Anion Gap Metabolic Acidosis Research Articles

An Unusual Cause of Acidosis in a Man With Clostridium difficile Colitis

An Unusual Cause of Acidosis in a Man With Clostridium difficile Colitis

Severe Hypertriglyceridemia Causing Pseudo-acidosis: A Case Report

Pseudo hypobicarbonatemia is a rare phenomenon associated with spuriously low bicarbonate levels in the presence of elevated triglycerides (TG). TG’s interfere with commonly used enzymatic assays in basic metabolic panel (BMP), giving falsely low bicarbonate levels. It adds to the diagnostic dilemma and possible extensive workup to identify the cause. Previous case reports have used plasmapheresis in these settings. We report the successful use of insulin infusion in managing a case of pseudo-acidosis secondary to severely high TG levels. Our patient was a 53-year-old female who presented with complaints of progressive fatigue. Her bicarbonate was 5 mmol/L on workup, anion gap was 30 mmol/L, with elevated TG levels (5904 mg/dL). Arterial blood gas analysis showed normal pH (7.32) and normal calculated bicarbonate (22.8 mmol/L). Insulin infusion was started along with adding fenofibrate and atorvastatin. TG levels decreased progressively to 509 mg/dL with an associated normalization of bicarbonate levels and anion-gap acidosis on BMP. The patient was discharged on day 8 of her hospital stay. Hyper TG can lead to pseudo hypobicarbonatemia, presenting as pseudo anion gap metabolic acidosis. It is essential to correlate the lab findings in the perspective of clinical findings to avoid over-testing and clinical misdiagnosis. In addition, these patients can be managed safely with insulin infusion in resource-limited settings.

ODP159 A Rare Case of Pembrolizumab Induced Diabetic Ketoacidosis

Abstract Introduction Immune checkpoint inhibitors (ICI), such as Pembrolizumab, have demonstrated excellent clinical outcomes in numerous solid organ malignancies. However, this new drug comes with unpredictable adverse reactions which are still under review in the medical literature. We are showcasing a cancer patient treated with an ICI and presenting to the hospital in diabetic ketoacidosis (DKA), despite no significant history of a formal diagnosis of Diabetes Mellitus. Case description The patient is a 69 year old male who presented to the hospital with generalized weakness. His past medical history was significant but not limited to, Hypothyroidism, Tobacco use disorder, Stage IV Siewert type 2 gastroesophageal junction adenocarcinoma (cT4N2M1, HER2/FGFR negative, PD-L1 positive) after completion of one year of chemotherapy. He was now undergoing immunotherapy with Pembrolizumab, with his first dose three weeks ago. Reviews of systems including fever, abdominal pain, nausea, vomiting, polyuria, polydipsia were negative. Vital signs were grossly normal. He gave no personal or family history of diabetes. On admission venous blood gas demonstrated a high anion gap metabolic acidosis (pH 7. 096, Blood glucose 762 mg/dL, Anion Gap 29 mmol/L, bicarbonate 9 mmol/L, Plasma osmolality 337 mOsm/kg). Serum Lipase was 23 U/L. HbA1c was found to be 5.9%. Urinalysis was significant for glucose >500 mg/dl and >80 mg/dl of ketones. The physical exam was only remarkable for dry mucous membranes. Given the presentation and lab findings, he was subsequently diagnosed with DKA. The patient was treated with standard guideline therapy for DKA including bolus fluids, maintenance fluids and intravenous (IV) Insulin. The Anion gap closed and glucose decreased to under 200. He was transitioned to a subcutaneous insulin regimen, and discharged on the same. Discussion Based on diagnostic workup and exclusion of probable aetiologies, the patient was diagnosed with pembrolizumab-induced DKA. In the acute care setting, an autoimmune workup was not done in our patient. A meta analysis review of 71 such cases from 56 publications showed the average HbA1c concentration was 7.84% + 1. 0% at presentation. The A1c finding of 5.9%, defined at pre-diabetes, in represents an outlier. Another meta-analysis of such patients demonstrated DKA as the first sign of diabetes in 30 out of 35. The pathophysiology of this side effect of ICI's remains unknown, however several mouse studies have shown PD-1/PD L1 blockade precipitating diabetes in prediabetic non-obese mice. Anti -PD-1 drugs might have the same effect, and the reduction of PD-1 might activate autoreactive T cells, resulting in an autoimmune response against pancreatic islet cells. As the use of immunotherapy is expected to increase, it is essential that clinicians become aware of DKA as a rare and life threatening side effects of immunotherapy and that blood glucose monitoring is strongly considered as a method of prevention. Presentation: No date and time listed

