ﺑﺎﺯﮔﺸﺖ ﺑﻪ ﺻﻔﺤﻪ ﻗﺒﻠﯽ
خرید پکیج
تعداد آیتم قابل مشاهده باقیمانده : 3 مورد
نسخه الکترونیک
medimedia.ir

Toxic plant ingestions in children: Management

Toxic plant ingestions in children: Management
Literature review current through: Jan 2024.
This topic last updated: Dec 20, 2023.

INTRODUCTION — The management of toxic plant ingestions in children will be reviewed here. Evaluation and clinical manifestations of potentially toxic plant or poisonous mushroom ingestions, the management of toxic mushroom poisoning, and contact dermatitis caused by poison ivy are discussed separately:

(See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation".)

(See "Clinical manifestations and evaluation of mushroom poisoning".)

(See "Management of mushroom poisoning (except amatoxin-containing mushrooms)".)

(See "Amatoxin-containing mushroom poisoning (eg, Amanita phalloides): Clinical manifestations, diagnosis, and treatment".)

(See "Poison ivy (Toxicodendron) dermatitis".)

(See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment".)

BACKGROUND — Children are frequently exposed to potentially toxic plants, both in the home and outdoors. 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 serious clinical effects. Most young children are asymptomatic or have minimal gastrointestinal toxicity after exploratory plant ingestions (eg, picking berries off a bush). Serious poisoning is associated with large ingestions of highly toxic plant species (table 1), which typically occur in the setting of suicidal ingestion, foraging mistakes, or intentional recreational use.

APPROACH — Patient management and disposition after ingestion of a potentially toxic plant depends upon the plant ingested, the amount ingested, and the clinical findings:

Asymptomatic

Nontoxic or minimally toxic plant ingestion – Patients with small ingestions of confirmed nontoxic or minimally toxic plant species (table 2) do not require any treatment. (See 'Mucosal irritation' below and 'Gastroenteritis' below.)

Unknown or potentially highly toxic plant ingestion – Patients with ingestions of unknown or potentially highly toxic plants (table 1), particularly consumption of large amounts, should receive medical evaluation, gastrointestinal decontamination with activated charcoal (AC) if accomplished within one to three hours, and observation for four to six hours after ingestion. In most instances, the child will remain asymptomatic and be discharged home. (See 'Gastrointestinal decontamination' below.)

Symptomatic

Mucosal irritation – Patients with oral mucosal irritation after chewing or ingesting plants of the Araceae family (eg, philodendron, dieffenbachia [dumbcane]) should receive skin decontamination around the mouth, pain management, and (if able to swallow and no airway compromise) cold milk, ice cream, popsicles, or ice. Dexamethasone is suggested for patients with significant lip, tongue, or other oral swelling. These patients warrant observation for signs of airway obstruction. (See 'Mucosal irritation' below.)

Gastroenteritis – Patients with vomiting or diarrhea that is not self-limited after ingestion of minimally toxic plants (table 2) may receive antiemetics (eg, ondansetron) and fluid repletion. Ondansetron should be avoided if plants known to cause prolonged QTc interval or torsades des pointes are ingested (eg Aconitum species [monkshood] or Taxus species [yew]). (See 'Gastroenteritis' below.)

Highly toxic plants – Patients with ingestions of highly toxic plants should receive:

-Stabilization of airway, breathing, and circulation; and supportive care with expectant management determined by plant identification (table 1) (see "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Plant identification')

-Gastrointestinal decontamination with AC (see 'Gastrointestinal decontamination' below)

-For patients with severe signs of anticholinergic, cardiac glycoside, or cyanide poisoning, antidotal therapy (see 'Anticholinergic poisoning' below and 'Cardiac glycoside poisoning' below and 'Cyanide poisoning' below)

In addition to medical management, patients who ingest highly toxic plants with intent of self-harm or for recreational purposes warrant evaluation for mental illness or drug abuse. (See 'Supportive care' below and 'Gastrointestinal decontamination' below.)

SUPPORTIVE CARE — Treatment recommendations for children with toxic plant ingestion are primarily derived from case series and reports and are based upon physical findings. Many exploratory plant ingestions in young children ultimately involve consumption of nontoxic species that require no therapy (table 2). Gastrointestinal irritation is the most common clinical effect associated with toxic plant ingestion in children and is typically self-limited.

Clinical findings and identification of the ingested plant are helpful in determining specific management. A regional poison control center should be contacted to assist with likely plant species ingested based upon clinical findings, identification of any available plant material, knowledge of regional native flora, and treatment of specific toxic effects. Most poison control centers maintain active call lists of botanists who are knowledgeable concerning local prevalence of plant species and can assist in identification. To obtain emergency consultation with a medical toxicologist, call the United States Poison Control Network at 1-800-222-1222; contact information for poison centers around the world is provided separately. (See 'Additional resources' below.)

