Printer Friendly

The syndromic classification, differential diagnosis, management, and prevention of potentially fatal plant poisonings in Louisiana and the Gulf South.

Through its Toxic Exposure Surveillance System (TESS), the American Association of Poison Control Centers (AAPCC) now reports more than 50,000 calls annually relating to plant exposures, usually ingestions in young adults, adolescents, and children. (1-2) In 2004, plant exposures were the seventh most frequently reported toxic exposures in children younger than age six years. (2) For children, the frequency of plant exposures is directly related to their common presence and abundance in households and public places. (3) Fortunately, most toxic plant exposures in children are unintentional and insignificant as compared to adolescents who may attempt suicide by ingesting poisonous plants or seek "legal" hallucinogenic plants, such as Salvia divinorum, often on the Internet. (4) In addition, adolescents may combine hallucinogenic plant ingestions with other abused substances and exhibit a higher rate of unintended medical complications. (4)

In 2010, Bohnert and co-investigators reported a dramatic increase of 108.5% between 1999 and 2006 in the mortality rate for unintentional poisonings in the United States (US), especially in males and in individuals aged 15-29 years. (5) In light of such recent trends in US poisoning cases, the objectives of this investigation will be to propose a rapid syndromic classification scheme for the initial evaluation of patients poisoned by indigenous and often unidentified toxic plants in Louisiana and the Gulf South. It will also discuss current strategies for the early diagnosis, management, and prevention of potentially lethal plant poisonings.


Initially, several search engines were queried for references using all key words listed as medical subject heading (MESH) words for searches. The sources of US cases of plant poisonings were provided by peer-reviewed, published case reports and series; descriptive studies; case-control studies; and morbidity and mortality weekly reports (MMWR) published by the US Centers for Disease Control and Prevention (CDC). Data sources were extracted to create a simple syndromic classification of plant poisonings based on target organ toxicities to better guide clinicians in establishing early diagnoses and implementing therapies, despite confusing ingestion histories and clinical presentations. The final four different syndromes, or more precisely, toxidromes, of plant poisonings included cardiotoxic, neurotoxic, cytotoxic, and gastrointestinal/hepatotoxic plant poisonings; all of which have caused fatalities worldwide following both intentional and unintentional ingestions. These toxidromes were then stratified by their mechanisms of toxicity and by regional plant species to assist clinicians in confirming diagnoses from patients or witnesses; in identifying causative plant species using easily available Internet images; in selecting the most effective antidotes, if available; and in providing proven supportive therapies.



The Epidemiology of Plant Poisoning in the United States

Although there are no formal national registries for plant poisonings, the AAPCC has operated a surveillance system (TESS) for telephone-reported poisonings in the United States for more than 20 years; and the CDC often reports regional clusters of plant poisoning. (4-5) In the 2004 AAPCC Annual TESS Report, plants were the 11th most frequently reported ingested substances in human exposures, responsible for 3% of all poison exposures. Plants were the seventh most frequently involved substance in pediatric exposures in children younger than 6 years of age and responsible for more than 4% of pediatric poison exposures in that age group in 2000. (2) When stratified by frequencies of exposures by plant types among all age groups, unintentional ingestions of seasonal, ornamental household plants with limited gastrointestinal toxicity--such as peace lily, holly, and poinsettia--were more common than exposures to potentially lethal plants, such as highly cardiotoxic foxglove and oleander species (Table 1, Figure 1). (2) In summarizing the epidemiology of plant poisonings today, passive surveillance systems and longitudinal studies have described increasing toxic plant exposures in adolescents and young adults, especially males. They have also detailed a relatively stable frequency of toxic plant exposures to common, ornamental household species in children under 6 years of age (Table 1). (1-5)

The General Management of Poisonings by Unknown Plants

Since most plant exposures are to nontoxic plants or to relatively nontoxic amounts of toxins in poisonous plants, the general management of poisonings by unknown plants should be expectant and based on presenting toxidromes as more history is obtained from patients and witnesses. (3) Potential plant poisonings are often shrouded in many uncertainties, including time elapsed since ingestions, amounts of ingested plant matter, plant parts ingested, causative plant toxins, and risk-benefit ratios of aggressive decontamination therapies. With the exception of animal-derived, digoxin-specific Fab antibodies to inactivate ingested plant-derived cardiac glycosides and physostigmine to reverse plant toxin-induced central anticholinergic syndromes, there are few remaining effective antidotes for most plant toxins. As a result, gastrointestinal decontamination techniques remain management mainstays for most plant poisonings and include induction of vomiting, activated charcoal administration, orogastric lavage, and whole-bowel irrigation.

