Glycol Ingestion Research Articles

Can endogenous ethylene glycol production occur in humans? A detailed investigation of adult monozygotic twin sisters

Introduction To the best of our knowledge, clinically significant endogenous ethylene glycol production has never been reported in humans, very seldom reported in other animals or microorganisms, and then only under rare and specific conditions. We describe the detailed investigations we undertook in two adult monozygotic twin sisters to ascertain whether they were producing endogenous ethylene glycol. Methods Two previously healthy monozygotic adult twin sisters presented with recurrent episodes of apparent ethylene glycol poisoning beginning at age 35, requiring chronic hemodialysis to remove ethylene glycol and its metabolites as well as to restore metabolic homeostasis. The sisters denied ingestion or exposure to ethylene glycol. At their request, they were admitted to hospital under strict supervision to exclude surreptitious ingestion of ethylene glycol and to evaluate the need for treatment. Hemodialysis was withheld during this prospective study. Twin A was admitted for 14 days and twin B for 11 days. Serial biochemical analyses were performed in blood and urine. Clinical exome sequencing and mitochondrial deoxyribonucleic acid sequencing were also completed. Results In both twins, ethylene glycol was detected in urine, along with intermittent increases in concentrations of lactate, glycolate, and glycine in blood and/or urine. Blood ethylene glycol concentrations, however, remained <62 mg/L (<1 mmol/L) but became positive soon after discharge. The oxalate concentration remained normal in blood and urine. Plasma and urine amino acid profiles showed intermittent small increases in glycine, serine, taurine, proline, and/or alanine concentrations. Exome sequencing and mitochondrial deoxyribonucleic acid sequencing were non-diagnostic. Neither twin has been admitted with metabolic acidosis nor ethylene glycol poisoning since chronic hemodialysis was started. Twin A developed a calcium oxalate dihydrate lithiasis. Discussion Mitochondrial disease, methylmalonic/propionic/isovaleric aciduria, primary hyperoxaluria, and analyte error were all excluded in these twins, as were obvious common environmental exposures. Conclusion Detailed investigations were performed in adult monozygotic twin sisters to ascertain whether they were producing endogenous ethylene glycol. Alternative explanations were excluded to the very best of our efforts and knowledge. Global metabolomics, gut microbiome analyses, and whole genome sequencing are pending.

Clinical manifestations and renal pathology of ethylene glycol.

Ethylene glycol (EG) poisoning is a critical medical emergency often associated with suicide attempts in adults. EG is metabolized by alcohol dehydrogenase, leading to the formation of toxic metabolites that cause metabolic acidosis, renal failure, hypocalcemia, aciduria, and disorders of the central nervous and cardiovascular systems. Calcium oxalate, a metabolite of EG, contributes to acute tubular necrosis. Despite limited reports on human renal pathology, we present a case detailing renal pathology following EG ingestion. A 44-year-old male, admitted due to loss of consciousness, had ingested a lethal dose of EG. Blood tests indicated metabolic acidosis, while urinary examination revealed calcium oxalate crystals. Continuous renal replacement therapy corrected the acidosis; however, nephrogenic diabetes insipidus subsequently developed. A renal biopsy on day 31 revealed calcium oxalate crystal deposition and tubulointerstitial damage. Notably, various stages of crystal deposition, adherence, and degradation were observed. This case underscores the importance of considering EG poisoning in cases of unexplained metabolic acidosis and renal dysfunction, with renal biopsy serving as a valuable diagnostic tool. Understanding the renal effects of EG is essential for timely intervention and effective management of poisoning cases.