In patients who have ingested highly toxic plants (table 1) or who present with signs of serious toxicity, the clinician should rapidly perform an initial assessment of clinical findings and support airway, breathing, and circulation as needed.

Antidotes are often necessary in symptomatic children who have ingested plants that cause anticholinergic, cardiac glycoside, or cyanide poisoning. (See 'Antidotes' below.)

Mucosal irritation — Children who chew plants of the Araceae family (eg, philodendron, dieffenbachia [dumbcane]) and other plants that contain calcium oxalate raphides (intracellular sharp projections) may develop mucosal irritation and swelling. However, most young children are asymptomatic or have only mild irritation [1]. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Mucosal irritation and swelling'.)

For symptomatic patients, treatment consists of [2]:

Wash the skin around the mouth with soap and water.

Treat pain:

Mild pain – Oral ibuprofen

Moderate pain – Oral opioids (eg, hydrocodone); duration of treatment should be limited to a few days

Severe pain – Intravenous (IV) or intranasal (IN) opioids (eg, IV morphine or IV/IN fentanyl)

For patients who can swallow, administer cold milk, ice cream, popsicles, or ice; some experts also recommend application of viscous lidocaine (no more than 4 mg/kg total dose) [3]. (See "Clinical use of topical anesthetics in children", section on 'Viscous lidocaine'.)

For patients with significant lip, tongue, or oral swelling, we suggest administration of dexamethasone (eg, IV dexamethasone 0.25 to 0.5 mg/kg, maximum dose 10 mg). Use of dexamethasone in these patients is supported by indirect benefit of dexamethasone for treatment of infectious and traumatic causes of upper airway swelling. (See "Management of croup", section on 'Glucocorticoids' and "Complications of pediatric airway management for anesthesia", section on 'Treatment of postintubation croup'.)

For patients with ocular exposure, perform extensive irrigation and evaluate for corneal abrasions; chemical conjunctivitis may occur. (See "Topical chemical burns: Initial evaluation and management", section on 'Water irrigation' and "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis".)

Observe for four to six hours to assure no progressive airway obstruction. Perform endotracheal intubation in patients with severe upper airway obstruction (eg, stridor, aphonia, and/or sniffing position) (table 3 and table 4) [4]. (See "Technique of emergency endotracheal intubation in children".)

Gastroenteritis — Vomiting and diarrhea may be caused by ingestion of any of the toxic plants [2,5]. Persistent vomiting after ingestion of minimally toxic plants (table 2) may be safely treated with antiemetics (eg, ondansetron). However, ondansetron may precipitate or exacerbate arrhythmias and should be avoided in patients who ingest plants associated with prolonged QTc interval and torsades des pointes (eg, monkshood, false hellebore, or yew) (table 1).

Antispasmodic agents (eg, loperamide) should be avoided in patients with diarrhea. IV fluids should be given based upon the clinical assessment of losses and evidence of volume depletion. Patients with signs of shock should receive prompt fluid resuscitation (algorithm 1). (See "Shock in children in resource-abundant settings: Initial management" and "Treatment of hypovolemia (dehydration) in children in resource-abundant settings".)

For patients with significant ingestion of plants that cause delayed gastroenteritis with systemic toxicity (eg, castor or jequirity bean [Ricinus communis or Abrus precatorius, respectively], autumn crocus [Colchicum autumnale], or May apple [Podophyllum peltatum]), activated charcoal (AC) without sorbitol is recommended. These patients also warrant hospital admission for observation and expectant management of severe gastroenteritis and multisystem organ failure. (See 'Gastrointestinal decontamination' below.)

Cardiac arrhythmias — Although rare, a variety of bradyarrhythmias and tachyarrhythmias can occur after ingestions of a number of toxic plants (eg, oleander, death camas, azalea, monkshood, yew, false hellebore) (table 1). (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Cardiac arrhythmias'.)

Cardiac glycosides — Patients with hyperkalemia or life-threatening or hemodynamically unstable arrhythmia (eg, ventricular tachycardia, ventricular fibrillation, asystole, complete heart block, Mobitz II heart block, or symptomatic bradycardia) caused by cardiac glycoside-containing plants such as foxglove (Digitalis purpurea), lily of the valley (Convallaria majalis), or oleander (Nerium oleander) warrant treatment with digoxin-specific antibody (Fab) fragments as discussed in detail separately. (See "Digitalis (cardiac glycoside) poisoning", section on 'Antidotal therapy with antibody (Fab) fragments'.)

Higher doses of digoxin-specific Fab fragments than typically given for digoxin poisoning are usually required. Quantitative digoxin or digitoxin serum levels obtained in patients poisoned with plants that contain cardiac glycosides do not correlate with clinical toxicity and should not be used to calculate the Fab fragment dose.

Bradyarrhythmias — Children with clinically significant bradyarrhythmias (eg, complete atrioventricular block) following ingestion of plant species not containing cardiac glycosides (table 1) should first be treated with atropine [6-8]. If bradycardia with hypotension persists, then the patient should receive treatment according to Pediatric Advanced Life Support (PALS) guidance for pediatric bradycardia (algorithm 2) [9].

