Severe Anion Gap Metabolic Acidosis Research Articles

Severe Anion and Non-Anion Gap Metabolic Acidosis in a Patient with Hereditary Periodic Paralysis

Severe Anion and Non-Anion Gap Metabolic Acidosis in a Patient with Hereditary Periodic Paralysis

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.

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

A CASE OF STATUS EPILEPTICUS SECONDARY TO BUPROPION OVERDOSE TREATED WITH IV LIPID EMULSION THERAPY

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Bupropion is a norepinephrine/dopamine reuptake inhibitor useful in depression and smoking cessation, with seizures being its most well-known adverse effect. Here, we present a case of status epilepticus secondary to Bupropion overdose (OD), successfully treated with intravenous lipid emulsion (ILE) therapy. CASE PRESENTATION: A 21-year-old female with a past medical history of depression, anxiety, PTSD, and polysubstance abuse, presented to the emergency room with bizarre behavior. Her roommate reported finding empty pill bottles of bupropion, gabapentin, and propranolol at her apartment. On arrival, vitals were HR: 140, BP: 119/59, RR: 18, SpO2: 98%, and GCS: 12. Soon after, the patient had a tonic-clonic seizure that initially subsided on administering 2mg of Lorazepam. Post-seizure, she was tachycardic, diaphoretic with dry oral mucosa, and had dilated pupils with conjunctival injection. Pertinent laboratory findings included an arterial blood gas analysis suggestive of severe high anion gap metabolic acidosis secondary to elevated lactate of 13.2 mmol/L. Her urine toxicology was positive for amphetamine. Salicylates, acetaminophen, and alcohol levels were undetectable. CT head was unremarkable. She was transferred to ICU and intubated for an increasing frequency of seizures and status epilepticus. Despite being on lorazepam drip, her seizures continued and were also resistant to phenobarbital, levetiracetam, valproate, fentanyl, and propofol. Ventricular tachycardias further complicated her course with hemodynamic instability, requiring electro cardioversion and multiple vasopressors. The history of empty bottles of bupropion, positive amphetamine in urine toxicology, along with seizures and ventricular tachycardias, led to a suspicion of bupropion overdose. Intravenous lipid emulsion (ILE) therapy was administered, consequently reversing bupropion toxicity evidenced by cessation of seizures, decreasing vasopressor requirement, improvement in mental status, and extubation. DISCUSSION: Seizures, ventricular tachycardias, and QT prolongation are well-known side effects of bupropion OD, which can occur at any dose with higher incidences noted at higher doses. Positive amphetamines on urine toxicology are expected with bupropion use as their metabolites have chemical structures similar to amphetamine. Intravenous lipid emulsion therapy (ILE) was used in our patient as salvage therapy for bupropion overdose in the setting of hemodynamic instability and status epilepticus with effective reversal of toxicity. The proposed mechanism of action involves ILE sequestering lipophilic drugs such as bupropion followed by its removal via biliary excretion into the gut. However, the use of ILE lacks high-powered evidence, and further investigation is warranted to expand and strengthen the antidotal uses of ILE. CONCLUSIONS: ILE therapy can be used as an antidote for severe bupropion toxicity. REFERENCE #1: Bornstein K, Montrief T, Anwar Parris M. Successful Management of Adolescent Bupropion Overdose with Intravenous Lipid Emulsion Therapy. J Pediatr Intensive Care. 2019;8(4):242-246. doi:10.1055/s-0039-1693483 REFERENCE #2: Stall N, Godwin J, Juurlink D. Bupropion abuse and overdose. CMAJ. 2014;186(13):1015. doi:10.1503/cmaj.131534 REFERENCE #3: Casey ER, Scott MG, Tang S, Mullins ME. Frequency of false positive amphetamine screens due to bupropion using the Syva EMIT II immunoassay. J Med Toxicol. 2011 Jun;7(2):105-8. doi: 10.1007/s13181-010-0131-5. PMID: 21191682; PMCID: PMC3724447. DISCLOSURES: No relevant relationships by Mubashir Ayaz Ahmed, source=Web Response No relevant relationships by Shayet Hossain Eshan, source=Web Response No relevant relationships by sami hussein, source=Web Response No relevant relationships by Sudha Misra, source=Web Response No relevant relationships by Chenyu Sun, source=Web Response

