Elevated Anion Gap Metabolic Acidosis Research Articles

The significance of precise diabetes diagnosis: a case of euglycemic diabetic ketoacidosis induced by the introduction of empagliflozin with simultaneous reduction of insulin dosage

Euglycemic diabetic ketoacidosis (euDKA) is a rare but severe metabolic complication of diabetes mellitus characterised by elevated anion gap metabolic acidosis despite normal or mildly elevated blood glucose levels. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have emerged as effective antidiabetic medications, yet their use is associated with an increased risk of euDKA, especially when coupled with insulin dose reduction. We present the case of a 50-year-old male with a 20-year history of diabetes mellitus, initially managed with insulin and metformin, who developed euDKA following the introduction of empagliflozin and sitagliptin alongside a reduction in insulin therapy. Despite normoglycaemia the patient exhibited symptoms of ketoacidosis, including chronic fatigue, polydipsia, and polyuria. Diagnostic workup revealed metabolic acidosis, elevated inflammatory markers, acute kidney injury and ketonuria. Subsequent specialised laboratory tests confirmed type 1 diabetes mellitus (T1DM) with the presence of anti-glutamic acid decarboxylase (anti-GAD) antibodies and the absence of C-peptide secretion. Management involved fluid therapy, intravenous insulin and glucose administration. This case underscores the diagnostic challenges of euDKA and emphasises the importance of differentiating between T1DM and T2DM, as management strategies vary significantly. Patient education on insulin therapy and injection techniques is crucial to prevent complications such as improper insulin delivery and dose reduction, which can precipitate euDKA. In conclusion, clinicians should be vigilant for euDKA in patients on SGLT2 inhibitors, particularly when insulin dose reduction is involved. Comprehensive patient education and accurate differentiation between diabetes types are essential for timely diagnosis and optimal management, thereby reducing the risk of severe complications.

Addison’s Crisis or Momordica Charantia Extract: Which Caused Shock?

Aim: Addison’s crisis is extremely rare entity that is difficult to diagnose in the emergency department. Here we present a case of Addison’s crisis diagnosed in the emergency department who complained of vomiting after consuming extract of Momordica charantia fruit for gastric pain.
 
 Case: A 29-year-old female was admitted to the emergency department with complaints of nausea and vomiting after consuming Momordica charantia extract for stomach pain. The patient had tachypnea, tachycardia, hypoglycemia, and hypotension. Blood tests revealed elevated anion gap (24 mEq/L) metabolic acidosis, +4 acetone, normokalemia, and hyponatremia. Although it was impossible to exclude intoxication immediately, 100 mg hydrocortisone was given IV due to possible Addison’s crisis after obtaining blood samples for hormone testing and excluding other causes of shock. The tests revealed very high ACTH (1.250 pg/mL) and low cortisol (1.23 ug/dL) levels, and the patient was diagnosed with primary adrenal insufficiency.
 
 Conclusion: This case illustrates the importance of comprehensive examination and management of profound hypotension and hypoglycemia in the emergency department and of emergency physicians diagnosing and initiating appropriate treatment for Addison’s crisis.

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.

Elevated Anion Gap Metabolic Acidosis With High Osmolar Gap and Increased Serum Acetone Level: A Case Report

Acetone poisoning, although not very common, can present with varied signs and symptoms. High acetone levels in serum can be due to exogenous exposure or endogenous production of acetone. Unlike certain alcohol toxicities, acetone does not cause high anion gap metabolic acidosis.A 69-year-old male presented to our service with shock and acute encephalopathy and required intensive care support. Initial laboratory investigation showed high anion gap metabolic acidosis with high osmolar gap. Serum acetone level was elevated. Clinicians need to be aware of how to elucidate such metabolic disturbances and associated toxicities.

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.

Organic Acidemias.

Organic Acidemias.

Obesity, Anion Accumulation, and Anion Gap Metabolic Acidosis: A Cohort Study.