Based upon calcium channel blocking activity in an animal model [10], some medical toxicologists have proposed calcium infusion as a potential treatment for bradyarrhythmias after human yew poisoning that are refractory to the above measures [5].

Tachyarrhythmias — Ventricular tachycardia or fibrillation and torsades de pointes are features of monkshood (aconitine), false hellebore, and yew toxicity (table 1). Ventricular arrhythmias may be initially treated with amiodarone (stable patients) [11,12]. Cardioversion (unstable patients) or defibrillation (pulseless patients) may also be performed according to PALS guidelines (algorithm 3 and algorithm 4) but are frequently ineffective [5,11,12].

Case reports suggest potential benefit from the following treatments:

Sodium bicarbonate – Monkshood, false hellebore, and yew toxins bind to sodium channels. Rapid administration of 1 to 2 mEq/kg of hypertonic sodium bicarbonate (7.5 to 8.4%) followed by a continuous infusion of approximately 1 mEq/kg per hour of isotonic sodium bicarbonate was associated with clinical improvement in an adult with large yew seed ingestion who had widening of the QRS interval and refractory ventricular tachycardia [13].

Magnesium sulfate – Magnesium sulfate (20 to 50 mg/kg, maximum single dose 2 g) is suggested for patients with torsades de pointes or other polymorphic ventricular arrhythmias caused by monkshood (Aconitum species) poisoning [12,14]. Magnesium administration has also been associated with successful conversion of ventricular bigeminy and prolonged QTc interval to sinus rhythm in an adult with a large ingestion of monkshood (Aconitum napellus) [15].

Flecainide – In a review of seven cases of monkshood (Aconitum species) poisoning in which flecainide was administered for ventricular arrhythmias, sinus rhythm was restored in six [12]. However, multiple simultaneous treatments were given in all of these cases. Thus, the direct contribution of flecainide in the termination of the arrhythmia is unclear.

Extracorporeal membrane oxygenation (ECMO) – Case reports describe the successful use of ECMO to support the circulation of patients with refractory ventricular arrhythmias and cardiogenic shock due to Taxus and Aconitum poisoning [12,16,17]. Although ECMO was associated with maintenance of hemodynamic stability while permitting time for toxin metabolism in these cases, this therapy is highly invasive and is usually not warranted.

Nicotine poisoning (muscarinic and/or nicotinic findings) — Nicotine is found in a variety of commercial products and plants. Exposure can cause muscarinic signs (eg, vomiting, diarrhea, bronchorrhea, salivation, and/or wheezing) and nicotinic effects (eg, muscle fasciculations, paralysis, coma, and seizures). The toxicology, clinical manifestations, and management of nicotine poisoning are discussed separately. (See "Nicotine poisoning (e-cigarettes, tobacco products, plants, and pesticides)".)

Agitation, delirium, and/or hallucinations — Central nervous system excitation with hallucinations may occur after ingestion of plants that contain lysergic acid diethylamide (LSD) congeners or atropine and related anticholinergic toxins. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Hallucinations' and "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Anticholinergic poisoning'.)

Patients with these findings should initially receive benzodiazepines (eg, lorazepam 0.05 to 0.1 mg/kg, typical maximum single dose 2 to 4 mg) and be placed in a quiet room. Physical restraints may be necessary. (See "Intoxication from LSD and other common hallucinogens", section on 'Agitation and dysphoria'.)

Physostigmine may be appropriate for selected patients with severe anticholinergic plant poisoning. (See 'Anticholinergic poisoning' below.)

Hypoglycemia and encephalopathy — Children who ingest unripe ackee fruit (Blighia sapida), commonly found in West Africa and the Caribbean, may develop a Reye-like syndrome with vomiting, hypoglycemia, encephalopathy, and seizures. A similar pathology has been observed in children who consume lychee [18]. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Hypoglycemia and encephalopathy'.)

Treatment is primarily supportive with close monitoring of the serum glucose and timely treatment of hypoglycemia with dextrose (table 5) [19].

Status epilepticus — Ingestion of Cicuta species (water hemlock) or Oenanthe crocata (hemlock water dropwort) is associated with recurrent seizures that may not be amenable to standard anticonvulsant therapy [2,20]. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Status epilepticus'.)

Seizures should be treated with benzodiazepines (eg, lorazepam) as first-line therapy. If seizures persist, levetiracetam, valproic acid, or phenobarbital is an appropriate second-line agent because fosphenytoin or phenytoin is less effective for the treatment of toxin-induced seizures (table 6). Treatment of refractory status epilepticus is summarized in the algorithm (algorithm 5) and discussed in detail separately. (See "Management of convulsive status epilepticus in children", section on 'Refractory status epilepticus'.)