Death by hand sanitizer: syndemic methanol poisoning in the age of COVID-19

Background The advent of COVID-19 increased attention to hand hygiene in prevention of disease transmission. To meet the increased demand for hand sanitizer during the pandemic, the US FDA issued an Emergency Use Authorization allowing new manufacturers and importers to enter the market. Some of the newly introduced hand sanitizer products contained methanol in lieu of ethanol or isopropanol. We describe five patients with fatal methanol poisoning resulting from hand sanitizers improperly containing methanol. Case summary Comparing a 5-month period from 2019 to the same time frame in 2020, the Arizona Poison and Drug Information Center has seen an increase of 124% in exposures to hand sanitizer. Of these cases, 28% involved methanol-contaminated hand sanitizer. Five of these patients died from methanol poisoning. All five cases had similar clinical features with severe high anion gap metabolic acidosis and, in four patients, elevated osmolal gap. Methanol concentrations were consistently very elevated, but these results were not available before the patients succumbed. Four of the patients received fomepizole and adjunctive care. Two patients received emergency extracorporeal therapy. All five died despite maximal treatment efforts. Conclusion During the pandemic in 2020, there was a proliferation of alcohol-based hand sanitizers which contained methanol. Exposure to these products, which failed to meet regulatory standards, led to increased harm and death. Challenges to treatment of methanol poisoning, especially in rural areas, include lack of access to timely laboratory measurement of methanol concentrations and lack of available emergency hemodialysis without transfer of the patient.

630: Burkitt Lymphoma Presenting as Isolated Severe Anion Gap Metabolic Acidosis

630: Burkitt Lymphoma Presenting as Isolated Severe Anion Gap Metabolic Acidosis

A NOT SO FUN-GI: AN RARE CASE OF AMANITA MUSCARIA MUSHROOM OVERDOSE

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Amanita muscaria (A. muscaria), commonly known as fly agaric is a poisonous fungus from the Amanitaceae family. The mushroom is taken to induce psychoactive effects and hallucinations also known as a “trip”. There are a few case reports in literature that highlight the toxic effects of this species as overall incidence is rare. We highlight a rare case that describes a patient admitted to the intensive care unit after ingesting the mushroom for its psychedelic effects. CASE PRESENTATION: A 56-year-old gentleman with no past medical history presented to the emergency department after being found down following purposeful ingestion of the A. muscaria mushroom. Vitals on admission were notable for a blood pressure of 136/112, heart rate 125, respiratory rate 22 and temperature of 96 degrees. The patient was encephalopathic, agitated and combative on arrival and subsequently intubated for airway protection. Later, the patient was noted to have myoclonic jerks. Labs were significant for creatinine of 2.17 mg/dL (unknown baseline), severe anion gap metabolic acidosis, lactate of 10.8 mmol/L, creatinine kinase over 1,500 U/L with mild elevation of liver function tests. Urine drug screen was negative and salicylate level was undetectable. Computed tomography head was negative. The patient was admitted to the intensive care unit for further monitoring and was treated with supportive measures. DISCUSSION: A. muscaria contains several distinct neurotoxins that can cause a variety of symptoms. The main neurotoxins are ibotenic acid and muscarine. Ibotenic acid is an excitatory neurotransmitter that is similar to glutamic acid and contributes to the hyperactive symptoms. Muscarine is a cholinergic agonist that causes atropine like effects including dry mouth, drowsiness and coma. Symptoms manifest between thirty minutes to two hours and include dizziness, confusion, and increased sensitivity to visual stimuli. Late effects include combativeness, seizures or coma. Complications include renal failure, rhabdomyolysis, cardiac and respiratory depression. Our case describes a fifty-year-old gentleman that manifested the same symptoms of hyperactivity followed by combativeness, respiratory depression and myoclonic jerks as well as renal failure and rhabdomyolysis. Treatment is often supportive and sometimes activated charcoal can be used to decrease absorption. Because of the variety of toxins present in the mushroom, there is no clear toxidrome and this drug does not show up on routine drug screening. Therefore, early detection with careful history taking and physical exam is essential to prevent the deadly complications. CONCLUSIONS: Our case describes a rare case of intentional A. muscaria overdose. There are few cases in literature that detail the prodrome of this drug and therefore it is important to highlight its effects. Supportive care is the mainstay of treatment and prompt identification is essential. Reference #1: Coma in the course of severe poisoning after consumption of red fly agaric (Amanita muscaria). Mikaszewska-Sokolewicz MA et al. Acta Biochim Pol 2016 Feb 1. Reference #2: Fly agaric (Amanita muscaria) poisoning, case report and review. Satora, L et al. Toxicon, Volume 45, Issue 7, 1 June 2005, Pages 941-943. Reference #3: Clinical symptoms and circumastances of acute poisonings with fly agaric (Amanita muscaria) and panther cap (Amanita pantherina). Łukasik-Głebocka M et al. Przegl Lek, 68(8):449-52. 2011. DISCLOSURES: No relevant relationships by Arjan Ahluwalia, source=Web Response No relevant relationships by Timothy Coyle, source=Web Response No relevant relationships by Christopher Lenivy, source=Web Response No relevant relationships by Reema Vaze, source=Web Response No relevant relationships by Andres Zirlinger, source=Web Response

