Osmolal Gap Research Articles

The Case | Unexplained stupor with a high osmolal and high anion gap metabolic acidosis

The Case | Unexplained stupor with a high osmolal and high anion gap metabolic acidosis

Hyperchloremic normal gap metabolic acidosis

Metabolic acidosis is defined as a pathologic process that, when unopposed, increases the concentration of hydrogen ions (H+) in the body and reduces the bicarbonate (HCO3-) concentration. Metabolic acidosis can be of a kidney origin or an extrarenal cause. Assessment of urinary ammonium excretion by calculating the urine anion gap or osmolal gap is a useful method to distinguish between these two causes. Extrarenal processes include increased endogenous acid production and accelerated loss of bicarbonate from the body. Metabolic acidosis of renal origin is due to a primary defect in renal acidification with no increase in extrarenal hydrogen ion production. This situation can occur because either the renal input of new bicarbonate is insufficient to regenerate the bicarbonate lost in buffering endogenous acid as with distal renal tubular acidosis (RTA) or the RTA of renal insufficiency, or the filtered bicarbonate is lost by kidney wasting as in proximal RTA. In either condition, because of loss of either NaHCO3 (proximal RTA) or NaA (distal RTA), effective extracellular volume is reduced and as a result the avidity for chloride reabsorption derived from the diet is increased and results in a hyperchloremic normal gap metabolic acidosis. The RTA of renal insufficiency is also characterized by a normal gap acidosis, however, with severe reductions in the glomerular filtration rate an anion gap metabolic acidosis eventually develops.

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.

SAT-269 URINE ESTIMATED AMMONIUM-TO-CREATININE RATIO IN PATIENTS WITH CHRONIC KIDNEY DISEASE.

Renal ammonium (NH4+) excretion plays a critical role in the elimination of acid. Recent studies have reported that the impairment in urinary NH4+ excretion is an important determinant of the development of metabolic acidosis and is an independent factor for predicting loss of renal function. However, urine ammonium measurements are not widely available in routine diagnostic laboratories, and its clinical significance is still unknown. We hypothesized that urine estimated ammonium-to-creatinine ratio (u-eNH4+/u-Cr), as an indicator of urinary NH4+excretion, would be surrogates for early metabolic acidosis in patients with CKD. We measured u-eNH4+/u-Cr in outpatients without overt metabolic acidosis (5.0< [urinary pH] <7.0, [HCO3-] >20 mEq/L, no medication of bicarbonate). The estimated ammonium concentration (u-eNH4+) from the osmolar gap was calculated as u-eNH4+=0.5x(osmolality-2[Na++K+]-[urea]/2.8-[glucose]/18). A total of 168 outpatients were identified (Mean age; 63.1 ± 18.0 years old, Male; 59.5%, CKD; 54.8%, Hypertensives; 74.4%, Diabetes; 35.1%). Although u-eNH4+/u-Cr showed a positive correlation with eGFR (P = 0.0151) (Fig.1), no associations were observed between eNH4+/u-Cr with age, BMI, uPCR, pH, HCO3-, BE, or Anion gap. Interestingly, eNH4+/u-Cr was significantly lower in CKD stage 3-5 than in non-CKD groups (Fig 2), even though there were no overt metabolic acidosis.Fig. 2View Large Image Figure ViewerDownload Hi-res image Download (PPT) u-eNH4+/u-Cr is easily measured in clinical practice and would be more tightly linked with ammonium excretion than serum bicarbonate and other acid-base indicators.