Patients with status epilepticus after plant poisoning should also have repeated evaluation of serum creatine kinase, urinalysis, and urine myoglobin to monitor for the development of rhabdomyolysis and myoglobinuria [9]. The primary treatment goals consist of fluid repletion, management of hyperkalemia, and monitoring for hypocalcemia, which are similar to rhabdomyolysis from other causes and are discussed in detail elsewhere. (See "Prevention and treatment of heme pigment-induced acute kidney injury (including rhabdomyolysis)".)

GASTROINTESTINAL DECONTAMINATION — For patients who are alert and acutely present for care after ingestion of a potentially highly toxic plant or ingestion of an unknown plant, we suggest administration of activated charcoal (AC). Because diarrhea often occurs after toxic plant ingestion, the use of a cathartic (eg, sorbitol) with AC should be avoided. The greatest benefit occurs if AC is given within one hour. However, AC administration more than one hour after ingestion may be appropriate in selected patients depending upon the degree of toxicity and specific plant. Consultation with a regional poison control center is advised. The efficacy of AC as a function of time from ingestion is discussed in detail separately. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Activated charcoal'.)

AC should not be given in patients who are sedated and may not be able to protect their airway unless endotracheal intubation is performed first. However, endotracheal intubation should not be performed solely for the purpose of giving AC.

Children who ingest nontoxic or minimally toxic plants (table 2) do not require AC. Plants that are nontoxic or minimally toxic (eg, philodendron, dieffenbachia, poinsettia) do not cause serious effects that are prevented by AC. Thus, AC administration is not necessary, and the risk of aspiration, although low, may outweigh the benefits. (See 'Mucosal irritation' above and 'Gastroenteritis' above.)

The recommendation for AC administration following highly toxic plant ingestion derives from indirect evidence of benefit in volunteers who ingested other substances and in animal studies, as well as from evidence of benefit following ingestions of other medications. Plant toxins, like most complex xenobiotics, bind well to AC. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Evidence of efficacy and adverse effects'.)

Gastric emptying with lavage has no role in the management of plant poisoning because plant matter is not effectively removed by lavage. In adults, endoscopic removal of gastric material after potential life-threatening plant poisonings has been suggested [21]. However, its efficacy is unclear and, given the higher risk in children, should not be routinely performed. (See "Gastrointestinal decontamination of the poisoned patient", section on 'Gastric lavage'.)

In addition, syrup of ipecac is no longer recommended as a means of gastrointestinal decontamination in the poisoned patient (see "Gastrointestinal decontamination of the poisoned patient", section on 'Syrup of Ipecac'). Syrup of ipecac may cause more symptoms than no gastric emptying in children who ingest nontoxic or minimally toxic plants and should be avoided. As an example, in a poison center-based trial of 96 children who ingested fewer than six potentially toxic berries, the administration of syrup of ipecac led to significantly more vomiting, diarrhea, and sedation than observation alone [22].

ELIMINATION ENHANCEMENT — In general, plant toxins are not amenable to elimination enhancement including multiple-dose activated charcoal (MDAC), plasma exchange, hemodialysis, or charcoal hemoperfusion [2,5,9].

However, the efficacy of MDAC in yellow oleander (Cascabela thevetia, formerly Thevetia peruviana) ingestion is not clear since two randomized trials had different results. In the largest trial of 1647 patients poisoned by yellow oleander, MDAC provided no mortality benefit when compared with a single dose of activated charcoal (AC) or placebo (6.3 versus 6.8 percent, odds ratio [OR] 0.96) [23]. This is in contrast to a smaller trial in 401 patients who ingested yellow oleander in which MDAC was associated with a significant reduction in mortality compared with single-dose AC (2.5 versus 8 percent) [24].

Plasma exchange therapy was used to treat seven children who each consumed between 5 and 12 castor beans (Ricinus communis). All children survived and had improved laboratory findings and symptoms within 48 hours of plasma exchange. While encouraging, in the absence of a comparison group, no recommendation on plasma exchange can be provided [25].

ANTIDOTES — For most serious plant poisonings, supportive care is the mainstay of treatment. However, antidotal therapy may be lifesaving in selected patients with anticholinergic, cardiac glycoside, or cyanide poisoning.

Anticholinergic poisoning — For children and adolescents who develop anticholinergic toxicity after plant ingestion with agitated delirium, benzodiazepines are the mainstay of treatment. Selected patients may benefit from careful administration of physostigmine as discussed separately. Before physostigmine is given, the patient should be placed on a cardiac monitor, and atropine and resuscitative equipment should be available at the bedside. Physostigmine should not be given to patients with known or suspected cyclic antidepressant poisoning, to patients with a QRS interval that is ≥100 msec, or to patients with normal or low heart rate [26].

The suggested dose and method of administration is 0.02 mg/kg intravenously (IV; maximum single dose 0.5 mg) slowly over five minutes. If no response, may repeat every 5 to 10 minutes until improvement up to a maximum total dose of 2 mg. (See "Anticholinergic poisoning", section on 'Antidotal therapy with physostigmine for severe toxicity'.)

