Section

Poisons, Poisoning Syndromes, and Their Clinical Management

This section includes detailed scientific and clinical toxicological information. For nonphysicians, this scientific and medical information should be utilized for informational purposes only; certain medical terms utilized in this section terms are not defined. For physicians, clinical care should not simply focus on the potential plant exposure, although this information is obviously helpful in many situations. Rather, clinical care should take into account the patient's current and prior medical history, physical examination, appropriate diagnostic testing, response to therapy, and all other factors normally utilized in the provision of clinical care. That is, the patient should be managed based on his or her clinical condition rather than just on the knowledge of an exposure or suspicion of a toxin. Appropriate clinical judgment should be exercised in the management of all patients. The information in this section should be supplemented by consultation with a Poison Control Center, medical toxicologist or other expert, or the use of a medical textbook or other appropriate reference.

General initial medical management strategies that are required for all plant-exposed patients include, but are not necessarily limited to, vital sign assessment, consideration of the need for immediate interventions (e.g., ventilation and oxygenation, blood glucose), determination of the need for laboratory or other diagnostic testing, and the consideration of the need for gastrointestinal decontamination (see Section 4). Intervention at any point that is deemed appropriate to correct or prevent progression of a clinical abnormality is critical. Specific considerations and interventions follow. Additional information and references are found in the individual plant descriptions in Section 5.

Poisoning by Plants with Anticholinergic (Antimuscarinic) Poisons

Examples of plant genera associated with this syndrome: Atropa Brugmansia Datura

Hyoscyamus Solandra Solanum

Toxic Mechanism

Competitive antagonism of acetylcholine at the muscarinic subtype of the acetylcholine receptor, which is primarily located in the parasympathetic nervous system and the brain.

Clinical Manifestations

The classically described anticholinergic syndrome includes dry, warm, and flushed skin, parched mucous membranes, garbled speech, sinus tachycardia, adynamic ileus (absent bowel motility), urinary retention, and delirium with hallucinations. The hallucinations may be quite troubling to the patient, and patients may develop severe dysphoria or agitated delirium along with their sequelae. The patient's temperature may be slightly elevated, and is rarely above 102°F unless he or she is severely agitated or convulsing. Seizures may occur but generally only in patients who have other clinical findings consistent with anticholinergic poisoning. Complete clinical recovery even in the absence of complications may take many hours to days.

Specific Therapeutics

Given the common clinical presentation of altered mental status in association with elevated body temperature, patients should be evaluated for other medical problems, including sepsis and meningitis, unless the diagnosis is certain. Patients who are seriously poisoned by an antimuscarinic agent, particularly those with an appropriate confirmatory history, should receive either sedation with a benzodiazepine or reversal of their clinical syndrome with physostig-mine. This antidote, a cholinesterase inhibitor, raises intrasynaptic levels of acetylcholine by preventing the neurotransmitter's enzymatic metabolism by the enzyme cholinesterase and allows acetylcholine to successfully compete with the toxin for the muscarinic receptor. The initial dose of physostigmine is 1-2mg in adults (0.02mg/kg in children) administered intravenously over no less than 5 minutes. Lack of clinical improvement suggests that either the diagnosis is incorrect or the dose of physostigmine is insufficient. Failure to develop cholinergic findings (e.g., salivation, bradycardia) following physostigmine raises the likelihood of the diagnosis of anticholinergic poisoning, and administration of increasing doses of the drug (up to 5mg total dose in adults over 30 minutes) may be appropriate. The duration of action of some of the antimus-carinic alkaloids may be longer than that of physostigmine, and repeated administration of the latter may be required; alternatively, once the diagnosis is confirmed by an appropriate response to antidote, the patient may be sedated with a benzodiazepine and observed.

References

Burns MJ, Linden CH, Graudins A, Brown RM, Fletcher KE. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med 2000;35:374-81.

Howland MA. Physostigmine salicylate. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 794-797.

Poisoning by Plants with Calcium Oxalate Crystals

Examples of plant genera associated with this syndrome: Alocasia Arisaema Brassaia

Caladium Caryota Colocasia

Dieffenbachia Epipremnum Monstera

Philodendron Spathiphyllum

Calcium Oxalate Raphides Image

Calcium oxalate crystals at high magnification* Toxic Mechanism

Upon mechanical stimulation, as occurs with chewing, crystalline calcium oxalate needles, bundled in needle-like raphides, release from their intracellu-lar packaging (idioblasts) in a projectile fashion. These needles penetrate the mucous membranes and induce the release of histamine and other inflammatory mediators.