With the exception of witnessed ingestions of highly toxic plants, there are few indications for the induction of vomiting using syrup of ipecac. Ipecac administration is absolutely contraindicated in obtunded or seizing patients who have lost upper airway protective reflexes and are at risk of pulmonary aspiration. Ipecac administration is also contraindicated following ingestions of injurious plant species that can release their spines or launch calcium oxalate crystals and cause esophageal damage or perforation during emesis. Ipecac administration is relatively contraindicated following ingestion of cardiotoxic, highly vagomimetic plants that can cause nausea, vomiting, and bradycardia; often progressing to bradydysrhythmias, conduction blocks, and ventricular tachydysrhythmias. Finally, induction of emesis with ipecac could delay critical administration of activated charcoal solutions which have fewer adverse effects and bind many plant-derived toxins; most of which are uncharged, of relatively low molecular weight with extensive volumes of distribution, and not amenable to removal by hemodialysis. If possible, oral-activated charcoal should be administered within one hour of poison plant ingestions or within two hours of anticholinergic poison plant ingestions, which delay gastrointestinal activity. In addition, oral-activated charcoal solutions should only be administered to conscious patients who are not seizing or vomiting and have not ingested injurious plants containing sharp spines, nettles, or calcium oxalate crystals.

Orogastric (or nasogastric) lavage with sterile water to remove plant matter from the stomach should be reserved for patients who have recently ingested highly toxic plant matter likely to have serious consequences, such as chewed castor bean seeds containing ricin or crocus leaves containing colchicine. Orogastic lavage carries risks of esophageal damage or perforation and pulmonary aspiration and should be reserved for patients with intact airway protective reflexes or patients who have undergone endotracheal intubation.

Whole-bowel irrigation does offer an opportunity to completely cleanse the gastrointestinal tract of poisonous plant matter and should be reserved for patients who have ingested significant amounts of poisonous plant matter that will release toxins slowly over time in the gastrointestinal tract, such as apple or apricot kernels containing cyanogenic glycosides or oleander seeds containing cardiotoxic glycosides. In summary, the general management of patients who have ingested poisonous or injurious plants should be based on several simple rules, including (1) avoid harm to patients from over-aggressive gastrointestinal decontamination, (2) base initial therapies on presenting toxidromes, and (3) continue therapies with observed positive responses.

The Syndromic Diagnosis and Management of Plant Poisonings

Cardiotoxic Plants--The cardiotoxic plants have been mistaken for edible herbs (dandelion) and bulbs (wild onion) or intentionally ingested in suicide attempts (foxglove, Japanese yew, oleander). They also include cardiac glycosides, sodium channel activators, and dual sodium and calcium channel blockers. Poisonings following ingestions of plants containing cardiac glycosides resemble digoxin toxicity with initial nausea, vomiting, and abdominal pain, followed by bradycardia with predisposition to hyperkalemia and ventricular tachydysrhythmias. Since its discovery by William Withering in 1785, digoxin is still obtained from the foxglove plant, Digitalis lanata, and used to treat atrial fibrillation and congestive heart failure. (6) Digitoxin may be obtained from another species of foxglove, Digitalis purpurea. Blooming cardiac glycoside-containing foxglove plants are commonly found in flower arrangements and in English-style gardens, and their leaves have been mistaken for edible greens and herbs. In 1998, Slifman and co-investigators reported two cases of digoxin-like poisoning manifesting as severe bradycardia in women who had consumed several days of dietary herbal supplements containing ground Digitalis lanata leaves mistaken for edible plantain leaves. (7) Both patients had elevated digoxin levels, and one patient was treated with intravenous ovine digoxin Fab. (7) In 2004, Newman and co-authors reported the case of a 53-year-old woman who presented with nausea, vomiting, hyperkalemia, and profound sinus bradycardia (heart rate 36-38 bpm) following consumption of a salad containing presumed dandelion leaves plucked from an herb garden and later identified as Digitalis purpurea leaves. (8)