Obesity is associated with low serum bicarbonate, an indicator of metabolic acidosis and a CKD risk factor. To further characterize acid-base disturbance and subclinical metabolic acidosis in this population, we examined prospective associations of body mass index (BMI) with elevated anion gap and whether anion gap values in obesity associate with low bicarbonate. Data from adult outpatients (n=94,448) in the Bronx, New York were collected from 2010 to 2018. Mixed effects models and Cox proportional hazards models were used to examine associations of BMI with elevated anion gap and anion gap metabolic acidosis and of baseline anion gap with incident low bicarbonate and anion gap metabolic acidosis. Anion gap was defined using traditional and albumin-corrected calculations. Greater BMI was associated with higher anion gap over time and with progressively greater risk of developing an elevated anion gap (hazard ratio [HR] for body mass index [BMI]≥40 kg/m2 versus 18 to <25 kg/m2, 1.32; 95% confidence interval [95% CI], 1.23 to 1.42 for traditional and HR for BMI≥40 kg/m2 versus 18 to <25 kg/m2, 1.74; 95% CI, 1.63 to 1.85 for corrected). Higher BMI was also associated with increased risk of developing anion gap metabolic acidosis (HR for BMI≥40 kg/m2, 1.53; 95% CI, 1.39 to 1.69). Among patients with obesity, higher anion gap was associated with increased risk of incident low bicarbonate (HR for fourth versus first quartile, 1.29; 95% CI, 1.23 to 1.44 for traditional and HR for fourth versus first quartile, 1.36; 95% CI, 1.26 to 1.48 for corrected) and higher risk of anion gap metabolic acidosis (HR for fourth versus first quartile, 1.78; 95% CI, 1.59 to 1.99). Obesity is characterized by unmeasured anion accumulation and acid retention or overproduction. Modest elevations in anion gap among patients with obesity are associated with previously unrecognized anion gap metabolic acidosis.

S1595 A Curious Case of COVID-19-Induced Acute Severe Pancreatitis

Introduction: The COVID-19 virus causes a wide range of lung diseases. It has also been proven to affect other organ systems. Acute pancreatitis is defined as inflammation of the pancreas and has varied etiologies. SARS-CoV2 affects the pancreas by direct binding to ACE2 receptors and stimulation of an inflammatory cytokine storm. Here, we present a rare case of acute pancreatitis induced by COVID-19 in an healthy individual. Case Description/Methods: 35 y.o male with no medical history presented with altered mental status. He was noted to be hypothermic, hypotensive, and tachypneic. Labs revealed, elevated anion gap metabolic acidosis, leukocytosis, ketonuria with elevated blood glucose of 1056mg/dL. Treatment for DKA was started with insulin drip and IV fluids. Patient tested positive for COVID-19, however had no respiratory symptoms. HbA1c was 18. On the 4th day of admission, he developed emesis and epigastric abdominal pain. A CT abdomen revealed features of acute pancreatitis, no evidence of necrosis or fluid collection. Lipase was elevated to 1399. He began spiking intermittent fevers, was initiated on systemic antibiotic therapy. A workup for various etiologies of pancreatitis was performed. A thorough work-up and medication reconciliation ruled out many etiologies of pancreatitis, including alcohol, medications, triglycerides, biliary, and autoimmune pathologies. Abdominal pain continued with development of abdominal distention, therefore, TPN was initiated. Inflammatory markers were elevated. Patient was managed with bowel rest, IV fluids and pain control. A repeat CT abdomen showed persistent ongoing inflammation in the abdomen secondary to pancreatitis and ongoing retroperitoneal fluid. This patient presented with DKA, new onset diabetes mellitus and development of acute pancreatitis. While common causes were ruled out, one diagnosis to consider is COVID-19 induced acute pancreatitis. The absence of other causes, this remains a diagnosis of exclusion. Discussion: Etiologies of acute pancreatitis include alcohol use and gallstone disease. Diagnosis requires 2/3: abdominal pain, imaging of pancreatic inflammation, and lipase elevation. Several viruses have been implicated in the etiology of acute pancreatitis, SARS-CoV-2 also has its significance. Understanding of clinical manifestations of COVID-19 continues to evolve, this case demonstrates that SARS-CoV-2 can precipitate pancreatitis. It is important that clinicians remain cognizant of COVID-19 being a cause for acute pancreatitis.

Euglycemic diabetic ketoacidosis associated with SGLT2i use: Case series.