Clinical Manifestations

After biting or chewing, there is rapid onset of local oropharyngeal pain, which typically limits continued exposure, as well as local swelling and garbled speech. If swallowed, inflammation of the posterior oropharynx or larynx may rarely produce oropharyngeal edema and airway compromise. Endoscopic evaluation of the patient's airway, esophagus, or stomach may be necessary. Ocular exposure produces extreme pain, keratoconjunctival injection, and chemosis, with the potential for severe ocular damage and vision loss. Extensive dermal contact may produce pain and signs of irritation. In contrast to that occurring with soluble oxalate ingestion, in which profound hypocalcemia may occur, there is generally no associated systemic toxicity.

Specific Therapeutics

Airway assessment and management is of the highest priority following ingestion. Oropharyngeal or dermal pain may be managed with appropriate demulcents, viscous lidocaine, analgesics or with copious irrigation. Further evaluation of the patient's pharyngeal, respiratory, and gastrointestinal tract may be necessary. Eye exposure generally requires extensive irrigation and analgesia. Ophthalmologic consultation should be considered as needed.

References

*Franceschi VR, Nakata PA. Calcium oxalate in plants: Formation and function. Annu Rev Plant Biol. 2005;56:41-71.

Gardner DG. Injury to the oral mucous membranes caused by the common houseplant, Dieffenbachia. A review. Oral Surg Oral Med Oral Pathol. 1994;78:631-633.

Palmer M, Betz JM. Plants. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1577-1602.

Poisoning by Plants with Cardioactive Steroids/Cardiac Glycosides

Examples of plant genera associated with this syndrome: Acokanthera Adenium Adonis

Calotropis Cryptostegia Digitalis

Helleborus Ornithogalum Convallaria

Nerium Pentalinon Thevetia

Urginea Strophanthus Scilla

Toxic Mechanism

Cardioactive steroids, termed cardiac glycosides when sugar moieties are attached, inhibit the cellular Na+/K+-ATPase. The effect is to indirectly increase intracellular Ca2+ concentrations in certain cells, particularly myocardial cells. Therapeutically, this both enhances cardiac inotropy (contractility) and slows the heart rate. However, excessive elevation of the intracellular Ca2+ also increases myocardial excitability, predisposing to the development of ventricular dysrhythmias. Enhanced vagal tone, mediated by the neurotransmitter acetylcholine, is common with poisoning by these agents, and produces brady-cardia and heart block.

Clinical Manifestations

Ingestion of plants containing cardioactive steroids may cause abdominal pain and induce vomiting, which serves both as an early sign of toxicity and a mechanism to limit poisoning. Cardiovascular and electrocardiographic effects include sinus and junctional bradycardia as well as ventricular tachydysrhyth-mias, including ventricular tachycardia and ventricular fibrillation. Hyperkalemia may develop and is associated with poor patient outcome. Serum digoxin concentrations may be obtained but should not be relied upon to exclude toxicity as other cardioactive steroids will have unpredictable assay cross-reactivity. Consequently, treatment, if clinically indicated, should not await laboratory confirmation.

Specific Therapeutics

Most of the available clinical experience with cardioactive steroid poisoning is related to digoxin toxicity. In these patients, standard supportive medical management is often inadequate. Therefore, any patient with consequential digoxin poisoning should receive digoxin-specific Fab. This product contains the antigen-binding regions (Fab) of animal-derived antidigoxin antibodies. Although specifically designed for the management of digoxin poisoning, digoxin-specific Fab appears to have sufficient cross-recognition of other cardioactive steroids to warrant its administration in other nondigoxin cardioactive steroid poisonings. The empiric dose is 10 vials (400 mg) administered intravenously in both adults and children, with additional dosing based on clinical response or additional information. Indications for its use include significant bradycardia, tachydysrhythmias, or hyperkalemia, with or without an elevated serum digoxin concentration, in any patient seriously believed to be poisoned by a cardioactive steroid-containing plant.

References

Eddleston M, Persson H. Acute plant poisoning and antitoxin antibodies. J Toxicol Clin Toxicol 2003;41:309-315.