Although these patients recovered from cardiac glycoside poisonings following antidotal and supportive therapies, approximately 2,000 deaths occur each year in Sri Lanka following intentional self-poisoning with yellow oleander (Thevetia peruviana) seeds, which contain two highly cardiotoxic thevetin glycosides. (9) In Sri Lanka, ovine digoxin Fab is expensive and not uniformly available to treat cardiotoxic glycoside poisonings from yellow oleander ingestions. (9) In a case-control study of 401 patients with yellow oleander poisoning, deSilva and co-investigators found multiple-doses of activated charcoal to be highly successful in preventing ventricular tachydysrhythmias and death, with five deaths in the treatment group (n = 201) versus 18 deaths in the control group (n = 200) (p = 0.025). (9) Although specifically designed for the management of digoxin toxicity, digoxin-specific Fab antibodies may possess sufficient immunological cross-recognition capabilities to bind cardiac glycoside antigens from certain cardiotoxic plants. They are indicated in empiric intravenous doses (10-20 vials of 30-40 mg each) in cases with refractory bradycardia, hyperkalemia, and ventricular tachydysrhythmias, with or without elevated serum digoxin levels. (3)

Although poisonings with cardiotoxic plants containing sodium channel activators, such as monkshood (Aconitum spp.) and death camas (Zigadenus spp.), may mimic cardiac glycoside poisoning on initial presentation with bradycardia, heart blocks, and ventricular tachydysrhythmias sodium channel activator poisonings are often accompanied by hypotension and cardiovascular collapse; are refractory to reversal with digoxin-specific Fab; and may require inotropic support, temporary cardiac pacing, or temporary cardiopulmonary bypass. (10-11)

The leaves and seeds of Taxus or yew trees contain taxine alkaloids with both sodium and calcium channel blocking activity and digoxin toxicity-like effects, particularly a predisposition to hyperkalemia and ventricular tachydysrhythmias. The taxines in yew leaves and seeds are structurally similar to the digitalis-like plant glycosides, but their effects are refractory to reversal by digoxin-specific Fab. In 2009, Pierog and co-authors reported the case of attempted suicide in a 24-year-old male who chewed and swallowed 168 Japanese yew seeds (Taxus cuspidate) and presented with seizures, hypotension, and wide-complex ventricular tachycardia that would not electrically or pharmacologically cardiovert with amiodarone at the suicide attempt scene. Subsequently, the authors were able to close the QRS complexes and successfully cardiovert the patient with an intravenous bolus of sodium bicarbonate (100 mEq), followed by a continuous sodium bicarbonate infusion (37.5 mEq/hr). (12) The authors concluded that wide complex ventricular tachycardia following yew ingestions can respond to sodium bicarbonate therapy, which will reverse metabolic acidosis and promote sodium conductance through incompletely blocked myocardial sodium channels. (12) Intravenous calcium chloride and vasopressor support may also be required to treat simultaneous calcium channel blockade and restore blood pressure and tissue perfusion. (12) In summary, cardiotoxic plant poisonings may cause serious dysrhythmias and death and will require intensive care management with combinations of gastrointestinal decontamination with oral-activated charcoal, intravenous vasopressor support, anti-arrhythmics, temporary pacemaker or temporary cardiopulmonary bypass, and few specific antidotes, with the exception of digoxin-specific Fab in cases of confirmed cardiac glycoside poisonings.

Neurotoxic Plants--The neurotoxic plants have also been mistaken for edible herbs (Queen Anne's lace, parsnip, wild carrot) by foragers or intentionally ingested for their intoxicating or hallucinogenic effects and include the anti-cholinergic plants, hallucinogenic plants, nicotinic plants, and convulsant plants. In the southern US, anticholinergic plant poisoning is frequently caused by several species of three closely related plant genera (Brugmasia, Datura, and Solandra) from the nightshade or Solanaceae family that contain combinations of tropine alkaloids, including atropine, hyoscyamine, and scopolamine (Figure 2). The tropine alkaloids cause central and peripheral anticholinergic toxidromes when plant parts, especially seeds, are ingested in salads or stews or brewed into teas. The Datura (jimsonweed) species leaves resemble dandelion and mint and are considered noxious weeds compared to ornamental Brugmasia (trumpet or chalice plant) and Solandra (angel's trumpet) species (Figure 2).