Minding the osmol gap: a sentinel event and subsequent laboratory investigation

Introduction Many hospitals are unable to determine toxic alcohol concentrations in a clinically meaningful time frame. Thus, clinicians use surrogate markers when evaluating potentially poisoned patients. Index case A patient presented after an intentional antifreeze (ethylene glycol) ingestion with an osmol gap of −10.6 that remained stable one hour later. Further investigation revealed that the serum osmolality was calculated and not measured. The true osmol gap was 16.4, which correlated to a measured ethylene glycol concentration of 808 mg/L (80.8 mg/dL, 13.0 mmol/L). Survey A telephone survey of hospital laboratories in our catchment area was performed to investigate the potential for similar events. Results Thirty-eight (47 percent) hospitals responded. No laboratories were able to test for toxic alcohols. One hospital (2.6 percent) reported routinely calculating osmolality based on chemistries, while two hospitals (5.3 percent) reported scenarios in which this might occur. Thirty-five (92.1 percent) hospitals could directly measure osmolality. Two hospitals (5.3 percent) were reliant on outside laboratories for osmolality measurement. Limitations The 47 percent response rate and one geographic area are significant limitations. Discussion Over 10 percent of hospitals that responded could have significant difficulty assessing patients with toxic alcohol ingestion. Conclusions Until the standard of rapidly obtaining toxic alcohol concentrations is broadly implemented, we recommend that policies and procedures be put in place to minimize errors associated with the determination of the osmol gap.

Assessing the Role of Initial Serum Calcium Concentration in Patients with Ethylene Glycol Poisoning.

Assays for ethylene glycol (EG) with a rapid turn-around time are not routinely available. Clinicians must rely on historical features and readily available clinical tests, combined with clinical acumen, to guide the initial management of suspected EG poisoning. Hypocalcemia has been suggested as a clue supporting the diagnosis of EG poisoning in patients presenting with an unexplained high anion gap metabolic acidosis (HAGMA). A previous small study challenged this assumption. This was a retrospective case series of one state's poison control system of confirmed EG-poisoned patients between September 2017 and April 2021. The definition of EG poisoning was based on suspected EG ingestion and a serum EG concentration > 5 mg/dL. Patients who were suspected to have EG toxicity but did not have a confirmed EG concentration or the EG concentration was less than 5 mg/dL were excluded. Routine laboratory studies were recorded for all patients. Comparisons between serum calcium on presentation to presenting blood pH, bicarbonate, anion gap, and creatinine were assessed for correlation. There was no correlation between the presenting calcium and either pH or creatinine. There was a weak positive correlation between the initial serum calcium and anion gap, a weak negative correlation between the initial serum calcium and bicarbonate. On hospital presentation, hypocalcemia was not associated with EG poisoning, even in patients with a HAGMA. A normal serum calcium on presentation does not exclude the diagnosis of EG poisoning.

Neuroimaging in Acute Ethylene Glycol Toxicity (P8-4.006)

<h3>Objective:</h3> To describe unique neuroradiological features of Ethylene Glycol poisoning. <h3>Background:</h3> Ethylene Glycol (EG) is a sweet tasting, industrial compound that is ubiquitously found in various consumer products (antifreeze, paints, solvents, and cosmetics). Ingestion of EG results in toxicity with characteristic metabolic, pathological, and imaging findings. Toxicity classically presents with a severe anion gap metabolic acidosis, an osmolar gap, and multi-organ involvement. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> A 64-year-old man presented with acute onset nausea, recurrent vomiting, and ataxic gait. Within a few hours, he became progressively confused, lethargic, and eventually obtunded requiring intubation for airway protection. On physical examination, he was unresponsive but had preserved brainstem reflexes. Laboratory tests showed elevated high anion gap metabolic acidosis (HAGMA) with pH of 7.23, bicarbonate of 13 mmol/L, anion gap of 38 mmol/L, and lactic acid of 2.2 mmol/L. Ethanol, salicylates, acetaminophen, and ketones were undetectable. Further tests revealed methemoglobin level of 1%, increased serum osmolality 328 mOsm/kg, and osmolal gap 71 mOsm/kg. CT head was unrevealing. Due to the HAGMA with hyperosmolality suggesting a toxic alcohol ingestion, the patient was empirically treated with fomepizole 15 mg/kg. EEG showed severe diffuse cerebral dysfunction. He soon developed progressive renal failure requiring hemodialysis. MRI of the brain without contrast revealed bilateral and symmetric enlargement of the basal ganglia and thalami with T2-weighted hyperintensities, as well as T2-weighted hyperintensities involving the brainstem and scattered cortical areas. Ethylene glycol concentration from blood drawn on admission resulted at 1962 mg/dL confirming EG poisoning. <h3>Conclusions:</h3> This case highlights MRI brain findings of T2-weighted hyperintensities in deep gray matter structures in EG toxicity. Current scientific literature infrequently reports any neuroradiologic findings. Clinicians should be cognizant of these neuroradiologic features and use MRI as a supportive diagnostic tool in the proper clinical context while awaiting a definitive EG concentration. <b>Disclosure:</b> Dr. Hiana has nothing to disclose. Dr. Mulatu has nothing to disclose. Dr. Sharma has nothing to disclose. Dr. Askandaryan has nothing to disclose. Dr. Mulatu has nothing to disclose. Dr. Anziska has nothing to disclose.

