A 12-year-old male patient presented with a two-week history of muscle weakness in the right upper extremity. Upon further inquiry, the patient reported a history of accidental ingestion of benzalkonium chloride (BAC) approximately one month prior, having mistaken it for water. He vomited immediately afterward and was admitted to the emergency department, where he required endotracheal intubation for respiratory failure. His hospitalization included one week in the intensive care unit followed by one week in the general ward. Following discharge, two weeks after the BAC ingestion episode, the patient noticed weakness in the right upper extremity, with difficulty elevating his arm and performing daily activities. At presentation to our department, neurological examination revealed weakness in right shoulder abduction (Medical Research Council grade 3-/5), elbow flexion (4-/5) and wrist extension (4/5). The biceps and brachioradialis reflexes were hypoactive on the right side. These findings suggested a brachial plexus injury, likely involving the upper trunk. Magnetic resonance imaging demonstrated mildly increased signal intensity indicating edema in the C5 root of the right brachial plexus upper trunk (Figure 1). Electromyography, performed three weeks after the BAC ingestion, revealed acute partial denervation in the right C5–C6 myotomes, consistent with a severe partial lesion of the right upper trunk. Accordingly, a physical therapy program emphasizing strengthening exercises for the affected muscles was initiated. At one-week follow-up, the patient demonstrated marked improvement, with strength grades of 4/5 in shoulder abduction, 4+/5 in elbow flexion and 5/5 in wrist extension. Ongoing follow-up is being conducted to monitor recovery.

Figure 1.

Short Tau Inversion Recovery (STIR) – sequence magnetic resonance imaging of the brachial plexus demonstrates mildly increased signal intensity in the right C5 root (arrowheads), more prominent at the pre-truncal levels (A, B, C, D).

Figure 1 Long description

Panel A: A magnetic resonance imaging scan using the Short Tau Inversion Recovery (STIR) sequence shows the brachial plexus. An arrowhead points to the right C5 root, indicating mildly increased signal intensity. Panel B: Another view of the STIR sequence MRI, highlighting the same area with an arrowhead marking the right C5 root. Panel C: A different angle of the STIR sequence MRI, with an arrowhead indicating the right C5 root. Panel D: A further view of the STIR sequence MRI, with an arrowhead pointing to the right C5 root, showing increased signal intensity.

BAC, a quaternary ammonium compound, is widely used as a component of various substances, including surface disinfectants, floor cleaners, sanitizers and certain pharmaceutical products.^{Reference Kumar, Chetiwal and Rastogi1} BAC solutions with concentrations of 10% or higher are known to be toxic to humans.^{Reference Külbay, Çevik and Vural2} While lower concentrations (<10%) are generally not associated with significant injury, concentrated solutions (>10%) can cause severe upper gastrointestinal and respiratory tract damage.^{Reference Kumar, Chetiwal and Rastogi1} Clinical manifestations of BAC poisoning may include nausea, vomiting, dysphagia, corrosive gastrointestinal injury, dyspnea, bronchoconstriction, chemical pneumonitis, metabolic acidosis, renal failure and central nervous system depression.^{Reference Kumar, Chetiwal and Rastogi1} Prompt intervention and supportive management are crucial to prevent complications and unexpected outcomes. Several cases have been reported in the literature, predominantly involving pediatric patients.^{Reference Niţescu, Lescaie, Boghiţoiu and Ulmeanu3} Most of these cases presented with esophageal corrosive lesions and chemical lung injury.^{Reference Niţescu, Lescaie, Boghiţoiu and Ulmeanu3} The majority did not develop long-term sequelae, and all pediatric cases reported favorable outcomes.^{Reference Niţescu, Lescaie, Boghiţoiu and Ulmeanu3} However, clinical data regarding neurological involvement in BAC toxicity are extremely limited, with evidence derived primarily from a few animal studies.^{Reference Vitoux, Kessal and Melik Parsadaniantz4} In contrast to the existing literature, our patient developed brachial plexus involvement following BAC ingestion, which gradually resolved with conservative treatment. There are two potential mechanisms that may explain the development of brachial plexus injury in our patient. The first possibility is that the injury resulted from factors related to hospitalization, including a one-week stay in the intensive care unit, which may have involved malpositioning, traction forces, or other traumatic causes. The second possibility is that the injury was due to the neurotoxic effects of BAC. Considering the clinical timeline – BAC ingestion, one week in the intensive care unit, followed by one week in the general ward, the onset of weakness noted two weeks post-ingestion and electromyography conducted three weeks after the poisoning – the second scenario appears more likely. This is further supported by the fact that needle electromyography findings indicative of active or ongoing denervation typically become evident approximately three weeks after the onset of nerve injury.^{Reference Ginsberg, Morren and Levin5} In light of the aforementioned issues, the brachial plexus involvement was attributed to BAC-induced neurotoxicity. Therefore, to the best of our knowledge, this represents the first reported pediatric case of upper trunk brachial plexus injury caused by BAC poisoning.

In conclusion, this case highlights a previously unreported complication – brachial plexus involvement – following BAC exposure and emphasizes the need for further research into the potential neurotoxic effects of this compound. To this end, expanding our understanding of its impact on various organ systems, including the nervous system, is essential for anticipating and managing such unexpected clinical presentations, especially in the pediatric population.