Mid-to-late stage diquat accumulation in the central nervous system: A severe case of oral poisoning





Abstract


A 54-year-old woman in good health was admitted to our hospital with diquat poisoning. The patient drank an unknown dose of diquat, and acute kidney injury developed early. However, there were no obvious pulmonary abnormalities and no signs of central nervous system toxicity in the early stage. The woman underwent active treatment, which resulted in a significant decrease in blood diquat levels, but her lung condition progressively worsened and neurological symptoms developed. Fortunately, the patient survived after intensive hemoperfusion combined with continuous renal replacement therapy (CRRT), intracranial pressure reduction, and anti-infective treatment. This case report highlights the importance of being aware of the development of delayed pulmonary symptoms and neurologic complications when caring for patients poisoned with diquat, even in those with low diquat blood concentrations. Interestingly, we also detected the concentration of diquat in the cerebrospinal fluid (CSF) of patients with diquat poisoning, and found that the rate of decrease of diquat concentration in the CSF was considerably slower than that in the blood.Notably, a specific correlation was observed between the concentration of diquat in the CSF, rather than in the blood, and both the intracranial pressure (ICP) and the severity of cerebral edema in this patient.


Highlights




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    Neurological complications can occur in patients with diquat poisoning.


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    Patients with diquat poisoning are at risk for delayed neurological complications


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    A lumbar puncture aids in assessing diquat presence in the CNS and early detection of CNS toxicity.



1


Introduction


Recently, an increasing number of clinical researchers have been reporting cases of diquat poisoning accompanied by nervous system abnormalities [ , ]. However, the majority of these reports primarily focus on neuroimaging perspectives, with no existing documentation regarding the detection of diquat concentration in the cerebrospinal fluid (CSF) of diquat poisoning patients.


Our hospital recently treated an adult patient who had ingested an unknown dose of diquat. The patient developed acute kidney injury (AKI) shortly after ingestion, followed by severe pulmonary damage and neurological symptoms that appeared five days later. Notably, a lumbar puncture (LP) revealed a high concentration of diquat in the patient’s cerebrospinal fluid (CSF). Our case report serves as a reminder to clinicians about the potential for delayed onset of severe pulmonary and neurological complications in diquat poisoning patients, and highlights the need for further research into the diagnosis and treatment of diquat poisoning, particularly in cases involving the central nervous system (CNS).


2


Case report


A previously healthy 54-year-old female patient was admitted to our hospital on the fourth day after poisoning with an unknown dose of diquat. The patient had been treated at a local hospital, where acute kidney injury had been diagnosed. Upon admission to our hospital, the patient had no abnormal physical examination findings, remained conscious, and the chest CT showed only scattered inflammatory changes in both lungs. Blood tests using high-performance liquid chromatography-mass spectrometry (HPLC-MS/MS) detected a concentration of 187.25 ng/mL of diquat, and no trace of paraquat. The patient was promptly initiated on continuous renal replacement therapy (CRRT), hormonal therapy (corticosteroid pulse-therapy with 500 mg/day dexamethasone, followed by methylprednisolone [80 mg q8h], which was gradually tapered until discontinuation), anti-infective therapy (cefoperazone-sulbactam [2 g, q8d]), antioxidation, and organ protection (reduced glutathione, N -acetylcysteine, methylcobalamin). Despite the declining diquat concentration in the patient’s blood, the patient fell into coma on the fifth day after poisoning. Through LP, elevated intracranial pressure (460 mmH2O) was identified. Head CT was performed, and the result showed hypodensity in the pons. After implementing active treatment to reduce intracranial pressure (mannitol [20 g q8h]), we performed LP to collect CSF for biochemical and routine testing, as well as diquat concentration analysis, which revealed a concentration of 141.32 ng/mL of diquat. Meanwhile, the patient’s pulmonary condition deteriorated significantly. Given the pronounced decline in oxygenation and blood pressure, the patient underwent tracheal intubation and was assisted with ventilation. We subsequently conducted continuous monitoring of diquat concentration in the patient’s blood and intermittent monitoring in the CSF ( Table 1 ). Therapeutic strategies were adjusted gradually in response to changes in the patient’s condition. After 26 days of therapy, the patient was discharged in a stable condition, and follow-up lung CT scans showed improvement. Figs. 1, 2 and 3 display the patient’s clinical course and examination results.


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Mar 29, 2024 | Posted by in EMERGENCY MEDICINE | Comments Off on Mid-to-late stage diquat accumulation in the central nervous system: A severe case of oral poisoning

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