Oxidative stress and biochemical indicators in blood of patients addicted to alcohol treated for acute ethylene glycol poisoning.

Ethylene glycol (EG), in addition to its neurotoxic and nephrotoxic effects, evokes oxidative stress. The aim of this study was to assess the influence of the ethylene glycol on the biochemical indicators and oxidoreductive balance of patients treated for acute poisoning. The total study group consisted of 56 persons including 26 alcoholics who took EG as a substitute for ethyl alcohol in the course of alcohol dependence syndrome and 30 controls. Severity of poisoning, results of acid-base parameters, biochemical, and toxicological tests as well as biomarkers of the oxidative stress in blood were analyzed during the patients' hospitalization. The key issue was to assess the oxidative stress and biochemical disturbances caused by EG and the type of treatment applied in the course of poisoning. Significant changes in some parameters were found both at time of diagnosis and after treatment initiation (ethanol as an antidote and hemodialysis). The most important differences included the activity of hepatic parameters (aspartate aminotransferase, AST) and oxidative stress markers like catalase (CAT); correlation of the lipid peroxidation products level (TBARS) with urea concentration has been shown. On the last day of the hospitalization, in some cases, the mutual correlation between the evaluated markers were observed, for example, between alanine transaminase (ALT) and glutathione reductase (GR), and urea concentration and glutathione level (GSH/GSSG). The concentration of ions (H+) had a major impact on the oxidoreductive balance, correlating with the elevated GR and GSH/GSSG levels.

Unexpected Mycoplasma hominis infection in two renal transplant recipients traced back to the same donor by whole-genome sequencing.

Mycoplasma hominis is a common colonizer of the lower genitourinary tract. Although its clinical relevance for causing urogenital infections in immunocompetent individuals is controversial, this bacterium has been involved in severe invasive infections in allograft recipients. In this report, we describe two cases of M. hominis infection in two young renal transplant recipients within the first month post-transplant. Although at first no epidemiological link between the two cases had been suspected, whole-genome sequencing (WGS) analysis showed that both isolates were identical, highly suggestive of an origin with the common organ donor.

Life-threatening triclopyr poisoning due to diethylene glycol monoethyl ether solvent.

INTRODUCTION: Triclopyr is a synthetic auxin-like herbicide. It is considered to have low toxicity and there are few reports of poisoning. We report two cases of life-threatening toxicity following ingestions of 250 mL of 50 g/L triclopyr co-formulated with diethylene glycol monoethyl ether (DEGEE). CASE REPORTS: A 79-year-old male with a background of hypertension and atrial fibrillation presented two hours after ingestion with sedation, a severe high anion gap metabolic acidosis, raised osmolar gap and an aspiration pneumonitis. He was ventilated and dialysed for 10 h with resolution of the acidaemia. He was discharged home on day 33. A 66-year-old male with a past history of alcoholism and hypertension presented following a collapse. He had sedation, a severe high anion gap metabolic acidosis with a raised osmolar gap, acute kidney injury and vasodilatory shock. He was ventilated and received dialysis for 43 h. He had poor neurological recovery and died on day 10. DISCUSSION: Ingestion of triclopyr formulations can produce life-threatening toxicity. In large poisonings of triclopyr co-formulated with DEGEE, a high anion gap metabolic acidosis appears to be due to the glycol ether solvent rather than triclopyr itself. Management should focus on good supportive care including dialysis for significant metabolic acidosis.

A neonate with metabolic acidosis: Intentional ethylene glycol poisoning.

We present a rare case of the intentional poisoning of a neonate. An 8-day old child presented to an academic pediatric emergency department (ED) with respiratory distress and decreased intake. In the ED the patient was stabilized, and workup uncovered an anion gap metabolic acidosis. Blood, urine, and CSF cultures were negative at 48 h and a metabolic screen revealed elevated glycine. Calcium oxalate crystals were later found in the urinalysis, raising concern for ethylene glycol poisoning. The patient's father admitted to mixing antifreeze with the child's formula. The workup of an ill or distressed neonate should be methodical, ruling out sepsis, inborn errors of metabolism, cardiac disease, trauma, and less common etiologies such as intestinal catastrophes, renal or hepatic disease, neurologic disease, drug withdrawal, non-accidental trauma, formula mixing errors, and poisoning.

Intoxicación por etilenglicol, fisiopatología y enfrentamiento clínico / Ethylene glycol poisonin: an update

Toxic alcohols can produce severe poisoning with multiple organic involvement and even death. The most common form is ethylene glycol. The diagnosis can be extremely difficult if there is no history of its consumption. Its clinical presentation can simulate other conditions. Ethylene glycol poisoning is characterized by an initial rise in plasma osmolal gap that decreases during the evolution, while alcohol is metabolized to acids. This last condition causes a metabolic acidosis with elevated anion gap. The clinical manifestations are diffuse neurological involvement initially, followed by hemodynamic alterations due to myocardial damage associated with hypocalcemia and acidemia. Subsequently, severe tubular renal damage appears, which may require renal replacement therapy, and finally, focal neurological alterations. To treat this poisoning, it is necessary to inhibit the transformation of alcohol into acids, increase the metabolism of the latter or withdraw them directly with hemodialysis.