ODP150 Hypertriglyceridemic Induced Acute Pancreatitis with Diabetic Ketoacidosis Treated with Insulin: A Case Report

Abstract Introduction Acute pancreatitis due to hypertriglyceridemia with DKA is a unique entity. The diagnosis of acute pancreatitis in DKA is challenging as most patients present with abdominal pain, and elevated amylase, and lipase are quite common in DKA. Hypertriglyceridemia-induced pancreatitis (HTGP) accounts for 1 to 35 percent of all cases of acute pancreatitis. Pancreatitis may occur in DKA with high anion gap metabolic acidosis. Lack of insulin results in lipolysis with release of free fatty acids. Increased free fatty acids presented to the liver, causes increased VLDL, which inhibits lipoprotein lipase in peripheral tissues and results in elevated triglycerides. Case presentation A 29-year-old morbidly obese male with Asperger's syndrome, prediabetes, and hyperlipidemia presented with a 3-day history of sharp, non-radiating, and progressively worsening right upper abdominal pain, associated with nausea, non-bilious vomiting, and shortness of breath. His past medical history was notable for a prior bout of gallstone pancreatitis, for which he underwent a laparoscopic cholecystectomy. On his arrival in the emergency department, he was afebrile, but tachycardic (HR 139), mildly hypertensive (BP 149/98) with a Kussmaul breathing saturating 98% on room air. His lung sounds were clear but diminished and his abdomen was soft but diffusely tender, without peritoneal signs. Initial laboratory tests showed a neutrophilic leukocytosis of 12K, glucose of 867 mg/dL, hyponatremia (corrected 131), ketonuria, with elevated lipase 1,164 U/L. Venous blood gas showed a pH of 7.18 and PCO2 24 mmHg. He also had severe hypertriglyceridemia with a total triglyceride level of > 9,000 mg/dL. His CT abdomen showed peripancreatic inflammation consistent with acute pancreatitis. He was admitted to the ICU, and initially managed with aggressive intravenous fluids and pain control, then was started on an insulin drip for diabetic ketoacidosis and hypertriglyceridemia. His hospital course was notable for the development of acute kidney injury requiring hemodialysis. His triglyceride level gradually decreased and was 396 U/L on hospital day #9. He was discharged on fenofibrate, Lantus 20 units daily and insulin lispro 10 units with meals. Conclusion Hypertriglyceridemia is an uncommon but a well-established cause of acute pancreatitis leading to significant morbidity and mortality. In this case, a prediabetic patient presented with DKA and further investigation revealed HTGP. There is currently a paucity of data to support an optimal treatment for this condition; however, both insulin and plasmapheresis have been successfully employed. Plasmapheresis helps remove plasma lipoproteins and reduces triglyceride more rapidly than insulin and has been recommended for severe cases. In our case, insulin infusion alone significantly reduced the triglyceride level. Presentation: No date and time listed

