Poisoning by Plant Resin 

Updated: Feb 12, 2019
Author: Hagop A Isnar, MD, FACEP; Chief Editor: Asim Tarabar, MD 

Overview

Practice Essentials

Plants have evolved highly complex systems of defense against most of their natural enemies (eg, insects, animals). At the very least, these defenses make many plants unpalatable; however, some can be fatal to the inexperienced forager.[1]  Resins represent one form of plant defense. See the image below.

Hemlock. Photo by Cornell University Poisonous Pla Hemlock. Photo by Cornell University Poisonous Plants Informational Database.

Throughout human history, plants have played pivotal roles as medicines and poisons. Our medical predecessors may not have known the exact mechanisms involved, but they did recognize various plants as instrumental for medical treatment and as instruments of murder. With current technology, we finally are able to peer into plants and see their vast arsenal of chemicals, including glycosides, alkaloids, oxalates, and resins.

A rapid toxidromic classification of plant poisonings has been developed for use by first responders and other urgent-healthcare providers to assist in rapid identification of poisonous plant–induced toxidromes and to reduce confusion among highly toxic, less toxic, and nontoxic plants. The resultant 4 specific toxidromes of plant poisonings identified in the scientific literature are stratified as cardiotoxic, neurotoxic, cytotoxic, and gastrointestinal/hepatotoxic poisonings, all of which have caused fatalities worldwide after both intentional and unintentional ingestions.[2]

When considering poisoning by plant resin, always be aware of possible co-intoxicants, which may blur the clinical picture. Such co-intoxicants include pharmaceutical and illicit drugs, herbicides, fungicides, insecticides, fertilizers, and artificial plant hormones.

Examples of unintentional toxic plant ingestion include the following:

  • Hikers who mistake poisonous plants for nutritious ones

  • Herbalists who seek natural remedies or natural highs and end up with poisonous concoctions

  • Children who are attracted to brightly colored fruits and leaves of poisonous plants (this group accounts for the most calls to poison centers regarding plant toxicity)

See 11 Common Plants That Can Cause Dangerous Poisonings, a Critical Images slideshow, to help identify plant reactions and poisonings. For patient education information, see the First Aid and Injuries Center, as well as Poisoning and Activated Charcoal.

Pathophysiology

Resins are a diverse group of chemical compounds that share chemical characteristics, such as insolubility in water, solidity at room temperature, and lack of a nitrogen group. Resin compounds formed with sugars are called glycoresins; those formed with oils are called oleoresins. Latex is a term used to describe these toxins when found in emulsions (ie, urushiols, which are catechol derivatives)[3] in ducts of plants. They are released and activated when structural damage to the plant occurs.

Epidemiology

While some individuals ingest toxic plants to attempt suicide, most present to the emergency department after unintentional toxic plant ingestion.

The 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS) documented 46,782 plant exposures. The 25 most commonly involved plant species and categories account for 40.6% of all reported plant exposures. Three of the top 5 categories are for unknown plants and comprise 10.6% of exposures. This reflects the difficulty in identification. See the following[4] :

  • Cherry (not otherwise specified) – 2006 exposures
  • Plants, general unknown – 1986
  • Unknown botanical name (unknown toxic types or unknown if toxic) – 1627
  • Botanical terms unknown – 1338
  • Phytolacca americana (L) – 1300
  • Plants, toxicodendrol – 1131
  • Spathiphyllum spp – 862
  • Plants, pokeweed – 856
  • Plants (cardiac glycosides) – 832
  • Ilex spp (not otherwise specified) – 745
  • Berry (not otherwise specified) – 572
  • Malus spp – 524
  • Solanum nigrum – 503
  • Plants, oxalates – 472
  • Caladium spp – 461
  • Euphorbia tirucalli (L) – 458
  • Zantedeschia aethiopica – 444
  • Philodendron spp – 433
  • Unknown botanical name (non-toxic) – 417
  • Solanum dulcamara – 405
  • Mold, food related – 384
  • Epipremnum areum – 381
  • Solanum tuberosum  – 300
  • Crassula argentea  – 276
  • Taxus canadensis  – 265

Approximately 60% of plant exposures reported to poison centers in 2017 involved children younger than 6 years.[4]

 

Presentation

History

Most plants involved in exposures reported to poison control centers are identified. However, plants often remain unidentified when patients come to the ED because of concern regarding plant ingestion or symptoms following plant ingestion or exposure.