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.

Acetaminophen Use Concomitant with Long-Lasting Flucloxacillin Therapy: A Dangerous Combination.

Acetaminophen and flucloxacillin both interfere with the γ-glutamyl cycle. Long-lasting concomitant use of flucloxacillin and acetaminophen can lead to 5-oxoproline accumulation and severe high anion gap metabolic acidosis. Females and patients with sepsis, impaired kidney and/or liver function, malnutrition, advanced age, congenital 5-oxoprolinase deficiency and supratherapeutic acetaminophen and flucloxacillin dosage are associated with increased risk. Therefore, a critical attitude towards the prescription of acetaminophen concomitant with flucloxacillin in these patients is needed.We present the case of a 79-year-old woman with severe 5-oxoprolinaemia after long-lasting treatment with flucloxacillin and acetaminophen, explaining the toxicological mechanism and risk factors, and we make recommendations for acetaminophen use in patients with long-lasting flucloxacillin treatment.LEARNING POINTSAlthough rare, long-lasting treatment with flucloxacillin concomitant with acetaminophen can lead to severe high anion gap metabolic acidosis.When prescribing long-lasting flucloxacillin therapy in combination with acetaminophen, regular blood gas analysis is needed to evaluate pH and the anion gap.In cases of 5-oxoproline-induced high anion gap metabolic acidosis in patients with long-lasting acetaminophen and flucloxacillin therapy, acetaminophen prescription should be stopped immediately. Replacing flucloxacillin with another antibiotic agent should be considered.

Minding The Gap: Severe Anion Gap Metabolic Acidosis Associated With 5-Oxoproline Secondary To Chronic Acetaminophen Use

AbstractAn 89-year-old man with multiple comorbidities presented to the emergency department with diffuse abdominal pain and dyspnea. He was found to have a severe anion-gap metabolic acidosis with the normal osmolar gap. An initial panel of investigations for common causes of anion-gap metabolic acidosis was unremarkable. Further history revealed long-term daily acetaminophen use. A presumptive diagnosis of 5-oxoprolinemia secondary to chronic acetaminophen use was made. Despite supportive care, the patient did not survive. There is emerging literature on elevated anion gap metabolic acidosis induced by the accumulation of 5-oxoproline, an intermediate organic acid in the gamma-glutamyl cycle. A quantitative profile of urinary organic acids to measure 5-oxoproline is valuable in confirming the diagnosis. Treatment is largely supportive, consisting of cessation of acetaminophen, alkali therapy, and N-acetylcysteine. Clinicians should consider 5-oxoprolemia in patients who present with an otherwise unexplained anion gap metabolic acidosis and a history of chronic acetaminophen use.&#x0D; RESUMEUn homme de 89 ans souffrant de comorbidités multiples s’est présenté à l’urgence avec douleur abdominale diffuse et dyspnée. On a découvert qu’il souffrait d’une acidose métabolique grave à anions nuls avec un écart osmolaire normal. Un premier groupe d’études sur les causes courantes d’acidose métabolique à intervalle anionique n’a pas été remarquable. D’autres antécédents ont révélé une utilisation quotidienne à long terme de l’acétaminophène. Un diagnostic présumé de 5-oxoprolinémie secondaire à l’utilisation chronique d’acétaminophène a été posé. Malgré des soins de soutien, le patient n’a pas survécu. Il existe une littérature émergente sur l’acidose métabolique à intervalle anionique élevé induite par l’accumulation de 5-oxoproline, un acide organique intermédiaire dans le cycle gamma-glutamyle. Un profil quantitatif d’acides organiques urinaires pour mesurer la 5-oxoproline est utile pour confirmer le diagnostic. Le traitement est largement favorable, consistant en l’arrêt de l’acétaminophène, un traitement alcalin et de la N-acétylcystéine. Les cliniciens devraient envisager l’administration de 5-oxoprolemia chez les patients qui présentent une acidose métabolique par gap anionique autrement inexpliquée et des antécédents d’utilisation chronique d’acétaminophène.

