Osmolal Gap Research Articles

TOXIC ALCOHOL POISONING: A CASE REPORT

During the COVID-19 pandemic, toxic alcohol poisoning, notably from methanol, has emerged as a significant concern due to increased consumption of illicit liquor amidst lockdown restrictions. We present a case of a middle-aged man who developed altered consciousness, metabolic acidosis, and shock two days after ingesting hospital spirit. Although initial qualitative tests only detected ethanol, subsequent MRI findings showed classical signs of methanol poisoning, including basal ganglia abnormalities. Prompt management with dialysis, ventilatory support, and adjunctive therapy successfully addressed the acute phase despite the patient remaining delirious for seven days. This case underscores the importance of considering methanol toxicity even in the absence of direct evidence, necessitating comprehensive diagnostic approaches. Awareness and incorporating point-of-care assessments such as arterial blood gas analysis and osmolar gap evaluation in suspected cases are crucial, especially in resource-limited settings. Recognizing unexplained high anion gap metabolic acidosis with a high osmolar gap and characteristic MRI findings can aid in the early diagnosis and management of toxic alcohol poisoning

Suggested guide to using lactate gap as a surrogate marker in the diagnosis of ethylene glycol overdose.

Ethylene glycol (EG) poisoning, if not diagnosed rapidly, can lead to poor patient outcomes. Gas Chromatography (GC) is primarily used for EG quantitation which is rarely available, and the turn-around time may be prolonged. Most lactate results from point-of care (POCT) methods are falsely elevated in EG poisoning compared with automated chemistry analyser results. In combination the lactate gap (POCT-Automated chemistry) can be used as surrogate marker in just about all laboratories to indicate likely EG toxicity and guide treatment. A male presented by ambulance to hospital with severe agitation requiring mechanical ventilation to facilitate ongoing management. Venous blood gas analysis confirmed a high anion gap metabolic acidosis (HAGMA) with an elevated lactate. The lactate and osmolarity measured in the laboratory showed a normal lactate and high osmolarity, giving a large osmolar gap. The patient was immediately commenced on renal replacement therapy for presumed EG poisoning to minimize kidney injury, and the treatment continued for 19 hours. A very high EG concentration was confirmed by GC the next day. An elevated lactate gap along with a HAGMA and osmolar gap can provide rapid surrogate laboratory data indicating EG poisoning enabling timely treatment and better patient outcomes.

Elevated osmol gaps in patients with alcoholic ketoacidosis.

The use of the osmol gap as a surrogate marker of toxic alcohol poisoning is common. Unfortunately, many patients with alcoholic ketoacidosis have elevated osmol gaps and are misdiagnosed with toxic alcohol poisoning. We aimed to characterize the range of osmol gaps in patients with alcoholic ketoacidosis. This was a retrospective poison center study. Data from 24 years were reviewed using the following case definition of alcoholic ketoacidosis: (1) documented alcohol use disorder; (2) presence of urine or serum ketones or an elevated blood beta-hydroxybutyrate concentration; (3) an anion gap ≥14 mmol/L. Potential cases of alcoholic ketoacidosis that failed to fulfill all three criteria were adjudicated by three toxicologists. Exclusion criteria included (1) detectable toxic alcohol concentration, (2) hemodialysis and/or multiple doses of fomepizole, (3) no osmol gap documented, (4) other diagnoses that lead to a metabolic acidosis. Demographics, pH, anion gap, lactate concentration, and osmol gap were extracted. Of 1,493 patients screened, 55 met criteria for alcoholic ketoacidosis. Sixty-four percent were male, and their median age was 52 years. The median osmol gap was 27 [IQR 18-36]. The largest anion gap was 57 mmol/L, and the lowest pH was 6.8. Forty-five (82%) of the patients with alcoholic ketoacidosis had osmol gaps >10; 38 (69%) had osmol gaps >20; 24 (44%) had osmol gaps >30; 11 (20%) had osmol gaps > 40. The large range of osmol gaps in patients with alcoholic ketoacidosis often reaches values associated with toxic alcohol poisoning. The study is limited by the potential for transcribing errors and the inability to identify the cause of the osmol gap. In this retrospective study, patients with alcoholic ketoacidosis had a median osmol gap of 27. Given that alcoholic ketoacidosis is easily and inexpensively treated, proper identification may prevent costly and invasive treatment directed at toxic alcohol poisoning.

Hyperosmolarity in children with hyperammonemia: a risk of brain herniation at the start of renal replacement therapy.