1,4-Butanediol overdose mimicking toxic alcohol exposure

Context: 1,4-butanediol (1,4-BD) is a gamma-hydroxybutyrate (GHB) analogue with a similarly narrow therapeutic window that is becoming a more common cause of recreational overdose. Reports of confirmed exposures are limited.Case details: A 44 year-old man who had consumed alcohol subsequently became unconscious after ingesting what was thought to be GHB. The presentation was not entirely consistent with GHB poisoning, including a longer duration of unconsciousness and features that mimicked toxic alcohol exposure including a high anion gap metabolic acidosis (HAGMA) and osmol gap. The patient was treated supportively with intubation, haemodiafiltration and intravenous ethanol until the diagnosis was refined using specific laboratory testing. The concentration of 1,4-BD was the highest reported in the literature and the outcome favourable.Discussion: This case highlights pharmacokinetic issues peculiar to 1,4-BD, including the interaction with ethanol which delays the onset of psychoactive effects from 1,4-BD’s metabolite GHB, and dose-dependent pharmacokinetics. In overdose, 1,4-BD can induce a HAGMA and other features of toxic alcohol poisoning. Managing an unconscious patient with these features can prompt certain treatments until the diagnosis is refined, which can require specific laboratory testing to identify the culprit. The actual risk of toxic alcohol and other causes is adjusted on a case-by-case basis from the history of exposure and local epidemiology of substance use and poisoning.

The Diagnosis and Management of Toxic Alcohol Poisoning in the Emergency Department: A Review Article.

Context:This review discusses the range of clinical presentations seen with poisonings by the major toxic alcohols--methanol, ethylene glycol, and isopropyl alcohol. It outlines a straightforward diagnostic strategy and discusses in detail the current treatment recommendations.Evidence acquisition:The authors conducted a literature search of primary and secondary sources related to the topic. For treatment recommendations, search restrictions included articles published between 2008 and 2019. For background information, search restrictions included articles written from 1990 – present.Results:This review discusses in detail how the diagnosis can be made via clinical signs, symptoms, and laboratory values as well as the most recent treatment recommendations. This paper will also discuss the limitations of the emergency department workup and how the absence of particular laboratory findings does not necessarily rule out the diagnosis.Conclusion:Poisoning with methanol, ethylene glycol, and isopropanol present diagnostic and therapeutic challenges to emergency physicians. Toxic alcohol poisonings lead to an elevated osmolar gap and, with the exception of Isopropanol, a metabolic acidosis. In order for the timely initiation of life-saving treatment, emergency physicians need a solid understanding of the pathophysiology, clinical presentation, laboratory workup, and treatment.

Sustained low-efficiency dialysis (SLED) therapy following ingestion of isopropanol in a pediatric patient

Introduction: Cardiovascular collapse due to large ingestions of isopropanol is rare. We report a case of a pediatric patient who had severe CNS and respiratory depression and cardiovascular collapse and was not hemodynamically stable enough to undergo hemodialysis.Case report: A 14-year-old 50 kg male was initially reported to have ingested an unknown amount of HEET® gas line antifreeze about 1 h prior to emergency department (ED) arrival. Despite severe CNS and respiratory depression and cardiovascular collapse, the patient was not initially acidotic. The patient did have an elevated osmolar gap. Approximately 6 h post-ingestion relatives updated the history to reflect that the product was in fact called ISO-HEET® which contains 99% isopropanol. Based on these concerns, a serum isopropanol and acetone levels were obtained that resulted at 475 and 75 mg/dL, respectively. Nephrology was consulted and it was decided to start the patient on sustained low-efficiency dialysis (SLED) which commenced 11 h post-ingestion. Serum and ultrafiltrate concentrations for isopropanol and acetone decreased to normal range over the course of SLED therapy.Discussion: SLED was instituted in this patient primarily for the treatment of elevated serum lactate, isopropanol, and acetone concentrations. The patient’s systemic clearance was calculated as 26.9 mL/min. During SLED therapy, the patient was able to clear isopropanol and acetone at 41.21 mL/min and 29.74 mL/min, respectively. SLED therapy is a viable treatment option when a patient is hemodynamically unstable and hemodialysis is not an option.