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.

Rrefractory Metabolic Acidosis in a Diabetic Patient : A case of Unsuspected Methanol Intoxication

We present a case of a 45 years old male, diabetic and hypertensive who was admited into hospital with a history ofrestlessness, blurring of vision and breathlessness for one day. Inspite of conservative treatment for 10 hours, hisgeneral condition gradually detoriated and he was shifted to ICU. He was kept on mechanical ventilator. Hislaboratory results showed severe high anion gap metabolic acidosis not corrected by sodibicarb and adequate fluidresuscitation. MRI of brain showed bilateral putamenal lesion suspecting methanol intoxication. His acidosis persistedand after giving 3 sessions of Sustained Low Efficiency Dialysis (SLED), metabolic acidosis was corrected withnormalization of renal function. After six months in a follow-up, patient complained of total blindness and fundalphotography showed bilateral optic atrophy.&#x0D; Bangladesh Crit Care J September 2019; 7(2): 111-112

ARTERIAL VS SERUM LACTIC ACID DISCREPANCY

SESSION TITLE: Unusual Cases and Treatments in the ICU SESSION TYPE: Fellow Case Reports PRESENTED ON: 10/22/2019 3:45 PM - 4:45 PM INTRODUCTION: We are presenting a case where a significant difference was noticed between lactate levels measured by arterial blood gas (ABG) analyzer and serum chemistry analyzer; Lactate gap. Why does that happen? How does it help in supporting a diagnosis and monitoring a treatment? CASE PRESENTATION: A 46-year-old female was brought to the Emergency Department (ED) after her family called 911 for altered mental status and abnormal behavior. Emergency Medical Services personnel found the patient next to an empty bottle of Oxycodone/Acetaminophen and beer cans. In the ED, She was oriented only to person, unable to provide significant history regarding her medication/alcohol consumption. She denied homicidal or suicidal ideation. Few hours later, she progressively became more lethargic prompting intubation for airway protection. Physical exam was within normal limits except for the lethargy and tachypnea. Initial blood workup showed severe high anion gap metabolic acidosis, serum bicarbonate level of 5, anion gap of 24, calculated serum osmolality of 281, measured serum osmolality of 334, making an osmolal gap of 53. Serum lactate 1.2, Serum alcohol, acetone, salicylate and acetaminophen levels were undetectable. ABG, with lactate level, revealed a pH of 7.0, PaCO2 of 13, PaO2 of 151, bicarbonate of 3.2 and lactate of 20. Serial lactate discrepancies were noticed between measuring lactate by the ABG and the serum chemistry analyzers. Due to encephalopathy, high anion gap and osmolar gap, there was a high suspicion that she ingested methanol or ethylene glycol, so she was started on Sodium bicarbonate drip, fomepizole infusion and an emergent hemodialysis was initiated. After 1 session, her mental status improved and was extubated. Lactate gap, anion gap, osmolar gap and metabolic acidemia normalized. DISCUSSION: Ethylene glycol toxicity is known to cause a high anion gap and osmolal gap, especially early in presentation. The new thing to our knowledge, which was confirmed by published literature was that it may cause a lactate gap; a discrepancy between lactate levels measured by the ABG analyzer and the serum chemistry analyzer. This discrepancy is explained by the cross reactivity of the ABG analyzer with glycolate, a byproduct of ethylene glycol, resulting in high ABG lactate levels. This false positive result of lactate gap by the ABG analyzer can help to support the diagnosis of the ethylene glycol toxicity and monitor the treatment, that includes administration of Sodium bicarbonate to correct the severe academia, fomepizole to prevent conversion of ethylene glycol to the toxic metabolites and emergent dialysis to clear these metabolites before they cause acute tubular necrosis resulting in acute renal failure. CONCLUSIONS: Lactate gap noted through discrepancy between Lactate level on ABG and serum chemistry analyzers can be used to diagnose and monitor treatment for Ethylene Glycol toxicity. Reference #1: DOI:https://doi.org/10.1016/S0140-6736(01)06799-X DISCLOSURES: No relevant relationships by Moayyad Alziadat, source=Web Response No relevant relationships by Mohd Hazem Azzam, source=Web Response No relevant relationships by Anish Samuel, source=Web Response

