Conium maculatum 19.May.2019-Expires: 7 days - Do not archive IDENTIFICATION The correct identification of this plant is imperative. If the identity is uncertain, seek clarification from a reliable source such as a garden center or botanist.   Different Conium species cause different toxic effects. Generalizations should never be made as to symptoms expected. “Hemlock” may refer to Conium maculatum or Cicuta spp.. Both are highly toxic but have very different effects.[1][2]   FAMILY NAME Umbelliferae GENUS NAME Conium   SPECIES NAME Conium maculatum   IMAGE Click here for full-size image   Click here for full-size image   Click here for full-size image   HABITAT Grows in damp, cooler places and open woods. Weed of roadsides, ditches, edges of cultivated fields, and waste areas.[3][4][5]   Conium maculatum is native to Europe and West Asia. It has been introduced to America, North Africa, Australia, and New Zealand.   USES Extracts of this species were used both as a sedative and an antispasmodic. However, because of the plants toxicity, it was discontinued by the early 20th century.[6]   This species has no known uses and is classified as a weed. INTERVENTION CRITERIA Intervention Level Child and Adult Decontamination, if appropriate, and monitoring is recommended: - For all known or suspected ingestions of hemlock   With environmental exposures involving dermal contact, management depends on clinical presentation. Refer all symptomatic cases to an appropriate health care facility.   Observation Period Observation at Home All patients require medical attention.   Medical Observation If medical observation is required the patient must be monitored for 4 hours following exposure for onset or worsening of symptoms.   If the patient is asymptomatic at the end of the observation period, and if they have been appropriately decontaminated and any investigations have been completed, they may be: Discharged into the care of a reliable observer, or Referred for psychological assessment if the overdose or exposure was with intent to self-harm   Investigations Levels A mousy odor is associated with Conium maculatum; this odor on the breath or in the urine can be used as a diagnostic clue. However, absence of this odor does not rule out exposure.   Coniine (or other plant alkaloids) blood levels are not readily available, nor necessary for clinical management. Admission Criteria Admission to an intensive care facility is required for those suffering significant signs of toxicity including: CNS depression Convulsions Respiratory depression Hypotension Bradycardia   TREATMENT TREATMENT SUMMARY Administration of activated charcoal may be considered within one hour of ingestion; however, benefit is unproven, and risks of seizure, vomiting, and aspiration potentially out-weigh gain.[1] There are no specific antidotes and no methods for enhancing elimination can be recommended.   Supportive care is the mainstay of management with primary emphasis on cardiovascular and respiratory support. In severe cases, particular care should be given to airways management and respiratory support is vital in obtaining a positive outcome, as death is usually due to respiratory paralysis. Routine supportive care should be used for the treatment of other effects.   Nausea and vomiting may persist requiring symptomatic care with IV rehydration or antiemetic drugs, appropriate fluid and electrolyte balance must be maintained. Hypotension usually responds to intravenous fluids, sympathomimetics may be needed. Rarely cardiac dysrhythmias occur and should be managed using standard electrical and/or pharmacological methods. Extreme agitation or seizures can be a complicating feature and should be treated with a benzodiazepine. Atropine may be used to control manifestations from parasympathetic stimulation, such as diarrhea, urination, bronchospasm, emesis, lacrimation, and sweating. Monitor for rhabdomyolysis and acute renal failure.   Emergency Stabilization Ensure adequate cardiorespiratory function Seizure Emergency monitoring Decontamination Ingestion Single dose activated charcoal Skin Irrigate Eye Irrigate immediately Antidote(s) None recommended Enhanced Elimination Not recommended Supportive Care Monitoring Gastrointestinal Gastrointestinal irritation Neurologic Coma Seizure Respiratory Respiratory failure Cardiovascular Bradycardia Musculoskeletal Rhabdomyolysis Renal Acute renal failure EMERGENCY STABILIZATION Ensure Adequate Cardiopulmonary Function Airway Ensure the airway is protected if compromised (intubation may be necessary).   Cardiovascular Immediately establish secure intravenous access.   Seizure Administer a benzodiazepine as first-line treatment to patients with seizure activity.[7]   Blood glucose concentration should be promptly determined. If the result indicates hypoglycemia, or is unobtainable, supplemental dextrose should be administered IV.   Emergency Monitoring Heart rate Respiratory rate Seizure activity DECONTAMINATION Ingestion Single Dose Activated Charcoal Decontamination with activated charcoal is recommended for recent ingestions of hemlock. However, as hemlock commonly produces vomiting, CNS or respiratory depression, the time frame for successful administration is limited and risks pulmonary aspiration. In symptomatic patients general supportive measures should take precedence over decontamination.[1]   Administer activated charcoal up to 1 hour following a potentially toxic ingestion.[8]   Single dose activated charcoal[9] CHILD 1 to 2 g/kg orally ADULT 50 to 100 g orally   Nasogastric Administration Nasogastric instillation of activated charcoal is not recommended unless the ingestion is considered potentially severely toxic and oral administration is not successful. Accurate placement of the nasogastric tube and protection of the airway must be ensured.   