SUN-LB030 Empagliflozin Causing Euglycemic Diabetic Ketoacidosis

Background: Empagliflozin is a sodium glucose co-transporter 2 (SGLT-2) inhibitor that works in the proximal renal tubules reducing resorption of glucose and increasing urinary glucose excretion. It effectively lowers glycated hemoglobin (HbA1C) values and reduces risks of adverse cardiovascular events compared to other antidiabetic medications. Common side effects include urinary frequency, genital mycotic infection, and urinary tract infection. A less common, but potentially life-threatening side effect, is euglycemic diabetic ketoacidosis (euDKA). Clinical Case: We present a 60-year-old woman with a history of poorly controlled Type 2 diabetes with a HbA1C of 10.7% on empagliflozin and glipizide, who presented with a nine day history of lethargy, fever, chills, myalgia, and nausea with poor oral intake. Two days prior, she was diagnosed with Influenza A. Initial laboratory results revealed evidence of a metabolic acidosis with a bicarbonate level of 6 (21-31 mmol/L), anion gap of 27 (3-15 mmol/L), and a blood glucose level of 189 (70-100 mg/dL). Urinalysis showed glycosuria and ketones. A venous blood gas was significant for a pH of 7.00 (7.31-7.41) and pCO2 of 22 (41-51 mmHg). Serum osmolality was 331 (289-309 mosm/kg) and a serum acetone level was high at 0.058% (0.0-0.010%). Serum ethanol, methanol, and isopropanol were negative thus ruling out possible ingestion as a source of osmolar gap. The patient was diagnosed with euDKA secondary to empagliflozin with precipitating factors being acute illness and decreased oral intake.Within 42 hours, treatment with normal saline and insulin infusion, the metabolic acidosis, anion gap, and osmolar gap normalized. Empagliflozin was discontinued upon discharge. Conclusion: A review of current literature suggests euDKA from empagliflozin is rare with only four cases reported to date. As SGLT-2 inhibitors continue to be increasingly prescribed, awareness of this potential complication in the setting of misleading blood glucose levels and an osmolar gap is integral for the early detection and treatment of euDKA. Patient counseling on this uncommon adverse event, especially during times of decreased oral intake and acute illness should be provided. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. s presented at a news conference are embargoed until the date and time of the news conference. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.

Toxic Alcohols

Although alcohols share a common metabolic pathway, the toxicity of each is unique. This review discusses the common toxic alcohols, including ethanol, isopropanol, methanol, and ethylene glycol, and summarizes the principles of toxicity, immediate stabilization, diagnosis and definitive therapy, and disposition and outcome for each. A special consideration is also given to diethylene glycol due to its historical significance as a contaminant of multiple different drugs. Figures show type B lactic acidosis; the Mellanby effect; the role of thiamine in aerobic metabolism; the metabolism of isopropanol, methanol, formate, and ethylene glycol; and the relationship between the osmol gap and the anion gap over time. Tables list treatment recommendations for Wernicke encephalopathy, alcoholic ketoacidosis, and alcohol withdrawal; the Clinical Institute Withdrawal Assessment–Alcohol Revised (CIWA-Ar); dosing recommendations for fomepizole and ethanol; serum alkalization; and indications for hemodialysis in ethylene glycol poisoning. This review contains 8 figures, 10 tables, and 54 references. Keywords: Poisoning, ethanol, isopropanol, ethylene glycol, methanol, fomepizole, withdrawal, Wernicke encephalopathy, alcohol dehydrogenase, aldehyde dehydrogenase

Characteristics of Laboratory Confirmed Ethylene Glycol and Methanol Exposures Reported to a Regional Poison Control Center

Ethylene glycol (EG) and methanol (MET) exposures are rare but can cause significant morbidity and mortality. Though frequently treated similarly, EG and MET exposures have characteristics that are not well differentiated in the literature. We sought to describe the clinical characteristics of EG and MET exposures, confirmed with quantitative serum levels. An IRB-approved retrospective review of the University of Kansas Health System Poison Control Center database from July 2005 to July 2015 identified all EG/MET exposures evaluated at a health care facility. Initial measurements were EG/MET levels, serum pH, serum creatinine, anion gap, serum ethanol level, max anion gap, max osmolar gap, therapy performed (hemodialysis, fomepizole, ethanol) and death. The search identified 75 cases, with 59 cases having only detectable EG levels and 15 cases having only detectable MET levels. The average EG level was 126 mg/dL (range 5 - 834). The average detectable methanol level was 78 mg/dL (range 5 - 396). The average maximum anion gap of the EG positive group was 20 mEq/L (range 8 - 35). The average maximum anion gap of the MET positive group was 14 mEq/L (range 6 - 34). One death was reported in the EG positive group, with an initial level of 266 mg/dL. In this study of EG/MET exposures, EG exposures were more common than MET exposures, but they had similar demographics, laboratory findings, and interventions. Continued studies are warranted to characterize these uncommon exposures further.