Euglycemic diabetic ketoacidosis (EuDKA) associated with Sodium-Glucose Cotransporter-2 inhibitor (SGLT2i) use has been described but remains poorly understood. Data on Emergency Department (ED) presentation, resource utilization, and safety outcomes for these patients are lacking. We report a case series of patients diagnosed with EuDKA in the ED. An electronic medical record search identified adult patients presenting to a large tertiary ED with EuDKA. They were screened for concurrent use of SGLT2i. Clinical presentation, resource utilization, safety, and disposition data were collected and described. Five patients were included for analysis. Median age [range] was 57 [43-73] years. Presenting symptoms included nausea, vomiting, fatigue, and altered mental status. Initial results included: serum glucose 191mg/dL [176-215], venous pH7.01 [6.95-7.30], serum HCO3 8mEq/L [6-13], anion gap 27 [26-31], serum beta-hydroxybutyrate 9.9mmol/L [9.2-12.3], and urine ketones 150 [150-150]. Patients remained on an insulin infusion for 18.77h [11.25-56.48]. There were zero episodes of hypoglycemia and one episode of hypokalemia while on insulin infusion. Time to resolution of metabolic acidosis was 23.82h [15.45-24.77]. We report a case series of ED patients with EuDKA associated with SGLT2i use, and describe presentation characteristics, resource utilization, and safety outcomes. Emergency physicians should be aware of the association between SGLT2i use and EuDKA. An appropriate work-up should be pursued for patients taking an SGLT2i who present with symptoms suggestive of DKA, including nausea, vomiting, malaise, and altered mental status, or are noted to have an unexplained elevated anion gap metabolic acidosis.

S2548 MDMA-Induced Rapidly Progressive Multiorgan Failure: A Rare Case of Full Recovery

INTRODUCTION: 3,4-methylenedioxymethamphetmamine (MDMA) is a synthetic drug that is known to be used for its euphoric effects via the release of serotonin, dopamine, and norepinephrine. It has been associated with multiple adverse effects, including seizures, serotonin syndrome, multiorgan failure, disseminated intravascular coagulation (DIC), and death. Here we report a rare case of rapidly reversible multiorgan failure after ingestion of a single tablet of MDMA and its subsequent management. CASE DESCRIPTION/METHODS: A 23-year-old female presented in a comatose state after ingesting 200 mg of MDMA. She was febrile to 109 °F, tachycardic, and hypotensive 69/42 mm Hg. Labs were initially notable for ALT 49 U/L, serum creatinine of 1.75 mg/dL, lactate 10.5 mmol/L, and an elevated anion gap metabolic acidosis. The patient was intubated for airway protection and placed under external cooling measures for hyperpyrexia. Repeat labs in the ICU revealed worsening transaminitis with AST/ALT of 2686/2239, and increasing creatine kinase of 36,350. Within 12 hours, her course worsened to acute decompensated DIC as the patient had epistaxis, platelets 35 K/uL, PT 29.3 sec, aPTT 40.7 sec, fibrinogen 129 mg/dL, and D-dimer 12,466 ng/mL, and INR 2.5 (Figure 1). Fresh frozen plasma and platelet transfusions were administered. The patient was initiated on N-acetylcysteine (NAC) infusions and transferred to a liver transplant center for further care and possible need for OLT (MELD Score 30). Her LFTs slowly improved over the next couple of weeks with overall improvement in clinical status with supportive care. She was ultimately discharged on hospital day 12. On outpatient follow-up day 21, she had complete restoration of her synthetic liver and renal function. DISCUSSION: Acute liver failure with DIC is one of many manifestations of MDMA toxicity, and it carries a 60% mortality rate. Its mechanism of hepatic injury is unclear – since a spectrum of severity exists, histology varies from a mild-moderate lobular hepatitis, to massive hepatic parenchymal collapse. The severity of liver damage appears to not be dose dependent, which suggests an idiosyncratic reaction. MDMA is primarily metabolized by the enzyme CYP2D6 and of note, the patient is Chinese – a population known to have a high prevalence of CYP2D6 polymorphisms, predisposing them to liver failure. This case is one of the few cases of full recovery from MDMA-induced multiorgan failure and it emphasizes the importance of aggressive supportive care in such patients.Figure 1.: Laboratory values by hospital day.

Serious Adverse Health Events, Including Death, Associated with Ingesting Alcohol-Based Hand Sanitizers Containing Methanol - Arizona and New Mexico, May-June 2020.