PSAT042 Adrenal Insufficiency Associated to Immune Checkpoint Inhibitors

Abstract Background Innovations in management of multiple malignancies have developed throughout the years. Despite benefits in immune checkpoint inhibitors there is an incidence of approximately 9.4% to 10.4% in endocrine immune related disorders. The challenge advocates to promptly recognize the clinical manifestations related to adverse effects. Clinical Case We report a case of a 61-year-old caucasian woman with Metastatic Lung Squamous Cell Carcinoma Stage IV on immunotherapy and radiotherapy who presented to ED with nausea and vomiting for the last 2 weeks. The review of the system pertinent for weight loss 18 pounds in the last 2 months, fatigue and decreased appetite. Medication history pertinent for active Pembrolizumab (started 6 months prior to presentation; cycle every 3 weeks); Radiotherapy (3 cycles) and steroid injections (last dose 1 month prior for bilateral knee pain). Upon arrival vital signs T 36.9C, HR 110/min, RR 18/min, BP 80/60mmHg, and StO2 98%. The physical examination pertinent for an acutely ill patient with tachycardia. Initial laboratory studies showed peripheral eosinophilia 14% (n <6%); high anion gap metabolic acidosis (AG 18), hypokalemia 2.8 mmol/L (n 3.5-5.0mmol/L). The patient was hospitalized with sepsis and intractable vomiting. Gastroenterology evaluated with EGD showed erosive gastritis and reflux esophagitis. CT abdomen with IV contrast showed numerous sclerotic bone lesions and single hepatic lesion suggestive of metastatic disease; unremarkable adrenal glands. Poor response to initial hydration and antibiotics as blood pressure remained fluctuant borderline low prompted evaluation. Random cortisol at 6: 50am showed hypocortisolism (1.6mcg/dl) and TSH 1.290 mcIU/mL (n 0.358- 3.74mcIU/mL); patient was started on stress dose steroids and endocrinology was consulted for suspected adrenal insufficiency. Cosyntropin stimulation test (n >18 mcg/dL) with baseline cortisol levels 1.6mcg/dl and ACTH less than 5mcg/dl; cortisol levels at 30 minutes after 250 mcg of Cosyntropin was 4.3mcg/dl and at 1 hour 6.8mcg/dl, confirming most likely secondary vs primary adrenal insufficiency. Within 24-48 hour stress dose steroids were weaned and the patient was then discharged home with hydrocortisone 20 mg am and 10mg pm for further outpatient management. Conclusion Pembrolizumab is a human programmed death receptor-1-blocking antibody that on October 2015 was FDA approved for treatment of non-small cell lung cancer. Adrenal Insufficiency can cause a broad nonspecific clinical scenario with reported incidence of 0.6-0.7% pembrolizumab-induced AI. This rare clinical entity adrenal insufficiency immune mediated endocrinopathy by pembrolizumab constitutes an emergency that prompts attention for early identification and initial management. Nevertheless increased morbidity and mortality is associated with acute adrenal crisis encouraging physicians to be aware of this particular risk. Presentation: Saturday, June 11, 2022 1:00 p.m. - 3:00 p.m.

LBODP019 Vitamin D Levels In A Population With Type 2 Diabetes

Abstract Background Little is known about the impact of over-the-counter ketone supplementation, used by patients to promote weight loss, on ketosis and serum ketone values. Recent literature suggests that acute ingestion of exogenous ketones leads to increased blood beta-hydroxybutyrate and decreased blood glucose1. Clinical Case A 61-year-old man with a history of type 2 diabetes mellitus, atrial fibrillation, hypertension, and hyperlipidemia presented as a transfer to the neurocritical care ICU from an outside hospital for subarachnoid hemorrhage secondary to intracranial saccular aneurysm. His admission hemoglobin A1c was 9.9% (ref 4.4-5.6), blood glucose was 205 mg/dL (ref 70-99), beta-hydroxybutyrate was markedly elevated at 26.2 mg/dL (ref 0-3), and urinalysis showed 80mg/dL ketones (ref 0). Serum toxicology screen was notable for detectable acetone 8mg/dL (ref: none detected). His lactate was 2 mmol/L (ref 0.5-1.9), Cr 0.99mg/dL (0.67-1.17), and HCO3 22 mmol/L (ref 22-27). Arterial blood gas showed pH of 7.37 (ref 7.38-7.47), and an anion gap metabolic acidosis (AGMA) of 15 mmol/L (ref <12). Given the patient's profound ketosis, hyperglycemia, and mild AGMA, the patient was started on an insulin drip for presumed diabetic ketoacidosis (DKA). After 4 hours, the patient's anion gap had decreased to 12mmcol/L. The following day, he was transitioned to basal/bolus insulin, and underwent embolization of his cerebral aneurysm. After further recovery, Endocrinology was consulted for insulin recommendations. The patient denied any prior history of DKA or use of any SGLT2-inhibitors, and denied decreased oral intake or vomiting prior to admission. He did report taking ketone supplements, "Keto Strong: Ketogenic Weight Management – Advanced Formulation," two tabs (700mg "proprietary keto blend") BID for 2-3 years with ingredients listed as: sodium beta-hydroxybutyrate, calcium beta-hydroxybutyrate, magnesium beta-hydroxybutyrate, medium chain triglyceride oil, L-arginine, alpha-ketoglutaric acid, and 7-keto-dehydroepiandrosterone. Given a lack of acidosis, mild hyperglycemia, and mild lactic acidosis without risk factors for euglycemic DKA, it was suspected his profound ketosis out of proportion to clinical picture was secondary to ketone supplementation with a misdiagnosis of DKA. Conclusion This is one of the first cases to report profound ketosis in a hospitalized patient likely secondary to exogenous ketone supplementation. Ketosis secondary to nutritional supplementation should be considered once more common etiologies are ruled out. Additional research is needed to determine the role of exogenous ketone use on metabolism and glycemic control.