Hack JB, Lewin NA. Cardioactive steroids. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 971-982.

Howland MA. Digoxin-specific antibody fragments. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 983-988.

Newman LS, Feinberg MW, LeWine HE. Clinical problem-solving: A bitter tale. N Engl J Med 2004;351:594-599.

Poisoning by Plants with Convulsant Poisons (Seizure)

Examples of plant genera associated with this syndrome: Aethusa Anemone Blighia

Caltha Caulophyllum Cicuta

Clematis Conium Coriaria

Gymnocladus Hippobroma Laburnum

Lobelia Menispermum Myoporum

Nicotiana Pulsatilla Ranunculus

Sophora Spigelia Strychnos

Toxic Mechanism

A convulsion is the rhythmic, forceful contraction of the muscles, one cause of which are seizures. Seizures are disorganized discharges of the central nervous system that generally, but not always, result in a convulsion. There are various toxicological mechanisms that result in seizures including antagonism of gamma-aminobutyric acid (GABA) at its receptor on the neuronal chloride channel, imbalance of acetylcholine homeostasis, excitatory amino acid mimicry, sodium channel alteration, or hypoglycemia. Strychnine and its analogues antagonize the postsynaptic inhibiting activity of glycine at the spinal cord motor neuron. Strychnine results in hyperexcitability of the motor neurons, which manifests as a convulsion.

Clinical Manifestations

Unless an underlying central nervous system lesion exists, patients with plant-induced seizures generally present with generalized, as opposed to focal, seizures. Most patients develop generalized tonic-clonic convulsions, in which periods of shaking movement (convulsion or clonus) are interspersed with periods of hypertonicity. Occasionally, patients may not have overt motor activity (i.e., nonconvulsive seizure), or may present in the postictal period (partially or fully recovered from their seizure). The diagnosis in this situation may be difficult to determine. Patients who are having a generalized seizure should have loss of consciousness as a result of central nervous system dysfunction, and often have urinary or fecal incontinence, tongue biting, or other signs of trauma.

Conscious patients who are manifesting what appear to be generalized convulsions may have myoclonus or strychnine poisoning. Strychnine-poisoned patients manifest symmetrical convulsive activity, but because the activity is the result of spinal cord dysfunction, there is no loss of consciousness (i.e., no seizure) until metabolic or other complications intercede.

Specific Therapeutics

Once hypoglycemia and hypoxia have been excluded (or treated), a rapidly acting anticonvulsant benzodiazepine (e.g., diazepam, 5-10 mg in adults (0.1-0.3mg/kg in children) or lorazepam, 2mg in adults, or 0.1mg/kg in children), should be administered parenterally for persistent seizures. Although diazepam and lorazepam are nearly equivalent in time to onset, lorazepam has a substantially longer duration of anticonvulsant effect. Lorazepam can be administered intramuscularly, though this route is not ideal because of a slow absorptive phase. Dosing may be repeated several times as needed. Inability to expeditiously control seizures with benzodiazepines may necessitate the administration of barbiturates, propofol, or another anticonvulsant medication. There is generally no acute role for phenytoin or other maintenance anticonvulsants in patients with toxin-induced seizures.

References

Chan YC. Strychnine. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1492-1496.

Philippe G, Angenot L, Tits M, Frederich M. About the toxicity of some Strychnos species and their alkaloids. Toxicon 2004;44:405-416.

Wills B, Erickson T. Drug- and toxin-associated seizures. Med Clin North Am 2005;89: 1297-1321.

Poisoning by Plants with Cyanogenic Compounds

Examples of plant genera associated with this syndrome: Eriobotrya Hydrangea Malus

Prunus Sambucus

Toxic Mechanism

Cyanogenic compounds, most commonly glycosides, must be metabolized to release cyanide. Cyanide inhibits the final step of the mitochondrial electron transport chain, resulting rapidly in cellular energy failure.

Clinical Manifestations

Because the cyanogenic glycosides must be hydrolyzed in the gastrointestinal tract before cyanide ion is released, the onset of toxicity is commonly delayed. Abdominal pain, vomiting, lethargy, and sweating develop initially, followed shortly by altered mental status, seizures, cardiovascular collapse, and multisystem organ failure. Laboratory testing may reveal an elevated blood lactic acid; cyanide levels are not generally available rapidly. Thiocyanate, a metabolite of cyanide, may be measured in the patient's blood, and although often confirmatory in retrospect, immediate results are not readily available.