Alcohol-based hand sanitizer is a liquid, gel, or foam that contains ethanol or isopropanol used to disinfect hands. Hand hygiene is an important component of the U.S. response to the emergence of SARS-CoV-2, the virus that causes coronavirus disease 2019 (COVID-19). If soap and water are not readily available, CDC recommends the use of alcohol-based hand sanitizer products that contain at least 60% ethyl alcohol (ethanol) or 70% isopropyl alcohol (isopropanol) in community settings (1); in health care settings, CDC recommendations specify that alcohol-based hand sanitizer products should contain 60%-95% alcohol (≥60% ethanol or ≥70% isopropanol) (2). According to the Food and Drug Administration (FDA), which regulates alcohol-based hand sanitizers as an over-the-counter drug, methanol (methyl alcohol) is not an acceptable ingredient. Cases of ethanol toxicity following ingestion of alcohol-based hand sanitizer products have been reported in persons with alcohol use disorder (3,4). On June 30, 2020, CDC received notification from public health partners in Arizona and New Mexico of cases of methanol poisoning associated with ingestion of alcohol-based hand sanitizers. The case reports followed an FDA consumer alert issued on June 19, 2020, warning about specific hand sanitizers that contain methanol. Whereas early clinical effects of methanol and ethanol poisoning are similar (e.g., headache, blurred vision, nausea, vomiting, abdominal pain, loss of coordination, and decreased level of consciousness), persons with methanol poisoning might develop severe anion-gap metabolic acidosis, seizures, and blindness. If left untreated methanol poisoning can be fatal (5). Survivors of methanol poisoning might have permanent visual impairment, including complete vision loss; data suggest that vision loss results from the direct toxic effect of formate, a toxic anion metabolite of methanol, on the optic nerve (6). CDC and state partners established a case definition of alcohol-based hand sanitizer-associated methanol poisoning and reviewed 62 poison center call records from May 1 through June 30, 2020, to characterize reported cases. Medical records were reviewed to abstract details missing from poison center call records. During this period, 15 adult patients met the case definition, including persons who were American Indian/Alaska Native (AI/AN). All had ingested an alcohol-based hand sanitizer and were subsequently admitted to a hospital. Four patients died and three were discharged with vision impairment. Persons should never ingest alcohol-based hand sanitizer, avoid use of specific imported products found to contain methanol, and continue to monitor FDA guidance (7). Clinicians should maintain a high index of suspicion for methanol poisoning when evaluating adult or pediatric patients with reported swallowing of an alcohol-based hand sanitizer product or with symptoms, signs, and laboratory findings (e.g., elevated anion-gap metabolic acidosis) compatible with methanol poisoning. Treatment of methanol poisoning includes supportive care, correction of acidosis, administration of an alcohol dehydrogenase inhibitor (e.g., fomepizole), and frequently, hemodialysis.

Pseudo-anion gap metabolic acidosis from severe hypertriglyceridemia corrected by plasma exchange .

Falsely low or even unmeasurable serum bicarbonate has been described in patients with severe hypertriglyceridemia or paraproteinemia. This phenomenon, known as pseudo-hypobicarbonatemia, is believed to be due to interference by these components when the commonly used enzymatic assay is utilized for serum bicarbonate measurement. The calculated bicarbonate derived from blood gas machines is not affected. This can lead to a misdiagnosis of a severe anion gap metabolic acidosis along with an extensive and expensive work-up. We review a series of 5 patients with severe hypertriglyceridemia who presented with pseudo-hypobicarbonatemia and an elevated anion gap metabolic acidosis. Membrane-based therapeutic plasma exchange was utilized. Following aggressive lowering of the triglycerides, there was an immediate resolution of the pseudo-hypobicarbonatemia and anion gap metabolic acidosis. Recognition of lipemic serum in the setting of an otherwise unexplained anion gap metabolic acidosis should prompt the clinician to obtain a blood gas sample for true determination of the acid-base status. Doing so may avoid an extensive and expensive metabolic work-up.