Anticholinergic plant poisonings typically occur in two at-risk groups recent immigrants foraging for greens for salads and stews that resemble familiar ones in their native countries and adolescents experimenting with plant hallucinogens. (1-4) The tropine alkaloids inhibit acetylcholine receptors in the brain and parasympathetic nervous system, producing a classic toxidrome of flushed, dry skin, lowgrade fever, tachycardia, mydriasis, ileus, urinary retention, agitation, vertigo, and dysphoria; later progressing to aggression, confusion, dysarthria, hallucinations, and, potentially fatal coma. (13,14) The management of anti-cholinergic poisonings may include a timely opportunity in conscious patients for orogastic lavage and oral-activated charcoal decontamination afforded by delayed gastric emptying. Sedation with benzodiazepines is often indicated later; and physostigmine, 1-2 mg intravenously and repeated as indicated every 30-60 minutes (to a maximum total dose of 5-6 mg), can reverse a central anti-cholinergic syndrome in severe cases with coma and tachydysrhythmias. (15-18) Most patients will recover within 24 hours with benzodiazepine sedation alone for agitation and restlessness. (15-18) Recently, two cases of anisocoria were described in pre-teens who simply handled Brugmasia flowers and developed painless unilateral mydriasis unresponsive to light and accommodation with blurred vision. (19-20) In both cases, anisocoria resolved within two to three days. (19-20)

Although now banned by several countries and controlled by Schedule 1 status in several US states, including Louisiana, Salvia or diviner's sage (Salvia divinorum) is marketed on the Internet as a legal alternative to marijuana and other abused drugs. (4) Both Salvia leaves and morning glory seeds contain powerful hallucinogenic compounds that continue to be used in ritual ceremonies performed by Mazatec shamans in the state of Oaxaca, Mexico. (21) The psychoactive agent in Salvia is salvinorin A, a diterpene and selective kappa-opioid receptor agonist, which produces psychomimetc effects on ingestion of teas brewed from leaves, resembling the adverse effects caused by serotonergic agonists, selective serotonin reuptake inhibitors, or n-methyl-d-aspartate glutamate (NMDA) antagonists. (21) In its 2006 Annual National Survey on Drug Use and Health in the US, the Substance Abuse and Mental Health Services Administration reported that 1.8 million persons aged 12 or older had used Salvia in their lifetimes, and of these, 750,000 persons had used Salvia divinorum that year. (22) By 2007, the annual number of Salvia users in the US aged 12 or older had increased to 1 million. (22)

The psychoactive agents in morning glory seeds include the ergot alkaloids, ergonovine and lysergic acid amide (LSA), that resemble lysergic acid diethylamide (LSD) structurally and cause similar psychomimetic effects. Morning glory seeds, like Salvia divinorum, may also be purchased on the Internet, but, unlike Salvia, have not been criminalized. The psychedelic effects of Salvia leave teas and morning glory seeds or brews are similar and include blunted affect, deja vu, dissociation, uncontrollable laughter, multi-dimensional motion sensation, merging objects, colorful visual hallucinations, and paranoia. (21) There are no antidotes for Salvia and morning glory seed intoxication, and sedation with benzodiazepines and antipsychotics are often indicated. (21)

The epileptogenic plants cause more serious poisonings and deaths following unintentional ingestions than most other poisonous plants worldwide every year because they are perennial weeds that resemble many frequently foraged, edible herbs, including Queen Anne's lace, parsnip, wild celery, and carrots. (23) Epileptogenic plants cause generalized tonoclonic seizure activity through several mechanisms, including massive nicotinic receptor stimulation (poison hemlock, wild tobacco), gamma-aminobutyric acid (GABA) antagonism in the CNS (water hemlock), postsynaptic inhibition of inhibitory glycine receptors in the spinal cord (strychnine), and profound hypoglycemia (imported unripe ackee or breadfruit tree fruit).

The poison hemlock plant (Conium maculatum) contains several toxic piperidine alkaloids, primarily coniine, and has been used since antiquity as an intentional poison--most notably by the Athenians to execute Socrates. Nicotinic plant poisoning following ingestion of poison hemlock will result in initial CNS stimulation, with myoclonus and hyperreflexia progressing to generalized tonoclonic convulsions followed rapidly by weakness, paralysis, and respiratory failure.