Because physostigmine is uncommonly used and unfamiliar to many clinicians, practitioners may choose to consult with a medical toxicologist or regional poison center. In the United States, the nearest available poison control center can be reached by calling 1-800-222-1222. Contact information for poison centers around the world is provided separately. (See 'Additional resources' below.)

Patients who ingest plants with atropine and related anticholinergic toxins (eg, jimson weed [Datura stramonium]) often develop severe agitation and delirium that may not be well controlled by supportive measures such as physical restraints or benzodiazepines [27,28]. Successful and safe use of physostigmine after jimson weed poisoning has been documented in several case reports and series [27-29]. Administration of physostigmine to such patients can result in rapid return to baseline mental status and avoid serious complications of anticholinergic poisoning including hyperthermia, tachycardia with hemodynamic instability, seizures, or rhabdomyolysis.

Cardiac glycoside poisoning — Multiple cardiac glycosides similar to digitalis or digitoxin are found in a number of common ornamental plants (eg, common oleander [Nerium oleander], yellow oleander [Cascabela thevetia, formerly Thevetia peruviana], foxglove [Digitalis purpurea]) [2,5,30]. Toxicity includes vomiting, diarrhea, abdominal pain, weakness, confusion, hyperkalemia, and bradyarrhythmias, especially high-grade atrioventricular block. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Cardiac glycosides (eg, oleander, foxglove)'.)

Indications for digoxin-specific Fab — Digoxin-specific antibody (Fab) fragments bind to naturally occurring cardiac glycosides, including those found in plants, and reverse toxicity in human poisoning [2,5,31]. We recommend that children who ingest cardiac glycoside-containing plants (table 1) and develop life-threatening arrhythmias (eg, atrioventricular node and/or severe sinus node block) or serum potassium >5 to 5.5 mEq/L receive digoxin-specific Fab fragments as discussed separately. (See "Digitalis (cardiac glycoside) poisoning", section on 'Indications and general approach'.)

The following evidence supports the use of digoxin-specific Fab fragments for patients with serious plant-derived cardiac glycoside poisoning:

A trial of 66 patients with yellow oleander (Cascabela thevetia, formerly T. peruviana) poisoning found faster resolution of bradyarrhythmias and elevated potassium in patients who received digoxin-specific Fab fragments versus placebo (71 versus 16 percent at eight hours) [32].

Case reports have also documented successful treatment of cardiotoxicity with digoxin-specific Fab fragments in patients who ingested foxglove extract, common oleander (Nerium oleander), and an herbal extract containing an unknown plant-derived cardioactive steroid [33-36].

Quantitative digoxin or digitoxin serum levels obtained in patients poisoned with plants that contain cardiac glycosides do not correlate with clinical toxicity and should not be used to calculate the Fab fragment dose.

Dose of digoxin-specific Fab — Because binding of digoxin-specific Fab fragments to naturally occurring cardiac glycosides is less efficient than in patients with digoxin or digitoxin poisoning, doses of digoxin-specific Fab fragments higher than typically given for digoxin poisoning may be necessary to achieve comparable efficacy. As an example, experts suggest that patients with common oleander (Nerium oleander) or yellow oleander (Cascabela thevetia, formerly T. peruviana) poisoning receive a starting dose of 400 mg (10 vials) of digoxin-specific Fab fragments over 20 minutes followed by 400 to 800 mg (10 to 20 vials) regardless of patient age infused over four to eight hours [31]. These higher doses of digoxin-specific Fab fragments may be associated with a higher frequency of adverse allergic reactions (eg, hives, angioedema, or bronchospasm). Thus, the clinician should have equipment and emergency medications to treat anaphylaxis (table 7) immediately available during digoxin-specific Fab fragment administration.

This dosing regimen for oleander poisoning is based, in part, upon a dose-finding study and subsequent trial of digoxin-specific Fab fragments in patients with yellow oleander poisoning. Findings from this study include [32]:

Ten of 12 patients who received doses of 800 to 1600 mg (20 to 40 vials) of digoxin-specific Fab fragments had conversion of arrhythmia to normal sinus rhythm or reversal of hyperkalemia compared with one of four patients who received a dose of 400 mg (10 vials).

The subsequent trial demonstrated significantly faster reversal of clinical toxicity (bradyarrhythmia, elevated potassium) among the 34 patients who received 1200 mg (30 vials) of digoxin-specific Fab fragments when compared with the 32 patients who received placebo (71 versus 16 percent at eight hours).

Adverse allergic reactions (eg, pruritus, hives, angioedema, bronchospasm) occurred in 23 percent of patients who received digoxin-specific Fab fragments during the dosing study or the trial.