Because toxic principles of plants may vary greatly by season and geography, systematic evaluation is invaluable for determining the etiology of the patient's symptoms and identifying the potential plant toxin. Generally, this is the case when describing circumstances surrounding the toxicity to the poison center or consulting toxicologist over the telephone.

Emergency physicians must obtain accurate history to determine extent of exposure and subsequent risk of disease. The following items may provide important information:

  • Name of plant (note that common names vary considerably by region)

  • Actual plant (if available, allows for detailed description of features)

  • Amount ingested or exposed

  • Duration of time since exposure

  • Initial symptoms and time between exposure and symptom onset

  • Past medical history, current medication, and allergies (These may alter host response and risk.)

Physical Examination

A thorough examination focusing on existence or development of toxidromes (eg, anticholinergic syndromes, nicotinic syndromes) may be helpful in identifying the general class of toxin(s). It is very important to repeat this evaluation over time (generally several hours) to follow the evolution of symptoms and response to treatment.

Many plants cause nonspecific gastrointestinal upset. Possible poison hemlock ingestion (see image below) is suggested when gastrointestinal upset is accompanied by early onset of increased secretions followed by nicotinic syndromes such as respiratory difficulty, altered mental status, and possibly seizures.

Hemlock. Photo by Cornell University Poisonous Pla Hemlock. Photo by Cornell University Poisonous Plants Informational Database.

Plant ingestion alone is unlikely to cause isolated altered mental status.

Physicians must always consider other causes of acute altered mental status, such as hypoglycemia, co-ingestants, concomitant trauma, or infection.

 

DDx

 

Workup

Laboratory Studies

Laboratory studies have little use in the treatment of any patient with acute plant poisoning; however, the studies may be helpful in attempts to exclude other causes of a patient's presentational signs and symptoms.

Evaluate any alteration in mental status with a rapid glucose determination, assessment of oxygenation status, and investigation of other potential causes such as trauma or infection.  Other studies, such as electrolyte determination, renal and hepatic function tests, and urinalysis, may be useful in certain situations but rarely alter treatment of exposure to a known toxic plant.

Obtaining a serum acetaminophen concentration is recommended for any suicidal ingestion. In absence of significant signs or symptoms, a urine drug screen rarely is useful clinically.

Other Tests

Electrocardiogram (ECG) and rapid potassium determination are indicated when bradycardia and/or hypotension are present.

 

Treatment

Prehospital Care

Plant parts or information regarding surroundings obtained by prehospital providers may be helpful in identifying the suspected toxin.

Rinse mouth in cases of mucosal irritation to help alleviate symptoms. Induced vomiting with ipecac syrup is discouraged, particularly in cases with potential for altered mental status.

Emergency Department Care

Airway, breathing, and circulation must, above all else, be ensured. Remove any remaining toxin. Ipecac syrup is not recommended. Gastric lavage is unlikely to be effective for removal of plant parts. Activated charcoal may be of benefit, particularly if administered within the first several hours; however, it may be of little benefit with rapidly absorbed substances such as teas.

Hemodialysis has not been proven clinically effective in removing any plant toxin.

Carefully monitor urine output in systemically ill patients because many plant toxins result in GI fluid losses and/or third-spacing of fluid.

Toxicodendron species

An estimated 70% of the population are sensitized to allergens found in the Toxicodendron species, which include poison ivy (see first and second images below), poison oak (see third image below), and poison sumac (see last image below).[5]

Poison ivy. Photo by Cornell University Poisonous Poison ivy. Photo by Cornell University Poisonous Plants Informational Database.
Poison ivy. Photo from the Centers for Disease Con Poison ivy. Photo from the Centers for Disease Control and Prevention.
Poison oak. Photo by Cornell University Poisonous Poison oak. Photo by Cornell University Poisonous Plants Informational Database.
Poison sumac. Photo by Cornell University Poisonou Poison sumac. Photo by Cornell University Poisonous Plants Informational Database.