Renal replacement therapy (RRT) is used in hyperammonemia to reduce the concentration of ammonia in the blood. In the case of plasma hyperosmolarity, RRT can also rapidly decrease plasma osmolarity, which may increase cerebral edema in these patients and favor the occurrence of brain herniation. We conducted a retrospective clinical study in a tertiary care university-affiliated hospital. All patients admitted in a Pediatric Intensive Care Unit (PICU), less than 18 years old with ammonemia >150 µmol/L and who underwent RRT between January 2015 and June 2023 were included. We collected data on plasma osmolarity levels, osmolar gap and blood ammonia levels before and during RRT. Eleven patients were included (10 with acute liver failure and 1 with a urea cycle disorders). Their mean age was 36.2 months. Before RRT, the median highest measured osmolarity was 320 (305-324) mOsm/L, whereas the median calculated osmolarity was 303 (293-314) mOsm/L, corresponding to an osmolar gap of 14 mOsm/L. Ammonia blood level over 400 µmol/L are significantly associated with higher plasma osmolarity (P-Value <0.001). In one case, a patient had a brain herniation episode after a quick osmolar drop. This episode was reversed by the administration of hyperosmolar agents and the temporary suspension of RRT. This study highlights the hyperosmolarity and high osmolar gap that occur in children with hyperammonemia. A careful monitoring and control of plasma osmolarity evolution may alert clinician on the risk of occurrence of neurological complication such as brain herniation.

Osmolar gap in hyponatraemia—an exploratory study

Hyponatraemia has indeed been extensively studied from multiple angles, including volume status, tonicity, and aetiology; however, the specific consideration of the osmolar gap (OG) within the context of hyponatraemia and its potential impact on their overall outcomes received limited attention in research. The current study represents an effort to address this gap in our understanding. This prospective exploratory study was conducted on adults aged 14 years and older at the Indus Hospital, Karachi, from 2017 to 2020. The study involved categorising severity of hyponatraemia and volume status. The osmolar gap (OG) was calculated and categorised as either increased (OG&gt;10) or normal (OG&lt;10). Among the 262 patients included in the study, there were 139 females and 123 males. Elevated OG was observed in 141(53.8%) patients. There were 28 (10.7%) recorded fatalities and majority of these individuals had an elevated OG. ---Continue

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.

Methanol Formation, Toxicity and its Impact on the Human Nervous System and Liver

Methanol poisoning is a severe public health issue that causes disease and death, particularly in developing countries. Exposure can occur intentionally or unintentionally through several industrial products such as cleansers, solvents, antifreeze, perfumes, and paints. The toxic dose of methanol is approximately 1g/kg, emphasizing its potent toxicity. Methanol intoxication is chiefly caused by the harmful metabolites which are formed during its breakdown. These metabolites encourage metabolic acidosis. Formic acid, a methanol breakdown product, troubles mitochondria, distressing cytochrome oxidase and ATP production. Methanol-related problems include neurological disorders, vision problems, liver impact, Alzheimer’s, and Parkinson's. Key lab tests, including osmolality and anionic gap, aid in recognizing alcohol harm. Furthermore, detecting a faint smell of methanol in the breath, observing visual disturbances, and altered sensory neurons, seeing a history of abdominal pain, and conducting routine checkups support the early diagnosis of methanol poisoning. Treatment using prompt gastric lavage, sodium bicarbonate given intravenously, management with ethanol, folate-dependent folate systems suggest, dialysis, competent ADH inhibitor “pyrazole”, specific antidote “Fomepizole” can be used to treat methanol poisoning. Regular toxicologist check-ups are critical in such cases. Definite symptoms like basal ganglia issues and eye problems require consultations with neurologists and ophthalmologists. For cases needing hemodialysis or liver tissue recovery, consulting a nephrologist is essential. It is suggested to immediately act to prevent harm, especially for industrial workers, rural alcohol sellers, those with alcoholism, and vulnerable youth vulnerable to methanol poisoning.

Emerging progressive atypical acute kidney injury in young children linked to ethylene glycol and diethylene glycol intoxication.