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

A False-Positive Gamma-Hydroxy Butyric Acid Urine Screening in a Patient with High Anion Gap Metabolic Acidosis Due to Ethylene Glycol Poisoning.

A young woman with a history of several suicide attempts was admitted to the hospital after suspicion of a new intoxication without definite identification of the causing agent. The patient had a high anion gap metabolic acidosis (HAGMA) with respiratory compensation, a lactate gap and an osmolar gap at admission. Initial toxicological screening showed no abnormalities except for a weak positive gamma-hydroxy butyric acid (GHB) enzymatic screen in urine. This finding could not be confirmed using chromatographic analysis nor be explained by the presence of known cross-reacting substances like ethanol. In this case, falsely elevated urinary GHB screening was caused by the ingestion of ethylene glycol. To confirm that the interference was due to ethylene glycol or its metabolites, we performed a spiking experiment. Cross reactivity was linked to ethylene glycol and was low in our experiments (0.1-0.2%). Substantial amounts of ethylene glycol are required to slightly elevated GHB results, depending on the endogenous cutoff used. We can conclude that ethylene glycol can give rise to falsely elevated urinary GHB levels at ethylene glycol concentrations that are typically found in intoxications.

Symptomatic Diethylene Glycol Ingestion Successfully Treated with Fomepizole Monotherapy

BackgroundDiethylene glycol (DEG) is an industrial solvent with many uses, including brake fluids. It has also caused mass poisonings after use as an inappropriate substitute for propylene glycol or glycerin, though individual ingestions are rare. Like other toxic alcohols, DEG is metabolized by alcohol dehydrogenase and aldehyde dehydrogenase, with toxicity likely mediated by the resulting metabolites. Fomepizole, an alcohol dehydrogenase inhibitor, is used to prevent metabolite formation with other toxic alcohol exposures. Fomepizole is recommended for DEG poisoning, though supporting clinical evidence is limited. Case ReportA 31-year-old man presented after ingestion of DEG-containing brake fluid and hydrocarbon-containing “octane booster.” He was noted to be clinically intoxicated, with a mildly elevated anion gap metabolic acidosis and no osmolar gap. DEG level was later found to be elevated, consistent with his ingestion. He was treated with fomepizole alone, with resolution of metabolic acidosis and clinical findings over the next 2 days. No delayed neurologic sequelae were present at 52-day follow-up. Our case provides additional evidence supporting the use of fomepizole for DEG poisoning. Consistent with other toxic alcohols, DEG poisoning, especially early presentations, may benefit from empiric fomepizole administration. Why Should an Emergency Physician Be Aware of This?DEG poisoning is potentially life threatening, but treatable if identified early. An ingestion can be toxic despite a normal osmolar gap, leading to false reassurance. Finally, it is rare, so emergency physicians must be made aware of its potential dangers.

Protective effect of bee pollen in acute kidney injury, proteinuria, and crystalluria induced by ethylene glycol ingestion in rats

Oxidative stress plays a role in hyperoxaluria-induced kidney injury and crystallization. Bee pollen is a hive product with a high content of antioxidants. The antioxidant content and protective effect of bee pollen extract (BPE) against ethylene glycol (EG) induced crystalluria, and acute kidney injury (AKI) were investigated. The effect of BPE on the EG-induced liver injury and proteinuria was also examined. Ten groups of male Wister rats were treated daily with vehicle, cystone, BPE (100, 250, and 500 mg/kg b.wt.), and group 6–9 treated with EG, EG + BPE (100, 250, and 500 mg/kg b.wt.) and group 10 EG + cystone. The dose of EG was 0.75% v/v, and the dose of cystone was 500 mg/kg b.wt. On day 30, blood and urine samples were collected for analysis. Kidneys were removed for histopathological study. The antioxidant activity of BPE was assessed, and its total phenols and flavonoids were determined. EG significantly increased urine parameters (pH, volume, calcium, phosphorus, uric acid, and protein), blood urea, creatinine, and liver enzymes (P < 0.05). EG decreased creatinine clearance and urine magnesium and caused crystalluria. Treatment with BPE or cystone mitigates EG's effect; BPE was more potent than cystone (P < 0.05). BPE increases urine volume, sodium, and magnesium compared to the control and EG treated groups. BPE reduces proteinuria and prevents AKI, crystalluria, liver injury, and histopathological changes in the kidney tissue caused by EG. BPE might have a protective effect against EG-induced AKI, crystalluria, proteinuria, and stone deposition, most likely by its antioxidant content and activity.

