· Hemlock belongs to the family Umbelliferae of genus Cicuta, and is a biennial herb that grows erect to an average height of 1 to 3 metres (Fig 21.6).
· The larger stems are hollow and bear numerous purple spots that are very distinctive.
· Leaves are fine, light-green, and fern-like. When crushed, they give off an unpleasant “mousy” smell.
· Fruits are smooth skinned with crenate ribs, and are binocu-lated, measuring about 9 mm long, and 6 mm across.
The toxins of poison hemlock are simple piperidine alkaloids: coniine and gamma-coniceine. They are structurally similar to nicotine and possess similar clinical features in toxicity.
The mode of action is two-fold. The most serious effect occurs at the neuromuscular junction where these alkaloids act as non-depolarising blockers causing respiratory failure due to flaccid paralysis. The second effect at the auto-nomic ganglia is nicotinic in nature resulting in salivation, mydriasis, and tachycardia, followed by bradycardia. Less commonly, rhabdomyolysis and acute tubular necrosis can occur.
· Nausea, vomiting, abdominal pain.
· Stimulant phase: tachycardia, tremors, sweating, mydriasis,convulsions.
· Depressive phase: bradycardia, ascending motor paralysis,and coma.
· Aggressive GI decontamination: lavage and activated charcoal.
· Benzodiazepines for convulsions.
· Respiratory support.
· Forced diuresis may help in preventing renal failure.
· Hemlock was popular in ancient times as a means of execu-tion. The most famous personality executed in this fashion was Socrates, who was condemned to death for his “crime” of introducing new divinities.
· Today, most cases of hemlock poisoning result from accidental circumstances due to mistaken identity with edible vegetables such as wild carrot, parsley, or anise seeds.
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