TCAS-ASSOCIATED WITH PERSISTENT WIDE COMPLEX VENTRICULAR TACHYCARDIA

SESSION TITLE: Monday Abstract Posters SESSION TYPE: Original Investigation Posters PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Amitriptyline is a tricyclic antidepressant (TCA) that has been used for over 50 years. TCAs are notorious for cardiotoxicity and neurotoxicity, and it is widely used medication for suicide. The incidence of ventricular tachycardia (VT) and ventricular fibrillation (VF) is approximately 4% in TCA overdose patients. It is mostly noted in patients with severe acidosis, hypotension, and prolonged QRS duration. Here, we present a patient with prolonged wide-complex ventricular tachycardia secondary to amitriptyline overdose. CASE PRESENTATION: A 50 year old female with history of Ehlers-Danlos syndrome and fibromyalgia was brought to the ED by her husband because of a reported seizure at home. Pertinent home medications included Amitriptyline, fentanyl patch, and hydromorphone. Patient denied any prior history of heart disease or neurological problems. On arrival to the ED, Glasgow Coma Scale was 3. Pertinent vital signs were blood pressure of 61/35 mmHg. The patient was emergently intubated. ECG on admission showed slow wide complex VT (80 bpm with QRS duration 217 msec. Admission labs showed elevated anion gap metabolic acidosis. Lactic acid was 20.0 mmol/L. ABG post intubation showed pH 7.17, pCO2 44, pO2 240 with base excess of -12. Urine toxicology demonstrated TCAs and opiates. Naloxone 4 mg IV was given twice with no improvement in symptoms. Repeat ECG 2 hours later showed wide complex ventricular tachycardia 158 bpm with QRS prolongation 178 msec. This was initially thought to be sinus tachycardia with prolonged QRS complex. ICU was consulted and the patient was immediately cardioverted upon arrival to the MICU. Sinus rhythm was achieved, but the patient remained tachycardic. EEG was obtained which confirmed 7 left and 5 right mid-temporal lobe seizures. Patient was started on bicarbonate gtt and Ativan gtt. ECG and ABG were obtained every 4 hours. Her QRS duration normalized and the acidosis has resolved after 12 hours. Brain MRI with and without contrast did not show any acute intracranial pathology. The patient was discharged home safely after a 7-day hospitalization. DISCUSSION: TCAs have been used for over 50 years for the treatment of depression and neuropathic pain. It has many side effects including cardiotoxic and neurotoxic adverse outcomes. The severity of cardiotoxic effects are also imperative to recognize; particularly, it is important to suspect TCA toxicity in a patient with persistent wide complex ventricular tachycardia. Patients with VT secondary to TCA overdose, should promptly treated with the ACLS protocol. These patients should be closely monitored in the ICU and should receive sodium bicarbonate gtt, ABG, and EKG every four hours. CONCLUSIONS: Early recognition and aggressive intervention is warranted in patients presenting with TCA overdose in order to improve patient outcomes. Reference #1: Goldberg RJ, Capone RJ, Hunt JD. Cardiac complications following tricyclic antidepressant overdose. Issues for monitoring policy. JAMA 1985; 254:1772. Reference #2: Khandker Mohammad Nurus Sabah, Abdul Wadud Chowdhury, Mohammad Shahidul Islam, Bishnu Pada Saha, Syed Rezwan Kabir, and Shamima Kawser. Amitriptyline-induced ventricular tachycardia: a case report. BME Res Notes. 2017;10:286. https://doi.org/10.1186/s13104-017-2615-8 DISCLOSURES: No relevant relationships by Abdisamad Ibrahim, source=Web Response No relevant relationships by Mohamed Labedi, source=Web Response No relevant relationships by Ruby Maini, source=Web Response No relevant relationships by Nitin Tandan, source=Web Response

Chronic Salicylate Toxicity Simulation.