Unintentional ingestions of the water hemlock plant, Cicuta maculata, causes most of the fatalities attributed to the misidentification of poisonous plants in the United States because the plant resembles many edible herbs and roots, is lethal in small quantities, and grows in low-lying areas throughout the US. (24) Water hemlock is considered the most toxic plant in the country, and its primary toxin, cicutoxin, is present in all of its parts and reaches its highest concentrations in roots and stems. (24) Oral mucosal contact with toy whistles made from the hollow stems of water hemlock have been associated with deaths in children. (24-25) Water hemlock poisoning will produce initial abdominal pain and nausea within 15-90 minutes, followed by vomiting, flushing, diaphoresis, salivation, vertigo, bronchorrhea, dyspnea, and cyanosis. Loss of consciousness, seizures, and status epilepticus may follow initial symptoms and, if not lethal, may result in rhabdomyolysis, myoglobinuria, and acute renal failure. (26)

Although derived from a non-native Asian plant, Strychnos nux-vomica, strychnine is now cultivated in Hawaii and has been used for decades in the United States as a rodenticide, medicinal and antipyretic folk remedy, and heroin adulterant. (27) Strychnine poisoning is unique among epileptogenic plant poisonings because it causes initial CNS stimulation manifested by fasciculations and hyperreflexia followed by severe tonoclonic muscle spasms with opisthotonic posturing without loss of consciousness. (27) Severe muscular spasms can result in tendon ruptures and vertebral fractures and are often associated with hyperpyrexia, rhabdomyolysis, and acute renal failure. (27) There are no antidotes for the epileptogenic plant poisonings, and successful management strategies have included early airway protection; multi-dose activated charcoal; sedation and muscular relaxation with benzodiazepines and neuromuscular blockers, especially in strychnine poisoning; ventilatory support; intravenous hydration; and hemofiltration or hemodialysis for renal failure. (27)

Cytotoxic Plants--The cytotoxic plants are popular household (crocus) and garden (crocus, vinca) plants that have been used to make anti-inflammatory drugs (colchicine from crocus), jewelry (castor bean, jequirty, or rosary pea), and to treat cancer (vinblastine and vincristine from vinca, podophyllotoxin from may apple). The cytotoxic plants include (1) the toxalbumins, the toxin (ricin) of which one, the castor bean (Ricinus communis), has been weaponized; (2) the mitotic inhibitors, many of which are highly effective as cancer chemotherapeutics; and (3) the cyanogenic glycosides contained in the kernels of several fruits, including apples, apricots, cherries, peaches, and plums (Table 1).

The toxalbumins are all plant lectins usually concentrated in seeds that inhibit protein synthesis by binding to intracellular 60S ribosomal subunits and resulting in initial gastrointestinal toxicity, followed by multi-organ failure after significant exposures. The indigenous toxalbumin containing plants include the castor bean plant (Ricinus communis), formerly grown commercially in the South for castor oil-containing pharmaceuticals; the jequirty pea or rosary plant (Abrus precatorius), a Caribbean tropical vine introduced into South Florida; the balsam apple (Mormordica species), a creeping vine that often chokes fences but remains revered as a folk medicine in Louisiana for wounds and diabetes; and several varieties of mistletoe (Phoradendron spp.), the parasitic epiphytes of deciduous trees popular as Christmas decorations. Ricin and abrin can be released in highly toxic amounts when their hard seeds are chewed, swallowed, and ingested, or when these toxalbumins are weaponized for injection or for aerosolization. In 1978, Georgi Markov, a Bulgarian dissident, was assassinated by Bulgarian agents in London by a ricin pellet fired into his leg from a modified umbrella-pellet gun. (28) Both castor bean and jequirty pea seeds are still used by Caribbean folk artists to make colorful jewelry and rosary beads that are frequently imported and may be accidently ingested by children (Figures 3 and 4). As long as seeds are not chewed prior to ingestion, they will not release their toxalbumins and cause significant gastrointestinal toxicity (Figures 3 and 4). There are no antidotes for toxalbumin toxicity and management of poisonings must begin immediately with activated charcoal, antiemetics, intravenous fluid resuscitation, and vasopressor support for cardiovascular collapse.

