Conium maculatum 23.Jul.2018-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   COMMON NAME(S) California fern Carrot fern Deadly hemlock Giftkjets Hemlock Nebraska fern Poison hemlock Poison parsley Skarntyde Spotted hemlock Winter fern     NB: The common names of Conium maculatum are also used to refer to other genera in the Umbelliferae family. Botanic identification is crucial.   “Hemlock” most commonly refers to Conium maculatum (poison hemlock) but can refer to Cicuta spp. (water hemlock), which are related and significantly toxic, but contain different toxic components. Although many symptoms overlap, differentiation is important; in severe poisoning Conium maculatum causes respiratory paralysis, whereas Cicuta spp. plants result in profound seizures and potentially status epilepticus.[1][2]   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 carried out, 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 Most toxic seizures are short-lived and often do not require intervention.[7]   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, 50% dextrose should be administered IV (preceded by thiamine in adults).   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.   ENHANCED ELIMINATION Enhanced Elimination Not Recommended Dialysis or perfusion may be indicated for secondary complications, such as acidosis or renal failure, but not for toxin removal alone.   SUPPORTIVE CARE Monitoring Heart rate Blood pressure ECG (12 lead) Cardiac monitoring Respiratory function Arterial blood gases (if compromised respiratory function) Neurological status Serum electrolytes Renal function On-set of paralysis   Gastrointestinal Gastrointestinal Irritation Due to nicotinic receptor over-stimulation gastrointestinal distress is common. Vomiting and diarrhea contribute to hypotension and fluid and electrolyte imbalances, potassium loss may increase the risk of cardiac dysrhythmia. Patients may require symptomatic care with antiemetic medication, IV fluids, and electrolyte replacement.[1]   Observe patient for: Nausea Vomiting Abdominal pain Hematemesis Diarrhea   Monitor: Blood pressure Fluid balance Serum electrolytes (if severe) Acid-base (if severe)   Manage gastrointestinal irritation following standard treatment protocols.   Neurologic Coma The sedation phase of hemlock toxicity can lead to reduced levels of consciousness and coma.[10]   Closely monitor level of consciousness.   Follow standard protocols for the management of coma.   Seizures Seizures may develop after the ingestion of hemlock,[6] though this has not been described in most case reports. Seizures should be treated with a benzodiazepine.   Observe the patient closely for onset of seizure activity.   Toxic seizure may be managed following these (hyperlinked) recommendations.   Respiratory Respiratory Failure The sedation phase of hemlock toxicity will cause weakness and paralysis, which includes muscle weakness. This can lead to respiratory arrest.[10] Intense respiratory support, when needed, constitutes the most vital supportive measure in preventing a poor outcome. Respiratory failure is usually the most common cause of death.   Monitoring for respiratory failure should include: Chest auscultation Oxygen saturation Arterial blood gases   Treat using standard protocols for respiratory failure.   Cardiovascular Bradycardia The late inhibitory phase of conium toxicity will result in bradycardia.[10]   Monitor: Heart rate/rhythm Blood pressure ECG   Manage bradycardia following standard treatment protocols.   Musculoskeletal Rhabdomyolysis The toxic effect of conium may result in the paralysis of skeletal muscles, which may lead to rhabdomylosis;[11] this is characterized by an increase in muscle enzymes and the urine becoming red-brown, due to the presence of myoglobin.   Examine patient for muscle tenderness/pain and weakness. Monitor: Serum creatine kinase (increased CK-MM isoenzyme) Urinalysis: Myoglobin pH   Rhabdomyolysis may be managed following these (hyperlinked) recommendations.   Renal Acute Renal Failure Acute renal failure can occur as a result of rhabdomylosis.   Patients should be monitored for the onset of renal failure: Urine output Serum creatinine Blood urea nitrogen (urea) Proteinuria Hematuria Loin pain may occur   Manage following standard treatment protocols for acute renal failure.   DISCHARGE CRITERIA Patients may be discharged from hospital care when clearly asymptomatic and fully recovered from any complications. Appropriate psychiatric intervention may be necessary depending on the circumstances of the exposure.   FOLLOW UP Medical follow-up is unlikely to be required. Psychiatric intervention may be necessary depending on the circumstances of the exposure.   PROGNOSIS Following appropriate supportive care the prognosis is good.   