There had been a sudden surge of unusually severe and rapidly progressing acute kidney injury (AKI) incidence in Indonesia since August 2022 which did not correspond to the rise of COVID-19 incidence. We suspected this was related to ethylene glycol (EG) and diethylene glycol (DEG) intoxication. This study is aimed at describing the clinical and laboratory characteristics of AKI related to D(EG) intoxication in order to spread awareness of the possibility of intoxication in cases of rapidly progressing AKI with unknown etiology. We conducted a cross-sectional study by collecting secondary data from the pediatric AKI registry at a national referral hospital in Jakarta, Indonesia. Data on children admitted from January to November 2022 with diagnosis of stage 3 AKI based on KDIGO criteria were included. Data regarding demographics, symptoms prior to anuria, laboratory results, infection panel including COVID-19 status, treatment administered, and mortality were analyzed. Sixteen patients tested positive for EG and DEG, all with history of consuming syrup-based medications. High anion gap metabolic acidosis was observed in majority of patients with mean pH 7.33 ± 0.07 and mean anion gap 15.6 ± 7.8mEq/L. No patient had high osmolal gap (mean osmolal gap 3.46 ± 4.68). One deceased patient, who had kidney biopsy performed, showed severe damage and calcium oxalate crystals in the kidney tissue. Mortality was recorded in six patients (37.5%). Careful history taking of patient's clinical course, including consumption of syrup-based medications and laboratory findings, might aid clinicians to establish a working diagnosis of D(EG) intoxication without needing to wait for blood toxicology test. Early diagnosis and therapy are crucial to prevent substantial mortality.

Elevated Osmolal Gap in a Case of Multiple Myeloma

BackgroundThe estimated serum osmolality is a measurement of solutes in the blood, including sodium, glucose, and urea, but also includes ethanol and toxic alcohols (e.g., methanol, ethylene glycol, diethylene glycol, isopropyl alcohol, propylene glycol) when present. These rarely measured toxic alcohols can elevate the serum osmolality, giving the true measured osmolality. The difference between that and a calculated osmolality is the osmolal gap, which can be elevated in many clinical scenarios such as renal failure, ingestion of toxic alcohols, diabetic ketoacidosis, shock, and others. Case ReportWe report a patient with a history of alcohol use disorder who came to the Emergency Department with an abnormally elevated osmolal gap in the setting of altered mental status. The patient's increased osmolal gap was further investigated while he was promptly treated with fomepizole, thiamine, and urgent hemodialysis. Why Should an Emergency Physician Be Aware of This?We discuss the differential diagnosis for substances that increase the osmolal gap with respective ranges of elevation. This case demonstrates that although osmolal gap elevation is often attributed to the presence of toxic alcohols, other common etiologies may account for the gap, including acute renal failure and multiple myeloma.

#5852 EFFECT OF DIET ON THE COLLECTOR DUCT BEHAVIOUR: RELEVANCE IN PRECLINICAL DRUG DEVELOPMENT

Abstract Background and Aims Drug induced syndrome of inadequate antidiuretic hormone secretion (SIADH) is a common problem in clinical practice. Early detection of this side effect at a preclinical level would improve safety and efficiency. We investigate the role of different diets in preclinical detection of SIADH. Method Animals were divided into two groups (n = 4 each), one receiving standard pellet based diet, and the other one a diluted hyposodic gelified liquid diet. After one week, both groups were administered daily intraperitoneal (i.p.) injections of desmopressin acetate (ddAVP; 0.4 μg/kg) and a volume of distilled water equivalent to 2.5% of body weight for 7 days. Animals were placed in metabolic cages for 24h at the end of each period to collect and analyse the urine, and a blood sample from the tail vein was obtained. Weight, water and food intake were measured on a daily basis. Results Differences in water and electrolyte balance are shown in Table 1. Pellet fed animals presented an increased water intake and produced a more concentrated urine compared to those on a hyposodic diet. When analysed in detail, urinary osmolality was mainly driven by ionic osmoles in pellet fed animals (42,25 ± 4,72 vs 266,30 ± 17,32 mOsm/kg, p&amp;lt;0,005). Of note, there seems to be an occult osmole, especially prominent in the pellet group (osmol gap 20,40 ± 3,18 vs 99,89 ± 9,81 mOsm/kg, p = 0,017). All of the above suggest there is a net retention of water, sodium and potassium in those animals fed with a conventional pellet diet. Daily administration of ddAVP/water induced a mild transient hyponatremia that was recovered 24h later in both groups; this situation was repeated over a 7 day period. Pellet fed animals did not modify water intake, diuresis, free water clearance or urinary osmolality after ddAVP/water treatment, suggesting that hyperosmolar diets significantly increase urinary osmolality fixating urinary water losses and impairing further urinary concentration. On the contrary, animals on a hyposodic diet did present antiaquaresis, as shown by an increase in water intake, a decrease in diuresis and free water clearance and an increase in urinary osmolality. Animals fed with hyposodic diet progressively lost weight, while pellet fed animals did not. However, this trend was reversed after 4 days of treatment with ddAVP/water, again suggesting a degree of water retention. It is remarkable that we have found signs of water retention despite the fact that the induced hyponatremia is mild and transient. Conclusion The antiaquaretic effect of ddAVP is overridden by the amount of urinary osmoles excreted when on a pellet diet, which seem to fixate the amount of water in the urine. Therefore, the use of hyposodic diets in preclinical drug development is essential when SIADH is likely to be expected, as its effects will be unnoticed if a standard diet is used.

