Datura stramonium L. (DS) is a wild-growing herb known as Jimson weed [1]. It also has several slang names; the most common in our context is "sak el ghoul." The whole plant, particularly the foliage and seeds, is toxic because it contains the tropane alkaloids atropine, L-hyoscyamine and L-scopolamine, which are responsible for anticholinergic syndrome resulting from the inhibition of central and peripheral muscarinic neurotransmission by these toxic components [1]. Causes of DS intoxication include medication overdose, improper preparation of edible vegetables, deliberate abuse as a hallucinogen, use for homicide or robbery (we approve this correction), and accidental intoxication [2]. Most of the cases reported in the literature occurred among teenagers after voluntary ingestion of the plant for its hallucinogenic and euphoric effects [1, 3–6]. To our knowledge, our patient is the youngest case of DS poisoning reported in the literature. The occurrence of this poisoning in our patient was facilitated by an abnormal dietary behavior called geophagia or pica, characterized by a perverted appetite for substances inappropriate for consumption, such as clay and earth [7]. Pica can lead to serious health complications such as iron deficiency anemia, electrolyte and metabolic disorders, parasitic infections, tooth wear, and intestinal obstruction. This condition has been observed in men and women of all ages and ethnicity, but is more prevalent among lower socioeconomic classes, pregnant women, and small children [7]. Our geophagous child developed a typical form of DS poisoning characterized mainly by a toxic delirium occurring rapidly after ingestion. Typical symptoms of DS intoxication are those of atropine intoxication, which are dry skin and mucosa, flushing, mydriasis, sinus tachycardia, hyperpyrexia, decreased bowel sounds, urinary retention, and neurological disorders with ataxia, impaired short-term memory, disorientation, confusion, hallucinations (visual and auditory), psychosis, agitated delirium, seizures, and coma. In severe forms, respiratory failure and cardiovascular collapse have been reported [1–6]. Rarely, rhabdomyolysis and fulminant hepatitis have also been described [8]. DS toxicity usually occurs within 60 min after ingestion, and clinical symptoms may persist for 24 to 48 h because the anticholinergic effects delay gastric emptying, resulting in a prolonged duration of action. Children have a special susceptibility to atropine toxicity; even a small amount may produce severe central nervous system manifestations [9]. Despite the young age of our patient, a rapid improvement of the neurological manifestations was obtained, probably because the diagnosis was evident and gastric decontamination was carried out soon after ingestion. The diagnosis of DS poisoning is essentially clinical, but tropane alkaloids may be detected by gas chromatography and mass spectrometry [1]. The treatment is essentially supportive and consists of gastric decontamination with activated charcoal by mouth or tube, control of agitation with benzodiazepines, and hyperpyrexia control (fluids and other cooling measures). Tachycardia usually responds to crystalloids [10]. Although physostigmine is the antidote for anticholinergic toxicity, its use is controversial despite recent reports of it being a safe treatment. Physostigmine is recommended when the patient has severe agitation or psychosis not controlled with bezodiazepines or has intractable seizures or tachydysrhythmias with hemodynamic compromise [1]. Phenothiazines for agitated delirium should be avoided due to their anticholinergic properties, and barbiturates can be administered in the case of seizures refractory to benzodiazepines [1, 10]. The prognosis of DS intoxication is usually favorable, as in our case, but it may be fatal, especially during massive intoxications meant to be autolytic or the result of toxicomania [6].