The mitotic inhibitors all contain similar cytotoxic plant alkaloids that can inhibit the polymerization of microtubules and cause metaphase arrest of mitosis, especially in rapidly dividing cells in the gastrointestinal tract and bone marrow. The indigenous plants containing mitotic inhibitors include crocus (Colchium autumnalis), vinca or periwinkle (Catharanthus roseus), and may apple (Podophyllum pelatum). Cytotoxic alkaloids derived from these plants have been used to treat gout (colchicine), condylomata acuminata (podophyllin), and cancer (vinblastine, vincristine, paclitaxel, podophyllotoxin). Ingestions of any parts of these plants will cause initial oropharyngeal pain, followed by severe gastrointestinal symptoms within hours, including intense abdominal pain and severe, profuse, and persistent diarrhea that may lead to volume depletion and electrolyte imbalance. Delayed toxic effects may include bone marrow toxicity, manifesting initially as leukocytosis, followed by leucopenia, peripheral neuropathy, ataxia, seizures, and encephalopathy. Death may result from direct toxic effects, cardiovascular collapse, or latent sepsis. There are no antidotes for mitotic inhibitor toxicity and management of poisonings must begin immediately with multi-dose activated charcoal, intravenous fluid resuscitation, and vasopressor support for cardiovascular collapse. Bone marrow toxicity may require blood and platelet transfusions and hematopoietic colony-stimulating factors.

Many edible fruits of the Malus (apple, crabapple) and Prunus (apricots, cherries, peaches, plums) species contain cyanide-releasing glycosides within their kernels. In addition, some ornamental plants, especially hydrangeas throughout the South, and trees (elderberry) also contain cyanogenic glycosides in their flowers (hydrangeas) or leaves and stems (elderberry). (29) Following ingestions of toxic parts of cyanogenic plants, cyanogenic glycosides have to be hydrolyzed in the gastrointestinal tract before releasing cyanide ion, which inhibits the final step in the mitochondrial electron transport chain and causes cytotoxicity from cellular energy failure. (29) After an incubation period of several hours, a constellation of lethargy, diaphoresis, abdominal pain, nausea, and vomiting ensues and is followed by mental status changes, ataxia, vertigo, stupor, seizures, cardiovascular instability, and multisystem organ failure. Laboratory results will demonstrate lactic acidosis and elevated thiocyanate levels. Initial management should include correction of acidosis, inotropic support, and antidotal therapy with prepackaged cyanide antidote kits (inhaled amyl nitrite ampoule initially or intravenous sodium nitrate, 10 ml; followed by intravenous 25% sodium thiosulfate, 50 ml) or a combination of sodium thiosulfate and hydroxocobalamin (5g intravenously over 15 min.). (30)

Plants Causing Gastrointestinal Toxicity--The plants causing gastrointestinal toxicity include the hepatotoxic pyrrolizidine alkaloids and the calcium oxalate injectors, which are popular household plants and include many popular cultivars of Caladium, Dieffenbachia, Philodendron, Schefflera, and Spathiphyllum (Table 1). Since intense oropharyngeal pain from mucosal injection of calcium oxalate crystals will limit further ingestion, chewing, and swallowing, most calcium oxalate plant ingestions can be managed with copious irrigation, demulcents, viscous lidocaine, and oral analgesics. Although calcium oxalate injectors rarely cause potentially fatal poisonings, they are responsible for the most frequent plant ingestions and have been used in suicide attempts (Dieffenbachia spp.), sometimes with serious consequences, including aortoesophageal fistula and massive gastrointestinal hemorrhage. (1-2,31)

Chronic low-dose ingestions of plant pyrrolizidine alkaloids in herbal teas and dietary supplements may result in insidious hepatotoxicity from veno-occlusive disease indistinguishable from the Budd-Chiari syndrome. (32) The indigenous plants containing pyrrolizidine alkaloids in all parts include the popular ornamental garden species of Crotalaria (yellow rattlebox) and Sesbania (scarlet rattlebox). Following ingestion, pyrrolizidine alkaloids are hepatically metabolized to highly alkaline pyrroles, which can cause caustic burns of the lining epithelium of hepatic sinusoids and, less commonly, of pulmonary vessels. (32) Massive acute ingestions can cause right upper quadrant pain, acute hepatitis, ascites, elevated liver enzymes, and coagulopathy. (32) Chronic low-level exposures may result in cirrhosis and in hepatic veno-occlusive disease more commonly than in pulmonary vascular occlusion with pulmonary hypertension. (32) There are no antidotes for pyrrolizidine toxicity; supportive management may allow time for hepatic regeneration; hepatic transplantation may be indicated for acute or chronic liver failure. (32)