Fatal poisoning with diethylene glycol in an unusual setting.

Morphological findings in cases of intoxication are relatively rare in forensic pathology. In this article we report on a 26-year-old man who drank clear fluid from a tequila bottle that was given to him by a friend. Afterwards, the clear fluid was assumed to be smoke fluid containing diethylene glycol (DEG). The man died eight days later. Macroscopic and microscopic examination of the kidneys and the liver at forensic autopsy revealed findings typical of a DEG intoxication. In addition, the clinical course showed the typical triphasic pattern of symptoms. Toxicological analysis confirmed the presence of DEG in both the original smoke fluid and the tequila bottle. In conclusion, death was due to fatal intoxication by DEG. While most DEG intoxications have been mass poisoning incidents attributed to pharmaceutical products, the present case describes an unusual example of a single decedent.

Intoxicación por etilenglicol, fisiopatología y enfrentamiento clínico.

Toxic alcohols can produce severe poisoning with multiple organic involvement and even death. The most common form is ethylene glycol. The diagnosis can be extremely difficult if there is no history of its consumption. Its clinical presentation can simulate other conditions. Ethylene glycol poisoning is characterized by an initial rise in plasma osmolal gap that decreases during the evolution, while alcohol is metabolized to acids. This last condition causes a metabolic acidosis with elevated anion gap. The clinical manifestations are diffuse neurological involvement initially, followed by hemodynamic alterations due to myocardial damage associated with hypocalcemia and acidemia. Subsequently, severe tubular renal damage appears, which may require renal replacement therapy, and finally, focal neurological alterations. To treat this poisoning, it is necessary to inhibit the transformation of alcohol into acids, increase the metabolism of the latter or withdraw them directly with hemodialysis.

Human health assessment for long-term oral ingestion of diethylene glycol.

Diethylene glycol (DEG) is an organic chemical that is used mostly as a chemical intermediate and has minor uses as a solvent or antifreeze in consumer products; these minor uses could result in potential human exposure. Potential short and long-term human exposures also occur from misuses. The considerable reporting of DEG misuses as a substitute for other solvents in drug manufacturing and summaries of important events in the history of DEG poisonings are reviewed. Given the potential for human exposure, the disposition and toxicity of DEG were examined, and a health assessment was performed. Toxicokinetics and metabolism studies are evaluated, along with a discussion on the renal toxicity mode of action in the rat. Additionally, in-depth assessments of the key animal research studies on the toxic effects of DEG from oral ingestion for various exposure time periods are presented with determination of NOAELs and LOAELs from the long-term exposure animal studies. These are applied in the derivation of a reference dose for a non-cancer endpoint from chronic exposure, resulting in a value of 0.3 mg DEG/kg bw.

Toxic Alcohol Ingestion: Prompt Recognition And Management In The Emergency Department.

Identifying patients with potential toxic alcohol exposure and initiating appropriate management is critical to avoid significant patient morbidity. Sources of toxic alcohol exposure include ethylene glycol, methanol, diethylene glycol, propylene glycol, and isopropanol. Treatment considerations include the antidotes fomepizole and ethanol, and hemodialysis for removal of the parent compound and its toxic metabolites. Additional interventions include adjunctive therapies that may improve acidosis and enhance clearance of the toxic alcohol or metabolites. This issue reviews common sources of alcohol exposure, basic mechanisms of toxicity, physical examination and laboratory findings that may guide rapid assessment and management, and indications for treatment.

Antidotes for poisoning by alcohols that form toxic metabolites.

The alcohols, methanol, ethylene glycol and diethylene glycol, have many features in common, the most important of which is the fact that the compounds themselves are relatively non-toxic but are metabolized, initially by alcohol dehydrogenase, to various toxic intermediates. These compounds are readily available worldwide in commercial products as well as in homemade alcoholic beverages, both of which lead to most of the poisoning cases, from either unintentional or intentional ingestion. Although relatively infrequent in overall occurrence, poisonings by metabolically-toxic alcohols do unfortunately occur in outbreaks and can result in severe morbidity and mortality. These poisonings have traditionally been treated with ethanol since it competes for the active site of alcohol dehydrogenase and decreases the formation of toxic metabolites. Although ethanol can be effective in these poisonings, there are substantial practical problems with its use and so fomepizole, a potent competitive inhibitor of alcohol dehydrogenase, was developed for a hopefully better treatment for metabolically-toxic alcohol poisonings. Fomepizole has few side effects and is easy to use in practice and it may obviate the need for haemodialysis in some, but not all, patients. Hence, fomepizole has largely replaced ethanol as the toxic alcohol antidote in many countries. Nevertheless, ethanol remains an important alternative because access to fomepizole can be limited, the cost may appear excessive, or the physician may prefer ethanol due to experience.