LBODP035 When Is Ketosis Just Ketosis?

Abstract Background Little is known about the impact of over-the-counter ketone supplementation, used by patients to promote weight loss, on ketosis and serum ketone values. Recent literature suggests that acute ingestion of exogenous ketones leads to increased blood beta-hydroxybutyrate and decreased blood glucose1. Clinical Case A 61-year-old man with a history of type 2 diabetes mellitus, atrial fibrillation, hypertension, and hyperlipidemia presented as a transfer to the neurocritical care ICU from an outside hospital for subarachnoid hemorrhage secondary to intracranial saccular aneurysm. His admission hemoglobin A1c was 9.9% (ref 4.4-5.6), blood glucose was 205 mg/dL (ref 70-99), beta-hydroxybutyrate was markedly elevated at 26.2 mg/dL (ref 0-3), and urinalysis showed 80mg/dL ketones (ref 0). Serum toxicology screen was notable for detectable acetone 8mg/dL (ref: none detected). His lactate was 2 mmol/L (ref 0.5-1.9), Cr 0.99mg/dL (0.67-1.17), and HCO3 22 mmol/L (ref 22-27). Arterial blood gas showed pH of 7.37 (ref 7.38-7.47), and an anion gap metabolic acidosis (AGMA) of 15 mmol/L (ref <12). Given the patient's profound ketosis, hyperglycemia, and mild AGMA, the patient was started on an insulin drip for presumed diabetic ketoacidosis (DKA). After 4 hours, the patient's anion gap had decreased to 12mmcol/L. The following day, he was transitioned to basal/bolus insulin, and underwent embolization of his cerebral aneurysm. After further recovery, Endocrinology was consulted for insulin recommendations. The patient denied any prior history of DKA or use of any SGLT2-inhibitors, and denied decreased oral intake or vomiting prior to admission. He did report taking ketone supplements, "Keto Strong: Ketogenic Weight Management – Advanced Formulation," two tabs (700mg "proprietary keto blend") BID for 2-3 years with ingredients listed as: sodium beta-hydroxybutyrate, calcium beta-hydroxybutyrate, magnesium beta-hydroxybutyrate, medium chain triglyceride oil, L-arginine, alpha-ketoglutaric acid, and 7-keto-dehydroepiandrosterone. Given a lack of acidosis, mild hyperglycemia, and mild lactic acidosis without risk factors for euglycemic DKA, it was suspected his profound ketosis out of proportion to clinical picture was secondary to ketone supplementation with a misdiagnosis of DKA. Conclusion This is one of the first cases to report profound ketosis in a hospitalized patient likely secondary to exogenous ketone supplementation. Ketosis secondary to nutritional supplementation should be considered once more common etiologies are ruled out. Additional research is needed to determine the role of exogenous ketone use on metabolism and glycemic control.