Importance of sample volume to the measurement and interpretation of plasma osmolality.

BackgroundSmall sample volumes may artificially elevate plasma osmolality (Posm) measured by freezing point depression. The purpose of this study was to compare two widely different sample volumes of measured Posm (mmol/kg) to each other, and to calculated osmolarity (mmol/L), across a physiological Posm range (~50 mmol/kg).MethodsPosm was measured using freezing point depression and osmolarity calculated from measures of sodium, glucose, and blood urea nitrogen. The influence of sample volume was investigated by comparing 20 and 250 μL Posm samples (n = 126 pairs). Thirty‐two volunteers were tested multiple times while EUH (n = 115) or DEH (n = 11) by −4.0% body mass. Protinol™ (240, 280, and 320 mmol/kg) and Clinitrol™ (290 mmol/kg) reference solutions were compared similarly (n = 282 pairs).ResultsThe 20 μL samples of plasma showed a 7 mmol/kg positive bias compared to 250 μL samples and displayed a nearly constant proportional error across the range tested (slope = 0.929). Calculated osmolarity was lower than 20 μL Posm by the same negative bias (−6.9 mmol/kg) but not different from 250 μL Posm (0.1 mmol/kg). The differences between 20 and 250 μL samples of Protinol™ were significantly higher than Clinitrol™.ConclusionsThese results demonstrate that Posm measured by freezing point depression will be ~7 mmol/kg higher when using 20 μL vs 250 μL sample volumes. Approximately half of this effect may be due to plasma proteins. Posm sample volume should be carefully considered when calculating the osmole gap or assessing hydration status.

Young man with severe metabolic acidosis after transformer oil ingestion: a case report

BackgroundTransformer oil is used in oil-filled transformers for its insulating as well as coolant properties. Transformer oil ingestion for attempted suicide is seldom heard of. Our patient’s case presented us with a major diagnostic as well as treatment challenge because we encountered such a case for the first time and were totally unaware of the fact that methanol might make up the main component of an aged transformer oil.Case presentationA 19-year-old Pakistani/Asian man was brought to our hospital with altered sensorium. He was found to have elevated anion gap acidosis, increased osmolal gap, and acute kidney injury. He had no evidence of rhabdomyolysis or hemolysis. Computed tomography of his head showed cerebral edema. He was resuscitated with intravenous fluids and bicarbonate. Three days later, he confessed taking transformer oil with suicidal intention. His clinical picture mimicked acute methanol intoxication. With an initial improvement in his neurological status, he started complaining of constant headache with episodes of agitation and delirium. His renal function continued worsening despite an adequate urine output. He showed a remarkable improvement in his neurological state after just one session of hemodialysis.ConclusionsThere is evidence that aged transformer oil contains methanol, and a patient who consumes it can present with features mimicking acute methanol intoxication.

The Hypothesis of Circulus Hypoxicus and Its Clinical Relevance in Patients With Methanol Poisoning - An Observational Study of 35 Patients.

