Brain death with calcium oxalate deposition in the kidney: Clue to the diagnosis of ethylene glycol poisoning

Takahashi, Shirushi; Kanetake, Jun; Kanawaku, Yoshimasa; Funayama, Masato

doi:10.1016/j.legalmed.2007.05.010

Cited by 18 publications

(7 citation statements)

References 9 publications

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“…The seventh and eight cranial nerves are commonly involved and it has been suggested to call this phase ”facial-auditory nerve oxalosis“ [16,17]. There have also been documented cases of deficits in other cranial nerves such as VI, IX, and X which result in visual disturbances and dysphagia [18,19]. Our patient also displayed a neurological sequel which involved several cranial nerves similar to the case reports described.…”

Section: Discussionsupporting

confidence: 76%

Severe Oxalosis With Systemic Manifestations

et al. 2012

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Ethylene glycol toxicity can have various clinical presentations with different organ system involvements. These presentations are independent of the level of toxicity. We describe a 31 years old male who presented with ethylene glycol toxicity manifesting as anuric renal failure who subsequently developed neurological sequela of its toxicity. Ethylene glycol is known to be metabolized to various metabolites and is ultimately converted to oxalate which results in crystal deposition the renal parenchyma causing renal failure. Oxalate deposition can occur in various organs including the nervous system as seen in our patient. The majority of patients do not recover from severe oxalosis despite the supportive care of hemodialysis in removing the parent compounds. Despite severe oxalosis, our patient was fortunate enough to be left with minimal neurological sequelae, and eventually was able to cease hemodialysis treatments.KeywordsEthylene glycol; Oxalate; Oxalosis; Glyoxylic acid

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Section: Discussionsupporting

confidence: 76%

Severe Oxalosis With Systemic Manifestations

et al. 2012

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“…Multi-colored birefringence and various forms of crystals were observed under the polarized light microscopic examination ( Fig. 2 B) [8] .…”

Section: Discussionmentioning

confidence: 97%

“…EG intoxication can be life-threatening, but early diagnosis and aggressive treatment are essential to prevent permanent disability or death [1] , [8] . Most of the absorbed EG is metabolized in the liver (80%), and the remaining (20%) is excreted by the kidney without being metabolized [2] , [4] .…”

Section: Discussionmentioning

confidence: 99%

“…1 ) with a urine output of 0.4∼0.5 mL/kg/hour. In many cases, EG intoxication is followed by kidney injury, like in this case [1] , [2] , [8] , [10] . Although this case showed rather typical manifestations of EG intoxication, we did not test EG levels, so we felt it was necessary to perform a kidney biopsy to make a definite etiologic diagnosis of metabolic acidosis with AKI.…”

Section: Discussionmentioning

confidence: 99%

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Acute oxalate nephropathy caused by ethylene glycol poisoning

Seo

Lee

Son

et al. 2012

Kidney Research and Clinical Practice

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Ethylene glycol (EG) is a sweet-tasting, odorless organic solvent found in many agents, such as anti-freeze. EG is composed of four organic acids: glycoaldehyde, glycolic acid, glyoxylic acid and oxalic acid in vivo. These metabolites are cellular toxins that can cause cardio-pulmonary failure, life-threatening metabolic acidosis, central nervous system depression, and kidney injury. Oxalic acid is the end product of EG, which can precipitate to crystals of calcium oxalate monohydrate in the tubular lumen and has been linked to acute kidney injury. We report a case of EG-induced oxalate nephropathy, with the diagnosis confirmed by kidney biopsy, which showed acute tubular injury of the kidneys with extensive intracellular and intraluminal calcium oxalate monohydrate crystal depositions.

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“…Depending on the timing of the initial test, head CT may be normal (as was the case with our patient) or exhibit cerebral edema. 12,16,17,[19][20][21][22][23] Various descriptions of EG effects on CT of the brain exist throughout the literature. Typical findings include hypodensities or hemorrhage within the basal ganglia, thalami, midbrain, pons, and temporal lobes.…”

Section: Discussion Clinical Progression Of Ethylene Glycol Toxicitymentioning

confidence: 99%

Reversibility of Severe Cerebral Magnetic Resonance Imaging Changes Associated with Ethylene Glycol Toxicity

Owen

Calhoun

McDonald

2017

J Pediatr Intensive Care

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Ethylene glycol (EG), commonly found in antifreeze and deicing solutions, continues to be a cause of morbidity and mortality in the pediatric population. EG metabolism produces toxins that cause metabolic acidosis and calcium oxalate deposition throughout the body. Deposition in the central nervous system is associated with significant neurologic sequelae, including altered mental status, seizures, and cerebral edema. We present a case of intentional EG poisoning in a 17-year-old male with resulting cerebral edema and coma. Neuroimaging studies were initially normal but eventually demonstrated diffuse abnormalities on both cranial computed tomography and magnetic resonance imaging (MRI). The patient ultimately made a complete recovery with resolution of the MRI abnormalities noted at the peak of illness. While neuroimaging is often incorporated into the management of EG poisoning, this is the first case report to show the evolution of EG-related MRI changes before, during, and after the resolution of EG-induced intracranial hypertension.

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Brain death with calcium oxalate deposition in the kidney: Clue to the diagnosis of ethylene glycol poisoning

Cited by 18 publications

References 9 publications

Severe Oxalosis With Systemic Manifestations

Severe Oxalosis With Systemic Manifestations

Acute oxalate nephropathy caused by ethylene glycol poisoning

Reversibility of Severe Cerebral Magnetic Resonance Imaging Changes Associated with Ethylene Glycol Toxicity

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