Version May 2024
INTRODUCTION — Children are frequently exposed to potentially toxic plants both in the home and outdoors. Since children are curious and readily explore their environment, it is no surprise that they often ingest plant parts such as leaves, seeds, berries, and flowers. While these exposures rarely result in clinically significant poisoning, it is important for health care providers to be aware of the limited number of plants that have the potential to cause significant poisoning and their clinical effects.
This topic will discuss the clinical manifestations and evaluation of toxic plant ingestion in children. The treatment of plant or mushroom poisoning and the clinical manifestations and evaluation of mushroom poisoning are discussed separately. (See "Toxic plant ingestions in children: Management" and "Management of mushroom poisoning (except amatoxin-containing mushrooms)" and "Clinical manifestations and evaluation of mushroom poisoning" and "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment".)
EPIDEMIOLOGY — Potentially toxic plant ingestions occur frequently in children, but serious toxicity is rare as indicated by the following longitudinal studies:
●Of approximately 500,000 toxic plant ingestions in children ≤5 years of age reported to United States poison control centers over 10 years, more than 90 percent of children had minimal or no effects, and only one child died as a result of an exploratory ingestion [1].
●Of almost 60,000 potentially toxic plant ingestions in children under 15 years of age reported to German poison information centers, 90 percent had no effects at the time of the call, 9 percent had minimal effects, and less than 1 percent had moderate or major effects [2].
●Among 25,000 cases of plant exposure reported to the Swiss Toxicological Information Center, 99 percent of patients remained asymptomatic, had minor effects, or had unknown outcomes. Severe plant poisoning occurred in only 152 patients [3].
●Of over 2700 plant poisoning calls to a regional poison control center in Australia, most patients were asymptomatic or had mild toxicity. Moderate or severe toxicity occurred in <1 percent of cases and typically occurred in adults [4].
The most common plant ingestions reported to United States poison control centers include peace lily, holly, philodendron, and poinsettia (table 1) [1]. These and the other most frequently ingested potentially poisonous plants produce few, if any, significant toxic side effects. Approximately 95 percent of unintentional potentially toxic plant ingestions reported to United States poison control centers are managed at home [1].
Serious toxicity, including death, occurs most frequently in adolescents and adults. Common scenarios include:
●Recreational use or accidental foraging of atropine-containing plants (eg, Atropa belladonna, Datura species [jimsonweed, angel's trumpet]) [1-3,5]
●Mistaking the roots of the epileptogenic plants Cicuta maculata (water hemlock) or Oenanthe crocata (hemlock water dropwort) for wild carrots, parsnip, ginseng, or turnip [6-8]
●Ingestion of known toxic species (eg, yellow oleander [Thevetia peruviana]) with suicidal intent [1,9]
PLANT TOXICITY — Toxic plants contain numerous chemical components, such as toxic alkaloids, glycosides, terpenes, proteins, lectins, phenols, and phenylpropanoids [10]. The amount of toxin ingested is determined by several factors, including:
●Part of the plant consumed – For many poisonous plants, the roots and stems have higher concentrations of toxins than flowers or berries [11]. However, notable exceptions include:
•The skin of the castor bean (Ricinus communis) has high levels of the deadly toxin ricin, while the flesh of the seed is used to make castor oil.
•Rhubarb stems (Rheum rhabarbarum) are frequently eaten, but their leaves are toxic.
●Method of consumption – In some instances, boiling portions of a plant into a tea extracts and concentrates the toxin (eg, pokeweed [Phytolacca americana]) [12]. In other cases, mastication of seeds releases the toxin, such as amygdalin from apricot pits or ricin from castor bean seeds (Ricinus communis) [13,14]. Plant toxins from poisonous flowers (eg, Digitalis purpurea [foxglove]) may also contaminate water in vases [15].
●Local conditions – Within species, plant toxicity may vary by season, soil conditions, and region.
●Growth stage of the plant – The toxicity of various parts of some plants changes depending on the age of the plant. As an example, ackee fruit (Blighia sapida) is far more toxic when the fruit is not ripe [16]. (See 'Hypoglycemia and encephalopathy' below.)
Specific plant toxins lead to recognizable plant poisoning syndromes as described below.