The Prevention of Potentially Fatal Plant Poisonings

Most plant poisonings can be prevented by education and enforcement strategies. Education strategies include plant identification training in order to avoid selecting poisonous greens and herbs when foraging and choosing poisonous ornamental plants for gardens and households, especially in homes with children and pets. Enforcement strategies include scheduling and criminalizing the possession and use of hallucinogenic plants by state governments.

Although many plants contain toxins, plants provide more than 70% of new drugs today and continue to provide new therapies for infectious diseases (e.g., ciprofloxacin from the Chinese star anise plant) and cancer (e.g., paclitaxel from the Pacific yew tree). (33) More leisure time spent outdoors seeking natural foods and surfing the Internet for legal substances to abuse will create more opportunities for plant poisonings among high-risk groups, such as immigrants foraging for greens and adolescents experimenting with natural hallucinogens.


(1.) Watson WA, Litovitz TL, Rodgers GC Jr, et al. 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposures Surveillance System. Am J Emerg Med 2004; 22: 335-404.

(2.) Watson WA, Litovitz TL, Rodgers GC Jr, et al. 2004 Annual Report of the American Association of Poison Control Centers Toxic Exposures Surveillance System. Am J Emerg Med 2005; 23: 589-666.

(3.) Nelson LS, Shih RD, Balick MJ. Handbook of Poisonous and Injurious Plants, Second Edition. Springer, New York, New York, 2007, pp. XIV-XVII.

(4.) Vohra R, Seefeld A, Cantrell FL, Clark RF. Salvia divinorum: exposures reported to a statewide poison control system over 10 years. J Emerg Med 2009; September 16, 2009, epublished ahead of print. Available at

(5.) Bohnert AS, Fudalej S, Ilgen MA. Increasing poisoning mortality rates in the United States, 1999-2006. Pub Health Rep 2010; 125: 542-7.

(6.) Wade OL. Digoxin 1785-1985. I. Two hundred years of digitalis. J Clin Hosp Pharm 1986; 11: 3-9.

(7.) Slifman NR, Obermeyer WR, Aloi BK, et al. Contamination of botanical dietary supplements by Digitalis lanata. N Engl J Med 1998; 39: 806-11.

(8.) Newman LS, Feinberg MW, LeWine HE. A bitter tale. N Engl J Med 2004; 351: 594-9.

(9.) DeSilva HA, Fonseka MMD, Alahakone DGS, et al. Multiple-dose activated charcoal for treatment of yellow oleander poisoning: a single-blind, randomized, placebo-controlled trial. The Lancet 2003; 361: 1935-8.

(10.) Ohuchi S, Izumoto H, Kamata J, et al. A case of aconitine poisoning saved with cardiopulmonary bypass. Japan J Thoracic Surg 2000; 53: 541-4.

(11.) West P, Horowitz BZ. Zigadenus poisoning treated with atropine and dopamine. J Med Toxicol 2009; 5: 214-7.

(12.) Pierog JE, 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: 84-9.

(13.) McHenry LE, Hall RC. Angel's trumpet: lethal and psychogenic aspects. J Florida Med Assoc 1978; 65: 192-6.

(14.) Urich RW, Bowerman DL, Levitsky JA, et al. Datura stramonium: a fatal poisoning. J Forensic Sci 1982; 27: 948-54.

(15.) Jimsonweed poisoning associated with a homemade stew--Maryland, 2008. MMWR Morb Mort Week Rep 2010; 59: 102-4.

(16.) Spina SP, Taddei A. Teenagers with jimsonweed (Datura stramonium) poisoning. Can J Emerg Med Care 2007; 9: 467-8.

(17.) Greene GS, Patterson SG, Warner E. Ingestion of angel's trumpet: an increasingly common source of toxicity. South Med J 1996; 89: 365-9.

(18.) Francis PD, Clarke CF. Angel trumpet lily poisoning in five adolescents: clinical findings and management. J Paediatr & Child Health 1999; 93-5.