These plants cause potentially severe contact dermatitis. The allergenic substance of Toxicodendron species is found in the milky white sap that is distributed throughout the plant, seed, flowers, and berries. A unique characteristic of the emulsion found in all Toxicodendron species is the color change from milky white to black lacquer upon exposure to air for several minutes. This spot test is not recommended for routine identification because of inherent risk of exposure (see Plant Poisoning, Toxicodendron).

Contact dermatitis develops within 48 hours for most exposures. Highly sensitized individuals develop eruptions within 8 hours. Eruptions often appear in a linear pattern, indicating that a portion of bruised plant was rubbed across the skin when handled or trampled.

Poison oak rash. This photograph depicts an indivi Poison oak rash. This photograph depicts an individual's arm with a blistering poison oak rash. Note the linear pattern to the lesions. Hardin Library for the Health Sciences, University of Iowa Public Domain Picture (http://www.lib.uiowa.edu/haRDIN/MD/cdc/4484.html) and Centers for Disease Control and Prevention.

Symptoms at presentation range from mild erythema to papules, vesicles, and bullae. Although once believed to contain the allergen, vesicular fluid cannot transmit contact dermatitis. Systemic distribution of toxin may cause diffuse urticaria or erythema multiforme[6] .

In mild cases involving only erythema and papules, a topical lotion of calamine or steroid cream and an oral antihistamine may be used.

Severe cases require more aggressive therapy. Topical therapy for such cases includes the following:

  • Aluminum sulfate (1:10 diluted in water) compressed for 30 minutes 3 times a day to dry blisters and relieve itching

  • Potassium permanganate soaks to dry blisters (one-half tablespoon in a tub of water for 20 min/d)

In severe cases, oral corticosteroids may be required and should be tapered over 2-3 weeks. A shorter duration of therapy is associated with rebound dermatitis.

Symptoms in severe cases should be cleared within 3 weeks; symptoms in milder cases may last only 10 days.

Possible sequelae include hyperpigmentation over the area of eruption.

After contact with poison ivy, washing the exposed area as well as hands and clothes with soap and water within 30 minutes of exposure greatly reduces the risk of developing contact dermatitis.[7]

Weekly follow-up visits are recommended to document the progress of treatment.

Water hemlock

Cicuta maculate and most other species of Cicuta are similar in appearance and grow to heights of 6 ft. The sap is a yellow oily compound with a parsnip scent and contains cicutoxin, a long chained aliphatic alcohol. Cicutoxin is distributed throughout the plant, with the highest concentration in the tuberous roots. One mouthful of root is sufficient to kill a grown man, and toxicity has been documented after dermal contact. These plants are found in wet swamplands throughout the United States and are the most toxic plants in Alaska (see image below).

Hemlock. Photo by Cornell University Poisonous Pla Hemlock. Photo by Cornell University Poisonous Plants Informational Database.

Cicutoxin has a parasympathomimetic action when ingested and produces symptoms in 15-60 minutes. Muscarinic actions manifest as abdominal pain, vomiting, diarrhea, trismus, and hypersalivation. More central effects manifest as central nervous system depression, respiratory distress, and possibly tonic-clonic seizures. Death is usually secondary to respiratory arrest. In a symptomatic patient, close monitoring of respiratory status is essential.

Pay particular attention to the patient's airway and respiratory status. Treatment is mostly supportive. Benzodiazepines are recommended for control of seizures. Treatment with anticholinergics has not been proven effective in animal models.

Consider creatine kinase measurements; the combination of seizures with resultant rhabdomyolysis and gastrointestinal fluid losses place the patient at risk for oliguric renal failure. Given the GI losses, closely monitoring the patient's fluid balance is needed.

Chinaberry

Melia azedarach is a tree that may grow to a height of 50 ft. The leaves are serrated with 2-inch long leaflets. The flowers are scented, purplish, and grow in clusters. Chinaberry trees produce yellow berries that persist after the leaves are shed; they contain 3-5 smooth black seeds. Chinaberry trees grow in the South from Virginia to Florida to Texas and Hawaii.

