Clinical toxicology (Philadelphia, Pa.) · 2025
Hyperbaric oxygen therapy for diquat-induced toxic brain injury in the subacute or chronic phase.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
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Wang Ping, Luo Cui-Fei, Li Ting, Lin Li-Ying, Song Cong-Ying, Lu Yuan-Qiang
Аннотация
INTRODUCTION: Diquat-induced toxic brain injury is a challenging clinical issue, characterized by oxidative stress and neuroinflammation, which causes extensive damage to the central nervous system and has a poor prognosis.
METHODS: We conducted a retrospective analysis of three patients diagnosed with diquat-induced toxic brain injury who underwent hyperbaric oxygen therapy in the subacute or chronic phase. Clinical data, laboratory findings, and neuroimaging were reviewed to assess their response to treatment.
RESULTS: Three young adults were admitted following ingestion of diquat solution (20 g/L) and developed transient multiorgan dysfunction, managed with supportive interventions. All patients exhibited altered consciousness, such as somnolence or coma, elevated intracranial pressure, and central nervous system lesions on imaging. After stabilization of vital signs and oxygenation, hyperbaric oxygen therapy was administered. Post-treatment neuroimaging demonstrated lesion reduction. At final follow-up, two patients showed improvements in their Neurofunctional Scores and modified Barthel Indices, achieving clinical independence, while the third patient discontinued treatment for financial reasons.
DISCUSSION: These observations suggest a potential association between hyperbaric oxygen therapy and neurological improvement in the subacute or chronic phase of diquat-induced toxic brain injury. Possible underlying mechanisms may include improved tissue oxygenation and modulation of inflammatory responses.
CONCLUSIONS: These preliminary findings suggest a possible benefit of hyperbaric oxygen therapy in the subacute or chronic phase of diquat-induced toxic brain injury. However, due to the limited sample size and lack of a control group, larger and prospective studies are needed to verify its efficacy and safety.
METHODS: We conducted a retrospective analysis of three patients diagnosed with diquat-induced toxic brain injury who underwent hyperbaric oxygen therapy in the subacute or chronic phase. Clinical data, laboratory findings, and neuroimaging were reviewed to assess their response to treatment.
RESULTS: Three young adults were admitted following ingestion of diquat solution (20 g/L) and developed transient multiorgan dysfunction, managed with supportive interventions. All patients exhibited altered consciousness, such as somnolence or coma, elevated intracranial pressure, and central nervous system lesions on imaging. After stabilization of vital signs and oxygenation, hyperbaric oxygen therapy was administered. Post-treatment neuroimaging demonstrated lesion reduction. At final follow-up, two patients showed improvements in their Neurofunctional Scores and modified Barthel Indices, achieving clinical independence, while the third patient discontinued treatment for financial reasons.
DISCUSSION: These observations suggest a potential association between hyperbaric oxygen therapy and neurological improvement in the subacute or chronic phase of diquat-induced toxic brain injury. Possible underlying mechanisms may include improved tissue oxygenation and modulation of inflammatory responses.
CONCLUSIONS: These preliminary findings suggest a possible benefit of hyperbaric oxygen therapy in the subacute or chronic phase of diquat-induced toxic brain injury. However, due to the limited sample size and lack of a control group, larger and prospective studies are needed to verify its efficacy and safety.