LBSUN289 Ketonuria — A Possible Early Indicator Of Impending Euglycemic DKA In Setting Of Recent SGLT-2 Inhibitor Use And Acute Stress

Abstract Introduction - Euglycemic DKA is a notorious entity; previously thought to be primarily afflicting type 1 diabetics and rarely type 2 diabetics in a state of relative insulin deficiency, it has now become a major cause of concern and lead to the issuance of FDA warning in 2015 with regards to its link with SGLT-2 inhibitors. Although DKA is characterized by hyperglycemia, metabolic acidosis and ketogenesis, euglycemic DKA poses a diagnostic challenge as it remains disguised under the cover of euglycemia. Moreover, in the setting of recent SGLT-2 inhibitor use, this definition becomes even more of a paradox as SGLT-2 inhibitors, by the virtue of their action, promote ketogenesis thereby further adding to this enigma. Case presentation - A 67 year old male with hypertension and diabetes mellitus type 2 (on Metformin and Empagliflozin) presented to the emergency room with dizziness. He woke up to go to the bathroom that day and felt weak, dizzy and like he was going to fall. He endorsed nausea and vomiting but denied headache, fever, chills, chest pain, shortness of breath, abdominal pain, and problems with urination/bowel movements. He was afebrile and hemodynamically stable. On examination, left sided dysmetria, loss of coordination, and axial imbalance were noted. No motor/sensory deficits. Labs were significant for WBC count 10 k/mm cu (4 - 11), Creatinine 0.78 mg/dL (0.7 - 1.3), Glucose 279 mg/dL (70 - 99), Bicarbonate 21 mmol/L (21 -31), Anion gap 19 mmol/L (6 - 14), and Lactate 3.2 mmol/L (0.7 - 2). Urinalysis showed glucosuria (glucose >500 mg/dL) and ketonuria (ketones 20 mg/dl). CT head was negative but MRI brain showed left inferior cerebellar peduncle acute ischemic infarct. Stroke protocol was initiated and he transferred to telemetry. The next day, labs showed Glucose 166, Bicarbonate 13, Anion gap 21, and Ketones 5.6 mmol/L (<0.6). Since blood glucose levels remained less than 250 mg/dl with concurrent anion gap metabolic acidosis in the setting of recent Empagliflozin use, he was transferred to ICU for insulin infusion for management of euglycemic diabetic ketoacidosis. Subsequently, he was transitioned to a basal-bolus insulin regimen and transferred to the floors. Discussion - SGLT-2 inhibitors reduce renal tubular glucose reabsorption, causing glycosuria, and promote ketonemia directly by enhancing ketogenesis via glucagon secretion from the pancreatic alpha cells and indirectly by decreasing the renal clearance of ketone bodies. In the setting of acute stress, such as stroke in our patient, and recent SGLT-2 inhibitor use, the presence of ketonuria should be recognized as an early ominous warning sign for euglycemic DKA. A targeted approach detailing diagnostic and therapeutic interventions should be designed to halt its progression in its track before it transforms into the dreaded euglycemic DKA. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

Anion Gap Metabolic Acidosis due to Lactate Production in the Setting of Metformin Poisoning

Anion Gap Metabolic Acidosis due to Lactate Production in the Setting of Metformin Poisoning