CLINICAL MANIFESTATIONS OF POISONING — Most young children are asymptomatic or have minimal gastrointestinal toxicity after exploratory plant ingestions. Serious poisoning is associated with a large ingestion of highly toxic plant species (table 2), which is typically in the setting of suicidal ingestion, foraging mistakes, or intentional recreational use.
Nontoxic — Many exploratory plant ingestions in children ultimately involve consumption of nontoxic species (table 3). Even when potentially toxic plants are ingested, most small exploratory exposures in children result in minimal or no toxicity.
Gastrointestinal toxicity — Gastrointestinal irritation is the most common clinical effect associated with toxic plant exposure in children. In most patients, symptoms are mild and self-limited [15].
Mucosal irritation and swelling — Plants of the Araceae family (eg, philodendron, dieffenbachia [dumbcane]) and others such as Spathiphyllum species (peace lily), Arisaema triphyllum (Jack-in-the-pulpit), rhubarb (leaf only), Colocasia esculenta (elephant ear), and Symplocarpus foetidus (skunk cabbage) contain calcium oxalate in the form of intracellular sharp projections called raphides [17,18]. In some plants (eg, dieffenbachia), many raphides are bundled with proteolytic enzymes into idioblasts. When the plant is chewed, the raphides are injected into the mucosa along with proteolytic enzymes and can cause localized irritation and swelling. Most typical exposures in children are asymptomatic or result in only minor, temporary irritation [17,19,20]. Rarely, significant oral swelling, dysphagia, and drooling with concern for airway obstruction can occur [21]. In one child, esophageal lesions progressed to stricture after ingestion of philodendron [22].
Minor gastrointestinal irritation — Many plants can cause self-limited nausea, vomiting, and diarrhea, which either require no therapy or respond to supportive measures. The most common of these toxic plants include:
●Bulbs of the Amaryllidaceae family (narcissus, daffodil, and amaryllis) [23,24]
●Plant berries from Ilex (holly), Phoradendron flavescens (American mistletoe), and Pyracantha species; ingestion of fewer than six berries typically requires no therapy [25,26]
●Poinsettia [27]
Acute gastroenteritis — Ingestion of uncooked leaves or unripe berries of the pokeweed plant (Phytolacca americana) can cause severe gastroenteritis and, occasionally, hemorrhagic gastritis [10,11,28-30]. Symptoms typically occur within six hours of consumption. Most serious poisonings involve drinking concentrated teas as a folk remedy for rheumatism or eating improperly prepared salad greens. Pokeweed also contains a mitogen that can cause a self-limited plasmacytosis occurring up to four days after poisoning [31]. Pokeweed can be eaten without toxicity if it is parboiled (cooked in boiling water that is discarded, reboiled, and then rinsed).
Gastroenteritis with systemic toxicity — Although rarely associated with serious poisoning, the following plants contain toxins that can cause gastroenteritis and other systemic effects:
●Castor bean (Ricinus communis) – Castor beans are used in the production of castor oil and are also found in decorative necklaces. Castor beans contain the cellular toxin ricin, which binds to ribosomes and inhibits protein synthesis in rapidly dividing cells [14,32,33]. Ricin requires mastication of the seeds to be released. Oral ingestion of whole beans typically causes no symptoms. When chewed, castor beans frequently cause nausea, vomiting, diarrhea, and abdominal pain [34]. Severe gastroenteritis with dehydration and shock may occur [14]. Rarely, gastrointestinal bleeding, hemolysis, and mild elevations of creatinine or liver enzymes may also be seen. Raw castor beans are also highly allergenic, and anaphylaxis has been described after repeated exposure to a decorative necklace [35]. When synthesized into the crystalline form, ricin is extremely toxic, and inhalation, ingestion, or injection of as little as 500 mcg can be lethal [36].
●Jequirity beans (Abrus precatorius) – Similar to the castor bean, these decorative beans contain the cellular toxin abrin, which binds to ribosomes and inhibits protein synthesis [37]. Children who ingest intact beans typically remain asymptomatic. If chewed, the jequirity bean can cause severe gastroenteritis with hematemesis and hematochezia, dehydration, and shock [38]. Seizures and demyelinating encephalitis have also been described [39].