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.

Mind the gap: Measured and Calculated Osmolarity are not interchangeable in Diabetic Hyperglycemic Emergencies.

INTRODUCTION Small case series have reported that diabetic ketoacidosis is associated with elevated osmolar gap, while no previous studies have assessed the accuracy of calculated osmolarity in the hyperosmolar hyperglycemic state. The aim of this study was to characterize the magnitude of the osmolar gap in these conditions and assess whether this changes over time. METHODS Retrospective cohort study using two publicly available intensive care datasets: Medical Information Mart of Intensive Care (MIMIC) IV and the eICU Collaborative Research Database. We identified adult admissions with diabetic ketoacidosis and the hyperosmolar hyperglycemic state who had measured osmolality results available contemporaneously with sodium, urea and glucose values. Calculated osmolarity was derived using the formula 2Na + glucose + urea (all values in mmol/L). RESULTS We identified 995 paired values for measured and calculated osmolarity, originating from 547 admissions (321 diabetic ketoacidosis, 103 hyperosmolar hyperglycemic state and 123 mixed presentations). A wide variation in osmolar gap was seen, including substantial elevations as well as low and negative values. There was a greater frequency of raised osmolar gaps at the start of the admission which tends to normalize by around 12-24hr. Similar results were seen regardless of the admission diagnosis. CONCLUSIONS Osmolar gap varies widely in diabetic ketoacidosis and the hyperosmolar hyperglycemic state and may be highly elevated especially at the time of admission. Clinicians should be aware that measured and calculated osmolarity values are not interchangeable in this population. These findings should be confirmed in a prospective study.

Low Serum Bicarbonate in a Patient With Diabetes Mellitus:: A Quiz

Low Serum Bicarbonate in a Patient With Diabetes Mellitus:: A Quiz

Moderate hyperosmolar hyponatremia caused by excessive off-label use of icodextrin during peritoneal dialysis

Icodextrin use during the long dwell of a peritoneal dialysis (PD) regimen is commonly used to increase ultrafiltration. Its use may cause a mild and clinically insignificant degree of hyponatremia. We describe a patient who was admitted twice to our medical center on an atypical continuous ambulatory peritoneal dialysis (CAPD) regimen utilizing solely icodextrin with 2 exchanges (12-hour dwells). On both admissions, he had hyperosmolar hyponatremia in the 120-mmol/L range with a large osmolal gap. After icodextrin was stopped and his PD prescription was switched to dextrose solutions, both hyponatremia corrected and the osmolal gap quickly disappeared. The accumulation of osmotically active solute in extracellular fluids results in efflux of water from the cellular compartment and produces both hyponatremia and hypertonicity [1]. This tonic effect occurs most frequently with hyperglycemia, but other substances can also cause this, including mannitol, sorbitol, glycine, and maltose [1, 2]. In this report, we present a patient with end-stage renal disease (ERSD) on an atypical off-label PD regimen utilizing solely icodextrin solutions who developed hyperosmolar hyponatremia in the 120-mmol/L range, with a large osmolal gap. This appeared to be due to absorbed metabolites of icodextrin, mainly maltose.

Mass Poisoning From Ethylene Glycol at a U.S. Military Base.

