Water Bead Ingestion Linked to Neurotoxicity

Water bead toys have the potential to cause not only intestinal obstruction in children who ingest them, but also neurotoxicity, a case study suggested.

A 13-month-old female who was previously healthy presented to the emergency department with vomiting, lethargy, and weight loss over several weeks along with insomnia and facial dermatitis, reported a group led by Ashley Haugen, of the nonprofit advocacy organization That Water Bead Lady and the mother of the patient.

During an exploratory laparotomy, a mass consisting of water beads was removed from the child’s distal small intestine, Haugen and colleagues noted in Pediatrics.

Following removal of the mass, the patient’s facial dermatitis resolved. However, her speech along with gross and fine motor, sensory, and neurological functions continued to worsen. A second surgical procedure removed multiple fragments of water bead material from the child’s large intestine.

“This is an essential area for pediatric medical awareness because the dangers of water beads extend beyond what is commonly understood,” Haugen told MedPage Today in an email. “While physical obstructions are often the focus, the potential chemical toxicity of water beads, including neurotoxic and systemic effects have been largely overlooked.”

These beads are made of polymerized acrylamide monomer, which can be toxic at high levels. And they can clump together into a gelatinous mass.

“In cases where beads remain in the body for prolonged periods, chemical exposure could exacerbate the injury even beyond the physical obstruction,” Haugen added. “The material may contain residual monomers, degrade over time, impact digestive tract function, or disrupt gut microbiota — factors that cannot be fully replicated in testing or reliably predicted. Our paper highlights the importance of clinicians recognizing the duality of risk — both physical and chemical — which is often overlooked and should be an integral part of the clinical evaluation process.”

Along with marketing to children generally as toys, water bead sales are also targeted to children with autism and sensory processing disorders as sensory-based therapies, noted Patrick Reeves, MD, and Eric Pasman, MD, both of the Uniformed Services University of the Health Sciences in Bethesda, Maryland, in a commentary accompanying the case study in Pediatrics

“Without [pending] consumer protections, pediatrics should counsel families, including those at high risk based on age or developmental status, on the dangers of water bead ingestion,” they wrote. “There must be continued advocacy with the [Consumer Product Safety Commission] to mitigate the dangers posed by water beads.”

Overall, reports of children swallowing water beads have risen in the last decade, according to a systematic review presented at the American Academy of Pediatrics’ annual meeting in Orlando in September. And members of the American Medical Association House of Delegates also have called attention to reported injuries from the products.

In the case study by Haugen and colleagues, the patient had a normal developmental trajectory prior to water bead ingestion, meeting standard milestones like walking and speaking, as well as normal hearing.

However, at age 17 months, 3 months after surgical removal of the water bead mass, the patient’s pediatrician and medical records indicated that she demonstrated the following: motor incoordination, tremor, myoclonus, muscle weakness (minimal use of right hand), extremity hypotonia, gait abnormality, expressive receptive language delay, sensory processing issues with temperature and resistance to items touching feet and hands, delayed problem solving, and abnormal hearing.

Meanwhile, the patient’s brain MRI and chromosomal microarray were normal, “ruling out structural and genetic etiology,” Haugen and colleagues reported. And her parents confirmed with the water bead retailer and manufacturer that the products were made of polyacrylamide.

Because the patient’s symptoms and clinical progression were consistent with acrylamide exposure, her developmental pediatrician made a presumptive diagnosis of encephalopathy associated with acrylamide toxicity.

At age 20 months (6 months after surgery), formal assessment indicated the patient’s gross motor age was 18 months, her fine motor age was 16 months, her receptive language age was 10 months, and expressive language age was 12 months. And at 22 months of chronological age, histopathology of the colon showed mild eosinophilic inflammation and lymphoid aggregates consistent with an immune response.

Starting at age 17 months, the patient received specialized skills training four times per month for more than 3 months, which was aimed at addressing lack of coordination and fine motor skill challenges. Starting at 22 months, the patient received speech therapy eight times per month. And the patient also was initiated on a low-dose regimen of the sodium channel blocker oxcarbazepine (Trileptal) to mitigate hyperexcitability of damaged nerves.

At around 6 years of age, the patient was recommended to start 20 to 30 minutes of speech therapy five times a week and to get special education services in a general education setting to address functional deficits. At 8 years of age, the patient had made significant progress and speech therapy dropped to twice a week.

Limitations of the case study included lack of free acrylamide monomer blood level measurement, which is typically available only in research contexts, Haugen and colleagues noted. And “significant delay” between surgical intervention and identification of exposure “further precluded the possibility of obtaining accurate measurements.”

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