●Solanaceous plants – Solanaceous steroidal glycoalkaloids (eg, solanine, chaconine) are present in cultivated and wild plants including unripe potatoes and potato eyes, tomatoes, Solanum torvum (susumber berry), Solanum dulcamara (woody or climbing nightshade), Solanum nigrum (black nightshade), and Solanum pseudocapsicum (Jerusalem cherry) [10,24,40]. Exploratory ingestion of one or two berries of Solanum dulcamara is the most common exposure in young children and typically results in no symptoms or limited vomiting and/or diarrhea. Delayed gastroenteritis with central nervous system effects may occur if large amounts of toxic plant material is ingested:
•In a report of a mass poisoning at a school, 78 boys were fed old potatoes with a high concentration of solanine and developed gastroenteritis starting 8 to 10 hours after consumption. In 17 patients, altered mental status, including hallucinations and coma, occurred [41].
•Delayed gastroenteritis, weakness, facial droop, dysarthria, and blurry vision occurred in several family members in two separate events after ingestion of cooked susumber berries that had been personally picked and exported out of Jamaica [40].
●Autumn crocus (Colchicum autumnale) – The autumn crocus (also known as wild saffron) contains the microtubular toxin colchicine [42]. Ingestion by young children is rare. However, cases of severe poisoning with delayed gastroenteritis, multisystem organ failure, and death have been described among eastern European and Japanese adult foragers who mistook autumn crocus for wild garlic [43,44].
●May apple (Podophyllum peltatum) – This plant is a source of the microtubular toxin podophyllin [10]. Although serious pediatric poisoning is very rare, ingestion of concentrated podophyllin by adults has caused esophageal, gastric, and duodenal mucosa necrosis; coma; and polyneuropathy [45,46].
Cardiac arrhythmias — Cardiotoxicity after toxic plant ingestion is unusual. However, several common ornamental plants contain cardiac glycosides or substances that affect sodium channel activity and can cause serious arrhythmias after ingestion.
Cardiac glycosides (eg, oleander, foxglove) — Multiple cardiac glycosides similar to digitalis or digitoxin are found in a number of common ornamental plants, including [10,24,47,48]:
●Convallaria majalis (lily of the valley)
●Digitalis purpurea (foxglove)
●Nerium oleander (common oleander)
●Cascabela thevetia (syn. Thevetia peruviana, yellow oleander)
●Cebera odollam (pong-pong)
Of these plants, poisoning with N. oleander or C. thevetia is most frequently reported [49]. T. peruviana poisoning is most prevalent in India and Southeast Asia, where intentional ingestion of the seeds by suicidal adolescents and adults commonly occurs. Ingestion of 5 to 15 N. oleander leaves or 8 to 10 C. thevetia seeds can be fatal in an adult [49]. Exposures in young children are typically limited to one flower or leaf, and serious toxicity is less common.
Toxicity after acute ingestion of cardiac glycoside-containing plants is similar to medicinal digitalis poisoning. Vomiting, diarrhea, weakness, and confusion are typical.
Reversible inhibition of the Na+/K+ ATPase pump leads to hyperkalemia, which, in acute ingestions, correlates with cardiac toxicity [50]. Patients may develop bradycardia with atrioventricular block, atrial tachycardias, ventricular tachycardia including bidirectional ventricular tachycardia (waveform 1), and ventricular fibrillation. (See "Digitalis (cardiac glycoside) poisoning", section on 'Clinical features and diagnosis' and "Digitalis (cardiac glycoside) poisoning", section on 'Laboratory and ECG evaluation'.)
The treatment of cardiac glycoside poisoning following plant ingestion is discussed in detail separately. (See "Toxic plant ingestions in children: Management", section on 'Cardiac glycoside poisoning'.)
Grayanotoxins (eg, azalea, rhododendron) — Grayanotoxins are found in Kalmia latifolia (mountain laurel), rhododendron and azalea species, and Zigadenus (death camas). These toxins bind to sodium channels and place them in a partially open state [51]. Serious toxicity is rare after exploratory ingestions of less than one blossom from an azalea, rhododendron, or mountain laurel [52]. However, when honey contaminated with grayanotoxins from these plants is ingested (also known as "mad honey poisoning"), patients commonly develop bradycardia, hypotension, vomiting, dizziness, blurred vision or diplopia, and altered mental status [51,53]. Fatalities are rare.