Ethylene glycol (EG) toxicity is an important cause of toxic alcohol poisoning in the USA with over 5,000 exposures reported annually. While classically characterized by solitary accidental or intentional ingestions, mass toxic alcohol poisoning outbreaks and more rarely collective consumptions (typically of methanol) have been described. We describe an ethylene glycol poisoning from collective ingestion that involved soldiers presenting at William Beaumont Army Medical Center in El Paso, Texas. Eleven soldiers presented to the emergency department over a 12-h period after ingestion of an unknown substance. The first two patients exhibited severe neurologic symptoms, while the remainder were asymptomatic. As serum EG levels were not immediately available, treatment decisions were based on surrogate laboratory values. Two patients received immediate hemodialysis, and fomepizole (FOM) because of severe acidosis with elevated anion and osmolal gaps. These patients developed acute kidney injury with renal recovery within a 3-week period. Two patients with elevated lactate received bicarbonate-based intravenous (IV) fluids and FOM. Two patients received IV fluids only and required prolonged observation for worsening acidosis and/or acute kidney injury. Five patients with normal laboratory values were treated with IV fluids and observation. All patients received cofactors including thiamine and pyridoxine. All patients survived. The outbreak occurred in the setting of limited dialysis resources, limited FOM availability, and in a resource-limited community. Additional guidelines are needed to determine allocation of limited resources, optimal dialysis and FOM treatment course, and comorbid conditions, which may prolong recovery.

LBODP038 Metformin-Associated Severe Lactic Acidosis: A Case Study Of The Perfect Storm

Abstract Background Metformin carries a rare risk of lactic acidosis. Medications that can increase the concentration of metformin in the serum can increase the risk of lactic acidosis. Similarly, kidney dysfunction leads to decreased clearance of the drug, hence potentiating its adverse effects. Clinical Case A 62-year-old male with HIV (undetectable viral load) on dolutegravir, atazanavir/cobicistat, rilpivrine, type 2 DM (A1C 7.2%) on metformin and dulaglutide presented with 1 day history of dyspnea. He had a respiratory rate of 28 and heart rate of 131. Blood glucose was 43 mg/dL (nl 74-99 mg/dL). Labs were also notable for lactate 23.6 mmol/L (nl 0.4-2 mmol/L), severe anion gap metabolic acidosis with pH &amp;lt;6.8, bicarbonate 5 mmol/L (nl 21-32 mmol/L). Creatinine was 2.29 mg/dL (nl 0.5-1.3 mg/dL) with a normal baseline kidney function. Beta-hydroxybutyrate was elevated at 0.73 mmol/L (nl 0. 02-0.27 mmol/L). Osmolar gap was 17.3 mOsm, ethanol level was 22 mg/dL (nl &amp;lt;10 mg/dL), ethylene glycol was not detected. Patient reported drinking four beers daily but endorsed binge drinking the previous night with associated emesis. Review of records showed that the patient was started on dulaglutide recently and he endorsed nausea and diarrhea with initiation of the medication. He otherwise had no changes in his metformin dose or antiretroviral regimen. He was admitted to the ICU for further management of his severe lactic acidosis. Patient's antiretroviral regimen, dulaglutide, and metformin were held on admission. Medical toxicology was consulted, and metformin associated lactic acidosis was suspected. He was initiated on dialysis and his lactic acidosis resolved within 24 hours. His antiretroviral regimen was resumed prior to discharge when his creatinine improved to 1.38 mg/dL. Metformin was discontinued and he was discharged on dulaglutide with endocrinology follow up. Conclusion This case demonstrates how multiple factors such as alcohol use, kidney injury, and other medications can increase the, otherwise rare, risk of lactic acidosis in patients taking metformin. The patient had experienced GI losses due to emesis from his increased alcohol intake as well as diarrhea with the initiation of dulaglutide leading to dehydration and acute kidney injury. The latter can give rise to decreased metformin clearance. In addition, dolutegravir increases metformin plasma exposure. Together, the constellation of factors had likely led to increased metformin plasma levels and associated severe lactic acidosis. Patients should be counseled on the use of alcohol while taking metformin. Additionally, drug interactions should be monitored, and dose reductions of metformin should be considered in patients taking dolutegravir. Presentation: No date and time listed

Methanol toxicity in a pediatric patient treated with fomepizole and hemodialysis.

Methanol toxicity is an important cause of toxic alcohol exposure resulting in morbidity and mortality in both adult and pediatric populations. Methanol is metabolized into formaldehyde and formic acid: toxic metabolites that can cause altered mental status, visual disturbances, multisystem organ failure, and death. Recognition of methanol intoxication and rapid treatment are critical for the prevention of long-term sequelae. We present the case of a 16-year-old male with a past medical history of depression who intentionally ingested windshield wiper fluid containing methanol. Based on the patient's osmolal gap, he was estimated to have a serum methanol level of 374mg/dL; a send-out laboratory measurement later revealed a serum methanol level of 436mg/dL. Therapy included two hemodialysis treatments as well as fomepizole and supportive care. The patient recovered remarkably with no long-term sequelae. This case demonstrates the effectiveness of swift recognition and treatment of methanol ingestion. Optimization of methods of measuring serum methanol and evidence-based guidelines for therapy are needed to improve the care of patients with methanol intoxication.

