the journal of emergency medicine volume 15 issue 1 1997 [doi 10.1016%2fs0736-4679%2896%2900244-2]...

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ELSEVIER The Journal of Emergency Medicine, Vol 15, No II pp 65-69. 1997 Copyright 0 1997 Elsevier Science Inc. Printed in the USA. All rights reserved 0736-4679/97 $17.00 + .Gil PIT SO736-4679( % ) 00244-2 Topk Toxkdogy ANTtCHOLtNEfGtC TOXtCt-tY FROM NtWUSMDE BERRY POtSOHM RESPONStVE TO PHYSOSTKWWE L. J. Ceha, MD,* C. Presperin, RN, MPH, E. Young, PharmD, M. Allswede, DO,and T. Erickson, MD, FACEP *Cook County Hospital Department of Emergency Medicine, University of Illinois College of Pharmacy, Ingalls Memorial Hospital, Toxikon Consortium Section of Clinical Toxicology and Department of Emergency Medicine, University of Illinois at Chicago, Chicago, Illinois Reprint Address: Timothy B. Erickson, MD, FACEP, Offices of Emergency Medicine (M/C 724), University of Illinois at Chicago. 618 College of Medicine West, 1819 West Polk Street, Chicago, IL 6061 Z-7354 Cl Abstract-The woody nightshade, Sohum dulca- mara, belongs to the genus Solanum and its primary toxin is solauine. We report a large nightshade ingestion in a 4-yr-old girl who presented to the emergency depart- ment in acute anticholhtergic crisis. The child was given 0.2 mg of intravenous physostigmine (0.02 mg/kg). Within 50 min, the patient received two additional equal doses with complete resolution of symptoms. After 36 h of observation, the child was discharged. Our patient presented with symptoms more suggestive of the deadly nightshade species, Atropa belludonna , which is native to Europe; however, a detailed laboratory analysis of the suspect berries revealed no atropine or hyoscyamine. Analysis did reveal sterols consistent with sohmhte. Thii is a unique case presentation of woody nightshade, S. dulcamura, poisoning presenting with anticholinergic cri- sis and responding to physostigmine. Copyright 0 1997 Elsevier Science Inc. 0 Keywords-anticholhxugic toxicity; nightshade berry; physostigmine INTRODUCTION The woody nightshade, climbing nightshade, or bitter- sweet nightshade is a hearty shrub or vine with purple Presented at the North American Congress of Toxicology, Salt Lake City, UT, September 1994. flowers. The berries are green to bright orange-red, depending on their maturity. The plant is commonly found in the eastern and northern central IJnited States (Figure 1, left) and its primary toxin is solanine. Nightshade plant ingestion is a common poisoning. In the 1993 annual report of the American Association of Poison Control centers, 1853 solanine-containing plant exposures were reported and 754 casesinvolved woody nightshade berries. The majority of casesoccur in children younger than 6 yr ( 1). Ingestion of woody nightshade typically causesself- limited gastrointestinal symptoms. Severe toxicity presents with tachycardia or bradycardia, weakness, headache, fever, diaphoresis, and central nervous sys- tem (CNS) and respiratory depression (2 ‘1. CASE REPORT A 4-yr-old girl was brought to the emergency depart- ment with signs and symptoms consistent with anticho- linergic poisoning. The mother suspectedan ingestion 15 min prior to arrival of multiple orange-and-red ber- ries from a climbing vine located in the backyard. The patient was found supine and uttering incomprehensi- Toxicology is coordinated by Kenneth Kulig, MD, of Denver, Colorado RECEIVED: 18 December 1995; FINALSUBMISSIONRECEIVED: 24 April1996; ACCEPTED : 21 May 1996 65

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  • ELSEVIER

    The Journal of Emergency Medicine, Vol 15, No II pp 65-69. 1997 Copyright 0 1997 Elsevier Science Inc. Printed in the USA. All rights reserved