Aconitine (monkshood, wolfbane) — Aconitine and related alkaloids are found in Aconitum napellus (monkshood) and other Aconitum species. These plants are widely used by traditional medicine providers in China and India as herbal remedies and can cause life-threatening toxicity by binding and maintaining sodium channels in the open position [54-56]. The plant itself contains high levels of toxins in all parts, especially the roots. Processing of the roots and tubers into a tincture of aconite reduces the amount of toxic alkaloids by 90 percent, but these preparations have still been associated with serious morbidity and mortality after ingestion of as little as eight drops.
Cardiotoxicity consists of ventricular arrhythmias (eg, ventricular tachycardia or fibrillation, torsades de pointes), bradycardia, hypotension, and asystole [54,57]. Other clinical features include vomiting, diarrhea, paresthesias, numbness, weakness, diaphoresis, and altered mental status. Death may occur in up to 12 percent of patients [58].
Veratridine (false hellebore) — Similar to aconitine, veratridine opens sodium channels in skeletal muscle, nerves, and cardiac tissue. Pediatric poisoning from exploratory ingestions is rare. However, Veratrum parviflorum has been mistaken for ramps (wild leeks) [59], and, in Europe, Veratrum album (white hellebore) may be mistaken for yellow gentian (Gentiana lutea) or wild garlic (Allium ursinum) by adult foragers [60,61]. Typical cardiac toxicity consists of sinus bradycardia, atrioventricular block, and hypotension. Other signs of poisoning include vomiting, diarrhea, paresthesias, transient blindness, syncope, and seizures. Mortality rarely occurs following unintentional ingestion.
Taxine (yew) — Taxine toxins block sodium and calcium channels in the heart. Exploratory ingestions of one or two seeds or leaves of the yew (Taxus baccata) occur commonly in children and typically result in no symptoms [47]. Intentional ingestions in adults have been associated with life-threatening cardiotoxicity, including atrioventricular block, ventricular tachycardia, and refractory ventricular fibrillation [62-65]. Vomiting, diarrhea, seizures, and coma may also occur.
Nicotinic poisoning — Several plants contain alkaloids that have nicotinic effects, including (see "Nicotine poisoning (e-cigarettes, tobacco products, plants, and pesticides)", section on 'Tobacco and other nicotinic plants'):
●Conium maculatum (poison hemlock)
●Nicotiana tabacum (wild tobacco)
●Lobelia inflata (Indian tobacco)
●Laburnum anagyroides (golden chain)
●Cytisus laburnum (golden chain tree)
●Baptisia australis (blue wild indigo or blue false indigo)
Clinical manifestations of nicotinic plant poisoning include secondary muscarinic symptoms (salivation, lacrimation, vomiting, diarrhea, wheezing, bradycardia, diaphoresis, and small pupils) and primary nicotinic signs (muscle fasciculations, weakness, paralysis, coma, seizures, tachycardia, and hypertension). Green tobacco sickness refers to nicotine toxicity caused by dermal absorption from tobacco leaves in field workers and is discussed in detail separately. (See "Nicotine poisoning (e-cigarettes, tobacco products, plants, and pesticides)", section on 'Clinical features of poisoning'.)
Anticholinergic poisoning — Ingestion of jimson weed (Datura stramonium), angel trumpet (Brugmansia species), deadly nightshade (Atropa belladonna), henbane (Hyoscyamus niger), or improperly prepared lupine (Lupinus species) food products [66] can produce anticholinergic toxicity because they contain significant concentrations of belladonna alkaloids (hyoscyamine, hyoscine, atropine, and scopolamine). Topical exposure to plant material can cause localized symptoms (ie, unilateral mydriasis from ocular exposure) [67]. Ingestion of jimson weed seeds or drinking teas made from angel trumpet flowers are promoted as legal hallucinogenic highs among adolescents [1,68,69]. Use of Datura or Brugmansia species for medicinal purposes without the guidance of a Chinese medical practitioner constitutes another important cause of poisoning [70].