Chronic salicylate toxicity is an uncommon, potentially life-threatening poisoning that requires high clinical suspicion in order to make the diagnosis. We created a simulation case that challenges learners to analyze case information, construct a differential diagnosis of an elevated anion gap metabolic acidosis with respiratory alkalosis, and initiate treatment for this toxicity. The simulation case was designed for emergency medicine residents and pediatric emergency medicine fellows. The activity began with a brief overview of the monitors, equipment, and simulation experience. For interns, a team of two learners comanaged the case; for senior learners, the case was managed solo. The learners had 15 minutes to complete a focused history and physical exam, request and interpret labs and studies, and initiate specific treatments. The simulation was followed by a 15-minute facilitated debrief session that included an overview of key learning points and learner performance based on an evaluation checklist. Residents completed a postparticipation questionnaire consisting of six questions rated on a 5-point Likert scale. Overall, residents reported a high degree of satisfaction with the simulation experience. The case and debrief were effective in meeting the educational objectives and proved to be an effective modality to fill this educational gap. This simulation exercise was effective in showing residents the uncommon presentation of chronic salicylate toxicity. Learners reported increased confidence in recognizing and managing this ingestion. The simulation experience closed an identified education gap and provided an experiential learning opportunity that accomplished the targeted learning objectives.

An Unusual Case of Elevated Anion Gap Metabolic Acidosis Secondary to Chronic Acetaminophen Toxicity: A Case Report and Review of Literature

An Unusual Case of Elevated Anion Gap Metabolic Acidosis Secondary to Chronic Acetaminophen Toxicity: A Case Report and Review of Literature

Saved by the Collaterals: A Case of Chronic Mesenteric Ischemia

A 59-year-old male with a history of peripheral vascular disease came to the hospital with worsening, dull but diffuse abdominal pain for one month. The pain was worsened after eating and associated with episodes of loose, non-bloody bowel movements. He had a decreased appetite and steadily lost about 20lbs of weight over the past few months. On initial presentation, he was frail and ill appearing with hypothermia of 36°C, tachypnea of 24bpm and tachycardia around 120bpm. He was otherwise awake with stable blood pressures. His abdomen was diffusely tender on palpation but soft with normal bowel sounds and no guarding, rebound or rigidity. He was found to have leukocytosis of 21x103/uL and a lactate of 15.9mmol/L. He had an elevated anion gap metabolic acidosis with a gap of 44, bicarbonate of 5mmol/L, pCO2 of 15mmHg and pH 7.11. He was immediately started on aggressive fluid resuscitation in an effort to clear his lactic acidosis. A CTA of the abdomen revealed a celiac artery occlusion, proximal SMA occlusion and occlusion of the IMA by his aorto-bifemoral bypass graft. It was diagnostic of mesenteric ischemia. Fortunately, he had collateral circulation supplying his liver and colon, which protected him from complete necrosis of the bowel and ischemic liver disease. The left gastric artery and iliac collaterals to the distal colon provided much of the circulation. He underwent angiography and stenting of his SMA. There was atherosclerotic disease with an acute thrombus overlapping. He improved after the surgery and fluid stabilization with his lactate declining to 1.3mmol/L, acidemia, anion gap and white blood cell count improving back to normal range. He was anticoagulated with heparin to warfarin bridging and then later discharged to a short-term rehab facility. Chronic mesenteric ischemia is episodic or constant hypo-perfusion of the intestines usually caused by stenosis or occlusion. Atherosclerosis of the mesenteric vessels is fairly common in the general population. 18 percent of the population above 65 is eventually found to have significant stenosis. Clinical manifestations are usually rare due to the development of a large collateral circulation network over time. Patients usually present with dull, cramping, post-prandial pain with gradual weight loss. An acute thrombosis can set off acute mesenteric ischemia requiring prompt revascularization usually with angiography and stenting. Close follow-up is needed, as restenosis is common.

Euglycemic Diabetic Ketoacidosis in a Patient with Cocaine Intoxication.

Diabetic ketoacidosis (DKA) is characterized by elevated anion gap metabolic acidosis, hyperglycemia, and elevated ketones in urine and blood. Hyperglycemia is a key component of DKA; however, a subset of DKA patients can present with near-normal blood glucose, an entity described as “euglycemic DKA.” This rare phenomenon is thought to be due to starvation and food restriction in insulin dependent diabetic patients. Cocaine abuse is considered a trigger for development of DKA. Cocaine also has anorexic effects. We describe an interesting case of euglycemic DKA in a middle-aged diabetic female presenting with elevated anion gap metabolic acidosis, with near-normal blood glucose, in the settings of noncompliance to insulin and cocaine abuse. We have postulated that cocaine abuse was implicated in the pathophysiology of euglycemic DKA in this case. This case highlights complex physiological interplay between type-1 diabetes, noncompliance to insulin, and cocaine abuse leading to DKA, with starvation physiology causing development of euglycemic DKA.