Unintentional ethylene glycol ingestions in children

ABSTRACT Background: Toxic alcohol poisoning may result in severe acidemia and death. Previous work from our regional poison center (RPC) revealed that most pediatric unintentional methanol exposures are benign and do not require alcohol dehydrogenase (ADH) blockade or hemodialysis. Methods: We retrospectively reviewed all ethylene glycol (EG) cases in patients less than 6 years of age reported to our RPC over a 19 year period. We included unintentional ingestions with measured EG concentrations. Results: Twenty-nine cases met inclusion criteria. EG concentrations were undetectable in 25 cases (86%). No patient became symptomatic or acidemic. No EG concentration warranted treatment with ADH inhibition or hemodialysis. However, 21 patients (72%) received fomepizole or ethanol. Fifteen patients (52%) transferred from a community hospital to a pediatric specialty hospital. All 27 children admitted to the hospital went to a pediatric intensive care unit (PICU) while awaiting EG results. Conclusions: No child during the 19-year period required either antidote or hemodialysis. Unintentional EG exposures in typical pediatric patients may warrant nothing more than repeat laboratory testing (electrolytes, pH) to exclude evolving toxicity. Timely availability of EG laboratory test results would likely reduce unnecessary and expensive use of antidote, transport, and PICU resources.

Acute poisonings presenting to King Edward VIII hospital intensive care unit in Durban, South Africa.

Background Acute poisoning is a potentially preventable burden on the healthcare systems and a significant cause of morbidity and mortality worldwide. Improved knowledge of the patterns of poisoning, the clinical course and outcomes of these cases may help create better preventive and management approaches. Objectives To describe the demographics, clinical characteristics and outcomes of patients with acute poisonings who were admitted to a multidisciplinary intensive care unit (ICU) at King Edward VIII Hospital, Durban, South Africa. Methods A retrospective observational chart review of patients admitted to the study ICU with acute poisoning over a 24-month period (1 July 2015 - 30 June 2017). Results A total of 85 patients with acute poisoning were admitted to the ICU during the study period. There was a female preponderance (55%) with a median age of 28 years. ICU mortality was 16.5% with a median ICU length of stay of 3 days. Tricyclic antidepressants (TCA) were the most common toxin identified (16.5%). The ingestion of amphetamines was associated with a statistically significant increase in mortality (100.0% v. 13.4%; p=0.04). Ethylene glycol was a commonly ingested toxin (9.4% of admissions) and had a high mortality rate of 37.5% that was not statistically significant (p=0.121). Referral for inotropic support, a Glasgow Coma Scale ≤5 and metabolic acidosis on admission were associated with higher ICU mortality. Conclusion Acute poisoning results in potentially preventable ICU admission and mortality. TCA poisoning was the most common presentation and this warrants review of TCA prescription practice. Ingestion of illicit drugs, ethylene glycol or presentation with a markedly reduced level of consciousness, shock or metabolic acidosis should alert treating physicians to a possible elevated risk of adverse outcomes. Contributions of the studyThis is the first study to describe acute poisoning patterns in KwaZulu-Natal from a critical care perspective. This will increase knowledge of common toxins and the presentations that lead to critical care referral. Furthermore, prescription practices for common toxins like TCAs need to be reviewed as a prevention strategy.