Clinical findings of anticholinergic plant ingestion consist of the classic anticholinergic (atropine-like) toxidrome (see "Anticholinergic poisoning", section on 'Clinical features of overdose'):
●Tachycardia
●Hot, flushed, dry skin
●Dilated pupils and blurry vision
●Disorientation, bizarre behavior, paranoia, delirium, visual hallucinations, and, in severe cases, seizures
●Decreased bowel sounds and urinary retention
Status epilepticus — Ingestion of Cicuta species (water hemlock) and Oenanthe crocata (hemlock water dropwort) usually result from the misidentification of these plants as wild parsnip, carrots, parsley, or turnips by adult foragers. The primary toxin is cicutoxin, a gamma-aminobutyric acid (GABA) antagonist that is found in all parts of the plant, with the highest concentrations occurring in the root [71].
Ingestion results in severe, recurrent seizures that may not be amenable to standard anticonvulsant therapy [10,72]. Accompanying symptoms may include nausea, vomiting, abdominal pain, delirium, diaphoresis, bronchorrhea, salivation, flushing, bradycardia, and hypotension [71]. Prolonged seizure activity may also lead to rhabdomyolysis with myoglobinuria, severe lactic acidosis, cerebral edema, and death.
Hypoglycemia and encephalopathy — Ackee fruit (Blighia sapida) is a common food source in West Africa and the Caribbean, especially among impoverished and malnourished children [16]. Although edible when ripe and properly prepared, the unripe fruit contains high concentration of the toxin hypoglycin A, which, when metabolized, inhibits long-chain fatty acid breakdown and transport into the mitochondria [73,74]. Toxicity manifests as a Reye-like syndrome with vomiting, hypoglycemia, seizures, and coma occurring between 2 and 48 hours after ingestion of unripe ackee fruit. Without rapid correction of hypoglycemia, the death rate approaches 100 percent [75,76]. Pathologic findings on liver biopsy include cholestasis and centrilobular necrosis.
Lychee fruit consumption followed by fasting also has been associated with outbreaks of hypoglycemia and encephalopathy with high mortality in the region of India, where cultivation of lychee fruit is concentrated [77,78]. Metabolites of hypoglycin A and methylenecyclopropylglycine were found in two-thirds of urine specimens from the victims.
Hallucinations — Ipomea violacea (morning glory), Argyreia nervosa (baby woodrose), Merremia tuberosa (woodrose), and Lopophora williamsii (peyote) are plants that contain lysergic acid diethylamide (LSD) congeners. These plants are frequently used recreationally by adolescents and cause visual hallucinations, vomiting, nausea, and abdominal pain. (See "Intoxication from LSD and other common hallucinogens", section on 'LSD and other lysergic acid derivatives'.)
Cyanide poisoning — Many fruit pits and seeds (eg, cherry, apricot, peach, plum, pear, almond, apple) contain cyanogenic glycosides such as amygdalin that are converted to hydrogen cyanide by gut bacteria after ingestion of masticated seeds or pits [10,15]. Numerous seeds or pits have to be crushed or chewed to cause toxic side effects. Thus, acute cyanide poisoning from exploratory toxic plant ingestion is extremely rare in children [15]. However, amygdalin and laetrile (a chemical congener of amygdalin) are sold as alternative treatments for cancer in adults, and cyanide poisoning from unintentional laetrile ingestion has been described in a four-year-old child [79].
The clinical findings of cyanide poisoning are delayed several hours after toxic ingestion of amygdalin-containing seeds or herbal preparations and include cherry-red skin, vomiting, abdominal pain, tachypnea, tachycardia, ventricular arrhythmias, confusion, coma, and seizures. Poisoned patients also demonstrate severe lactic acidosis. Rebound toxicity after initial treatment has been described in an adult patient following amygdalin ingestion [80]. The clinical presentation and diagnosis of cyanide poisoning are discussed in greater detail separately. (See "Cyanide poisoning", section on 'Clinical presentation' and "Cyanide poisoning", section on 'Diagnosis'.)
EVALUATION — When the ingested plant is unknown, clinical findings may suggest a specific toxic plant. A regional poison control center should be contacted to discuss likely plant species ingested based upon clinical findings, identification of any plant parts available for analysis, and treatment of specific toxic effects. Most poison control centers maintain active call lists of botanists who are knowledgeable concerning local prevalence of plant genera and species and can assist in plant identification.
To obtain emergency consultation with a medical toxicologist, in the United States, call 1-800-222-1222 or the nearest regional poison center. Contact information for regional poison centers around the world is provided separately. (See 'Clinical manifestations of poisoning' above and 'Additional resources' below.)