Heart transplant complicated by metformin induced lactic acidosis

Introduction Mild lactic acidosis following heart transplant is a known laboratory finding that generally does not require treatment. However, we encountered a case in which a diabetic patient on metformin underwent a heart transplant and developed a profound rise in lactate which caused a severe anion gap metabolic acidosis and refractory vasoplegia. Methods Case Report. Results A 52 year old man with a past medical history of type 2 diabetes mellitus managed with metformin, chronic kidney disease, and coronary artery disease underwent an LVAD explant and a heart transplant utilizing bicaval anastomosis technique. Twenty minutes after separating from bypass, an arterial blood gas was notable for a lactate of 7.8 mmol/L. Over the next two hours, the patient developed vasoplegia and a severe anion gap metabolic acidosis with a lactate that peaked at 18.0 mmol/L. TEE and surgical visualization agreed that cardiac function was excellent and without evidence of tamponade. The patient's hyperdynamic cardiac function was confirmed by the cardiac output values nearing 14 L/m via Swan-Ganz thermodilution. The patient's preoperative medication history was once more analyzed and metformin induced lactic acidosis was added to our working differential diagnosis. A dialysis line was placed, and continuous veno-venous hemofiltration (CVVH) was initiated in the OR, followed by a downtrend of lactate and improvement in hemodynamics. CVVH was continued in the ICU resulting in resolution of lactemia. Discussion Metformin induced lactic acidosis is rare and a diagnosis of exclusion. We ruled out hypovolemia due to a CVP of 14-15 mmHg and ischemic bowel by benign abdominal exam and normal AST, ALT, amylase, and lipase. Sepsis was considered less likely due to lack of infectious source/fever and maintenance of scheduled antibiotic prophylaxis. We had established that the donor cardiac function was excellent. Due to the unpredictable nature of heart transplant, our patient received metformin within 48 hours of surgery. The patient's known chronic kidney disease, potentially exacerbated by cardiopulmonary bypass, likely contributed to metformin induced lactic acidosis.

Recurrent Anion Gap Metabolic Acidosis.

Background:Metabolic acidosis refers to any process that increases the hydrogen ions in the body and reduces the bicarbonate concentration. Metabolic acidosis is subdivided based on presence of anion gap (AG), and AG metabolic acidosis is most often due to ketoacidosis, lactic acidosis, renal failure, or toxic ingestions. AG metabolic acidosis is frequently encountered in the clinical practice. Rarely, the underlying cause of the AG metabolic acidosis is considered a diagnostic dilemma as the established algorithm allows the physicians to identify the etiology.Case presentation:A fifty-three-year-old Black woman with well-controlled human immunodeficiency virus (HIV), hypertension, and asthma presented with recurrent episodes of severe anion gap metabolic acidosis. The patient’s AG metabolic acidosis always corrected with the administration of intravenous normal saline. Laboratory studies were always negative for common causes of acidosis.Conclusion:Nucleoside reverse transcriptase inhibitors-associated lactic acidosis has been reported in the literature. The shift to anaerobic mitochondrial metabolism induced by the HIV medications used in this patient could be explain the recurrent severe metabolic acidosis.

CME: Ethylene Glycol Intoxication

CME: Ethylene Glycol Intoxication Abstract. Ethylene glycol is a sweet-tasting alcohol used in common antifreeze and other industrial solutions. Without appropriate therapy, intoxication with ethylene glycol can result in severe metabolic acidosis, acute renal failure, and in death. After gastrointestinal resorption, hepatic metabolism starts with oxidation by alcohol dehydrogenase and results in severe anion gap metabolic acidosis. Other metabolic products are calcium oxalate crystals, which can deposit in several tissues like the kidneys and lead to acute tubular necrosis with reversible renal failure. The crucial therapeutic step is rapid inhibition of alcohol dehydrogenase with fomepizole or ethanol to avoid the formation of toxic metabolites. Additionally, haemodialysis is the most effective way to eliminate ethylene glycol as well as its toxic metabolites. If therapy is initiated rapidly, prognosis is favorable.

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.