Specific Therapeutics

Initial management includes aggressive supportive care, intravenous fluid therapy, and correction of consequential metabolic acidosis using intravenous sodium bicarbonate as appropriate. Antidotal therapy, available in the form of a prepackaged cyanide antidote kit, should be administered to any patient believed to be suffering from cyanide poisoning. Before the establishment of an intravenous line, an amyl nitrite pearl may be broken and held under the patient's nose for 30 seconds each minute. In patients with intravenous access,

10 ml of 3% sodium nitrite in an adult, or in an appropriate pediatric dose (guidelines supplied with the kit), should be administered intravenously; this should be followed rapidly by 50 ml of 25% sodium thiosulfate intravenously in an adult, or 1.65 ml/kg in children. In certain circumstances, for example, when the diagnosis is uncertain, administration of only the sodium thiosulfate component of the antidote kit may be appropriate. Outside of the United States, hydroxocobalamin, an alternative antidote, may be available.

References

Holstege CP, Isom G, Kirk MA. Cyanide and hydrogen sulfide. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1716-1724.

Howland MA. Nitrites. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1725-1727.

Howland MA. Sodium thiosulfate. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1728-1730. Vetter J. Plant cyanogenic glycosides. Toxicon 2000;38:11-36.

Poisoning by Plants with Gastrointestinal Toxins

Many and various plant genera are associated with this syndrome.

Toxic Mechanism

Several different mechanisms are utilized by plant toxin to produce gastrointestinal effects, generally described as either mechanical irritation or a pharma-cologic effect. Irritant toxins indirectly stimulate contraction of the gastrointestinal smooth muscle. The pharmacologically active agents most commonly work by stimulation of cholinergic receptors in the gastrointestinal tract to induce smooth muscle contraction [e.g., cholinergic (including nicotinelike)] alkaloids. Some plant toxins (e.g., mitotic inhibitors, toxalbumins) alter the normal development and turnover of gastrointestinal lining cells and induce sloughing of this cellular layer. Hepatotoxins may directly injure the liver cells, commonly through the production of oxidant metabolites. Indirect hepatotox-icity may occur, as with the pyrrolizidine alkaloids (see "Poisoning by Plants with Pyrrolizidine Alkaloids", p 31).

Clinical Manifestations

Nausea, vomiting, abdominal cramping, and diarrhea are the hallmarks. Vomiting may be bloody or may contain acid-degraded blood ("coffee grounds") leaked secondary to gastric irritation. Extensive diarrhea and vomiting may produce acid-base, electrolyte, and fluid abnormalities, leading to hypokalemia and profound volume depletion. Small children in particular may become rapidly volume depleted and it may be more difficult to diagnose than in adults. Certain plant toxins that produce prominent gastrointestinal findings may subsequently produce systemic toxicity following absorption. For agents in this group (e.g., mitotic inhibitors, toxalbumins), the gastrointestinal manifestations serve as a warning for potential systemic toxicity.

Specific Therapeutics

Vomiting may be mitigated by antiemetic agents such as metoclopramide; occasionally, resistant emesis may require a serotonin antagonist such as ondansetron. Specific treatment of a patient's diarrhea (e.g., loperamide) is generally unnecessary. Assessment for and correction of volume depletion and metabolic changes are critical. For most patients, intravenous rehydration should be initiated using normal saline or lactated Ringer's solution and adjusted based on clinical or laboratory criteria. Oral rehydration therapy may be attempted in patients with minor clinical abnormalities. Electrolyte and acid-base derangements usually resolve with supportive care but may occasionally require specific therapy. Phar-macotherapies for the prevention of treatment of hepatotoxicity are varied, but empiric therapy with N-acetylcysteine is often suggested.

References

Palmer M, Betz JM. Plants. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1577-1602.

Poisoning by Plants with Mitotic Inhibitors

Examples of plant genera associated with this syndrome: Bulbocodium Catharanthus Colchicum

Gloriosa Podophyllum

Toxic Mechanism

These agents interfere with the polymerization of microtubules, which must polymerize for mitosis to occur, leading to metaphase arrest. Rapidly dividing cells (e.g., gastrointestinal or bone marrow cells) typically are affected earlier and to a greater extent than those cells that divide slowly. In addition, micro-tubules are important in the maintenance of proper neuronal function.

