Chodorowski, Z., Anand, J. S., Salamon, M., Waldman, W., Wnuk, K., Ciechanowicz, R., and Swiatek-Brzezinski, K. [Evaluation of illicit drug use among students from universities in Gdansk]. Przegl.Lek. 2001;58(4):267-271. View abstract.
Shervette, R. E., III, Schydlower, M., Lampe, R. M., and Fearnow, R. G. Jimson “loco” weed abuse in adolescents. Pediatrics 1979;63(4):520-523. View abstract.
Uses & Effectiveness
Groszek, B., Gawlikowski, T., and Szkolnicka, B. [Self-poisoning with Datura stramonium]. Przegl.Lek. 2000;57(10):577-579. View abstract.
The appropriate dose of jimson weed depends on several factors such as the user's age, health, and several other conditions. At this time there is not enough scientific information to determine an appropriate range of doses for jimson weed. Keep in mind that natural products are not always necessarily safe and dosages can be important. Be sure to follow relevant directions on product labels and consult your pharmacist or physician or other healthcare professional before using.
Stomach and intestinal infections: Jimson weed might slow down the emptying of the stomach and intestines. As a result, “bad” bacteria and the toxins they produce could remain in the digestive tract longer than usual. This could make infections caused by these bacteria worse.
Diets containing 0.5, 1.58 and 5.0% jimson weed seed were fed to male and female rats (20/group) in a 90-day subchronic feeding study. The alkaloid content was 2.71 mg atropine and 0.66 mg scopolamine/g of seed. Gross clinical observations, body weights and feed and water intakes were recorded weekly. Tear production and pupil dilation measurements were made throughout the study. At 90 days, all of the animals were autopsied and clinical-chemistry analyses, complete haematology and bone-marrow evaluation for evidence of clastogenic effects were performed. Tissues from control (0% seed) and high-dose animals were examined histologically. The principal effects of jimson weed seed were: decreased body-weight gain, serum albumin and serum calcium; increased liver and testes weights (as a percentage of body weight), serum alkaline phosphatase and blood urea nitrogen. Female rats showed more marked responses to jimson weed seed than did males. In addition to the effects seen in both sexes, the females developed decreased serum total protein and cholesterol, and increased serum glutamic-pyruvic transaminase and chloride, red blood cell count, haemoglobin concentration and packed red cell volume. No histological lesions were associated with ingestion of jimson weed seed at 5.0%. It is concluded that jimson weed seed at concentrations of 0.5% or more in the diet produced adverse physiological changes in rats.
Absorption of jimson weed may be minimized either by using an agent that binds to the toxins or through removal of gastric contents by inducing emesis or administering gastric lavage. Activated charcoal binds to the toxins in jimson weed and decreases overall absorption of these toxins.5 The usual oral dose of activated charcoal for adults is 1 g/kg. If medical attention is sought within several hours after ingestion or if the patient has been intubated, removal of the ingested plant by gastric lavage can be considered. Emesis may be induced by using syrup of ipecac if the patient is awake and relatively alert. The usual dose of ipecac is 30 mL for adults and 15 mL for children.3,5
The anticholinergic effects of jimson weed are attributed to the atropine, hyoscyamine, and scopolamine components. Symptoms of jimson weed toxicity usually occur within 30 to 60 minutes after ingestion. Initial symptoms include hallucinations, dry mucous membranes, thirst, dilated pupils, blurred vision, and difficulty speaking and swallowing. 2 Subsequent effects may include tachycardia, urinary retention, and ileus. Rarely, late symptoms may include hyperthermia, respiratory arrest, and episodes of seizure.6 Slowing of gastrointestinal motility may prolong elimination of the toxin, thus causing symptoms to persist for 24 to 48 hours.
A toxicology screen is useful to rule out concomitant use of other drugs. Most documented lethal cases of jimson weed ingestion occur in persons with polysubstance abuse, including use of jimson weed combined with alcohol, marijuana, or cocaine.7 Drug screens usually do not detect pure anticholinergic poisons, and other laboratory tests are usually not helpful for identifying jimson weed as the cause of symptoms.3
Effective treatment of jimson weed poisoning requires a primary survey, clinical evaluation and recognition, elimination of the poison, supportive treatment, and continuing observation. 8 The primary survey includes assessment of the ABCs—ie, airway, breathing, and circulation. Although rare, some patients with jimson weed intoxication may be seen for episodes of seizure or coma. If compromise of the airway is suspected, prompt intubation and mechanical ventilation are indicated.
In the ED, the patient received several doses of lorazepam intravenously as treatment for agitation. He was admitted to the hospital for observation and for monitoring. The patient remained stable, and his mental status improved. At a subsequent interview, the patient admitted that he and his friends had consumed jimson weed deliberately: They had tried it for the first time after hearing that it was hallucinogenic. After 36 hours of observation, the patient was discharged from the hospital.
Benzodiazepine therapy is the main treatment for acute agitation, and use of restraints may be necessary to avoid injury to the patient or hospital staff. Clinicians must remember that drugs with anticholinergic properties (eg, some antipsychotic and sedative drugs) can worsen symptoms of jimson weed poisoning. Agents such as haloperidol or chlorpromazine can exacerbate agitation, and psychosis and should therefore be avoided.12
Results of an emergent fingerstick blood glucose test, complete blood count, chemistry panel, and urinalysis were normal. Results of a toxicology screen were negative for alcohol, benzodiazepines, amphetamines, marijuana, tricyclic antidepressant agents, opiate agents, and phencyclidine. An electrocardiogram showed sinus tachycardia without other abnormality. Cranial structures appeared normal on computed tomography scans administered without contrast medium.
Routine use of physostigmine to treat jimson weed intoxication remains controversial. Closely monitored use of physostigmine in very small doses to prevent cholinergic excess may be safe: When used to treat a series of 23 patients with hallucinations from jimson weed intoxication, physostigmine had no adverse effects.11 Physostigmine can quickly reverse signs and symptoms of central and peripheral nervous system dysfunction and can assist diagnosis of anticholinergic excess.12 However, most cases of jimson weed poisoning have a benign outcome after treatment with only supportive care and observation; use of physostigmine is therefore not routine and should be reserved for patients who have clinically significant symptoms or complications.