Lethal diquat poisoning manifesting as central pontine myelinolysis and acute kidney injury: A case report and literature review

Diquat is a nonselective herbicide that is used as a contact and preharvest desiccant to control terrestrial and aquatic vegetation. Increasing numbers of cases of diquat poisoning have recently been reported. Organs commonly affected by diquat poisoning include the kidney, liver, and lung. Neurological involvement of diquat poisoning is relatively rare. A 21-year-old man ingested 100 mL of diquat (20 g/100 mL) 5 hours before admission. Fifteen minutes after ingestion, he developed nausea and vomiting. The patient was sent to the emergency intensive care unit, and gastric lavage was performed. Continuous renal replacement therapy and continuous venovenous hemodiafiltration with hemoperfusion were performed, and methylprednisolone was administered. Five days after admission, the patient developed disturbance of consciousness and positive bilateral Babinski signs. Head computed tomography demonstrated hypodensity in the pons. At 11 days after admission, brain magnetic resonance imaging showed acute pontine demyelination. At 15 days after admission, the patient died of multiple organ dysfunction syndrome. We encountered a case of diquat poisoning with central pontine myelinolysis and acute kidney injury. This case highlights the clinical value of neuroimaging examination for early diagnosis of central pontine myelinolysis.

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Central pontine myelinolysis during treatment of hyperglycemic hyperosmolar syndrome: a case report

Clinical Diabetes and Endocrinology ◽

10.1186/s40842-020-00111-6 ◽

2020 ◽

Vol 6 (1) ◽

Author(s):

Koshi Kusumoto ◽

Nobuyuki Koriyama ◽

Nami Kojima ◽

Maki Ikeda ◽

Yoshihiko Nishio

Keyword(s):

Risk Factors ◽

Disseminated Intravascular Coagulation ◽

Thrombus Formation ◽

Central Pontine Myelinolysis ◽

Bed Rest ◽

Severe Illness ◽

Intravascular Coagulation ◽

Disturbance Of Consciousness ◽

Pontine Myelinolysis ◽

Central Pontine

Abstract Background Central pontine myelinolysis (CPM) is a non-inflammatory demyelinating lesion of the pons. CPM and extrapontine demyelination (EPM) are together termed osmotic demyelination syndrome (ODS), a known and serious complication of acute correction of hyponatremia. Conversely, hyperglycemic hyperosmolarity syndrome (HHS) develops in patients with type 2 diabetes who still have some insulin secretory ability due to infection, non-compliance with treatment, drugs, and coexisting diseases, and is often accompanied by ketosis. HHS represents a life-threatening endocrine emergency (mortality rate, 10–50%) associated with marked hyperglycemia and severe dehydration. HHS may develop ODS, and some cases have been associated with hypernatremia. Case presentation The patient was an 87-year-old woman with hyperglycemia, dehydration, malnutrition, and potential thrombus formation during long-term bed rest. HHS was suspected to have developed due to progression of hyperglycemia and dehydration caused by pneumonia. Furthermore, ketoacidosis developed from ketosis and prerenal renal failure associated with circulating hypovolemia shock, which was also associated with disseminated intravascular coagulation. Treatment was started with continuous intravenous injection of fast-acting insulin and low-sodium replacement fluid. In addition, ceftriaxone sodium hydrate, heparin sodium, thrombomodulin α, human serum albumin, and dopamine hydrochloride were administered. Blood glucose, serum sodium, serum osmolality, and general condition (including vital, infection/inflammatory findings, and disseminated intravascular coagulation) improved promptly, but improvements in disturbance of consciousness were poor. Diffusion-weighted imaging of the brain 72 h after starting treatment showed no obvious abnormalities, but high-intensity signals in the midline of the pons became apparent 30 days later, leading to definitive diagnosis of CPM. Conclusions Fluctuation of osmotic pressure by treatment from hyperosmolarity due to hyperglycemia and hypernatremia in the presence of risk factors such as malnutrition, severe illness, and metabolic disorders may be a cause of CPM onset. When treating HHS with risk factors, the possibility of progression to ODS needs to be kept in mind.

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Central pontine myelinolysis in a chronic alcoholic: A clinical and brain magnetic resonance imaging follow-up

Vojnosanitetski pregled ◽

10.2298/vsp1308785d ◽

2013 ◽

Vol 70 (8) ◽

pp. 785-788 ◽

Cited By ~ 2

Author(s):

Irena Dujmovic ◽

Jelena Vitas ◽

Natasa Zlataric ◽

Jelena Drulovic

Keyword(s):