Acil Servise Başvuran Metil Alkol Zehirlenmelerinin Geriye Dönük Analizi

Objective: Methyl alcohol poisoning remains a significant cause of mortality and morbidity. This poisoning is still one of the important reasons for admission to emergency services. We aimed to examine the admission complaints, laboratory findings, treatment methods, clinical outcomes and examine the factors affecting the mortality of patients diagnosed with methyl alcohol poisoning in the emergency department.&#x0D; Methods: In this retrospective descriptive study, we analysed the patients who were considered to be diagnosed with methyl alcohol intoxication among those who came to our emergency department due to alcohol intoxication from June 1, 2018 to June 1, 2020.&#x0D; Results: The study included 20 (4.86%) individuals with methyl alcohol poisoning among 411 people who presented to the emergency department due to ethyl and methyl alcohol intake and resulting effects.The mean age of the patients was 47.35±14.2 years and 85% (n=17/20) were male. Upon reviewing the patients' admission symptoms, 70% were observed to have visual problems, 60% complaints of vomiting, 45% shortness of breath, and 40% changes in consciousness. In the study, it was revealed that 18.2%(n=2/11) females and 81.8%(n=9/11) males died, and the mortality rate was calculated as 55%(n=11/20).&#x0D; Conclusions: The presence of visual problems, hypotension, and coma in clinical findings, high anion gap metabolic acidosis, marked osmolar gap, an increase in lactate level, and hyperglycemia in laboratory findings may be the early signs of mortality in patients with methyl alcohol poisoning. Therefore, patients with these signs should be followed up more closely and treated.

THE CLUE IS IN THE BLOOD GAS: A RARE MANIFESTATION OF LACTIC ACIDOSIS

THE CLUE IS IN THE BLOOD GAS: A RARE MANIFESTATION OF LACTIC ACIDOSIS

S2425 A Case Report of Volatile Ingestion-Induced Acute Esophageal Necrosis

Introduction: Acute esophageal necrosis (AEN), also known as black esophagus or acute necrotizing esophagitis, is a rare syndrome with diffuse circumferential black discoloration often of distal third esophageal mucosa due to relative hypovascularity and termination at the gastro-esophageal junction. It usually presents with upper GI hemorrhage. Despite controversial pathogenesis, there is strong consideration for a 2-hit hypothesis where an initial low-flow vascular state predisposes the mucosa to a severe topical injury. Chemical injury by gastric contents, toxin ingestion, severe infectious diseases, diabetic ketoacidosis and shock are associated with AEN. Advanced age, male gender and comorbidities like diabetes mellitus (DM), hypertension, cardiovascular disease, chronic kidney disease, malnutrition, chronic alcohol abuse, post-irradiation are predisposing risk factors for AEN. We present a patient with a favorable outcome of a generally rare, life-threatening condition due to early recognition and treatment. Case Description/Methods: A 74-year-old male presented to the hospital with shock and 3-day history of hematemesis. He had history of coronary artery disease, Type II Diabetes Mellitus, chronic obstructive pulmonary disease, esophageal adenocarcinoma post chemotherapy and radiation complicated by erosive esophagitis and alcoholism. Labs were significant for acute kidney injury (AKI), high anion gap metabolic acidosis (HAGMA), osmolar gap of 59 mOsm/kg and hemoglobin drop from 14 to 9 g/dL. Volatile panel not sent; drug-screen benign, infectious work-up negative. CT abdomen had distended stomach; thus, NG tube placed for decompression, yielding 700cc of coffee ground emesis. Upper endoscopy performed 2-days later showed Los Angeles Grade D esophagitis with entire esophagus with black appearance, gastric body erosions and superficial clean-based duodenal ulcers. Patient was continued on PPI twice daily for 8 weeks with planned repeat EGD (Figure). Discussion: This patient likely had volatile ingestion chemical injury given shock, hematemesis, AKI with HAGMA and osmolar gap. Despite AEN’s rarity with prevalence of 0.2 percent in autopsy states, given overall 32 percent mortality rate and 6 percent mortality rate directly attributed to complications of AEN, early recognition and prompt medical management is imperative for favorable outcomes. Treatment focuses on supportive therapy: namely resuscitation, PPIs, sucralfate, keeping the patient NPO and avoiding nasogastric tube to avoid esophageal perforation.Figure 1.: Proximal Acute Esophageal Necrosis.