Skin If necessary, remove contaminated clothing or jewelry. Flush the affected area with water as soon as possible. Continue to irrigate until all of the contaminant is removed.   Eye Remove contact lenses. Irrigate immediately with water or saline for at least 15 minutes. If the eye is contaminated with solid particles, the eyelid should be completely everted and any solid material removed as quickly as possible whilst continuing to irrigate. A topical anesthetic may be necessary in some patients, especially children, to enable the patient to open the lids sufficiently for effective irrigation.   If, following irrigation, any of the following are apparent: Ocular pain (other than mild and resolving) Erythema (other than mild and resolving) Decreased visual acuity Ocular discharge/crusting   A full ophthalmologic examination should be undertaken and any injury appropriately treated.   ANTIDOTE(S) There Are No Antidotes For This Substance There is no specific antidote for the treatment of this poisoning. Treatment is based on symptomatic and supportive care.   SIGNS AND SYMPTOMS The effects of coniine are similar to those of nicotine, but with more pronounced CNS and curare-like actions.   General signs are salivation, vomiting, dilation of the pupils, blurred vision, incoordination, myalgia, muscle fasciculations or flaccid paralysis, coldness of the extremities, and slow weak pulse. Subsequently the pulse may become rapid and thready followed by coma, convulsions, and eventually death from respiratory paralysis.[10][11] Rhabdomyolysis and subsequent renal failure have also been reported.[12]   Routes of Exposure Systemic symptoms can occur after ingestion of fresh hemlock plant material; drying is thought to somewhat reduce toxicity, but poisonings have still occurred. Seeds of hemlock are toxic whether fresh or dried. Although the active alkaloids are oily volatile liquids, deaths have been reported after drinking liquid from boiling hemlock leaves.[10] Poisoning has also transpired from use of the hollow stem as a musical instrument or pea shooter.[13] Meat of birds, which eat hemlock seeds during migratory flights, is also poisonous to humans.[14]   Onset/Duration of Symptoms Symptoms could be expected to appear quite promptly, due to rapid absorption and the onset of similar compounds such as nicotine. One report describes the onset of symptoms occurring within 30 minutes of eating hemlock leaves[15] whereas another case reports the death of a child 3 hours after ingesting plant leaves.[10] Effects usually persist for between 4 to 24 hours.[15][16]   Animal studies have shown an onset of 0.5 to 2 hours with duration of 3 to 7 hours.[17][18]   Severity of Poisoning Mild Conium maculatum Toxicity Moderate Conium maculatum Toxicity Severe Conium maculatum Toxicity GI effects Thirst Nausea Vomiting Agitation Severe GI effects Salivation Abdominal pain Mydriasis Muscle weakness Muscle fasciculations Myalgia Drowsiness Tachycardia Tachypnea Respiratory depression Bradycardia Hypotension Seizures Paralysis Rhabdomyolysis Renal failure Respiratory failure Coma    REFERENCES [1] Schep LJ, Slaughter RJ, Beasley DM. Nicotinic plant poisoning. Clin Toxicol (Phila) 2009 Sep; 47 (8): 771-81. [2] Schep LJ, Slaughter RJ, Becket G, Beasley DM. Poisoning due to water hemlock. Clin Toxicol (Phila) 2009 Apr; 47 (4): 270-8. [3] Cooper MR, Johnson AW. Poisonous plants in Britain and their effects on animals and man. London: Crown Copyright; 1984. p. 229. [4] Kingsbury JM. Poisonous plants of the United States and Canada. Englewood Cliffs (NJ): Prentice-Hall; 1964. p. 381. [5] Everist SL. Poisonous plants of Australia. Sydney: Angus & Robertson Publishers; 1981. p. 718. [6] Vetter J. Poison hemlock (Conium maculatum L.). Food Chem Toxicol 2004 Sep; 42 (9): 1373-82. [7] Chen HY, Albertson TE, Olson KR. Treatment of drug-induced seizures. Br J Clin Pharmacol 2016 Mar; 81 (3): 412-9. [8] Chyka PA, Seger D, Krenzelok EP, Vale JA. Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43 (2): 61-87. [9] Fountain JS, Beasley DM. Activated charcoal supercedes ipecac as gastric decontaminant. N Z Med J 1998 Oct 23; 111 (1076): 402-4. [10] Drummer OH, Roberts AN, Bedford PJ, Crump KL, Phelan MH. Three deaths from hemlock poisoning. Med J Aust 1995 Jun 5; 162 (11): 592-3. [11] Foster PF, McFadden R, Trevino R, Galliardt S, Kopczewski LA, Gugliuzza K, Gonzalez Z, Wright F. Successful transplantation of donor organs from a hemlock poisoning victim. Transplantation 2003 Sep 15; 76 (5): 874-6. [12] Rizzi D, Basile C, Di Maggio A, Sebastio A, Introna F Jr, Rizzi R, Scatizzi A, De Marco S, Smialek JE. Clinical spectrum of accidental hemlock poisoning: neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis. Nephrol Dial Transplant 1991; 6 (12): 939-43. [13] Everist SL. Poisonous plants of Australia. Sydney: Angus & Robertson Publishers; 1981. p. 717-20. [14] Lopez TA, Cid MS, Bianchini ML. Biochemistry of hemlock (Conium maculatum L.) alkaloids and their acute and chronic toxicity in livestock. A review. Toxicon 1999 Jun; 37 (6): 841-65. [15] Frank BS, Michelson WB, Panter KE, Gardner DR. Ingestion of poison hemlock (Conium maculatum). West J Med 1995 Dec; 163 (6): 573-4. [16] Biberci E, Altuntas Y, Cobanoglu A, Alpinar A. Acute respiratory arrest following hemlock (Conium maculatum) intoxication. [Letter] J Toxicol Clin Toxicol 2002; 40 (4): 517-8. [17] Short SB, Edwards WC. Accidental Conium maculata poisoning in the rabbit. Vet Hum Toxicol 1989 Feb; 31 (1): 54-7. [18] Jessup DA, Boermans HJ, Kock ND. Toxicosis in tule elk caused by ingestion of poison hemlock. J Am Vet Med Assoc 1986 Nov 1; 189 (9): 1173-5. Do Not Archive. This document is current on day of issue, NZ: 19.May.2019

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