A Case of Belladonna Poisoning With Late‐Onset Reappearance of Anticholinergic Toxicity

ABSTRACT

In a patient with belladonna poisoning, symptom recurrence was accompanied by a rebound in drug concentration. This suggests reabsorption of residual alkaloids during impaired intestinal peristalsis. The case emphasizes the importance of carefully monitoring bowel motility in the management of belladonna poisoning to prevent delayed or recurrent toxic manifestations.

On day 1, blood concentrations of atropine and scopolamine were extremely low, whereas urinary concentrations were elevated, suggesting rapid urinary excretion. Subsequently, urinary concentrations decreased; however, at symptom recurrence, the blood atropine concentration increased, suggesting redistribution into the bloodstream.

1. Introduction

Atropa belladonna (commonly known as deadly nightshade) is a poisonous plant in the Solanaceae family [1]. According to the review by Fatur and Kreft, numerous cases of belladonna poisoning have been reported, with the most common causes being misidentification or accidental ingestion by children [2]. Most Atropa belladonna intoxications are accidental, resulting from misidentification as an edible plant or attraction of children to its berries, accounting for 68.5% of cases in Switzerland between 1995 and 2009 [3] and 98% of pediatric cases in Van, Turkey between 1996 and 2003 [4]. Suicidal ingestion was less common, reported in 9.3% of Swiss cases between 1995 and 2009 [3]. Atropa belladonna has historically been employed cosmetically to dilate pupils, as a poison and ritual substance, and as a medicinal treatment for a variety of symptoms [2]. Its toxic effects are primarily due to tropane alkaloids, which interfere with the central and peripheral nervous systems through anticholinergic activity [5]. Neurological symptoms vary depending on the dose and may include drowsiness, agitation, impaired short‐term memory, purposeless hand movements, hallucinations, seizures, and even coma [5]. Peripheral manifestations can involve dilated pupils with blurred vision, dry mouth and mucous membranes, hyperactive reflexes, flushed skin, reduced bowel sounds or intestinal blockage, urinary retention, and fluctuations in blood pressure [5]. Despite its toxicity, reports of nightshade poisoning are rare [1, 4]. Furthermore, information on alkaloid metabolism in humans is scarce [6]. The relationship between toxic symptoms and changes in drug metabolism in patients following belladonna poisoning remains unclear.

Here, we report the time course of drug concentrations in a 15‐year‐old female patient with belladonna poisoning who experienced recurrence of toxic symptoms after hospitalization.

2. Case History/Examination

A 15‐year‐old girl (height, 158 cm; weight, 42 kg) presenting with nausea was brought to our Emergency Department after impulsively ingesting 74 tablets of Atropa belladonna following an argument with her younger sister. The formulation used was a pharmaceutical product, specifically Atropa belladonna extract tablets containing 10 mg per tablet. She had gradually ingested the tablets over approximately 2 h, ending about 1 h before hospital arrival. On arrival, her vital signs were as follows: blood pressure 136/85 mmHg, pulse 141 beats per minute, respiratory rate 20 breaths per minute, oxygen saturation 99% on room air, and body temperature 37.7°C. Her Glasgow Coma Scale score was 4 for eye opening, 5 for verbal response, and 6 for motor response. The blood test results at presentation are shown in Table 1.

TABLE 1.

Laboratory data at presentation.

Laboratory data	Value	Normal range, units
Blood test
pH	7.418	7.350–7.450
Bicarbonate	21.8	20.0–26.0	mmol/L
Partial pressure of carbon dioxide	34.6	35.0–45.0	mmHg
Lactic acid	1.6	0.5–2.0	mmol/L
Blood glucose	94	70–109	mg/dL
White blood cell	5.4	3.3–8.6	103/μL
Hemoglobin	13.2	13.7–16.8	g/dL
Platelet	247	158–348	103/μL
Total Bilirubin	0.3	0.4–1.5	mg/dL
Aspartate transaminase	20	13–30	U/L
Alanine transaminase	11	10–42	U/L
Amylase	116	44–132	U/L
Blood urea nitrogen	5.2	8.0–20.0	mg/dL
Creatinine	0.46	0.65–1.07	mg/dL
Creatinine kinase	148	59–248	U/L
Sodium	142	138–145	mmol/L
Potassium	4.1	3.6–4.8	mmol/L
C‐reactive protein	0.02	0.00–0.14	mg/dL
D‐dimer	0.5	< 1.0	μg/ml

3. Differential Diagnosis, Investigations, and Treatment

Physical examination revealed mydriasis with pupils measuring 7.0 mm bilaterally. Electrocardiography demonstrated sinus tachycardia. Although dryness of the skin and mucous membranes and urinary retention were not observed, she was in an agitated state. Based on these findings, a diagnosis of belladonna poisoning was made. Gastric lavage and administration of activated charcoal were performed immediately upon arrival. As she began vomiting and agitation could not be controlled, deep sedation with sedatives was required to safely manage the treatment; endotracheal intubation was carried out to secure the airway, and she was admitted to the intensive care unit for close monitoring. Fentanyl was used as the analgesic, and midazolam was administered as the sedative. Due to decreased intestinal peristalsis, a prokinetic agent was additionally administered on hospital day 2, consisting of continuous intravenous infusion of panthenol 1000 mg and metoclopramide 20 mg over 24 h. By hospital Day 3, bowel sounds were present. However, tachycardia and pupillary dilation reappeared on hospital Day 4. Subsequently, her symptoms improved, and she was successfully extubated. Changes in blood and urine concentrations of atropine and scopolamine are shown in Table 2. A psychiatric evaluation was conducted by a psychiatrist after extubation. She was diagnosed with bipolar disorder, and although suicidal ideation had been present before hospitalization, it had resolved during the admission.