PSUN251 Euglycemic DKA In A Patient Undergoing Major Surgery

Abstract Background Euglycemic DKA represents a diagnostic challenge as a lack of hyperglycemia can lead to a delay in recognition and administration of appropriate treatment. We present a case of euglycemic DKA in the setting of starvation and surgical stress in a patient with type 2 diabetes without SGLT2 inhibitor use. Clinical Case A 61-year-old type 2 diabetic woman presented with a two-day history of vomiting associated with abdominal pain. She was previously treated with glipizide, metformin, and sitagliptin, which had been discontinued months ago due to poor oral intake. CT imaging demonstrated a 12.4×11.2×10.5 cm pelvic mass with ascites and omental nodularity in the setting of a history of prior right granulosa cell tumor and mature cystic teratoma status post total abdominal hysterectomy with bilateral salpingo-oophorectomy. The patient subsequently developed hematemesis on hospital day 7, for which she was made NPO. She underwent EGD which demonstrated severe esophagitis and duodenitis. She was given an oral diet for one day, prior to resuming NPO status on hospital day 10 for exploratory laparotomy and tumor debulking. On hospital day 11, the patient's labs were notable for an anion gap metabolic acidosis (pH 7.26, n 7.4; CO2 16 mmol/L, n 20-31 mmol/L; anion gap 15 mmol/L, n 5-15 mmol/L), elevated beta-hydroxybutyrate (5.5 mmol/L, n 0.02-0.27 mmol/L), and a blood glucose range of 141-233 mg/dL (n 65-140 mg/dL). The patient was not on any scheduled insulin other than a low dose correctional scale with Lispro subcutaneously pre-meals and had not used SGLT2 inhibitors. There was no suspicion for alcohol toxicity or other poisoning given that the patient had been hospitalized. The lactate level was normal. Thus, the patient met criteria for euglycemic DKA likely secondary to prolonged fasting, exacerbated by the stress of major surgery. The patient was started on an insulin drip with dextrose infusion until the metabolic parameters improved, and she was transitioned to subcutaneous insulin. In diabetic patients unable to tolerate enteral nutrition or with enteral nutrition delays due to surgery, initiation of parenteral nutrition may prevent progression to euglycemic DKA. Ultimately, her pathology was consistent with metastatic granulosa cell tumor, and she was discharged to subacute rehabilitation. Conclusion Euglycemic DKA may be overlooked due to normoglycemia leading to a delay in the diagnosis and appropriate management. It is a medical emergency and should be treated with an intravenous insulin infusion and dextrose. It can be prevented in diabetic patients undergoing major surgical stress by ensuring adequate nutritional support.Reference: Modi, A., Agrawal, A. and Morgan, F., 2017. Euglycemic diabetic ketoacidosis: a review. Current diabetes reviews, 13(3), pp.315-321. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

ODP043 Hypokalemia in Autoimmune Polyglandular Syndrome: A Case of Newfound Type I (Distal) Renal Tubular Acidosis

Abstract Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy Type 1 (APECED) is a rare autosomal recessive disorder predisposing to early development of chronic mucosal candidiasis and progressive development of various endocrinopathies, such as Addison's disease, Primary Hypoparathyroidism, and Type 1 Diabetes (T1D). Few cases described in literature regarding renal involvement in this disorder, with most common manifestation being tubulo-interstitial nephritis, however, there is limited evidence regarding presentation of APECED with hypokalemia due to concomitant Type I Renal Tubular Acidosis (RTA). Case of a 47-year-old female with past medical history of APECED Type 1 (consisting of hypoparathyroidism, adrenal insufficiency, and chronic mucocutaneos candidiasis), T1DM on honeymoon, hypothyroidism, and nephrolithiasis presenting to the emergency department complaining of bilateral upper and lower extremity weakness of one week in evolution, but worsening on day of admission. Denies associated constitutional symptoms. Strong positive first-degree relative history for autoimmune diseases. Physical examination: 2/5 strength in all four extremities, deep tendon reflexes grossly intact, no gross sensory or motor deficits. Patient on oral steroid therapy for her Addison's, calcitriol supplementation for hypoparathyroidism, and potassium chloride supplementation since a prior hypokalemic episode 17 years ago. Laboratory workup results remarkable for sodium: 140 mmol/L (N: 135-144 mmol/L), chloride: 110 mmol/L (N: 95-105 mmol/L), potassium: 2. 0 mmol/L (N: 3.4-4.5 mmol/L), central bicarbonate: 18mmol/L (N: 23-31 mmol / L), anion gap: 12 (N: 10-12), glycosylated hemoglobin: 5.2% (N: 4.7-6.2%) and anti-glutamic acid decarboxylase antibodies >25,000 U/mL (N: <5 U/mL). Adrenal insufficiency was ruled out by laboratory findings, but she had normal anion gap metabolic acidosis (NAGMA) and hypokalemia. Urinalysis was negative for urinary tract infection but with pH: 7. 0 (N: 4.5-8. 0). Urine spots, measured to find the cause of her NAGMA, showed urine sodium: 92 mmol/L, urine potassium: 10 mmol/L, urine chloride: 90 mmol/L, and urine anion gap of 12 mEq/L, which is positive and suggests low urinary NH4+, consistent with Type I (Distal) RTA as the main etiology. Patient started on IV potassium replacement, which increased potassium to 3.8 mmol/L, and improved acidotic state, with central bicarbonate of 29mmol/L, and overall symptoms. Patient was discharged home with alkali therapy (Sodium citrate) for Type I (Distal) RTA. RTA is an underrecognized condition that may be inherited or acquired. Diagnosis is difficult but can be verified with a thoughtful workup. RTA should be considered for any patient with otherwise unexplained hyperchloremic metabolic acidosis and may be the presenting manifestation of autoimmune diseases. Regular renal monitoring for any APECED patient should be performed. We present this case as evidence for the coexistence of several different immune-mediated diseases in the clinical context of APECED with an unusual concomitant Type I (Distal) RTA, where there is few documented evidence of association with this disorder. Presentation: No date and time listed