    0736-4679/97 $17.00 + .Gil

    PIT SO736-4679( % ) 00244-2

    Topk Toxkdogy

    ANTtCHOLtNEfGtC TOXtCt-tY FROM NtWUSMDE BERRY POtSOHM RESPONStVE TO PHYSOSTKWWE

    L. J. Ceha, MD,* C. Presperin, RN, MPH, E. Young, PharmD, M. Allswede, DO, and T. Erickson, MD, FACEP

    *Cook County Hospital Department of Emergency Medicine, University of Illinois College of Pharmacy, Ingalls Memorial Hospital, Toxikon Consortium Section of Clinical Toxicology and Department of Emergency Medicine,

    University of Illinois at Chicago, Chicago, Illinois Reprint Address: Timothy B. Erickson, MD, FACEP, Offices of Emergency Medicine (M/C 724), University of Illinois at Chicago.

    618 College of Medicine West, 1819 West Polk Street, Chicago, IL 6061 Z-7354

    Cl Abstract-The woody nightshade, Sohum dulca- mara, belongs to the genus Solanum and its primary toxin is solauine. We report a large nightshade ingestion in a 4-yr-old girl who presented to the emergency depart- ment in acute anticholhtergic crisis. The child was given 0.2 mg of intravenous physostigmine (0.02 mg/kg). Within 50 min, the patient received two additional equal doses with complete resolution of symptoms. After 36 h of observation, the child was discharged. Our patient presented with symptoms more suggestive of the deadly nightshade species, Atropa belludonna , which is native to Europe; however, a detailed laboratory analysis of the suspect berries revealed no atropine or hyoscyamine. Analysis did reveal sterols consistent with sohmhte. Thii is a unique case presentation of woody nightshade, S. dulcamura, poisoning presenting with anticholinergic cri- sis and responding to physostigmine. Copyright 0 1997 Elsevier Science Inc.

    0 Keywords-anticholhxugic toxicity; nightshade berry; physostigmine

    INTRODUCTION

    The woody nightshade, climbing nightshade, or bitter- sweet nightshade is a hearty shrub or vine with purple

    Presented at the North American Congress of Toxicology, Salt Lake City, UT, September 1994.

    flowers. The berries are green to bright orange-red, depending on their maturity. The plant is commonly found in the eastern and northern central IJnited States (Figure 1, left) and its primary toxin is solanine.

    Nightshade plant ingestion is a common poisoning. In the 1993 annual report of the American Association of Poison Control centers, 1853 solanine-containing plant exposures were reported and 754 cases involved woody nightshade berries. The majority of cases occur in children younger than 6 yr ( 1).

    Ingestion of woody nightshade typically causes self- limited gastrointestinal symptoms. Severe toxicity presents with tachycardia or bradycardia, weakness, headache, fever, diaphoresis, and central nervous sys- tem (CNS) and respiratory depression (2 1.

    CASE REPORT

    A 4-yr-old girl was brought to the emergency depart- ment with signs and symptoms consistent with anticho- linergic poisoning. The mother suspected an ingestion 15 min prior to arrival of multiple orange-and-red ber- ries from a climbing vine located in the backyard. The patient was found supine and uttering incomprehensi-

    Toxicology is coordinated by Kenneth Kulig, MD, of Denver, Colorado

    RECEIVED: 18 December 1995; FINALSUBMISSIONRECEIVED: 24 April1996; ACCEPTED : 21 May 1996

    65

  • L. J. Ceha et al.

    WOODY NIGHTSHADE (BITTERSWEET) Solanuv Lh4lcamara

    DEADLY NIGHTSHADE (BELLADONNA) Atropo Belladonna

    Figure 1. Comparison of So/artum dulcamara (left) and Atmpa belladonna (right). Reprinted with permission from Grieve CV, A modern herbal, vol. II. New York: Dover, 1971.

    ble sounds in the garden. The patient vomited once en route to the hospital.