TABLE 2.

Atropine and scopolamine concentrations in the blood and urine.

	Serum concentration (ng/mL)		Urine concentration (ng/mL)
	Atropine	Scopolamine	Atropine	Scopolamine
Day 1	< 0.05	< 0.05	352.29	1.53
Day 2	< 0.05	< 0.05	63.58	0.57
Day 4	0.23	< 0.05	—	—
Day 5	—	—	4.83	< 0.05
Day 8	< 0.05	< 0.05	< 0.05	< 0.05

Note: Blood and urine concentrations of atropine and scopolamine were measured by LC–MS/MS (Liquid Chromatography–Mass Spectrometry), with calibration curves prepared in human serum (0.01–1 ng/mL) and urine (0.5–500 ng/mL), respectively.

4. Conclusion and Results (Outcome and Follow‐Up)

She was discharged home on hospital day 10 with referral to a psychiatric clinic where care could be provided in her native language. At a six‐month follow‐up, she was living without any problems, and no recurrence of overdose was reported. Written informed consent was obtained from the patient for publication of this case report.

5. Discussion

We measured drug concentrations in a 15‐year‐old female patient who experienced a recurrence of toxic symptoms during hospitalization for belladonna poisoning. The delayed intestinal motility resulting from the anticholinergic effects of belladonna may have led to reabsorption of the drug once gastrointestinal activity resumed. These findings highlight the importance of careful monitoring of bowel peristalsis in such cases.

The roots, leaves, and fruits of A. belladonna contain various alkaloids, including atropine, hyoscyamine, and scopolamine. After ingestion, most of the scopolamine is metabolized to atropine [7]. Consequently, atropine and scopolamine are considered the primary alkaloids in A. belladonna [7]. Atropine and scopolamine competitively block muscarinic receptors, causing anticholinergic symptoms such as tachycardia, mydriasis, dry mouth, urinary retention, gastrointestinal hypomotility, and CNS effects [8]. Both atropine and scopolamine are rapidly absorbed in the gastrointestinal tract, with scopolamine absorbed within 0.5 h and atropine within 1 h [6]. Furthermore, previous studies have shown that tropane alkaloids are efficiently absorbed by intestinal epithelial cells; however, their absorption by gastric epithelial cells is limited [6]. In addition, atropine and scopolamine are primarily metabolized hepatically with renal excretion (half‐lives: atropine 2–4 h, scopolamine 1–3 h) [8], with 33%–50% of atropine eliminated in a pharmacologically active form [6].

In our case, atropine and scopolamine concentrations were measured in both blood and urine, with changes over time shown in Table 2. At presentation, blood concentrations were extremely low, whereas urine concentrations were elevated, reflecting the high lipophilicity and tissue distribution of belladonna alkaloids. These findings thus suggest the rapid translocation of atropine and scopolamine from the bloodstream to the urine. Subsequently, urinary concentrations decreased over time; however, at the time of reappearance of mydriasis and tachycardia, the blood concentration of atropine increased to 0.23 ng/mL, suggesting the possibility of drug redistribution into the bloodstream. Other possible causes of tachycardia and mydriasis include sympathomimetic or anticholinergic agents, hyperthyroidism, and benzodiazepine withdrawal. However, the prokinetic agent was administered within the approved dosage range, and no other medications capable of inducing tachycardia or mydriasis were given. The patient had no history of hyperthyroidism, and benzodiazepines had been administered for sedation, making withdrawal an unlikely cause. Given that changes in heart rate and pupil diameter paralleled the blood concentration of belladonna alkaloids, recurrence of toxic manifestations is strongly suggested.

Notably, this case report demonstrated the recurrence of toxic symptoms during hospitalization following belladonna poisoning and allowed for simultaneous monitoring of changes in drug metabolism. Intestinal peristalsis was likely suppressed due to both excessive ingestion of belladonna alkaloids and the sedatives and analgesics administered for mechanical ventilation. The addition of a prokinetic agent restored intestinal motility, raising the possibility that belladonna components not yet absorbed in the stomach were subsequently reabsorbed.

In conclusion, in cases of belladonna poisoning, recurrent symptoms may result from drug reabsorption caused by delayed intestinal motility. Therefore, careful monitoring of bowel peristalsis is essential in such patients.

Author Contributions

Tatsuhiko Hayashi: writing – original draft. Ichiro Hirayama: writing – review and editing. Minaho Nonaka: resources. Hiromu Naraba: conceptualization. Tetsuhiro Yano: visualization. Mitsuru Ishii: supervision. Asuka Kaizaki‐Mitsumoto: investigation. Satoshi Numazawa: investigation. Yoshiteru Tominaga: supervision. Yoshito Kamijo: project administration.

Funding

The authors have nothing to report.

Ethics Statement

Our institution does not require ethical approval for reporting individual cases.

Consent

Written informed consent was obtained from the patient to publish this report in accordance with the journal's patient consent policy.

Conflicts of Interest

The authors declare no conflicts of interest.

Hayashi T., Hirayama I., Nonaka M., et al., “A Case of Belladonna Poisoning With Late‐Onset Reappearance of Anticholinergic Toxicity,” Clinical Case Reports 14, no. 1 (2026): e71869, 10.1002/ccr3.71869.

Data Availability Statement

The authors have nothing to report.