Urine ‘picket fence’ crystals in ethylene glycol poisoning

A 46-year-old woman intentionally ingested ethylene glycol and overdosed on paracetamol. She had clinical and laboratory features suggestive of ethylene glycol poisoning, and examination of the urine revealed calcium oxalate monohydrate, or ‘picket fence’, crystals. She responded well to therapy that included haemodialysis. Clinicians should be aware that these crystals appear late during the evolution of ethylene glycol poisoning and, along with other clinical and laboratory findings, should prompt the initiation of haemodialysis.

Acute chemical ingestion in the under 19 population in South Korea: A brief report.

Most people are frequently exposed to chemicals and chemical products. This study provides basic information on the outcomes of acute chemical ingestion of patients aged under 19 years. Patients aged under 19 years who had ingested chemicals and thus visited the emergency department between January 2011 and December 2016 were included in this study. In all, 1,247 patients included (1,145 in the unintentional group and 102 in the intentional group). The mean age was 3.27±4.77 in the unintentional ingestion group and 16.49±1.94 in the intentional group. In the unintentional group, detergents were most frequently ingested (by 219 patients), followed by hypochlorite-based agents, ethanol, sodium hydroxide, acetone, silica gel, and citric acid. Cases of boric acid (odds ratio [OR] = 6.131), ethylene glycol (OR = 6.541), glacial acetic acid (OR = 7.644), other hydrocarbons (OR = 4.496), hypochlorite-based agent (OR = 2.627), nicotine (OR = 5.635), and sodium peroxocarbonate (OR = 6.783) ingestion was associated with a significantly high admission rate. In the intentional group, there were 54 cases of ingestion of hypochlorite-based agent, followed by detergent, ethylene glycol, ethanol, methanol and sodium peroxycarbonate. The significant risk factors for admission in the intentional group were ingestion of ethylene glycol (OR = 37.333) and hypochlorite-based agent (OR = 5.026). There was no mortality case. The most commonly ingested substances were sodium hypochlorite (hypochlorite-related agent), surfactants (detergent and soap), and ethanol. The ingestion of hypochlorite or ethylene glycol was the main risk factor for admission. Intentional ingestion was higher in adolescents than in children.

SP2 Management of ethylene glycol poisoning in an adolescent: a clinical pearl

Situation16 year old girl admitted with suspected ingestion of ethylene glycol. She was treated with fomepizole and continuous renal replacement therapy (CRRT).How the Pharmacy Team ContributedEthanol was prescribed until fomepizole arrived. The volume of ethanol to be administered was calculated wrongly by the consultant due to confusion about the available strength. The Paediatric Intensive Care Unit (PICU) pharmacist intervened and the correct dosage information was given.PICU pharmacist used Toxbase to determine the correct treatment of ethylene glycol poisoning and advised on dosing regime, including adjustment due to CRRT. The pharmacist facilitated prescribing on the electronic system (added drug to system, set up administration instructions and assisted with prescribing – pharmacist was not an Independent Prescriber). This allowed medical staff to concentrate on resuscitation, monitoring cardiac function, inserting intravenous lines and obtaining access for CRRT.The PICU pharmacist and pharmacy technician co-ordinated initial supply of fomepizole. Fomepizole is usually ordered directly from the manufacturer during office hours. The patient presented in the early evening so further supply had to be obtained from a hospital hundreds of miles away after referring to the Rarely Used Medicines list. Pharmacist contacted appropriate on-call pharmacist and arranged for transfer of medicines via courier. Pharmacy technician arranged for further supply form the manufacturer the following day.Pharmacy technician arranged supply of additional dialysis fluids for CRRT due to the higher than usual administration rate.Without contribution from the pharmacy team the patient is likely to have been given the wrong dose of ethanol and fomepizole, and there would have been delay in initiation of treatment followed by an interruption, as it was wrongly assumed that it was kept as stock in the adjoining ‘adult hospital’ and subsequent supply from a local hospital would not have been sought by ward staff until original supply ran out.OutcomeEthylene glycol poisoning was confirmed on laboratory testing. Levels of ethylene glycol fell steadily over 36 hours, allowing CRRT and fomepizole to stop. Patient was discharged from PICU after 48 hours with no apparent long-lasting effects, but was referred to various specialities including renal, gastroenterology and psychology.Patient and family denied knowledge of intentional or accidental ingestion. Police investigation was inconclusive.Lessons to be LearnedLarger supplies of fomepizole are now kept in stock within Health Board. Supplies were missing from emergency cupboards when stock was needed, despite being on stock lists, necessitating courier fees to transfer stock from elsewhere. Procedures reviewed to ensure that stock is available in emergency cupboards at all times.This patient demonstrated that current (target) stock levels of fomepizole were inadequate for providing treatment during CRRT as the required doses are substantially higher (administered every four hours rather than every twelve hours) and would have lasted less than 12 hours for this average sized teenager. National Rarely Used Medicines list was updated to reflect actual stock levels and other hospitals increased their stockholding due to the realisation that existing stock was inadequate and that further supplies were hard to obtain out of working hours.