The doses of digoxin-specific Fab fragments used for oleander poisoning may not be appropriate for poisoning with other naturally occurring plant and animal cardiac glycosides, such as lily of the valley and bufotoxin. Use of digoxin-specific Fab fragments in such poisonings is empiric. (See "Dosing regimen for digoxin-specific antibody (Fab) fragments in patients with digoxin toxicity", section on 'Cardiac glycoside poisoning other than digoxin or digitoxin'.)

Yellow oleander poisoning is a common method of suicide in resource-limited countries in Southeast Asia where digoxin-specific Fab fragments are not always available for treatment of serious poisoning. In resource-limited settings, experts suggest the following modification for treatment of serious cardiac glycoside poisoning [31]:

For serum potassium >5.5 mEq/L, use insulin with dextrose infusion, sodium bicarbonate, and potassium-binding resin. Do not give calcium. (See "Treatment and prevention of hyperkalemia in adults".)

Treat severe atrioventricular block with atropine and, if not responsive to atropine, cardiac pacing.

Treat ventricular tachycardia with low-dose cardioversion (eg, 0.25 to 0.5 joules/kg) and ventricular fibrillation with low-dose defibrillation (eg, 2 joules/kg, maximum dose 100 joules).

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 (table 1). Cyanide poisoning also complicates ingestion of amygdalin and laetrile (a chemical congener of amygdalin) sold as alternative treatments for cancer.

The clinical findings of cyanide poisoning are delayed several hours after toxic ingestion of amygdalin-containing seeds or herbal preparations and include vomiting, abdominal pain, tachypnea, tachycardia, ventricular arrhythmias, confusion, coma, and seizures. Severe lactic acidosis can occur. There may be absence of cyanosis despite obvious respiratory distress. Cherry-red skin is an uncommon finding. (See "Potentially toxic plant ingestions in children: Clinical manifestations and evaluation", section on 'Cyanide poisoning'.)

Like other patients with probable cyanide poisoning, children who have ingested cyanogenic plants and have findings of cyanide poisoning warrant emergency treatment with IV hydroxocobalamin (70 mg/kg, maximum dose 5 g), sodium thiosulfate 25% (1.65 mL/kg [412.5 mg/kg]) may also be administered to patients with extreme toxicity refractory to hydroxocobalamin. This recommendation is based upon direct evidence of benefit of this combined regimen for the treatment of cyanide poisoning (see "Cyanide poisoning", section on 'Suspected cyanide intoxication'). Rebound toxicity 12 hours after initial treatment and requiring repeat administration of cyanide antidotes has been described in an adult patient following amygdalin ingestion [37].

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

Approach – Patient management after ingestion of a potentially toxic plant is determined by clinical findings and, when known, the plant ingested. (See 'Approach' above.)

Asymptomatic patients

Nontoxic or minimally toxic plant ingestion – Patients with small ingestions of confirmed nontoxic or minimally toxic plant species (table 2) do not require any treatment. (See 'Mucosal irritation' above and 'Gastroenteritis' above.)

Unknown or potentially highly toxic plant ingestion – Patients with ingestions of unknown or potentially highly toxic plants (table 1), particularly consumption of large amounts, should receive medical evaluation, gastrointestinal decontamination as described below, and observation for four to six hours. In most instances, the child will remain asymptomatic and be discharged home. (See 'Gastrointestinal decontamination' above.)

Symptomatic patients Treatment of a child who is symptomatic after a plant ingestion consists of local or gastrointestinal decontamination, supportive care based upon specific plant toxicity, and, in selected patients, antidotal therapy:

Mucosal irritation – Initial treatment of patients with oral mucosal irritation after chewing or ingesting plants of the Araceae family (eg, philodendron, dieffenbachia [dumbcane]) consists of (see 'Mucosal irritation' above):

-Skin decontamination around the mouth; gastrointestinal decontamination is not warranted

-If able to swallow and no airway compromise, cold milk, ice cream, popsicles, or ice chips

-Pain management (eg, oral ibuprofen or similar nonsteroidal antiinflammatory medication)

For patients with significant lip, tongue, or oral swelling, we suggest administration of dexamethasone (eg, intravenous [IV] dexamethasone 0.25 to 0.5 mg/kg, maximum dose 10 mg) (Grade 2C). These patients warrant observation for signs of airway obstruction.

Gastroenteritis – Patients with vomiting or diarrhea that is not self-limited after ingestion of minimally toxic plants (table 2) may receive antiemetics (eg, ondansetron) and fluid repletion as needed. Ondansetron should be avoided if plants known to cause prolonged QTc interval or torsades des pointes (eg, Aconitum species) are ingested. (See 'Gastroenteritis' above.)

Highly toxic plants – Clinical findings and, when possible, identification of the ingested plant guide specific management. A regional poison control center can provide expert assistance with plant identification. (See 'Additional resources' above.)

Management of patients with ingestions of highly toxic plants includes stabilization of airway, breathing, and circulation; gastrointestinal decontamination; and supportive care of toxicity that varies by plant ingested (table 1). (See 'Supportive care' above.)