Clinical Manifestations

Patients typically have early gastrointestinal abnormalities, including vomiting and diarrhea. Oral ulcers and frank gastrointestinal necrosis can occur. Multisystem organ failure may follow. Bone marrow toxicity typically manifests as an initial leukocytosis, due to release of stored white blood cells, followed by leukopenia. Death may occur from direct cellular toxic effects or from sepsis. Nervous system toxicity, including ataxia, headache, seizures, and encephalopathy, may develop initially, and peripheral neuropathy may develop in patients who survive.

Specific Therapeutics

Initial management includes aggressive supportive and symptomatic care. In patients with profound bone marrow toxicity, colony-stimulating factors may be beneficial. Consultation with appropriate specialists, such as a hematologist, should be strongly considered.

References

Mullins ME, Carrico EA, Horowitz BZ. Fatal cardiovascular collapse following acute colchicine ingestion. J Toxicol Clin Toxicol 2000;38:51-54.

Schier J. Colchicine and podophylline. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 580-589.

Poisoning by Plants with Nicotine-Like Alkaloids

Examples of plant genera associated with this syndrome: Baptisia Caulophyllum Conium

Gymnocladus Hippobroma Laburnum

Lobelia Nicotiana Sophora

Toxic Mechanism

These agents are direct-acting agonists at the nicotinic subtype of the acetyl-choline receptor in the ganglia of both the parasympathetic and sympathetic limbs of the autonomic nervous system (Nn receptors), the neuromuscular junction (NM receptors), and the brain.

Clinical Manifestations

Sympathetic stimulation, including hypertension, tachycardia, and diaphoresis, and parasympathetic stimulation, including salivation and vomiting, are common (NN). Hyperstimulation at the NM results in fasciculations, muscular weakness, and, rarely, depolarizing neuromuscular blockade. Seizures may occur as a result of effects at cerebral nicotinic receptors.

Specific Therapeutics

Control of the patient's autonomic hyperactivity is generally not needed unless secondary complications, such as myocardial ischemia, develop or are anti cipated. In this case, the vital sign abnormalities may be corrected through the judicious use of antihypertensive drugs, including nitroprusside or diltiazem, as appropriate. Neuromuscular symptoms cannot be effectively antagonized because effective agents (e.g., curare-like drugs) would also produce neuromuscular blockade. Patients with inadequate ventilatory effort should be managed supportively. Seizures should respond to intravenous benzodiazepine, such as lorazepam or diazepam.

References

Palmer M, Betz JM. Plants. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1577-1602.

Rogers AJ, Denk LD, Wax PM. Catastrophic brain injury after nicotine insecticide ingestion. J Emerg Med 2004;26:169-172.

Solomon ME. Nicotine and tobacco preparations. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1221-1230.

Vetter J. Poison hemlock (Conium maculatum L.). Food Chem Toxicol 2004;42: 1373-82.

Poisoning by Plants with Pyrrolizidine Alkaloids

Examples of plant genera associated with this syndrome: Crotalaria Echium Heliotropium

Senecio Sesbania

Toxic Mechanism

Pyrrolizidine alkaloids are metabolized to pyrroles, which are alkylating agents that injure the endothelium of the hepatic sinusoids or pulmonary vasculature. Endothelial repair and hypertrophy result in venoocclusive disease. Centrilob-ular necrosis may occur following acute, high-dose exposures, presumably caused by the overwhelming production of the pyrrole. Chronic use is also associated with hepatic carcinoma.

Clinical Manifestations

Acute hepatotoxicity caused by massive pyrrolizidine alkaloid exposure produces gastrointestinal symptoms, right upper quadrant abdominal pain, hepatosplenomegaly, and jaundice as well as biochemical abnormalities consistent with hepatic necrosis [e.g., aspartate ammotransferase (AST), bilirubin, increased international normalized ratio (INR)]. Prolonged, lower-level exposure produces more indolent disease, and patients may present with cirrhosis or ascites caused by hepatic venous occlusion. This syndrome is clinically and pathologically similar to the Budd-Chiari syndrome.

Certain pyrrolizidine alkaloids (e.g., that from Crotalaria spectabilis) produce pulmonary vasculature occlusion and the syndrome of pulmonary hypertension in animals, but it is not known whether there is an analogous human response.