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.[12][13] Rhabdomyolysis and subsequent renal failure have also been reported.[11]   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.[12] Poisoning has also transpired from use of the hollow stem as a musical instrument or pea shooter.[14] Meat of birds, which eat hemlock seeds during migratory flights, is also poisonous to humans.[15]   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[16] whereas another case reports the death of a child 3 hours after ingesting plant leaves.[12] Effects usually persist for between 4 to 24 hours.[16][17]   Animal studies have shown an onset of 0.5 to 2 hours with duration of 3 to 7 hours.[18][19]   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    ACUTE EFFECTS (ROUTE OF EXPOSURE) Skin Local dermatitis (with or without blisters)[20] Burning sensation[20] Numbness[20]   Systemic symptoms have not been reported following skin exposure.   ACUTE EFFECTS (ORGAN SYSTEM) Gastrointestinal Burning/numbness to mouth or throat[16][21][22] Nausea[23][22] Vomiting[16][12] Hypersalivation[16][21] Thirst[24] Abdominal pain[25]   Neurologic Ataxia[21] Agitation[21] Tremor[6][21] Nervousness[6] Dizziness[17][22] Headache[17] CNS depression[16] Dysarthria[17] Hypotonia[26] Hyperreflexia[26] Arreflexia[26] Absent oculocephalic reflex[26] Absent gag reflex[26] Muscle paralysis[25] Seizures[6] Coma[6][26]   Respiratory Tachypnea[6][26] Dyspnea[17] Hypoxia[26] Respiratory depression[17] Respiratory paralysis[6] Respiratory failure[17][13][25][22]   Cardiovascular Tachycardia[16][26][21] Hypertension[26] Bradycardia[13][22] Widened QRS[26] Weak and thready pulse[6] Asystole[13]   Musculoskeletal Tremor[21] Muscle fasciculations[16] Myalgia[16] Muscle edema[27] Muscle weakness[25][17][22] Decreased muscle tone[26] Skeletal muscle paralysis[25] Rhabdomyolysis[28][11]   Renal Urination[6] Acute tubular necrosis[28][11] Renal failure (secondary to rhabdomyolysis)[27]   Ocular Mydriasis[24][23][26][21] Blurred/double vision[22][17] Amblyopia[23]   Hematologic Elevated INR[21] Prolonged partial thromboplastin time[21] Metabolic Fever[26]   TOXICITY The toxic content of plants may vary from year to year due to various factors that affect growth such as available moisture and spring temperatures. Thus, it is difficult to establish an association between the severity of symptoms and the ingestion of a specific amount of plant material. Symptoms, especially post dermal contact, are more likely to occur following repeated contact with the anacardiaceae family ( this is particularly the case for toxcodendron spp.).   HUMAN The primary toxic effects of this plant are due to coniine, but the toxicity of this plant may vary considerable from that of its toxic component, due a number of different considerations, including toxic concentration, and growth factors of this plant. Poison hemlock has been responsible for many human fatalities because of the resemblance of the seed to Anise, the leaves to parsley or carrot, and the roots to parsnips. All parts, especially the seeds, should be regarded as poisonous, even when dried.    An adult lethal dose is 100 to 300 mg of the toxic alkaloids. [28]   This approximately corresponds to:   Root 40 g in a 60 kg adult 10 g in a 15 kg child Shoots 29 to 1000 g in a 60 kg adult 7 to 250 g in a 15 kg child Leaves 13 to 67 g in a 60 kg adult 3 to 17 g in a 15 kg child Flowers 20 g in a 60 kg adult 5 g in a 15 kg child Unripe fruit 7 to 30 g in a 60 kg adult 2 to 8 g in a 15 kg child Ripe fruit 20 to 100 g in a 60 kg adult 5 to 25 g in a 15 kg child Seeds 22 to 100 g in a 60 kg adult 6 to 25 g in a 15 kg child   Child Toxicity is likely to occur after any ingestion of this plant.   142 g of Hemlock(ingested) 3 year male: Unknown Treatment unknown[12] Fatal[12] Hemlock leaves(ingested) 4 year male: cns depression developed after 30 minutes and was unrousable for 2 hours. Vomiting occurred Decontamination and supportive care, including gastric lavage, activated charcoal, dextrose, and nalorphine infusions[16] Recovered and discharged after 2 days[16] Unknown amount of Hemlock(ingested) 6 year female: burning sensation in the mouth, sialorrhea, tremor, and ataxia 2 hours post-ingestion. Agitation, loss of motor function, mydriasis, sinus tachycardia, elevated INR and increased PTT also occurred Decontamination and supportive care, including gastric lavage, activated charcoal, IV crystalloid infusion, and fresh frozen plasma[21] Recovered and discharged after 3 days[21]   Adult Two adults died after ingesting an unknown amount of hemlock, which was prepared by boiling the leaves in water.[12]   Adults have become poisoned after ingesting the meat from birds that have ingested hemlock buds.