of poppies may result in narcotic effects from opiate alkaloids and papaverine, as well as hypotension and cardiovascular collapse.
Frequency
United States
Most of the isoquinolines are noxious in smell and taste and discourage ingestion; thus, human toxicity is rare. Interestingly, some domestic species tolerate ingestion of isoquinoline and other alkaloids, and humans can ingest toxic alkaloids from the milk of a poisoned animal and manifest symptoms.
Isolated American and European case reports exist of toxicity following ingestion of improperly washed lupini beans.
Incidence of alkaloid poisoning is low and probably underreported.
International
As mentioned above, outbreaks of argemone oil poisoning are relatively common in India, where it has been used to adulterate more expensive mustard oil. Outbreaks have also been reported in Mauritius, Fiji, Madagascar, and South Africa.
Laburnum poisoning is reported widely in Great Britain and Europe; 50 cases were documented in 1979. One group in Germany, recorded 892 exposures between 1998 and 2004, and, of these, 45 demonstrated moderate or major effects.4 Concern regarding the toxicity of this plant may greatly exceed actual clinical effects in many cases.5,6
Mortality/Morbidity
Mortality is rare. A single adult case of death by Laburnum poisoning was reported in a man with schizophrenia. Mescal bean and other quinolizidine and isoquinoline alkaloids have been documented with sporadic case reports of fatality. Epidemic outbreaks of argemone oil poisoning have led to numerous deaths.
Race
Isoquinoline and/or quinolizidine poisonings are not noted to have increased frequency in any particular race.
Sex
Effects of isoquinoline and/or quinolizidine poisoning are related to dose and not sex.
Age
The toxic alkaloids are concentrated in the pealike or brightly colored seeds in laburnum, mescal bean, and lupine, which children may consume resulting in serious morbidity and mortality.
Clinical
History
- For all ingestions, obtain as complete a history as possible, including the following:
- Medications
- Allergies
- Suspected ingestion
- Time of ingestion
- Possible co-ingestions
- Identify the plant ingested if possible. An on-site plant reference text and established relationship with an emergency plant taxonomy consultant are useful resources.
- Laburnum is a small tree, up to 30 feet tall, that bears golden sweet pea-shaped flowers and seeds in pealike pods. It is found in the southeastern United States and Europe.
- Mescal bean is a shrub or small tree with purple flowers and bright red seeds. It is found in the southwestern United States and Mexico.
- Patients with cytisine ingestion may complain of vomiting, diarrhea, GI cramping, palpitations, confusion, tremor, and weakness.
- Following Sophora root ingestion, patients may complain of excessive salivation, abnormal gait, shortness of breath, muscle spasm, dizziness, palpitations, nausea, vomiting, and constipation. Reduced libido and impotence have been reported, though the association is confounded by other herbs in the formulation. Three case reports of adverse effects after ingestion of 60 g of Sophora root extract suggest that significant toxicity may occur at that dose.7
- Following argemone oil poisoning, patients may complain of whole body swelling, headache, vomiting, diarrhea, and shortness of breath.
- Following ingestion of Lupinus alkaloids, patients may complain of anticholinergic symptoms such as blurry vision, dry mouth, confusion, palpitations, flushing, and fever.
- Following ingestion of poppy seed tea, patients may complain of drowsiness and weakness, which can progress occasionally to respiratory arrest and death.8
Physical
- Cytisine ingestion causes a nicotinic toxidrome with hyperactive bowel sounds, vomiting, diarrhea, fasciculations, weakness, diaphoresis, seizures, coma, and mydriasis.
- Sophora root ingestion may be associated with vomiting, CNS agitation or depression, ataxia, diaphoresis, seizures, and respiratory depression.
- Physical examination following argemone oil ingestion may reveal pitting edema of the extremities, rales or rhonchi consistent with pulmonary edema, and flushing of the skin. Hypotension, vomiting, and diarrhea may be present.
- Exposure to morphine and papaverine from poppy seeds can produce depressed mental status and respiratory failure, as well as miosis and mild hypotension and bradycardia typical of opioid toxidrome.8
Causes
Risk factors for quinolizidine and/or isoquinoline plant toxicity include use of medicinal herbs and/or preparations, recreational drug experimentation (most notably mescal bean and opium poppy), drinking of milk from animals that ingest toxic plants (rare), adulteration of mustard oil (international), and childhood ingestion of ornamental plants (most notably Laburnum).