(19.) Firestone D, Slone C. Not your everyday anisocoria: angel's trumpet ocular toxicity. J Emerg Med 2007; 33: 21-4.

(20.) Andreola B, Piovan A, DaDalt L, et al. Unilateral mydriasis due to angel's trumpet. Clin Toxicol 2008; 46: 329-31.

(21.) Singh S. Adolescent salvia substance abuse. Addiction 2007; 102: 823-4. 2007

(22.) Substance Abuse and Mental Health Services Administration (SAMSHA), Office of Applied Sciences, February 2008. The NSDUH Report: Use of Specific Hallucinogens. Available at www.

(23.) Schep LJ, Slaughter RJ, Becket G, Beasley DM. Poisoning due to water hemlock. Clin Toxicol 2009; 47: 270-8.

(24.) Water hemlock poisoning--Maine, 1992. MMWR Morb Mort Week Rep 1994; 43: 229-231.

(25.) Driesbach R. Handbook of Poisoning, Eighth Edition. Lange Medical Publications, Los Altos, California, 1974, p. 433.

(26.) Carlton BE, Tufts E, Girard DE. Water hemlock poisoning complicated by rhabdomyolysis and renal failure. Clin Toxicol 1979; 14: 87-92.

(27.) Philippe G, Angenot L, Tits M, Frederich M. About the toxicity of some Strychnos species and their alkaloids. Toxicon 2004; 44: 405-16.

(28.) Rozsa L, Nixdorff K. Biological weapons in non-Soviet Warsaw Pact countries. In: Wheelis M, Rozsa L, Dando M, Eds. Deadly Cultures: The History of Biological Weapons since 1945. Harvard University press, Cambridge, Massachusetts, 2006, pp. 157-68.

(29.) Poisoning from elderberry juice--California. MMWR Morb Mort Week Rep 1984; 33: 173-4.

(30.) Sutter M, Tereshchenko N, Rafii R, Daubert GP. Hemodialysis complications of hydroxocobalamin: A case report. J Med Toxicol 2010; 6: 165-7.

(31.) Snajdauf J, Mixa V, Rygl M, et al. Aortoesophageal fistula--an unusual complication of Dieffenbachia ingestion. J Pediatr Surg 2005; 40: 29-31.

(32.) Stewart MJ, Steenkamp V. Pyrrolizidine poisoning: a neglected area in human toxicology. Therapeu Drug Monitoring 2001; 23: 698-708.


Dr. Diaz is Professor of Public Health and Program Director, Environmental and Occupational Health Sciences, School of Public Health, and Professor of Anesthesiology, School of Medicine, LSU Health Sciences Center-New Orleans.
Table 1: Frequency of Plant Exposures by Plant Types (all ages)

Ranking    Botanical Name       Common Name      Frequency   Percent

1         Spathiphyllum      White peace lily,     2,972       5.4
          spp.               white anthurium
2         Ilex spp.          Holly                 2,597       4.7
3         Philodendron       Philodendron          2,421       4.4
4         Euphorbia          Poinsettia            2,206       4.0
5         Phytolacca         Pokeweed              1,697       3.1
6         Toxicodendron      Poison ivy            1,490       2.7
7         Ficus spp.         Weeping fig,          1,136       2.1
                             rubber tree
8         Solanum spp.*      Nightshade            1,046       1.9
9         Malus spp.*        Apple, crab            920        1.7
                             apple rubber
10        Schlumbergera      Christmas              918        1.7
          bridgesii          cactus
11        Crassula spp.      Jade plant             817        1.5
12        Nerium oleander*   Oleander               785        1.4

* Potentially lethal exposures.

Source: Toxic Exposure Surveillance System (TESS) 2004 Annual Report
of the American Association of Poison Control Centers.
COPYRIGHT 2012 Louisiana State Medical Society
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2012 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Diaz, James H.
Publication:The Journal of the Louisiana State Medical Society
Article Type:Report
Geographic Code:1U7LA
Date:Jul 1, 2012
Previous Article:A case series of Vibrio vulnificus infections in New Orleans, Louisiana.
Next Article:An unexpected silver lining to Katrina: elimination of inter-campus transfer delay in STEMI care.

Terms of use | Privacy policy | Copyright © 2021 Farlex, Inc. | Feedback | For webmasters |