[28] The birds themselves (robins, skylarks, chaffinches) were not susceptible to the alkaloids.   Unknown amount of Hemlock(ingested) 19 year female: dizziness, headache, double vision, difficulty speaking, muscular weakness, dysarthria, and tachypnea on arrival. Dyspnea and hypoxia developed after 10 minutes after arrival Supportive care, including mechanical ventilation and intubation[17] Recovered and discharged[17] Unknown amount of cooked Hemlock(ingested) 45 year male: nausea, perioral numbness, dizziness, blurred vision, limb weakness, and bradycardia 1 hour post-ingestion Supportive care, including IV fluids and activated charcoal[22] Recovered after 8 hours[22] Unknown amount of cooked Hemlock(ingested) 45 year female: nausea, perioral numbness, dizziness, blurred vision, and limb weakness developed 1 hour post-ingestion. Respiratory arrest occurred soon after admission Supportive care, including intubation and mechanical ventilation[22] Recovered and discharged after 4 days[22] Unknown amount of ground up Hemlock with amitriptyline and diazepam(ingested) 28 year male: unresponsive with GCS of 3, fever, tachycardia, mild hypertension, tachypnea, mydriasis, decreased muscle tone, arreflexia, widened QRS on arrival. Absent oculocephalic reflex occurred on day 2. Developed hyperreflexia on day 6 Supportive care, including intubation, IV etomidate, rocuronium, and IV sodium bicarbonate[26] Recovered after 14 days[26]   ANIMAL Acute Coniceine: LD50 Oral, Mouse 12 mg/kg12 mg/kg/[15] Coniine: LD50 Oral, Mouse 100 mg/kg100 mg/kg/[15] N-methylconiine: LD50 Oral, Mouse 204.5 mg/kg204.5 mg/kg/ Birds   Some small birds are not susceptible to coniine poisoning, consuming the seeds as a food source, and therefore may have the potential to cause toxicity in any species ingesting them. In contrast, deaths have resulted in other larger birds such as chickens and turkeys.[18][29]   Farm Animals   Severe poisoning and fatalities in cattle, goats, horses, sheep, and pigs have resulted from poison hemlock exposure. Symptoms generally involve movement problems, increased salivation and urination, tremor, vocalization, muscle weakness, and respiratory problems, all which can occur quite rapidly.[30][18][31]   Other animals including rabbits and elk are affected in a similar way to farm animals.   REPRODUCTION PREGNANCY It is unknown whether coniine crosses the placenta but poison hemlock is likely to affect the infant. Any exposure to poison hemlock should be avoided during pregnancy.   No human information is available however Conium maculatum appears to act as a teratogen and abortifacient in animal poisonings.   Malformations have been found in multiple species including cattle, sheep, horse, pigs, and goats after exposure to poison hemlock. These include limb and joint malformations, as well as cleft palate.[31][32][30]   LACTATION It is unknown if exposure to, or ingestion of, this plant results in excretion of toxic substances into breast milk.   FERTILITY It is unknown if exposure to, or ingestion of, this plant causes impaired fertility.   TOXIC COMPONENTS Piperazine plant alkaloids include: Conhydrine Coniine Gamma-Coniceine N-Methylconiine Pseudoconhydrine   Coniine and gamma-coniceine are found in the largest amounts and combined account for most of the plant’s toxic activity. Coniine is about 8 times more toxic than gamma-coniceine.[15]   These alkaloids are structurally related to nicotine, and could be expected to produce similar symptoms.   Plant Content All parts of the plant contain toxic piperidine alkaloids. Before flowering, the leaves contain the most alkaloids, but the greatest concentrations are found in the flowers and fruits/seeds. The roots, at all times, contain the least. Younger plants have 0.3 to 0.6% in leaves and 0.15% in other plant material (excluding flowers and fruit). Older plants contain approximately 1% in all parts of the plant.[33] The alkaloid content, however, does vary with the climatic conditions. In good growing seasons, the average weight of the fruits and thus the quantity of alkaloids can be twice that of normal. Drying the plant reduces the alkaloid content. TOXIC MECHANISM Coniine alkaloids affect the neurological junction where they act as non-depolarizing neuromuscular blockers, similar to curare.[34] However, they also act on autonomic nervous system ganglia with varying degrees of stimulator, and inhibitor (biphasic) effects (resembling the effects of nicotine).[1]   BIOLOGICAL LEVELS - TOXIC Coniine (or other plant alkaloids) blood levels are not readily available, nor necessary for clinical management. KINETICS No human pharmacokinetic data were found in the literature.   