Methanol mass poisoning is a global problem with high fatality rates and often severe sequelae in survivors. Patients typically present late to the hospital with severe metabolic acidosis followed by a rapid deterioration in their clinical status. The hypothesis 'Circulus hypoxicus' describes the metabolic acidosis following methanol poisoning as a self-enhancing hypoxic circle responsible for methanol toxicity. We wanted to test the validity of this hypothesis by an observational study based on 35 patients from the methanol outbreaks in Norway (2004) and the Czech Republic (2012). Comprehensive laboratory values, including S(serum)-methanol, S-formate, S-lactate, arterial blood gases, anion and osmolal gaps, were used in the calculations. Laboratory values and calculated gaps were compared to each other using linear regression. S-lactate and S-formate correlated better with the increased base deficit and anion gap than did S-formate alone. Base deficit rose to about 20 mmol/L and S-formate rose to 12 mmol/L prior to a significant rise in S-lactate - most likely caused by formate inhibition of mitochondrial respiration (type B lactacidosis). The further rise in S-lactate was not linear to S-formate most likely due to the self-enhancing pathophysiology, but may also be associated with hypotension in critically ill patients and variable ethanol drinking habits. Our study suggests that the primary metabolic acidosis leads to a secondary lactic acidosis mainly due to the toxic effects of formate. The following decline in pH will further increase this toxicity. As such, a vicious and self-enhancing acidotic circle may explain the pathophysiology in methanol poisoning, namely the 'Circulus hypoxicus'.

Evaluation of the effects of glucose on osmolal gap using freezing point depression and vapor pressure methods

The measurement of serum osmolality, and the calculation of osmolal gap (OG) from a calculated osmolality are widely used in clinical and emergency medicine. In this study, the possible effects of blood glucose on OG were investigated by freezing point depression and vapor pressure methods. The concentrations of sodium, glucose, blood urea nitrogen and osmolalities of 2640 samples were measured. There were two methods for calculating serum osmolality: freezing point depression method (n = 2399) and vapor pressure method (n = 241). The OG was positively associated with glucose in glucose 110–450 mg/dL (r = 0.191, p < 0.001) and glucose > 450 mg/dL (r = 0.372, p < 0.001), but not in glucose < 110 mg/dL (r = 0.017, p = 0.711) in freezing point depression method. However, OG had no correlation with glucose regardless of glucose level in vapor pressure method. In freezing point depression method, compared with the groups of glucose <110 and 110–450 mg/dL, the group with glucose >450 mg/dL had higher OG (p < 0.001) and higher prevalence of OG > 10 mOsm/Kg H2O (p < 0.001). Our study demonstrated that OG is impacted by increasing blood glucose concentration using freezing point depression method, special attention should be made to blood glucose concentrations when using freezing point depression method to determine OG.

A New Model for Non-Lipid Compounded Neonatal Parenteral Nutrition Solution Osmolality.

Osmotic stress is a physical risk factor for adverse events related to peripheral parenteral nutrition (PN) administration, such as infiltration. We sought to improve prediction of compounded PN osmolality utilizing basic nutrient solutions available to North American neonatal intensive care units. This study tested the hypothesis that calculated osmolarity underestimates osmolality in compounded PN. Osmolarity (mOsm/L) was calculated utilizing commercial software. Osmolality (mOsm/kg) was determined by a freezing-point depression micro-osmometer. The relationship between calculated osmolarity and measured osmolality was modeled from linear or polynomial regression analysis using the least squares method. Regression models were based upon calculated osmolarity and included various combinations of PN components. Calculated osmolarity significantly underestimated measured osmolality in all PN samples (n = 363). Based upon the osmolality of PN and the basic nutrient solutions, we determined a polynomial regression that effectively corrects for the osmolal gap (measured osmolality-calculated osmolarity) in the validation set (R2 = 0.99367). The unbiased analysis corrected for the osmolal gap based on individual solute behaviors, as well as the solute-solute interactions in compounded solutions. Calculated osmolarity (mOsm/L) significantly underestimates the osmolality (mOsm/kg) in compounded PN. We developed a new algorithm to more accurately predict PN osmolality based upon calculated osmolarity from commercial software and composition of neonatal basic nutrient solutions used in North America. We propose that use of this PN algorithm will facilitate future studies to determine whether a causal association exists between PN osmolality and adverse events, and to establish safe thresholds for PN concentration in neonates.