    On examination, the patient was nonverbal, re- sponding only to painful stimuli. The airway was in- tact. Vital signs were 130/80 mmHg for blood pres- sure, 160-190 beats/min for heart rate, 26 breaths/ min for respiratory rate, and a temperature of 395C (103.7F). Pulse oximetry was 100% in room air. The patient weighed 13 kg. On physical examination, the pupils were 7-8 mm in diameter and poorly responsive to light. No nystagmus was noted. Lung sounds were clear bilaterally. The heart rate was fast and regular, without ectopic beats or murmurs. There was sinus tachycardia on the monitor. The abdomen was unre- markable. Rigidity and tremor were apparent in the upper and lower extremities. Neurological examination showed appropriate withdraw1 to pain. The skin was hot and dry.

    Laboratory survey revealed a white blood cell count

    of 20,500 mm3, a hemoglobin of 12 g/dL, and a hema- tocrit of 37%. The chemistry was unremarkable except for a blood sugar of 150 mg/dL. The chest radiograph was negative.

    Intravenous access was established. The patient was lavaged with an 18 French Salem tube and given 12 g of activated charcoal with sorbitol. The aspirate con- tained 50 cc of orange-colored fluid with ricelike grains. A lOO-mg acetaminophen suppository was given for temperature control. The Poison Control Center was contacted for further recommendations. The plant and berries were identified as nightshade by telephone consultation with a local botanist. The botanist did not receive a live specimen of the plant. Due to the apparent acute anticholinergic crisis with altered mental status, 0.2 mg of physostigmine, 0.02 mglkg, slow intravenous push, was administered. This dose was repeated twice over 50 min. Twenty minutes after the third dose, the patient demonstrated a deceler-

  • Nightshade Berry Poisoning 67

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  • 68 L. J. Ceha et al.

    CNS depression, headache, fever, diaphoresis, and res- piratory depression ( 7,11- 13 ) .

    Treatment is supportive. Gut decontamination, gas- tric lavage, and charcoal administration are recom- mended for early presentation. Depending on the se- verity, monitoring of the cardiorespiratory status and maintenance of fluid and electrolyte balance may be required ( 11) .

    Atropa belladonna (Figure 1, right) is the only spe- cies of nightshade that does not contain solanine; it contains hyoscyamine, atropine, and scopolamine ( 14). The toxins predominate in roots and leaves fol- lowed by the berries of the plant.

    Accidental ingestion of deadly nightshade berries can induce an anticholinergic toxidrome ( 15 - 17) ; however, our detailed laboratory analysis of the sus- pect berries indicates that our patient was not poisoned by this deadly nightshade species or its hybrid form. Other compounds found in A. belladonna that may be structurally different from atropine or hyoscyamine might possess anticholinergic properties.

    Morphologically, A. belladonna and S. dulcamara are distinctly different. The A. belludonna fruits are purple-black, whereas the S. dulcumaru berries can be yellow, orange, red, or green, depending on the ripe- ness. The leaves of A. belladonna are oval, whereas the leaves of S. dulcumaru are heart shaped, with one or two opposite lobes at the base of the leaf (Figure 1). Atropa belladonna grows like a bush, branching freely, whereas S. dulcamaru grows like a shrubby climber or vine.

    Atropa belladonna is native to Europe and is culti- vated in the eastern United States as an ornamental plant. The plant rarely survives in wild form in the United States (2,11,18).

    Site investigation in this case revealed only the S. dulcamuru species. A local botanist identified the plant as S. dulcamara by verbal descriptions.

    The possibility of a coingestion was considered. The plant and berries may have been exposed to insecticides or herbicides previously; however, the clinical picture described is not consistent with organophosphate, carba- mate, or pyrethrum toxicity. It is also not likely that the child ingested anticholinergic drugs in the house before going outside because none were available at that time. The Napralert profile, a database of ethnomedical, phar-

    macological, and chemical information found for any given species, did not have a citation of atropinelike compounds in S. dulcumaru ( 19).