Ethylene glycol intoxication following brake fluid ingestion complicated with unilateral facial nerve palsy: a case report

BackgroundBrake oil is an automobile transmission fluid composed of a mixture of toxic alcohols such as ethylene glycols and glycol ethers. Both accidental and intentional ingestion cases have been reported and they can present with multisystem involvement. Life-threatening complications evolve from deleterious effects on cardiopulmonary and renal systems. Effects on neurological and gastrointestinal systems give rise to a multitude of complications although non-fatal in nature. The biochemical panel consists of a high concentration of ethylene glycol with severe metabolic acidosis, high anion gap, high osmolar gap, oxaluria, and hypocalcemia. The mainstay of treatment is enhanced elimination of ethylene glycol and its metabolites by hemodialysis, together with general supportive care, gastric decontamination, and vitamins such as thiamine and pyridoxine to minimize the adverse effects of intoxication.Case presentationA 26-year-old Sinhalese woman presented with reduced urine output, shortness of breath, reduced level of consciousness, abdominal pain, and vomiting with mild degree fever of 2 days’ duration. She had bilateral lower limb edema, crepitations over bilateral lower lung fields, and right-sided lower motor type facial nerve palsy. Investigations showed severe metabolic acidosis with high anion gap and high osmolar gap. With regular hemodialysis she made a complete recovery after 3 months.ConclusionEven without a clear history of poisoning, the presence of a high anion, high osmolar gap metabolic acidosis should prompt one to search for ethylene glycol ingestion. Uncommon manifestations like cranial neuropathies need to be examined and considered. Timely aggressive treatment leads to a better prognosis.

Induced Acute Renal Failure (Injury) by Administration of Ethylene Glycol (Antifreeze) in Cats

Etheylene glycol (EG) poisoning is highly dangerous in cats and a small dose of it could cause signs which are initially non-specific and may be easily missed. So,our study was preformed to determine the various effects of EG administration on cats. 10 cats of both sexes aging 1-3 years old were included in this experimental study. Cats were examined before starting the experiment clinically , physically and ultrasonographically to ensure their soundness, then EG was administrated at a dose of 1.4 ml/kg b.wt. orally by using of sterile syringe.clinical signs started with in 12 hours after adminstraion and 4 cases were died in the 2nd day after ingestion and the remaining 6 cats were followed up to 5th day of EG administration. Clinical, physical, , urine, ultrasonographic and post-mortem examinations were preformed on each cat before EG ingestion and on the 2nd and 5th day after EG ingestion . In addition, Blood samples wre collected from each cat for hematological and serum biochemical analysis. Our results revealed that, clinically the cats were depressed ,anorexic, unwilling to move with decreased rectal temperature and pulse rate while the respiratory rate was sigificantly increased at the 5th day of EG ingestion. Hematological analysis showed a significant increase of erythrocytic count while hemoglobin and PCV levels were significantly decreased at the 5th day of the experiment.The total leucocytic count was significanlty increased with significant neutrophilia and lymphocytopenia at the end of the experiment. Serum analysis of these cats showed azotemia, reduction in calcium, potassium and chloride with elevated phosphorus, sodium and magnesium levels. Urinalysis showed calcium oxalate crystalluria which could be noticed shortly after EG ingestion. It could be conculded that ethylene glycol ingestion could cause a sever renal damage in cats which may be fatal and methods of prevention of its ingestion by cats should be applied to avoid its serious effects.

Time-dependent changes in kidney histopathology in ethylene glycol poisoning.