History — Key elements of the history include:
●Name of the plant ingested – If the caregiver knows which plant was ingested but does not know its name, the clinician should attempt to obtain a plant sample, including, if possible, flower, leaves, and stem for identification.
●Part of the plant ingested – In general, roots and stems have higher concentrations of toxins than flowers or berries. (See 'Plant toxicity' above.)
●Amount of plant ingested – Ingestion of fewer than six berries, one leaf, or one flower rarely causes toxicity.
●Circumstances of the ingestion – Serious plant poisoning is often associated with an error in plant identification while foraging or intentional recreational ingestion.
●Time from ingestion to symptoms – Delayed toxicity is seen with the following plant species (see 'Gastroenteritis with systemic toxicity' above and 'Cyanide poisoning' above):
•Castor bean (Ricinus communis)
•Jequirity pea (Abrus precatorius)
•Solanaceous plants (eg, Solanum dulcamara, green potatoes)
•Autumn crocus (Colchicum autumnale)
•May apple (Podophyllum peltatum)
•Amygdalin-containing fruits (cyanide poisoning)
●Prominent symptoms – Mucosal burning, nausea, vomiting, and diarrhea are common features of many plant poisonings. Visual disturbances (eg, blurry vision, diplopia), dizziness, weakness, and altered mental status are associated with several of the highly toxic plant ingestions. (See 'Clinical manifestations of poisoning' above.)
Physical examination — Many children will be asymptomatic with a normal physical examination after ingestion of a potentially toxic plant.
Among symptomatic patients, potential physical findings include:
●Bradycardia
●Tachycardia
●Hypotension
●Hyperthermia
●Flushed, warm, or cherry-red skin
●Diaphoresis
●Dilated pupils
●Swelling of the oral mucosa, excessive oral secretions
●Seizures, muscle weakness, or fasciculations
●Decreased bowel sounds
Toxidromes — Symptomatic patients can be classified according to presenting features to guide therapy and identify the type of plant ingested as follows:
●Burning and swelling of the oral mucosa (see 'Mucosal irritation and swelling' above)
●Mild gastroenteritis without volume depletion (table 4) or other systemic abnormalities (see 'Minor gastrointestinal irritation' above)
●Significant gastroenteritis with volume depletion (table 4), hematemesis, or hematochezia (see 'Acute gastroenteritis' above and 'Gastroenteritis with systemic toxicity' above and "Clinical assessment of hypovolemia (dehydration) in children", section on 'Estimating degree of hypovolemia')
●Bradycardia and hypotension (see 'Cardiac arrhythmias' above)
●Tachycardia without anticholinergic or nicotinic signs (see 'Cardiac glycosides (eg, oleander, foxglove)' above and 'Aconitine (monkshood, wolfbane)' above and 'Taxine (yew)' above)
●Muscle weakness and fasciculations, excess oral and bronchial secretions, bronchospasm, diaphoresis (see 'Nicotinic poisoning' above)
●Delirium, hallucinations, dilated pupils, flushed and warm skin, decreased bowel sounds, hyperthermia, tachycardia, seizures (see 'Anticholinergic poisoning' above)
●Seizures that are severe and recurrent (see 'Status epilepticus' above and 'Anticholinergic poisoning' above and 'Cyanide poisoning' above)
●Hallucinations without anticholinergic findings (see 'Hallucinations' above)
●Cherry-red skin, marked tachypnea, tachycardia, and hypotension (see 'Cyanide poisoning' above)
Ancillary studies — Although specific plant toxins can be identified using techniques such as thin-layer chromatography, high-performance liquid chromatography, mass spectrophotometry, and ultraviolet absorption, these analytic methods are neither routinely available in most hospital laboratories nor timely enough to aid in management [24]. Thus, specific diagnosis usually relies upon clinical findings and identification of plant samples. (See 'Plant identification' below.)
Asymptomatic individuals with ingestions that are unlikely to be toxic may be observed without any testing. Ancillary studies in symptomatic children with potentially toxic plant ingestions are guided by the clinical presentation and, when possible, plant identification:
●Children with an altered mental status or seizures (delirium lethargy, coma):
•Rapid blood glucose
•Arterial or venous blood gas
•Complete blood count (CBC; especially if hematemesis or hematochezia)
•Serum electrolytes, blood urea nitrogen (BUN), and serum creatinine
•Creatine kinase, urine for myoglobin (especially patients with seizures, anticholinergic poisoning, or nicotinic findings)
●Children who have ingested plants that may cause cardiac arrhythmias:
•Electrolytes – Hyperkalemia suggests ingestion of plants that contain cardiac glycosides. (See 'Cardiac glycosides (eg, oleander, foxglove)' above.)