A recently identified neurotoxin (tetranortriterpene) and an unidentified gastroenteric toxin are concentrated in the berry and bark of chinaberry. Ingestion of 6-8 berries has been reported to cause fatality in a young child.

Prolonged latent period is followed by development of mental confusion, ataxia, dizziness, and stupor. Some patients may develop intense vomiting and bloody diarrhea, which results in hypovolemic shock. Reports of respiratory depression, seizures, and paralysis also exist. In some autopsies, fatty degeneration of the liver has been observed.

Supportive care with fluid and electrolyte replacement is indicated.

Given the possibility of hepatic fatty degeneration, monitoring liver function is important.

Daphne

Daphne are deciduous round shrubs growing to heights of 4-5 ft. Elliptical leaves with purple or white flowers grow in clusters before the appearance of leaves. Although most exposure is due to the yellow fruit and pits of daphne, the entire plant is poisonous. Ingestion of only a few daphne fruits can be fatal to a young child. Daphne are cultivated throughout the United States and are naturalized to the northeastern United States and Canada (see image below).

Daphne. Photo by Cornell University Poisonous Plan Daphne. Photo by Cornell University Poisonous Plants Informational Database.

Ingestion of daphne causes vesication and edema of the mouth, lips, and pharynx with secondary hypersalivation and dysphagia. Subsequent symptoms include extreme thirst, abdominal pain, vomiting, and bloody diarrhea.

Daphnetoxin may cause organ damage, usually due to hypovolemia and electrolyte imbalance; therefore, the kidneys are particularly at risk for damage secondary to acute tubular necrosis.

Fluid and electrolyte balance is critical to prevent a potentially lethal outcome.

Consultations

Consult a medical toxicologist and/or regional poison center for further assistance.

Prevention

Pharmaceutical companies and the United States military actively research protective agents to prevent contact dermatitis from resin skin exposure.

Hylands produces an over-the-counter barrier product called Ivyblock, which is reported to prevent dermatitis preexposure. The active ingredient is bentoquatam (5%). It must be applied before possible exposure and reapplied at least every 4 hours. It may give the user a false sense of security since it may wash or be wiped off easily. It should be applied 15 minutes before risk of exposure. In adults and children aged 6 years and older, apply every 4 hours for continued protection or sooner if needed.

Oral or injectable forms of the resin have been studied in the past in order to desensitize the individual. Results were inconsistent at best. Diluted forms of the resin for oral ingestion can be found in the food supplement section of pharmacies. This is not approved by the US Food and Drug Administration. Past reports have documented individuals chewing on the leaves in order to desensitize the individual, which clearly has potentially dangerous consequences.

 

Medication

Medication Summary

Medical care of poisoning is primarily symptomatic in nature. Gastric decontamination may benefit by reducing the absorbed dose.

GI decontaminants

Class Summary

These agents are the preferred method when GI decontamination is desired. They are generally mixed and given with a cathartic (eg, 70% sorbitol), except in young pediatric patients in whom electrolyte disturbances may be of concern.

Activated charcoal (Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.

For maximum effect, administer within 30 min of ingesting poison.

Antihistamines

Class Summary

Competitive histamine antagonists minimize severity of hypersensitivity response.

Diphenhydramine (Benadryl)

For symptomatic relief of symptoms caused by release of histamine in allergic reactions.

Hydroxyzine (Vistaril, Atarax)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Sedating, alternative to diphenhydramine.

Benzodiazepines

Class Summary

These agents are used to abort seizures, if present.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life.

By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.

Monitoring patient's blood pressure after administering dose is important. Adjust prn.

Corticosteroids

Class Summary

These agents are useful for contact dermatitis.

Prednisone (Deltasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Methylprednisolone (Solu-Medrol, Depo-Medrol)

Useful to treat inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.

Multiple corticosteroid preparations are available. Widely available in the ED because of its other uses (ie, acute asthma, spinal cord injury) and is supplied in both parenteral and oral formulations and is therefore discussed here as a typical drug of this class.