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 <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 <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

Radiology Findings in a Case of Acute Methanol Intoxication Complicated with Intracranial Hemorrhage

Aim: Methanol intoxication is rare and it can be fatal. This case report aimed to describe the radiological findings in acute methanol intoxication complicated with intracranial hemorrhage in a young patient. Case Report: A 32 year-old man applied to emergency department with a major complaints of nausea, vomiting, double vision, and confusion. Glascow coma score (GCS) was 7 at the initial referral. Laboratory tests showed high anion gap metabolic acidosis. Acute methanol intoxication was diagnosed by aid of the patient anamnesis. Diffusion-weighted MRI (DW-MRI) showed similar diffusion restriction lesions in the putamen and cingulate gyrus of both cerebral hemispheres. The patient had a cardiac arrest during follow-up in the emergency department. He was converted to sinus rhythm with the interventions, intubated, and taken to the intensive care unit. GCS reduced to 3 during follow- up at the 4th day. Cerebral intraparanchimal hemorrhage at the level of left basal ganglia was observed in the brain computed tomography (CT). He was operated however remained comatose after the operation and died at the 8th day of admission. Conclusion: Possibility of methanol intoxication should be included in the differential diagnosis in patients with altered consciousness, vision disturbances and a high anion gap admitted to the emergency service. DW-MRI may be helpful in diagnosis by detecting symmetrical diffusion restrictions at the basal ganglia. Additionally radiologic methods like CT can be used to determine complications such as bleeding that may occur during the follow-up of the cases.

Acil Servise Başvuran Metil Alkol Zehirlenmelerinin Geriye Dönük Analizi

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

ELEVATED ANION GAP AS A MARKER OF SEVERE SARS-COV-2 INFECTION IN PREGNANT PATIENTS WITHOUT DIABETES: A CASE SERIES

ELEVATED ANION GAP AS A MARKER OF SEVERE SARS-COV-2 INFECTION IN PREGNANT PATIENTS WITHOUT DIABETES: A CASE SERIES

A CASE REPORT OF SYNCHRONOUS MULTIFOCAL NECROTIZING FASCIITIS DUE TO CLOSTRIDIUM SEPTICUM IN AN IMMUNOCOMPROMISED HOST

A CASE REPORT OF SYNCHRONOUS MULTIFOCAL NECROTIZING FASCIITIS DUE TO CLOSTRIDIUM SEPTICUM IN AN IMMUNOCOMPROMISED HOST

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

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

RARE CASE OF A NONTRAUMATIC LEFT MAIN BRONCHIAL TEAR

RARE CASE OF A NONTRAUMATIC LEFT MAIN BRONCHIAL TEAR

RARE CASE OF SEVERE NECROTIZING PNEUMONIA DUE TO STREPTOCOCCUS PYOGENES RESULTING IN REFRACTORY HYPOXEMIA

RARE CASE OF SEVERE NECROTIZING PNEUMONIA DUE TO STREPTOCOCCUS PYOGENES RESULTING IN REFRACTORY HYPOXEMIA

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING

HOW LOW CAN YOU GO: RECOVERY AFTER A SERUM PH OF 6.62 DUE TO ETHYLENE GLYCOL POISONING