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Conium maculatum

Conium maculatum
22.Nov.2017-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
 

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
Decontamination
Ingestion
Skin
Eye
Antidote(s)
Enhanced Elimination
Supportive Care
Gastrointestinal
Neurologic
Respiratory
Cardiovascular
Musculoskeletal
Renal
 

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.
 

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 ToxicityModerate Conium maculatum ToxicitySevere 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.

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NZ: 22.Nov.2017

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