Treatment of Metformin Intoxication Complicated by Lactic Acidosis and Acute Kidney Injury: The Role of Prolonged Intermittent Hemodialysis

Metformin intoxication with lactic acidosis, a potentially lethal condition, may develop in diabetic patients when the drug dose is inappropriate and/or its clearance is reduced. Diagnosis and therapy may be delayed due to nonspecific symptoms at presentation, with severe anion gap metabolic acidosis and elevated serum creatinine values being the most prominent laboratory findings. Confirmation requires measurement of serum metformin by high-performance liquid chromatography-tandem mass spectrometry, but this technique is available only at specialized institutions and cannot be relied on as a guide to immediate treatment. Thus, based on strong clinical suspicion, renal replacement therapy must be started promptly to achieve efficient drug clearance and correct the metabolic acidosis. However, because metformin accumulates in the intracellular compartment with prolonged treatment, a rebound in serum concentrations due to redistribution is expected at the end of dialysis. We report a case of metformin intoxication, severe lactic acidosis, and acute kidney injury in a diabetic patient with pre-existing chronic kidney disease stage 3, treated effectively with sustained low-efficiency dialysis. We discuss the pathophysiology, differential diagnosis, and treatment options and highlight specific pharmacokinetic issues that should be considered in selecting the appropriate modality of renal replacement therapy.

A Patient With Alcoholic Ketoacidosis and Profound Lactemia

BackgroundAlcoholic ketoacidosis (AKA) is a complex syndrome that results from disrupted metabolism in the setting of excessive alcohol use and poor oral intake. Dehydration, glycogen depletion, high redox state, and release of stress hormones are the primary factors producing the characteristic anion gap metabolic acidosis with an elevated β-hydroxybutyrate (β-OH) and lactate. Case ReportWe present the case of a 47-year-old man who presented to the emergency department with metabolic acidosis and profoundly elevated lactate levels who had AKA. He recovered completely with intravenous fluids and parenteral glucose administration. Why Should an Emergency Physician Be Aware of This?Emergency physicians should always consider the immediately life-threatening causes of a severe anion gap metabolic acidosis and treat aggressively based on the situation. This case highlights the fact that AKA can present with an impressively elevated lactate levels. Emergency physicians should keep AKA in the differential diagnosis of patients who present with a similar clinical picture.

Hypertriglyceridemia Induced Acute Pancreatitis Associated with Diabetic Ketoacidosis and a Vaginal Estrogen Contraceptive Device (NuvaRing): Successfully Treated with Insulin Infusion, Plasmapheresis, and Ring Removal

We present a 27-year-old female with only past medical history of gestational diabetes, who presented to our hospital with abdominal pain. Physical exam was significant for mild tachypnea and tachycardia, dry mucous membranes, and moderate epigastric tenderness to light palpation. Blood work revealed an elevated glucose of 411 mg/dl, creatinine of 0.4 mg/dl, severe wide anion gap metabolic acidosis, lipase >6,000, triglycerides (TG) increased to 1,368 mg/dl. Computed tomography of abdomen and pelvis was consistent with acute pancreatitis. She was started on an insulin infusion and intravenous fluids. Her condition worsened rapidly with significant decline in mentation and severe tachypnea requiring intubation. Further blood work showed worsening creatinine at 1.5 with an arterial blood pH of 6.9. Insulin infusion continued and plasmapheresis was initiated given the worsening in her clinical status. Post plasmapheresis, her triglycerides decreased to 259 mg/dl, glucose trending in the 100 range, and anion gap closed. Her severely elevated triglyceride level was attributed to a combined effect of her new onset diabetes and vaginal estrogen ring, which was removed on presentation. Hypertriglyceridemia pancreatitis is a rare cause of pancreatitis. Usually a serum triglyceride (TG) level of more than 1,000 mg/dL is an inciting factor for the episode. In DKA, the deficiency of insulin activates lipolysis in adipose tissue releasing increased free fatty acids, which accelerates formation of VLDL in the liver. In addition, reduced activity of lipoprotein lipase in peripheral tissue decreases removal of VLDL from the plasma, resulting in hypertriglyceridemia. Furthermore, exogenous estrogen use can cause an increase in TG by induced stimulation of the secretion of hepatic triglyceride-rich lipoprotein. Plasmapheresis has been repeatedly shown in case reports and series to be effective in quickly removing TG from the serum of patients with hypertriglyceridemia pancreatitis. Although a clear benefit of plasmapheresis in reducing the severity and improving outcomes in such patients has not been conclusively shown, we report the possible benefit of such therapy as an add-on treatment modality in case the clinical situation deteriorates while they are on standard therapy.