Ethylene glycol (EG) may be acutely toxic following ingestion. In fatal cases, microscopic examination of urine and kidney specimens can establish a post-mortem diagnosis of EG poisoning. We describe the main renal histopathologic changes during different stages of EG poisoning, which might be helpful when dating the EG poisoning itself. A single-centre retrospective study conducted on all EG poisoning cases demonstrated that in an early stage of EG poisoning, fine dust-like crystals were deposited to the tubular cell basement membrane, followed by internalisation of calcium oxalate crystals into the epithelial cells. Later, the crystals formed larger aggregates within the epithelial cells. As the changes became advanced, pronounced tubular epithelial damage occurred, with detachment of epithelial cells from the basement membrane. In the final stage, coarse calcium oxalate crystals were recognised in the tubular lumen, with cellular debris from damaged epithelial cells. Our study shows that the time-dependent histological changes described follow the clinical stages of EG poisoning and may therefore provide a rough estimate of the time of EG ingestion before death.

Recurrent Ethylene Glycol Poisoning with Elevated Lactate Levels to Obtain Opioid Medications

BackgroundMalingering is when a patient feigns illness for secondary gain. While most patients with malingering manufacture or exaggerate symptoms, some patients may induce illness. Previous reports of malingering patients inducing illness include sepsis, kidney pain, migraine, and chest pain. However, acute poisoning as a manifestation of malingering appears to be rare. Case ReportWe describe the case of a 39-year-old man who presented to the emergency department complaining of diffuse body pain. The patient reported multiple admission at outside hospitals for “lactate” and said, “it feels like it is happening again because of how my body feels.” Laboratory findings were concerning for serum lactate of >20.0 mmol/L and ethylene glycol (EG) level of 19 mg/dL. A chart review found that the man had been admitted for elevated serum lactate 8 times to area hospitals in several years, often in the setting of EG poisoning. During these episodes he required intravenous fluids and frequent intravenous pain medications. When confronted about concern regarding the recurrent fallacious lactate levels in the setting of factitious EG ingestion, the patient often became combative and left against medical advice. The primary metabolite of EG, glycolic acid, can interfere with lactate assays, causing a false elevation. Our patient apparently recognized this and took advantage of it to be admitted and receive intravenous opioids. This is the only case known to us of malingering via EG ingestion. Why Should an Emergency Physician be Aware of This?Emergency physicians should be aware that metabolites of EG may interfere with serum lactate assay. In addition, they should be aware of possible malingering-related poisoning and plausible association with requests for intravenous opioid pain medications. This represents a risk to the patient and others if undiagnosed.

Deadly Alcoholic Fog: Unusual Source of Ethylene Glycol Ingestion in an Infant

Deadly Alcoholic Fog: Unusual Source of Ethylene Glycol Ingestion in an Infant

Protective Effect of Propolis in Proteinuria, Crystaluria, Nephrotoxicity and Hepatotoxicity Induced by Ethylene Glycol Ingestion

Propolis is a natural honeybee product with wide biological activities and potential therapeutic properties. The aim of the study is to evaluate the protective effect of propolis extract on nephrotoxicity and hepatotoxicity induced by ethylene glycol in rats. Five groups of rats were used. Group 1 received drinking water, group 2 received 0.75% ethylene-glycol in drinking water, group 3 received 0.75% ethylene-glycol in drinking water along with cystone 500mg/kg/body weight (bw) daily, group 4 received 0.75% ethylene-glycol in drinking water along with propolis extract at a dose of 100mg/kg/bw daily, and group 5 received 0.75% ethylene-glycol in drinking water along with propolis extract at a dose of 250mg/kg/bw daily. The treatment continued for a total of 30d. Urinalyses for pH, crystals, protein, creatinine, uric acid and electrolytes, and renal and liver function tests were performed. Ethylene-glycol increased urinary pH, urinary volume, and urinary calcium, phosphorus, uric acid and protein excretion. It decreased creatinine clearance and magnesium and caused crystaluria. Treatment with propolis extract or cystone normalized the level of magnesium, creatinine, sodium, potassium and chloride. Propolis is more potent than cystone. Propolis extract alleviates urinary protein excretion and ameliorates the deterioration of liver and kidney function caused by ethylene glycol. Propolis extract has a potential protective effect against ethylene glycol induced hepatotoxicity and nephrotoxicity and has a potential to treat and prevent urinary calculus, crystaluria and proteinuria.