Magnetic Resonance Imaging ◽

Magnetic Resonance ◽

Brain Mri ◽

Central Pontine Myelinolysis ◽

Brain Magnetic Resonance Imaging ◽

Resonance Imaging ◽

Pontine Myelinolysis ◽

Pontine Lesion ◽

Central Pontine

Introduction. Central pontine myelinolysis (CPM) is a noninflammatory, demyelinating lesion usually localised in the basis pontis. Chronic alcoholism is frequently associated with this condition which may have a variable clinical outcome. Until now, brain magnetic resonance imaging (MRI) follow-up in alcoholic CPM cases after alcohol withdrawal has been rarely described. Case report. We reported a 30- year-old male with a 12-year history of alcohol abuse, who presented with inability to stand and walk, nausea, vomiting and somnolence. Neurological examination revealed: impared fixation on lateral gaze, dysarthria, mild spastic quadriparesis, truncal and extremity ataxia, sock-like hypesthesia and moderate decrease in vibration sense in legs. Brain MRI showed a trident-shaped non-enhancing pontine lesion highly suggestive of CPM. After an eight-month alcoholfree follow-up period, the patient?s clinical status significantly improved, while the extent of MRI pontine lesion was merely slightly reduced. Conclusion. The presented case demonstrates that CPM in chronic alcoholics may have a benign clinical course after alcohol withdrawal, which is not necessarily associated with the reduction of lesions on brain MRI.

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Acute Psychosis as Main Manifestation of Central Pontine Myelinolysis

Case Reports in Neurological Medicine ◽

10.1155/2017/1471096 ◽

2017 ◽

Vol 2017 ◽

pp. 1-7 ◽

Cited By ~ 1

Author(s):

Mangala Gopal ◽

Melvin Parasram ◽

Harsh Patel ◽

Chike Ilorah ◽

Hrachya Nersesyan

Keyword(s):

Central Pontine Myelinolysis ◽

Laboratory Data ◽

Clinical Manifestations ◽

Brain Magnetic Resonance Imaging ◽

Neurological Deficits ◽

Pseudobulbar Palsy ◽

Acute Psychosis ◽

Pontine Myelinolysis ◽

Neuropsychiatric Manifestations ◽

Central Pontine

Central pontine myelinolysis (CPM) is an acute demyelinating neurological disorder affecting primarily the central pons and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy, and encephalopathy of various degrees; however, coma, “locked-in” syndrome, or death can occur in most severe cases. Rarely, CPM presents with neuropsychiatric manifestations, such as personality changes, acute psychosis, paranoia, hallucinations, or catatonia, typically associated with additional injury to the brain, described as extrapontine myelinolysis (EPM). We present a patient with primarily neuropsychiatric manifestations of CPM, in the absence of focal neurologic deficits or radiographic extrapontine involvement. A 51-year-old female without significant medical history presented with dizziness, frequent falls, diarrhea, generalized weakness, and weight loss. Physical examination showed no focal neurological deficits. Laboratory data showed severe hyponatremia, which was corrected rather rapidly. Subsequently, the patient developed symptoms of an acute psychotic illness. Initial brain magnetic resonance imaging (MRI) was unremarkable, although a repeat MRI two weeks later revealed changes compatible with CPM. This case demonstrates that acute psychosis might represent the main manifestation of CPM, especially in early stages of the disease, which should be taken into consideration when assessing patients with acute abnormalities of sodium metabolism.

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Central pontine myelinolysis

Archives of Internal Medicine ◽

10.1001/archinte.119.5.444 ◽

1967 ◽

Vol 119 (5) ◽

pp. 444-478 ◽

Cited By ~ 6

Author(s):

W. F. McCormick

Keyword(s):

Central Pontine Myelinolysis ◽

Pontine Myelinolysis ◽

Central Pontine

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Ayurvedic understanding of Central Pontine Myelinolysis - A Case Report

Journal of Ayurveda and Integrated Medical Sciences (JAIMS) ◽

10.21760/jaims.v3i3.12900 ◽

2018 ◽

Vol 3 (3) ◽

Author(s):

Anoop AS ◽

Lakshmiprasad L. Jadhav ◽

Sruthy Nair ◽

Rohan Mohandas

Keyword(s):

Serum Sodium Level ◽

Central Pontine Myelinolysis ◽

Chronic Alcoholism ◽

Serum Electrolyte ◽

Oral Medications ◽

Shoulder Joints ◽

Pontine Myelinolysis ◽

Chief Complaints ◽

Hyponatremic Encephalopathy ◽

Central Pontine

A 56 year old male patient was admitted to S.D.M Ayurveda Hospital, Hassan, Karnataka with the confirmed diagnosis of Central Pontine Myelinolysis (CPM) on 11/12/17. The chief complaints were weakness of both hands and legs, stiffness in both hands and legs, pain in both shoulder joints, slurred speech, difficulty in walking with gait changes. H/O chronic alcoholism. MRI brain showed pontine and basal ganglia diffusion restriction - Acute Pontine Myelinolysis. The serum electrolyte showed serum sodium level as 128 mmol/litre. This disease can be understood as Samana Avruta Vyana in hyponatremic encephalopathy stage and the stage of myelinolysis can be understood as Sarvanga Vata with Kapha Avruta Udana and Vyana. After clinical evaluation, Avarana Chikitsa was started followed by Kevala Vatika Chikitsa and significant improvement was seen. Significant result was observed in subjective and objective parameters after the treatment. The patient was discharged with oral medications for 1 month.

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