Five-year review of a UK 24 hour testing service for plasma ethylene glycol and diethylene glycol.

BACKGROUND: We present a 5-year review of our UK service for plasma ethylene glycol and diethylene glycol determination in cases of acute poisoning. METHODS: Ethylene glycol and diethylene glycol have been measured on all samples received for screening for toxicity by gas chromatography-flame ionization detection over a five-year period. A detailed audit of the results has been undertaken. RESULTS: In this period, we received 811 requests, 56% were for first-time screening and 44% repeat analysis where a positive sample has already been received. Of the first-time screen samples, 33.5% screened positive for glycol poisoning. The mean positive ethylene glycol concentration was 1204 mg/L (range 31 to 8666 mg/L). Diethylene glycol was present in 14% of ethylene glycol positive samples but never found alone. CONCLUSIONS: The data presented here suggest it is not essential to measure diethylene glycol since its inclusion is rarely likely to change patient management.

Toxic alcohol ingestion: prompt recognition and management in the emergency department [digest].

Identifying patients with potential toxic alcohol exposure and initiating appropriate management is critical to avoid significant patient morbidity. Sources of toxic alcohol exposure include ethylene glycol, methanol, diethylene glycol, propylene glycol, and isopropanol. Treatment considerations include the antidotes fomepizole and ethanol, and hemodialysis for removal of the parent compound and its toxic metabolites. Additional interventions include adjunctive therapies that may improve acidosis and enhance clearance of the toxic alcohol or metabolites. This issue reviews common sources of alcohol exposure, basic mechanisms of toxicity, physical examination and laboratory findings that may guide rapid assessment and management, and indications for treatment. [Points & Pearls is a digest of Emergency Medicine Practice].

Diethylene glycol poisoning from transcutaneous absorption.

A case of transcutaneous diethylene glycol poisoning with severe acute kidney injury, but a positive outcome, is described. A man without significant medical history was admitted to our hospital due to anuria, gastrointestinal symptoms, and hypertension. Ultrasonography excluded vascular damage and postrenal obstruction. Laboratory tests showed acute kidney injury and metabolic acidosis with increased anion gap; hemodialysis therapy was started. The brother of the patient reported that the patient had been smearing his skin with brake fluid containing diethylene glycol to treat a "dermatitis." Only supportive therapy was given due to the lack of a specific antidote. Continuous venovenous hemofiltration was performed. The kidney biopsy showed acute toxic proximal tubulonecrosis, without deposition of oxalate crystals. His neurologic condition worsened dramatically; supportive care was continued. Over time, acute kidney injury and neurologic damage gradually improved; 33 days after admission, he went to a rehabilitation unit for 5 months, with complete clinical recovery. Historically, diethylene glycol has been the cause of large-scale poisonings from ingestion of contaminated drugs. The clinical evolution is unpredictable. Treatment is not well defined; early hemodialysis treatment reduces levels of toxic metabolites, and fomepizole could be useful in cases with an early diagnosis. A comparison of the characteristics of diethylene glycol versus ethylene glycol poisoning is given.

Neurological manifestation of recreational fatal and near-fatal diethylene glycol poisonings: case series and review of literature.

Diethylene glycol is a common industrial solvent which is responsible for accidental and epidemic poisoning as early as the 1930s. Due to the unavailability and unaffordability of ethanol, people in Qatar among the low income group are consuming household chemicals, some of which contain diethylene glycol, for recreational purposes.The history of ingestion is usually not volunteered and the initial clinical presentation is usually nonspecific, making it difficult to diagnose from the clinical presentation. Moreover, the biochemical profile varies with time, making the diagnosis more difficult. The neurological course and toxicity is less well characterized than its renal counterpart. Moreover, reports in the literature of such recreational poisoning is lacking particularly in the region.Three cases of recreational diethylene glycol poisoning seen in Hamad General Hospital, Doha, Qatar from 2009 to 2012 are detailed here.These illustrate the clinical course with emphasis on the neurological sequelae that include encephalopathy and multiple cranial and peripheral neuropathies with fatal and near-fatal outcomes. Neuroimaging in 2 were initially normal, but follow-up imaging showed brain atrophy. The third patient's neuroimaging showed diffuse brain edema with evidence of transtentorial herniation. Nerve conduction studies were performed in 2 of the 3 cases and showed evidence of mixed sensorimotor neuropathy. The outcomes were death in 1 and severe neurological morbidity and disability in 2 cases.Diethylene glycol is a dangerous substance when ingested and can result in mortality and severe morbidity, particularly from the renal and neurological manifestations. Whereas the mechanism of damage is less well known, the damage is likely dose related. The typical clinical pattern of evolution of the poisoning in the absence of cost-effective ways to detect it in the serum can help clinicians in making the diagnosis.Neurological manifestations may include encephalopathy and multiple cranial and peripheral neuropathies with subsequent brain atrophy. Public awareness of the danger of such recreational use should be raised.