Differential Diagnoses
| Delirium, Dementia, and Amnesia | Toxicity, Caffeine |
| Hypoglycemia | Toxicity, Clonidine |
| Meningitis | Toxicity, Cocaine |
| Plant Poisoning, Alkaloids - Tropane | Toxicity, Hallucinogen |
| Plant Poisoning, Glycosides - Cardiac | Toxicity, Mushroom - Hallucinogens |
| Plant Poisoning, Herbs | Toxicity, Narcotics |
| Status Epilepticus | Toxicity, Theophylline |
| Toxicity, Amphetamine | Withdrawal Syndromes |
| Toxicity, Anticholinergic | |
| Toxicity, Antidepressant | |
| Toxicity, Antidysrhythmic |
Workup
Laboratory Studies
- Assays for isoquinoline or quinolizidine alkaloids are not routinely available.
- A toxicology screen may be helpful in excluding amphetamine ingestion, but false-positive results may occur.
- Blood chemistries may be useful in assessing for other potential intoxicating ingestions.
- Perform a fingerstick glucose test for altered mental status.
- Perform a complete blood count (CBC), urinalysis, and blood and urine cultures in febrile patients with altered mental status.
- Always consider acetaminophen and salicylate levels in any potential toxic ingestion.
- Always obtain serum or urine human chorionic gonadotropin (HCG) levels in women of childbearing age.
- Draw a baseline liver function panel and CBC if ingestion of C majus (greater celandine) is suspected.
Imaging Studies
- Consider a CT scan of the head in any patient whose altered mental status is not clearly due to toxicity of the ingested substance.
Other Tests
- Obtain an ECG in all patients with possible toxic ingestions to evaluate for tricyclic antidepressant toxicity.
Procedures
- Perform lumbar puncture on any febrile patient with altered mental status if meningitis is considered as a potential diagnosis.
Treatment
Prehospital Care
- Transport the patient to the nearest emergency facility with advanced life support (ALS) capabilities.
- Focus assessment and treatment on ABCs.
- Check serum glucose level and treat if hypoglycemic.
- Consider naloxone if symptoms suggestive of opioid toxidrome are present.
- Obtain intravenous access and provide oxygen and cardiac monitoring.
- Use benzodiazepines to treat seizures.
Emergency Department Care
Emergency care is primarily supportive, focusing in emergency medicine airway, breathing, circulation, disability, and exposure (ABCDEs).
- Provide supplemental oxygen. If CNS or respiratory depression is present, intubate and provide ventilatory support.
- Check serum glucose level and treat if hypoglycemic.
- Consider intravenous naloxone for any patient with altered mental status and an opiate toxidrome.
- The cornerstone of treatment is GI decontamination with activated charcoal (1 g/kg). A single dose usually is adequate.
- Induction of emesis with ipecac syrup provides little benefit and is associated with increased risk of aspiration if the patient's mental status declines.
- Gastric lavage is controversial but may provide maximum benefit when performed within 1 hour of ingestion.
- Supportive care generally is all that is required postdecontamination. Continuous cardiac monitoring and frequent vital sign determinations are warranted.
- The use of diuretics has been suggested for diffuse edema from argemone oil poisoning, but evidence of efficacy has not yet been established. Similarly, antioxidant therapy has been suggested though evidence of efficacy has not yet been established.
Consultations
Consulting a medical toxicologist or poison control center may prove helpful in developing differential diagnoses and identifying toxic ingestion.
Medication
The goals of pharmacotherapy are to reduce toxicity, reduce morbidity, and prevent complications.
GI decontaminant
Activated charcoal is the treatment of choice for all quinoline and/or isoquinoline plant ingestions. It is the most effective substance known for adsorbing most poisons. Ipecac syrup administered as a precursor to charcoal is no longer recommended, and gastric lavage has limited use.
Activated charcoal (Actidose-Aqua, Liqui-Char)
Adsorbs toxic alkaloids.
Dosing
Adult
1 g/kg PO or via NG tube; consider repeat dose 0.5 g/kg 3-4 h after initial dose (usually not indicated in plant toxicity); may administer first dose with sorbitol (cathartic)
Pediatric
<2 years: Not recommended
>2 years: 0.5-1 g/kg PO or via NG tube
Interactions
Repeat doses may enhance elimination of therapeutic drugs (eg, benzodiazepines)
Contraindications
GI obstruction
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Intubate patient prn for airway protection
Benzodiazepines
Benzodiazepines are agents of choice for cytisine-induced or other alkaloid-induced seizures.
Lorazepam (Ativan)
Beneficial for sedative and anticonvulsant effects.