Proposed laboratory surrogate markers for the management of acute kidney injury in ethylene glycol poisoning in resource-challenged countries; a Mayo Clinic Health System, Wisconsin, case analysis

Mass poisonings with diethylene glycol (DEG) usually ingested as an unintended component of pharmaceutical preparations have occurred in Nigeria, especially affecting children with nearly 100% mortality outcomes. Clearly, the unavailability of Specialty Toxicology laboratory testing facilities translates to non-diagnosis and therefore inappropriate management of these patients with resulting poor outcomes. In this case analysis, while utilizing a case report involving intentional DEG intoxication that we managed at the Mayo Clinic Health System in North-Western Wisconsin, we have demonstrated the utility of serial values of commonly available blood test parameters including serum bicarbonate and anion gap, blood ABG pH and CO2 values, together with the use of serum osmolality gap as surrogates to expedite early and appropriate treatment of such cases even in the absence of Toxicology confirmation of DEG as the poisoning agent. Based on the experience gained from this case report, we strongly recommend that the responsible governments in resource-challenged countries must ensure that these laboratory surrogate indices, at the minimum, become available in the hospitals. This would improve outcomes in general.

Abnormal Osmolality Gap Exists in Distal Symmetric Polyneuropathy.

Distal symmetric polyneuropathy, represented by chronic inflammatory demyelinating polyneuropathy, is a popular neurological condition. Some cases are known to be associated with genetic mutations or serum auto-antibodies, but the exact mechanisms in most cases are unknown. Recently, osmotic factors have been suggested to trigger some neurological disorders, such as neuromyelitis optica. The aim of the present study was to assess the possible association of osmotic factors in the pathogenesis of distal polyneuropathy. We prospectively measured the serum levels of osmolality, electrolytes, total protein, albumin, blood urea nitrogen, glucose, and osmolality gap in the patients with acute distal polyneuropathy before treatments (n = 12) and those with other comprehensive neurological disorders such as multiple sclerosis and neurodegenerative diseases (n = 176). Then, we compared each osmotic fraction between the two groups. As a result, all of the 12 patients with acute distal polyneuropathy, including 4 patients with chronic inflammatory demyelinating polyneuropathy, showed abnormally high or low values of osmolality gap, compared to the others (p < 0.0001, F-test). In the patients with other diseases, there were 2 patients with abnormally high osmolality gap values, which were attributable to their hyperlipidemia or high titer of serum autoantibody unrelated to polyneuropathy. In conclusion, serum osmolality gap would be elevated or decreased in the acute phase of distal symmetric polyneuropathy. Osmotic imbalance between the serum and nerve cells, based on abnormal excess or deficit of some unidentified serum osmolytes, may be one of the mechanisms in symmetric polyneuropathy with unknown causes.

Reversal of Severe Methanol Induced Visual Impairment Due to Prompt Hemodialysis

We report a case series of recovery from severe visual impairment due to methanol intoxication following treatment with fomepizol and prompt hemodialysis. Three adult males presented to our hospital few hours after unintended methanol intoxication. All patients reported weakness and dizziness, two of them suffered visual impairment with visual acuity loss and one of them presented complete blindness and unresponsive dilated pupils. Fundoscopy examination revealed edema of the disk margin. Their laboratory findings included severe high anion gap metabolic acidosis with elevated osmolar gap and methanol levels. All three patients were treated with fomepizole, folic acid IV, and 2-3 sessions of hemodialysis four hours each. The first session of dialysis was performed about 16 h after the methanol ingestion. They all exhibited a full recovery including the patient with the blindness who reported normal vision 20/20 with normal fundoscopic examination on discharge at the fifth day of hospitalization. This case report confirms the effectiveness of the combined treatment based on early dialysis with fomepizol in reversing the retinal impairment in methanol intoxication. The reversibility of retinal end organ damage demonstrated here raises doubts about the common thought regarding the poor outcome of methanol induced retinal end organ damage.

Ethylene glycol poisoning

Ethylene glycol poisoning

Two gaps too many, three clues too few? Do elevated osmolal and anion gaps with crystalluria always mean ethylene glycol poisoning?

A 60-year-old African-American man with a medical history significant for heavy alcohol abuse, hypertension, delirium tremens, nephrolithiasis and seizure disorder was brought to the hospital with altered mental status. He...