Antidotes may be necessary in rare situations:

-Anticholinergic toxicity – For children and adolescents who develop anticholinergic toxicity with agitated delirium after plant ingestion, benzodiazepines are the mainstay of treatment. Selected patients may benefit from careful administration of physostigmine as discussed separately. (See "Anticholinergic poisoning", section on 'Antidotal therapy with physostigmine for severe toxicity'.)

-Cardiac glycoside toxicity – Patients with hyperkalemia or life-threatening or hemodynamically unstable arrhythmia caused by ingestion of cardiac glycoside-containing plants warrant treatment with digoxin-specific antibody (Fab) fragments. Higher doses of digoxin-specific Fab fragments than typically given for digoxin poisoning are usually required. Quantitative digoxin or digitoxin serum levels in these patients do not correlate with clinical toxicity and should not be used to calculate the Fab fragment dose. (See "Digitalis (cardiac glycoside) poisoning", section on 'Antidotal therapy with antibody (Fab) fragments'.)

-Cyanide toxicity – Like other patients with probable cyanide poisoning, children who have ingested cyanogenic plants and who have findings of cyanide poisoning warrant emergency treatment with hydroxocobalamin, sodium thiosulfate may also be administered to patients with extreme toxicity that is refractory to hydroxocobalamin as discussed separately. (See "Cyanide poisoning", section on 'Suspected cyanide intoxication'.)

Rebound toxicity after initial recovery is possible and may require retreatment. (See 'Cyanide poisoning' above.)

Gastrointestinal decontamination – Activated charcoal (AC) is not necessary after ingestion of nontoxic or minimally toxic plants. For patients who are alert and acutely present for care after confirmed ingestion of a highly toxic plant or after ingestion of an unknown plant, we suggest administration of AC without sorbitol (Grade 2C). Because diarrhea often occurs after toxic plant ingestion, the use of a cathartic (eg, sorbitol) with AC should be avoided. AC should not be given in patients who are sedated and may not be able to protect their airway unless endotracheal intubation is performed first. (See 'Gastrointestinal decontamination' above.)

Mental health evaluation – In addition to medical management, patients who ingest highly toxic plants with intent of self-harm or for recreational purposes warrant evaluation for mental illness or substance use disorder. (See 'Supportive care' above and 'Gastrointestinal decontamination' above and 'Antidotes' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Brian A Bates, MD, who contributed to earlier versions of this topic review.