Dosing
Adult
0.05 mg/kg (2-4 mg) IV at 2 mg/min, titrate to effect
Status epilepticus: 4 mg IV over 2-5 min; may repeat second dose in 10-15 min prn
Pediatric
Children: 0.05 mg/kg IV (range 0.02-0.1 mg/kg)
Adolescents: Administer as in adults
Status epilepticus:
Neonates: 0.05 mg/kg over 2-5 min; may repeat in 10-15 min prn
Infants and children: 0.1 mg/kg over 2-5 min; second dose of 0.05 mg/kg IV at 10-15 min prn; single dose not to exceed 4 mg
Adolescents: 0.7 mg/kg IV slowly over 2-5 min; second dose in 10-15 min prn
Interactions
Toxicity in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs
Contraindications
Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Monitor neurologic status, protect airway, and monitor cardiovascular status; caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease; contains benzyl alcohol, which may be toxic to infants in high doses
Diazepam (Valium)
Also beneficial for sedative and anticonvulsant effects. Half-life relatively long; may give IM if no IV access.
Dosing
Adult
0.15 mg/kg IV; repeat in 10-15 min prn
Pediatric
0.15 mg/kg IV; may repeat dose in 10-15 min prn; alternatively, 0.3-0.5 mg/kg PR; may repeat in 4-12 h prn
Interactions
Additive sedative and hypotensive effects with narcotics, psychotropics, and many other drugs
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Monitor neurologic status, protect airway, and monitor cardiovascular status
Antidotes for opiate agonists
These agents are used in patients with altered mental status and opiate toxidrome.
Naloxone (Narcan)
Prevents or reverses opioid effects (hypotension, respiratory depression, sedation), possibly by displacing opiates from their receptors.
Dosing
Adult
0.4-2 mg IV/IM/SC q2-3min prn; use increments of 0.05-0.1 mg in patients with opioid dependency; may need to repeat dose q20-60min; if no response observed after administering 10 mg, question diagnosis
Pediatric
0.1 mg/kg IV/IM/SC; repeat q2-3min prn
Interactions
Decreases analgesic effects of narcotics
Contraindications
Documented hypersensitivity
Precautions
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cardiovascular disease; naloxone may precipitate withdrawal symptoms in patients with opiate addiction
Follow-up
Further Inpatient Care
- Patients with no signs of neurologic or cardiovascular involvement may be discharged from the hospital after 6 hours of observation.
- Admit any patient with altered mental status, seizure activity, or cardiovascular instability to an intensive care unit (ICU) setting for observation and further treatment as needed.
- Draw a baseline liver function panel and CBC if ingestion of C majus (greater celandine) is suspected, and refer the patient for follow-up repeat liver function test and CBC.
Further Outpatient Care
- Ensure close follow-up care with a pediatrician or internist and instruct a responsible individual to return the patient to the emergency department immediately if altered mental status, seizure, vomiting, or any other concerns arise.
- Caution against further ingestion of herbal medications. Family members of intoxicated children should be instructed to remove offending plants from their landscaping.
Complications
- Most patients with quinolizidine and/or isoquinoline plant ingestions do well and are discharged from the emergency department after a period of observation.
- Patients with systemic symptoms require admission and close observation to prevent morbidity or mortality.
- Rarely, seizure, cardiovascular collapse, and aspiration secondary to emesis may complicate care.
- Celandine has been reported to have significant hepatotoxicity.
Prognosis
- Most patients recover fully and are discharged from the emergency department.
Patient Education
- Educate families regarding common household plant toxicity. Tailor education to individual ingestions.
Miscellaneous
Medicolegal Pitfalls
- As with any ingestion, consider co-ingestions, especially those that are potentially serious and treatable (eg, tricyclics, acetaminophen).
- Consider all possible causes for altered mental status, including infectious diseases such as meningitis and encephalitis.
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Keywords
plant poisoning, plant toxicity, alkaloids, quinolizidine, isoquinoline, Baptisia species, false indigo, Cytisus species, scotch broom, Laburnum species, goldenchain, laburnum, Lupinus species, lupine, bluebonnet, Sophora species, mescal bean, frijolito, Argemone species, prickly poppy, Chelidonium species, celandine poppy, Corydalis species, fitweed, Dicentra species, dutchman's breeches, Papaver species, poppy, Sanguinaria species, bloodroot
Contributor Information and Disclosures
Author
David Vearrier, MD, Fellow, Department of Toxicology, Drexel University College of Medicine
David Vearrier, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and American College of Occupational and Environmental Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Richard J Hamilton, MD, FAAEM, FACMT, Chairman, Department of Emergency Medicine, Drexel University College of Medicine
Richard J Hamilton, MD, FAAEM, FACMT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Medical Editor
Michael S Beeson, MD, MBA, FACEP, Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine; Program Director, Emergency Medicine Residency, Summa Health System
Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Pharmacy Editor
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.
Managing Editor
Michael Hodgman, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare
Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society
Disclosure: Nothing to disclose.
CME Editor
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
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Chief Editor
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
Disclosure: Nothing to disclose.