•Serum digoxin level – While the immunoassay is specifically designed to measure digoxin, other cardiac glycosides can cross-react. Due to variable amounts of cross-reactivity, the level obtained is not prognostic and cannot be used to dose digoxin antibody (Fab) fragments. Although a detectable level is strongly suggestive of an acute exposure, the absence of a detectable level cannot exclude exposure.
•12-lead electrocardiogram and continuous cardiac monitoring.
●Patients with findings suggestive of cyanide poisoning:
•Cyanide level
•Serum lactate, which is often markedly elevated
Plant identification — Determination of the specific plant ingested helps guide management and patient disposition. Whenever possible, samples of the plant (including, if possible, flower, leaves, stem, and root) should be obtained. Consultation with a medical toxicologist and botanist is advised when attempting plant identification (call a United States regional poison control center at 1-800-222-1222 or find contact information for regional poison centers around the world provided separately (see 'Additional resources' below)). Digital photographs can be immediately sent for inspection. Alternatively, the plant can be copied and the image sent digitally [81].
Web and mobile based applications are intended to aid in plant identification. However, application accuracy varies. While many recognize the correct genus of a plant >50 percent of the time, a greater degree of diagnostic capability is often necessary after plant exposure, especially for patients who present with serious poisoning [82,83]. If used, they should be interpreted with caution and not solely relied upon for clinical decision-making.
ADDITIONAL RESOURCES
Regional poison control centers — Regional poison control centers in the United States are available at all times for consultation on patients with known or suspected poisoning, and who may be critically ill, require admission, or have clinical pictures that are unclear (1-800-222-1222). In addition, some hospitals have medical toxicologists available for bedside consultation. Whenever available, these are invaluable resources to help in the diagnosis and management of ingestions or overdoses. Contact information for poison centers around the world is provided separately. (See "Society guideline links: Regional poison control centers".)
SUMMARY AND RECOMMENDATIONS
●Epidemiology – Potentially toxic plant ingestions occur frequently in children (table 1), but serious toxicity is rare. (See 'Epidemiology' above.)
Many exploratory plant ingestions in children ultimately involve consumption of nontoxic species (table 3). Gastrointestinal irritation is the most common clinical effect associated with toxic plant exposure in children. (See 'Nontoxic' above and 'Gastrointestinal toxicity' above.)
●Clinical manifestations and evaluation – Small exploratory exposures to potentially toxic plants in children usually result in minimal or no toxicity. (See 'Clinical manifestations of poisoning' above and 'Mucosal irritation and swelling' above and 'Minor gastrointestinal irritation' above.)
When it occurs, serious plant poisoning typically arises from large ingestions of highly toxic plant species (table 2) due to ingestion for self-harm, foraging mistakes, or intentional recreational use.
When the ingested plant is unknown, clinical findings may suggest a specific toxic plant. A regional poison control center should be contacted to discuss likely plant species ingested based upon clinical findings, identification of any plant parts available for analysis, and treatment of specific toxic effects. Symptomatic patients can be classified according to presenting features to guide therapy and identify the type of plant ingested. (See 'Evaluation' above and 'Toxidromes' above.)
●Ancillary studies – Asymptomatic individuals with plant ingestions that are unlikely to be toxic may be observed without any testing. Ancillary studies in symptomatic children with potentially toxic plant ingestions are guided by the clinical presentation and, whenever possible, plant identification from samples of the leaf, roots, berries, and/or fruit. (See 'Ancillary studies' above.)
●Plant identification – A regional poison control center should be contacted to help determine the plant ingested, degree of plant toxicity, and treatment of specific toxic effects. To obtain emergency consultation with a medical toxicologist, in the United States, call 1-800-222-1222 or the nearest regional poison center. Contact information for regional poison centers around the world is provided separately. (See 'Plant identification' above and 'Additional resources' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Brian A Bates, MD and Margaret R Ugalde, RN, DrPH, who contributed to earlier versions of this topic review.
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