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Emergency Medicine > TOXICOLOGY
Plant Poisoning, Resins
Article Last Updated: Nov 30, 2006
AUTHOR AND EDITOR INFORMATION
Section 1 of 11  
Author: Hagop A Isnar, MD, FACEP, Associate Medical Director, Consulting Staff, Department of Emergency Medicine, Auburn Memorial Hospital
Hagop A Isnar is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine
Coauthor(s):
Charles McKay, MD, Chief, Toxicology Section, Department of Traumatology and Emergency Medicine, Hartford Hospital
Editors: Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; Michael Hodgman, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare; 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:
glycoresins, oleoresins, urushiols, poisonous plants, poisonous plant exposures, plant toxin, Toxicodendron species, poison ivy, poison oak, poison sumac, contact dermatitis, Cicuta maculata, water hemlock, cicutoxin, chinaberry, Melia azedarach, tetranortriterpene, daphne, daphnetoxin, plant poisoning, resins, plant resins, toxic plant ingestion, resin skin exposure
Background
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.
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.
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.)
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 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) in ducts of plants. They are released and activated when structural damage to the plant occurs.
Frequency
United States
While some individuals ingest toxic plants to attempt suicide, most present to the ED after unintentional toxic plant ingestion.
The American Association of Poison Control Centers (AAPCC) documented 74,811 plant exposures in 2004. This represented approximately 3.1% of all exposures reported to poison centers. Plant exposure was the 7th most commonly reported exposure in children younger than 6 years, and it was ranked 11th (3.1%) of all human exposure reports in 2004.
The following list details the top 20 plant exposures reported by the AAPCC in 1998. Note that only a few of these frequent plant exposures are considered to be significantly toxic (indicated by *); many cause only mucosal or gastrointestinal irritation.
Common name (reported exposures in 1998)
- Pepper (5374)
- Philodendron* (4061)
- Holly* (3441)
- Peace lily (3350)
- Poinsettia (3296)
- Pokeweed, inkberry (2861)
- Dumbcane* (2141)
- Poison ivy* (1697)
- Jade plant (1619)
- Pothos, devil's ivy* (1250)
- Chrysanthemum (1093)
- English ivy* (1083)
- Yew* (1046)
- Rhododendron, azalea* (1028)
- Eucalyptus* (1027)
- Dandelion (948)
- Christmas cactus (886)
- Climbing nightshade (876)
- Apple seeds (844)
- Pyracantha (830)
Mortality/Morbidity
Five deaths were reported in 2004, which represents 0.007% of all plant exposures.
- Of all plant exposures reported, only 30% had outcomes reported. Sixty-six percent of the reported outcomes were asymptomatic.
- Ninety-five percent of all plant exposures reported were unintentional.
Age
Approximately 74% of plant exposures reported to poison centers in 2004 involved children younger than 6 years.
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
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 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 (see Image 1).
- 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.
Alcohol and Substance Abuse Evaluation
Dermatitis, Atopic
Dermatitis, Contact
Dermatitis, Exfoliative
Erythema Multiforme
Gastroenteritis
Plant Poisoning, Herbs
Plant Poisoning, Oxalates
Plant Poisoning, Phytophototoxins
Toxicity, Anticholinergic
Toxicity, Organophosphate and Carbamate
Other Problems to be Considered
Plant poisoning
Essential (volatile) oils (irritants)
Lab Studies
- Laboratory studies have little use in the treatment of any patient with acute 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.
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.
- Generally, induced vomiting with ipecac syrup is not encouraged, 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 Images 3-4), poison oak (see Image 5), and poison sumac (see Image 6). 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. 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.
- 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.
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 1). 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.
- 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 2). 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.
Medical care of poisoning is primarily symptomatic in nature. Gastric decontamination may benefit by reducing the absorbed dose.
Drug Category: GI decontaminants
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.
| Drug Name | Activated charcoal (Liqui-Char) |
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| Description | 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. |
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| Adult Dose | 1 g/kg (30-100 g) PO |
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| Pediatric Dose | 1-2 g/kg (15-30 g) PO |
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| Contraindications | Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalies; unprotected airway with absent gag reflex |
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| Interactions | May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases adsorptive properties) |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administering activated charcoal; after emesis with ipecac, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; monitor for presence of bowel sounds to minimize risk of charcoal ileus |
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Drug Category: Antihistamines
Competitive histamine antagonists minimize severity of hypersensitivity response.
| Drug Name | Diphenhydramine (Benadryl) |
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| Description | For symptomatic relief of symptoms caused by release of histamine in allergic reactions. |
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| Adult Dose | 25-50 mg PO q4-6h |
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| Pediatric Dose | 5 mg/kg/d PO divided qid |
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| Contraindications | Documented hypersensitivity; MAOIs; anticholinergic plant toxicity |
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| Interactions | Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction; may cause drowsiness |
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| Drug Name | Hydroxyzine (Vistaril, Atarax) |
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| Description | Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Sedating, alternative to diphenhydramine. |
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| Adult Dose | 25-50 mg PO q4-6h |
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| Pediatric Dose | 2-4 mg/kg/d PO divided q6h |
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| Contraindications | Documented hypersensitivity |
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| Interactions | CNS depression may increase with alcohol or other CNS depressants |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Associated with clinical exacerbations of porphyria (may not be safe for patients with porphyria); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness |
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Drug Category: Benzodiazepines
These agents are used to abort seizures, if present.