Specific Therapeutics

Standard supportive care may allow for some spontaneous repair. There are no known specific therapies. Liver transplantation may be an option for patients with severe hepatotoxicity or cirrhosis.

References

Palmer M, Betz JM. Plants. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1577-1602.

Stewart MJ, Steenkamp V. Pyrrolizidine poisoning: A neglected area in human toxicology. Therapeutic Drug Monitoring 2001;23:698-708.

Poisoning by Plants with Sodium Channel Activators

Examples of plant genera associated with this syndrome: Aconitum Kalmia Leucothoe

Lyonia Pernettya Pieris

Rhododendron Schoenocaulon Veratrum

Zigadenus

Toxic Mechanism

These agents stabilize the open form of the voltage-dependent sodium channel in excitable membranes, such as neurons and the cardiac conducting system. This causes persistent sodium influx (i.e., persistent depolarization) and prevents adequate repolarization leading to seizures and dysrhythmias, respectively. In the heart, the excess sodium influx activates calcium exchange, and the intracellular hypercalcemia increases both inotropy and the potential for dysrhythmias.

Clinical Manifestations

Vomiting is very common and occurs through a central nervous systemmediated mechanism. Sodium channel effects on sensory neurons may produce paresthesias in a perioral and distal extremity distribution. Persistent depolarization of motor neurons produces fasciculations, motor weakness, and ultimately paralysis. In the heart, the effects of sodium channel opening have been compared to that of the cardioactive steroids: atropine-sensitive sinus brady-cardia, atrioventricular blocks, repolarization abnormalities, and, occasionally, ventricular dysrhythmias. However, although the clinical findings are similar, the underlying mechanisms and treatments may differ.

Specific Therapeutics

Normal saline should be rapidly infused into patients with hypotension, and atropine is often therapeutic for sinus bradycardia and conduction blocks. Hypotension may require pressor agents such as norepinephrine. Mechanism-based therapy suggests the use of sodium channel blocking drugs such as lido-caine or amiodarone. None has been proven superior, and the agent used should probably be based on the comfort level of the provider. Although the clinical presentation is similar to poisoning by cardioactive steroids, there is no defined role for digoxin-specific Fab.

References

Lewin NA, Nelson LS. Antidysrhythmics. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 959-971.

Lin CC, Chan TY, Deng JF. Clinical features and management of herb-induced aconitine poisoning. Ann Emerg Med 2004;43:574-579.

Palmer M, Betz JM. Plants. In: Flomenbaum NE, Goldfrank LR, Hoffman RS, Howland MA, Lewin NA, Nelson LS. Goldfrank's Toxicologic Emergencies, 8th Edition. McGraw-Hill. New York, NY. 2006. p. 1577-1602.

Poisoning by Plants with Toxalbumins

Examples of plant genera associated with this syndrome: Abrus Hura Jatropha

Momordica Phoradendron Ricinus

Robinia

Toxic Mechanism

The protein toxins derived from these plants work specifically by inhibiting the function of ribosomes, the subcellular organelle responsible for protein synthesis. The toxins typically have two linked polypeptide chains. One of the chains binds to cell-surface glycoproteins to allow endocytosis into the cell. The other chain upon cell entry binds the 60S ribosomal subunit and impairs its ability to synthesize protein.

Clinical Manifestations

Clinical manifestations depend largely on the route of exposure. Following ingestion, local gastroenteritis produces diarrhea and abdominal pain. Because the seed coat of many toxalbumin containing seeds is tough, chewing is generally a prerequisite for toxicity. Absorption of toxin into the systemic circulation allows widespread distribution and multisystem organ failure. Parenteral administration via injection similarly produces diffuse organ dysfunction. Following inhalation of aerosolized toxin, localized pulmonary effects are of greatest concern, although systemic toxicity is possible. Depending on the dose and route administered, the development of findings may be delayed.

Specific Therapeutics

Death from multisystem organ failure is best prevented through aggressive support of vital organ function and prevention of infection. Work is progressing on the use of antiricin antibodies, but it is not in current clinical use.

References

Audi J, Belson M, Patel M, Schier J, Osterloh J. Ricin poisoning: A comprehensive review. JAMA 2005;294:2342-2351.

Bradberry SM, Dickers KJ, Rice P, Griffiths GD, Vale JA. Ricin poisoning. Toxicol Rev 2003; 22:65-70.

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