    Physostigmine, an indirect parasympathomimetic alkaloid, is obtained from dried ripe seeds of the Phy- sostigma venenosum (calabar bean). This alkaloid acts as a reversible anticholinesterase agent and thus inhib- its the destructive action of acetylcholinesterase on acetylcholine. Physostigmine reverses CNS and toxic effects of agents, such as belladonna alkaloids, diphen- hydramine, and benztropine, that produce the anticho- linergic syndromes. Physostigmine can produce sei- zures and exaggerated parasympathetic responses, so atropine should be available to reverse its effects. Po- tential drug interactions exist with the choline esters bethanechol and methacholine and with neuromuscular blockers. In adults, recommended doses are OS-2 mg repeated every 20 min, slow intravenously, over 1 min, or intramuscularly until response or adverse reaction occurs. An additional l-4 mg may be given every 30- 60 min as needed to control symptoms. In children, 0.02 mg/kg intravenously or intramuscularly can be administered every 5- 10 min at less than 0.5 mg/min, not to exceed 2 mg (20).

    We do not recommend routine use of physostigmine in S. dulcamara exposures. The majority of these in- toxications are self-limiting and respond to supportive therapy. Physostigmine may be considered for intoxi- cations that present with anticholinergic crisis.

    CONCLUSION

    The cause of the anticholinergic reaction of our patient to the woody nightshade berry ingestion remains un- clear. Detailed analysis of the berries did not reveal atropine or hyoscyamine contents. There may have been other alkaloid agents not recognized by the ana- lytical techniques we used, as opposed to solanine be- ing the sole etiologic agent for this patients symptoms. Further animal studies could clarify this issue.

    Acknowledgments-We thank Ken Wood of the Rush Pres- byterian-St. Lukes Poison Control for his invaluable assis- tance in managing this case.

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    try and interrelationships, 6th ed. Cordus Press; 1991:271-85.

    4. Tolkachev ON, Shermyankin BV, Pronina NV. Isolation and purification of alkaloids. Chem Nat Comp. 1983; 19:387-401.

    5. Keeler RF, Baker DC, Garfield W. Spirosolane-containing S&z- num species and induction of congenital craniofacial malforma- tions Toxicon. 1990;28:873-84.

    6. Mclafferty PW, Stauffer DB. The important peak index of the

  • Nightshade Berry Poisoning

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    7. Dalvi RR, Bowie WC. Toxicology of solanine: an overview. Vet Hum Toxicol. 1983;25:13-15.

    8. Nishie K, Gumbmann MR, Key1 AC. Pharmacology of solanine. Toxic01 Appl Pharmacol. 1971; 19:81-92.

    9. Orgell WH, Vaidya KA, Dabm PA. Inhibition of human cholin- esterase in vitro by extracts of solanaceous plants. Science. 1958; 128:1136--7.

    10. Patil BC, Sharma RP, Salunkhe DK, Salunkhe K. Evaluation of solanine toxicity. Fed Cosmetol Toxicol. 1972; 10:395-g.

    1 1. Ellenhom MJ, Barceloux DG. Medical toxicology diagnosis and treatment of human poisoning. I st ed. New York: Elsevier; 1988:1229-33.

    12. Homfeldt CS, Collins JE. Toxicity of nightshade berries (Sola- num dulcumuru) in mice. Clin Toxicol. 1990;28:185-92.

    13. McMillan M. Thompson JC. An outbreak of suspected solanine poisoning in schoolboys: examination of criteria of solanine poisoning. Q J Med. 1979; 190:227-43.

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    14. Mack RB. Through all thy veins shall run a cold and drowsy humor nightshade poisoning. NCMJ 1987;48:2%-9.

    15. Opoku E, Hyaman 9. The deadly nightshade story. Nursing Mirror. 1972;42-4.

    16. Jo11 ME. Three cases of belladonna poisoning f 1916). Lancet. 1916;2:647.

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    18. Goldfrank LR, Weismann RS, Flomenbaum NE, et al. Toxico- logic emergencies. 5th ed. Norwalk, CT: Appleton & Lange; 1994:981-95.

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