Ethylene Glycol Poisoning: An Unusual Cause of Altered Mental Status and the Lessons Learned from Management of the Disease in the Acute Setting.

Ethylene glycol is found in many household products and is a common toxic ingestion. Acute ingestions present with altered sensorium and an osmolal gap. The true toxicity of ethylene glycol is mediated by its metabolites, which are responsible for the increased anion gap metabolic acidosis, renal tubular damage, and crystalluria seen later in ingestions. Early intervention is key; however, diagnosis is often delayed, especially in elderly patients presenting with altered mental status. There are several laboratory tests which can be exploited for the diagnosis, quantification of ingestion, and monitoring of treatment, including the lactate and osmolal gaps. As methods of direct measurement of ethylene glycol are often not readily available, it is important to have a high degree of suspicion based on these indirect laboratory findings. Mainstay of treatment is bicarbonate, fomepizole or ethanol, and, often, hemodialysis. A validated equation can be used to estimate necessary duration of hemodialysis, and even if direct measurements of ethylene glycol are not available, monitoring for the closure of the anion, lactate, and osmolal gaps can guide treatment. We present the case of an elderly male with altered mental status, acute kidney injury, elevated anion gap metabolic acidosis, and profound lactate and osmolal gaps.

Clinical Features of Reported Ethylene Glycol Exposures in the United States.

BackgroundEthylene glycol is highly toxic and represents an important cause of poisonings worldwide. Toxicity can result in central nervous system dysfunction, cardiovascular compromise, elevated anion gap metabolic acidosis and acute kidney injury. Many states have passed laws requiring addition of the bittering agent, denatonium benzoate, to ethylene glycol solutions to reduce severity of exposures. The objectives of this study were to identify differences between unintentional and intentional exposures and to evaluate the utility of denatonium benzoate as a deterrent.Methods and FindingsUsing the National Poison Data System, we performed a retrospective analysis of reported cases of ethylene glycol exposures from January 2006 to December 2013. Outcome classification was summed for intentionality and used as a basis for comparison of effect groups. There were 45,097 cases of ethylene glycol exposures resulting in 154 deaths. Individuals more likely to experience major effects or death were older, male, and presented with more severe symptoms requiring higher levels of care. Latitude and season did not correlate with increased exposures; however, there were more exposures in rural areas. Denatonium benzoate use appeared to have no effect on exposure severity or number.ConclusionDeaths due to ethylene glycol exposure were uncommon; however, there were major clinical effects and more exposures in rural areas. Addition of denatonium benzoate was not associated with a reduction in exposures. Alternative means to deter ingestion are needed. These findings suggest the need to consider replacing ethylene glycol with alternative and less toxic agents.

Diagnostic Challenge in a Patient with Severe Anion Gap Metabolic Acidosis.

The approach to the patient with acute renal failure and elevated anion and osmolal gap is difficult. Differential diagnoses include toxic alcohol ingestion, diabetic or starvation ketoacidosis, or 5-oxoproline acidosis. We present a 76-year-old female with type 2 diabetes mellitus, who was found at home in a confused state. Laboratory analysis revealed serum pH 6.84, bicarbonate 5.8 mmol/L, pCO2 29 mmHg, anion gap 22.2 mmol/L, osmolal gap 17.4 mOsm/kg, elevated beta-hydroxybutyrate (4.2 mmol/L), random blood sugar 213 mg/dL, creatinine 2.1 mg/dL, and potassium 7.5 mmol/L with no electrocardiogram (EKG) changes. Fomepizole and hemodialysis were initiated for presumed ethylene glycol or methanol ingestion. Drug screens returned negative for ethylene glycol, alcohols, and acetaminophen, but there were elevated urine levels of acetone (11 mg/dL). The acetaminophen level was negative, and 5-oxoproline was not analyzed. After 5 days in the intensive care unit (ICU), her mental status improved with supportive care. She was discharged to a nursing facility. Though a diagnosis was not established, our patient's presentation was likely due to starvation ketosis combined with chronic acetaminophen ingestion. Acetone ingestion is less likely. Overall, our case illustrates the importance of systematically approaching an elevated osmolal and anion gap metabolic acidosis.