| Drug Name | Diazepam (Valium) |
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| Description | Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. |
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| Adult Dose | 5-10 mg IV q10-15min until symptoms resolve; not to exceed 30 mg |
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| 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 |
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| Contraindications | Documented hypersensitivity; acute narrow-angle glaucoma |
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| Interactions | Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs |
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| Pregnancy | D - Unsafe in pregnancy
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| Precautions | Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity) |
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| Drug Name | Lorazepam (Ativan) |
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| Description | 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. |
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| Adult Dose | 2-8 mg IV/IM; titrate to effect |
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| Pediatric Dose | 0.05 mg/kg IV/IM |
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| Contraindications | Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma |
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| Interactions | Toxicity in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs |
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| Pregnancy | D - Unsafe in pregnancy
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| Precautions | Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease |
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Drug Category: Corticosteroids
These agents are useful for contact dermatitis.
| Drug Name | Prednisone (Deltasone) |
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| Description | May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. |
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| Adult Dose | 40-60 mg PO qd; taper over 2-3 wk |
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| Pediatric Dose | 1-2 mg/kg PO qd; taper over 2-3 wk |
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| Contraindications | Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease |
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| Interactions | Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics |
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| Pregnancy | B - Usually safe but benefits must outweigh the risks.
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| Precautions | Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use |
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| Drug Name | Methylprednisolone (Solu-Medrol, Depo-Medrol) |
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| Description | 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. |
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| Adult Dose | 2-60 mg PO qd
40-250 mg IV/IM q6h |
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| Pediatric Dose | 1-2 mg/kg PO qd
1-2 mg/kg IV/IM q6h |
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| Contraindications | Documented hypersensitivity; some evidence indicates fetal harm from corticosteroids, so benefits and risks should be considered for use during pregnancy; immunosuppressed patients receiving corticosteroids are at risk for dissemination, activation, or certain infections, and this should be considered when prescribing for these patients |
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| Interactions | NSAIDs may cause ulcers when taken concurrently; anticholinesterases may increase weakness in patients with myasthenia gravis when taken concurrently with steroids; risk exists of possible viral dissemination with live-virus vaccines |
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| Pregnancy | C - Safety for use during pregnancy has not been established.
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| Precautions | Short-term use of corticosteroids, even in large doses, has minimal harmful effects; long-term usage has multiple adverse effects
Possible complications include hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections |
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Further Inpatient Care
- Water hemlock
- Symptoms of cicutoxin should manifest within 2 hours of observation in the ED.
- In a symptomatic patient, close monitoring of respiratory status is essential.
- Care is mostly supportive with particular attention to fluid balance (because of GI loss); benzodiazepines are used for possible seizures.
Further Outpatient Care
- Toxicodendron
- With most cases involving outpatient treatment, complete resolution of symptoms should occur within 3 weeks of therapy.
- Complications include infection and hyperpigmentation of the involved area.
- Weekly follow-up visits are recommended to document the progress of treatment.
Deterrence/Prevention
- Currently, pharmaceutical companies and the United States military actively research protective agents to prevent contact dermatitis from resin skin exposure.
Patient Education
Medical/Legal Pitfalls
- Failure to consider, exclude, and treat other causes of acute altered mental status such as occult trauma or infection
- Failure to appreciate the potentially severe gastrointestinal and other toxicities that may result from exposure to plants such as chinaberry and nicotinic plant species
- Incorrectly identifying plants leading to inadequate observation, evaluation, and treatment
- In 1998, 19% of calls to American poison control centers regarding plant exposures were coded as "unknown plant."
- Plant identification over the telephone may be difficult.
- Identification of plant parts by individuals at plant nurseries and gardening stores is accurate in fewer than 50% of cases, and botanists are unable to identify approximately 25%, often secondary to inadequate sample.
- Relying on pictures in an atlas is just as problematic.
- While software programs exist that will guide the user through a systematic plant identification scheme leading to accurate classification in most cases, these programs are not widely available and are somewhat cumbersome for use in an emergency setting.
- In some cases, a cautious tentative identification can be made in consultation with poison control centers with special interest in botanical exposures. This is particularly worthwhile in cases with potentially delayed toxicity or lack of correlation of observed symptoms with the presumed identity of the plant.
- Failure to recognize significant toxicity related to toxic plants that are indigenous to the patient's geographic location
| Media file 1:
Hemlock. Photo by Cornell University Poisonous Plants Informational Database. |
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| Media file 2:
Daphne. Photo by Cornell University Poisonous Plants Informational Database. |
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| Media file 3:
Poison ivy. Photo by Cornell University Poisonous Plants Informational Database. |
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| Media file 4:
Poison ivy. Photo from the Centers for Disease Control and Prevention. |
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| Media file 5:
Poison oak. Photo by Cornell University Poisonous Plants Informational Database. |
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| Media file 6:
Poison sumac. Photo by Cornell University Poisonous Plants Informational Database. |
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Plant Poisoning, Resins excerpt Article Last Updated: Nov 30, 2006
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