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· Jamestown weed; Jimson weed; Thorn apple; Stinkweed; Devil’s weed; Angel’s trumpet.
· Datura stramonium, D. metel, D. fastuosa
· This is a small coarse shrub with a strong and rather unpleasant smell, belonging to family Solanaceae which grows wild all over the Indian countryside.
· It grows to a height of 3 to 5 feet, and has a handsome foliage of dark green ovate, pointed leaves, and large tubular (trumpet-shaped) flowers which may be white (alba) or purple (niger) (Fig 15.1).
· The fruit capsule is spherical with soft spines (Fig 15.2) and contains 50 to 100 dark brown reniform (kidney-shaped) seeds (Fig 15.3) which bear a superficial resemblance to chilly seeds.*
· The active principles have various uses in modern medicine (Table 15.2).
· All parts, especially seeds.
· Hyoscine (scopolamine), hyoscyamine, and traces of atropine, together referred to commonly as belladonna alkaloids.
Belladonna alkaloids competitively inhibit the muscarinic effects of acetylcholine. Sites of action are at the autonomic effectors innervated by postganglionic cholinergic nerves or on smooth muscles that do not contain cholinergic innervation. Central nervous system effects result from their central antimuscarinic actions, i.e. vagal stimulation and decrease in heart rate.
The toxicokinetics of atropine are mentioned in Table 15.3.
Summarised in the classic phrase: blind as a bat, hot as a hare,dry as a bone, red as a beetroot, and mad as a wet hen.
The important manifestations can be better remembered as a series of D’s:
· Dryness of mouth, thirst, slurred speech.
· Dilated pupils (with no reaction to light or accommodation).
· Dry hot skin, with flushing, hyperpyrexia.
· Drunken gait (ataxia), hyperreflexia, convulsions.
· Delirium with hallucinations, agitation, amnesia, incoher-ence.
· Dysuria, urinary retention, bladder distension.
· Death, preceded by tachycardia, arrhythmias, coma, and respiratory depression.
· About 50 to 100 datura seeds.
· About 10 to 100 mg of atropine (usually 60 to 75 mg). However, recovery has been recorded with 1000 mg of atropine.
· Even minute traces of atropine in blood (as low as 10 ng/ ml) can be detected by GC-MS (gas chromatography-mass spectrometry). However, there is little or no correlation between dose of atropine, plasma concentration, and observed clinical effects.
· Neutrophil leucocytosis is often encountered.
· Dilated pupils: If the pupils do not constrict within 15 to 30minutes after instillation of 2–3 drops of 1% pilocarpine, it is indicative of atropine or anticholinergic poisoning.
· Cat’s eye test: Instillation of a few drops of the patient’surine into the eyes of a cat results in rapid mydriasis.
· Treat the patient in a quiet and dark environment.
· Treat respiratory failure with endotracheal intubation and assisted ventilation. Tidal volume should be at least 10 to 15 ml/kg.
· Monitor ECG, pulse, and temperature continuously.
· Gut decontamination: Gastric lavage (after intubation),activated charcoal.
· Dialysis and haemoperfusion do not appear to be effective.
· Catheterise bladder.
· Administer IV fluids, keeping a close watch on intake and output and renal function.
· Agitation can be controlled with judicious use of diaz-epam. Do not use phenothiazines or antihistamines, since they can aggravate the anticholinergic effects.
· Hyperthermia can be managed by hydration and cooling measures.
· Antidote: Physostigmine is the antidote of choice, and shouldbe administered if the following indications are present:
4. Severe hypertension
The adult dose is 2 mg IV, slowly, repeated if required, in 20 minutes. Do not give it as a continuous infusion. Continuous cardiac monitoring is mandatory. The paedi-atric dose is 0.5 mg IV, slowly, repeating if required, at 5 minute intervals till a maximum of 2 mg.
Physostigmine is an effective but dangerous antidote, and can give rise to convulsions, asystole, hypotension, hypersalivation, and bradyarrhythmias, if administered without caution. Neostigmine and pyridostigmine being quaternary ammonium compounds do not traverse the blood-brain barrier, and therefore are not effective in countering atropine-induced CNS toxicity. Pilocarpine is also ineffective. Physostigmine is a tertiary amine that easily passes the blood-brain barrier.
· Drugs to be avoided in the treatment of datura poisoning: antihistamines, phenothiazines, tricyclics, quinidine, disopyramide, procainamide, and morphine.
· Accidental—Accidental poisoning may result from any one of the following ways:
o Mistaken identity involving capsicum seeds (Fig 15.4).
o Foraging children in the countryside chewing on the seeds (or other parts of the plant) out of curiosity.
o Therapeutic misadventures.
o Overenthusiastic use of atropine as an antidote for organophosphate or carbamate poisoning.
· Suicidal—Owing to easy accessibility, datura is not infre- quently reported in suicidal ingestions, especially in rural parts of India.
· Homicidal—There have been rare instances of murder being accomplished with one or the other belladonna alkaloids. accomplished with one or the other belladonna alkaloids. Stupefaction—The term “stupefaction” is loosely applied to the process of rendering a victim suddenly incapacitated by exposing him to a deliriant poison such as datura, in order to facilitate robbery or rape. An extract of the seeds is usually employed, which is mixed with food or drink and adminis- tered to the unsuspecting victim. Sometimes, stupefaction is induced by exposing the person to fumes of incense, by mixing datura with other constituents of an incense or joss stick (agarbathi). Even cigarettes may be adulterated in a similar fashion. Gullible railway or bus passengers are the usual victims who fall into the trap of accepting food, drink, or tobacco from “friendly” strangers.
· Datura abuse—The hypnotic and hallucinogenic proper-ties of datura have been known since ages.
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