  1. Mrvos R, Dean BS, Krenzelok EP. Philodendron/dieffenbachia ingestions: are they a problem? J Toxicol Clin Toxicol 1991; 29:485.
  2. Palmer M, Betz JM. Plants. In: Goldfrank’s Toxicologic Emergencies, 9th ed, Nelson LS, Lewin NA, Howland MA, Hoffman RS, Goldfrank LR, Flomenbaum NE (Eds), McGraw-Hill, New York 2011. p.1537.
  3. Nelson LS, Balick MJ. Poisons, poisoning, syndromes, and their clinical management. In: Handbook of Poisonous and Injurious Plants, 3rd edition, Springer and The New York Botanical Garden, New York 2020. p.19.
  4. Cumpston KL, Vogel SN, Leikin JB, Erickson TB. Acute airway compromise after brief exposure to a Dieffenbachia plant. J Emerg Med 2003; 25:391.
  5. Smolinske SC, Daubert GP, Spoerke DG. Poisonous plants. In: Haddad and Winchester's Clinical Management of Poisoning and Drug Overdose, 4th ed, Shannon MW, Borron SW, Burns MJ (Eds), Saunders Elsevier, Philadelphia 2007. p.473.
  6. Gunduz A, Turedi S, Russell RM, Ayaz FA. Clinical review of grayanotoxin/mad honey poisoning past and present. Clin Toxicol (Phila) 2008; 46:437.
  7. Festa M, Andreetto B, Ballaris MA, et al. [A case of Veratrum poisoning]. Minerva Anestesiol 1996; 62:195.
  8. Masom CP, Kane KE, Katz KD. A 2-Year-old Girl With Bradycardia and Lethargy: Is Perseus to the Rescue? Pediatr Emerg Care 2018; 34:e60.
  9. Froberg B, Ibrahim D, Furbee RB. Plant poisoning. Emerg Med Clin North Am 2007; 25:375.
  10. Tekol Y, Kameyama M. [Electrophysiology of the mechanisms of action of the yew toxin, taxine, on the heart]. Arzneimittelforschung 1987; 37:428.
  11. Tai YT, But PP, Young K, Lau CP. Cardiotoxicity after accidental herb-induced aconite poisoning. Lancet 1992; 340:1254.
  12. Coulson JM, Caparrotta TM, Thompson JP. The management of ventricular dysrhythmia in aconite poisoning. Clin Toxicol (Phila) 2017; 55:313.
  13. Pierog J, Kane B, Kane K, Donovan JW. Management of isolated yew berry toxicity with sodium bicarbonate: a case report in treatment efficacy. J Med Toxicol 2009; 5:84.
  14. Adaniya H, Hayami H, Hiraoka M, Sawanobori T. Effects of magnesium on polymorphic ventricular tachycardias induced by aconitine. J Cardiovasc Pharmacol 1994; 24:721.
  15. Gottignies P, El Hor T, Tameze JK, et al. Successful treatment of monkshood (aconite napel) poisoning with magnesium sulfate. Am J Emerg Med 2009; 27:755.e1.
  16. Panzeri C, Bacis G, Ferri F, et al. Extracorporeal life support in a severe Taxus baccata poisoning. Clin Toxicol (Phila) 2010; 48:463.
  17. Vardon Bounes F, Tardif E, Ruiz S, et al. Suicide attempt with self-made Taxus baccata leaf capsules: survival following the application of extracorporeal membrane oxygenation for ventricular arrythmia and refractory cardiogenic shock. Clin Toxicol (Phila) 2017; 55:925.
  18. Shrivastava A, Kumar A, Thomas JD, et al. Association of acute toxic encephalopathy with litchi consumption in an outbreak in Muzaffarpur, India, 2014: a case-control study. Lancet Glob Health 2017; 5:e458.
  19. Barceloux DG. Akee fruit and Jamaican vomiting sickness (Blighia sapida Köenig). Dis Mon 2009; 55:318.
  20. From the Centers for Disease Control and Prevention. Water hemlock poisoning--Maine, 1992. JAMA 1994; 271:1475.
  21. Buetler VA, Braunshausen AM, Weiler S, et al. Characteristics of emergency department presentations following ingestion of Taxus baccata (yew). Clin Toxicol (Phila) 2023; 61:104.
  22. Wax PM, Cobaugh DJ, Lawrence RA. Should home ipecac-induced emesis be routinely recommended in the management of toxic berry ingestions? Vet Hum Toxicol 1999; 41:394.
  23. Eddleston M, Juszczak E, Buckley NA, et al. Multiple-dose activated charcoal in acute self-poisoning: a randomised controlled trial. Lancet 2008; 371:579.
  24. de Silva HA, Fonseka MM, Pathmeswaran A, et al. Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomised, placebo-controlled trial. Lancet 2003; 361:1935.
  25. Wang CF, Nie XJ, Chen GM, et al. Early plasma exchange for treating ricin toxicity in children after castor bean ingestion. J Clin Apher 2015; 30:141.
  26. Arens AM, Kearney T. Adverse Effects of Physostigmine. J Med Toxicol 2019; 15:184.
  27. Amlo H, Haugeng KL, Wickstrøm E, et al. [Poisoning with Jimson weed. Five cases treated with physostigmine]. Tidsskr Nor Laegeforen 1997; 117:2610.
  28. Glatstein MM, Alabdulrazzaq F, Garcia-Bournissen F, Scolnik D. Use of physostigmine for hallucinogenic plant poisoning in a teenager: case report and review of the literature. Am J Ther 2012; 19:384.
  29. Glatstein M, Alabdulrazzaq F, Scolnik D. Belladonna Alkaloid Intoxication: The 10-Year Experience of a Large Tertiary Care Pediatric Hospital. Am J Ther 2016; 23:e74.
  30. Krenzelok EP, Jacobsen TD, Aronis J. Is the yew really poisonous to you? J Toxicol Clin Toxicol 1998; 36:219.
  31. Bandara V, Weinstein SA, White J, Eddleston M. A review of the natural history, toxinology, diagnosis and clinical management of Nerium oleander (common oleander) and Thevetia peruviana (yellow oleander) poisoning. Toxicon 2010; 56:273.
  32. Eddleston M, Rajapakse S, Rajakanthan, et al. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial. Lancet 2000; 355:967.
  33. Camphausen C, Haas NA, Mattke AC. Successful treatment of oleander intoxication (cardiac glycosides) with digoxin-specific Fab antibody fragments in a 7-year-old child: case report and review of literature. Z Kardiol 2005; 94:817.
  34. Barrueto F Jr, Jortani SA, Valdes R Jr, et al. Cardioactive steroid poisoning from an herbal cleansing preparation. Ann Emerg Med 2003; 41:396.
  35. Safadi R, Levy I, Amitai Y, Caraco Y. Beneficial effect of digoxin-specific Fab antibody fragments in oleander intoxication. Arch Intern Med 1995; 155:2121.
  36. Rich SA, Libera JM, Locke RJ. Treatment of foxglove extract poisoning with digoxin-specific Fab fragments. Ann Emerg Med 1993; 22:1904.
  37. Shively RM, Harding SA, Hoffman RS, et al. Rebound metabolic acidosis following intentional amygdalin supplement overdose. Clin Toxicol (Phila) 2020; 58:290.
Topic 16521 Version 47.0

References

آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