DESCRIPTION PLANT ATTRIBUTES General A coarse, erect, branched plant, that can be biennial (lives for two years and flowers in the second year), sometimes annual (lifecycle completed in one year) or perennial (lasting several years). It may exceed 2 m in height. The stem is hairless, slightly ridged and hollow with characteristic irregular purple blotches.   When the plant is crushed or bruised, it emits a mousy odor.[3][35][5] Leaves Leaves are up to 30 cm long, triangular in outline, with finely divided leaflets, arranged on either side of the stem, with deeply serrated edges. This gives the plant a delicate, lacy, fernlike appearance. Leaves lack hairs and are described as large and carrot-like.[36][35][5] Flowers Appear in almost flat-topped clusters of 2 mm white flowers. Each cluster is 2 to 5 cm in diameter.[3] Fruit Fruit consist of a pair of flattened, greyish-brown seeds, with five prominent wavy longitudinal ridges, which are about 3 mm long when ripe.[37][35][5] The root is generally a thick yellow or white tap root (similar to a parsnip), which may or may not have branches.[37] 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] Brent J, Wallace KL, Burkhart KK, Phillips SD, Donovan JW, editors. Critical Care Toxicology. Philadelphia (PA): Elsevier Mosby; 2005. p. 1321. [11] 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. [12] 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. [13] 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. [14] Everist SL. Poisonous plants of Australia. Sydney: Angus & Robertson Publishers; 1981. p. 717-20. [15] 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. [16] Frank BS, Michelson WB, Panter KE, Gardner DR. Ingestion of poison hemlock (Conium maculatum). West J Med 1995 Dec; 163 (6): 573-4. [17] 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. [18] Short SB, Edwards WC. Accidental Conium maculata poisoning in the rabbit. Vet Hum Toxicol 1989 Feb; 31 (1): 54-7. [19] 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. [20] Mitchell J, Rook A. Botanical dermatology: plants and plant products injurious to the skin. Vancouver: Greengrass; 1979. [21] Konca C, Kahramaner Z, Bosnak M, Kocamaz H. Hemlock (Conium Maculatum) Poisoning in a child. Turk J Emerg. 2014 [Epub ahead of print]. [22] Chen HY, Horng H, Rowley F, Smollin. Rapid respiratory arrest after ingestion of poison hemlock mistaken for wild celery. Clin Toxicol (Phila). 2017 [Epub ahead of print]. [23] Ober WB. Did Socrates die of hemlock poisoning? N Y State J Med 1977 Feb; 77 (2): 254-8. [24] Bruneton J. Toxic plants dangerous to humans and animals. Paris: Lavoisier Publishing; 1999. p. 108-13. [25] West PL, Horowitz BZ, Montanaro MT, Lindsay JN. Poison hemlock-induced respiratory failure in a toddler. Pediatr Emerg Care 2009 Nov; 25 (11): 761-3. [26] Lung DD, Scott BJ, Wu AHB, Gerona RR. Prolonged ventilatory failure and flaccid quadriparesis after ingestion of poison hemlock. Muscle Nerve. 2017 [Epub ahead of print]. [27] Scatizzi A, Di Maggio A, Rizzi D, Sebastio AM, Basile C. Acute renal failure due to tubular necrosis caused by wildfowl-mediated hemlock poisoning. Ren Fail 1993; 15 (1): 93-6. [28] Rizzi D, Basile C, Di Maggio A, Sebastio A, Introna F Jr, Rizzi R, Bruno S, Scatizzi A, De Marco S. Rhabdomyolysis and acute tubular necrosis in coniine (hemlock) poisoning. [Letter] Lancet 1989 Dec 16; 2 (8677): 1461-2. [29] Frank AA, Reed WM. Conium maculatum (poison hemlock) toxicosis in a flock of range turkeys. Avian Dis 1987 Apr-Jun; 31 (2): 386-8. [30] Panter KE, Bunch TD, Keeler RF, Sisson DV, Callan RJ. Multiple congenital contractures (MCC) and cleft palate induced in goats by ingestion of piperidine alkaloid-containing plants: reduction in fetal movement as the probable cause. J Toxicol Clin Toxicol 1990; 28 (1): 69-83. [31] Keeler RF. Coniine, a teratogenic principle from Conium maculatum producing congenital malformations in calves. Clin Toxicol 1974 Apr; 7 (2): 195-206. [32] Keeler RF, Balls LD. Teratogenic effects in cattle of Conium maculatum and conium alkaloids and analogs. Clin Toxicol 1978; 12 (1): 49-64. [33] CROMWELL BT. The separation, micro-estimation and distribution of the alkaloids of hemlock (Conium maculatum L.). Biochem J 1956 Oct; 64 (2): 259-66. [34] BOWMAN WC, SANGHVI IS. Pharmacological actions of hemlock (Conium maculatum) alkaloids. J Pharm Pharmacol 1963 Jan; 15 (): 1-25. [35] Kingsbury JM. Poisonous plants of the United States and Canada. Englewood Cliffs (NJ): Prentice-Hall; 1964. p. 379. [36] Cooper MR, Johnson AW. Poisonousp in Britain and their effects on animals and man. London: Crown Copyright; 1984. p. 229. [37] Cooper MR, Johnson AW. Poisonous plants in Britain and their effects on animals and man. London: Crown Copyright; 1984. p. 229-32. Do Not Archive. This document is current on day of issue, NZ: 23.Jul.2018

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