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Metformin Overdose Medscape

Fatal Metformin Overdose Presenting With Progressive Hyperglycemia

Fatal Metformin Overdose Presenting With Progressive Hyperglycemia

Author Affiliation Jeffrey R. Suchard, MD Department of Emergency Medicine, University of California, Irvine School of Medicine Thomas A. Grotsky, MD Department of Emergency Medicine, University of California, Irvine School of Medicine ABSTRACT A 29-year-old man with no history of diabetes ingested over 60 grams of metformin in a suicide attempt. He presented to the emergency department with acute renal insufficiency, severe lactic acidosis, and rapidly-progressive hyperglycemia. The patient’s peak serum glucose level of 707 mg/dL is the highest yet reported in a case of metformin toxicity. Treatment included sodium bicarbonate infusion and hemodialysis, but the patient suffered several cardiac arrests with pulseless electrical activity and ultimately expired 25 hours after the ingestion. INTRODUCTION Metformin is a biguanide anti-hyperglycemic drug which is the most commonly prescribed oral agent to treat diabetes mellitus.1 Metformin-associated lactic acidosis (MALA) occurs infrequently with therapeutic use, occurring in 0.03 cases per 1000 patient-years.2 This rate is substantially lower than the incidence of phenformin-associated lactic acidosis, which caused that biguanide drug to be withdrawn from the U.S. market in the late 1970s.2–4 In overdose situations, however, metformin is frequently associated with lactic acidosis.3,5–15 Because the biguanide drugs do not enhance insulin release, as occurs with the sulfonylurea and meglitinide classes of diabetes medications, disorders of glucose homeostasis are rare with metformin. Although hypoglycemia associated with metformin has been reported, it is uncommon and often ascribed to concurrent use of other diabetes drugs.3,14,16 Hyperglycemia associated with metformin toxicity is even more rare, and has previously Continue reading >>

Metformin - Oral, Glucophage

Metformin - Oral, Glucophage

are allergic to dapagliflozin or any of the ingredients in FARXIGA. Symptoms of a serious allergic reaction may include skin rash, raised red patches on your skin (hives), swelling of the face, lips, tongue, and throat that may cause difficulty in breathing or swallowing. If you have any of these symptoms, stop taking FARXIGA and contact your healthcare provider or go to the nearest hospital emergency room right away have severe kidney problems or are on dialysis. Your healthcare provider should do blood tests to check how well your kidneys are working before and during your treatment with FARXIGA Dehydration (the loss of body water and salt), which may cause you to feel dizzy, faint, lightheaded, or weak, especially when you stand up (orthostatic hypotension). You may be at a higher risk of dehydration if you have low blood pressure; take medicines to lower your blood pressure, including water pills (diuretics); are 65 years of age or older; are on a low salt diet, or have kidney problems Ketoacidosis occurred in people with type 1 and type 2 diabetes during treatment with FARXIGA. Ketoacidosis is a serious condition which may require hospitalization and may lead to death. Symptoms may include nausea, tiredness, vomiting, trouble breathing, and abdominal pain. If you get any of these symptoms, stop taking FARXIGA and call your healthcare provider right away. If possible, check for ketones in your urine or blood, even if your blood sugar is less than 250 mg/dL Kidney problems. Sudden kidney injury occurred in people taking FARXIGA. Talk to your doctor right away if you reduce the amount you eat or drink, or if you lose liquids; for example, from vomiting, diarrhea, or excessive heat exposure Serious urinary tract infections (UTI), some that lead to hospitalization, occu Continue reading >>

Overdose Of Oral Antidiabetic Medications And Insulin

Overdose Of Oral Antidiabetic Medications And Insulin

Overdose of Oral Antidiabetic Medications and Insulin Authors: Diana Strasburger, MD, RDMS, Attending Physician, Department of Emergency Medicine, Advocate Christ Medical Center, Oak Lawn, IL. Janna H. Villano, MD, Resident Physician, Department of Emergency Medicine, Advocate Christ Medical Center, Oak Lawn, IL. Peer Reviewer: Gina Piazza, DO, Associate Professor of Emergency Medicine, Georgia Health Sciences University, Augusta, GA. — Sandra M. Schneider, MD, Editor Treating the hypoglycemia and metabolic derangements caused by antidiabetic medications, especially in massive overdose, are dynamic as new agents are introduced. Emergency physicians should know potential pitfalls in order to effectively and safely manage these patients, avoiding rebound hypoglycemia and premature discharge without appropriate monitoring. This article will review the clinical presentation and management of toxicity from commercially available antidiabetic agents in the United States, including oral hypoglycemic agents such as sulfonylureas and oral antihyperglycemic agents such as biguanides, as well as novel antidiabetic agents and insulin. Introduction Diabetes mellitus (DM) is an ever-increasing epidemic facing the current health care system. Its prevalence is increasing worldwide from an estimated 30 million in 1985 to 150 million in 2000, 171 million in 2007, and an anticipated 366 million in 2030.1,2 Medications used to treat diabetes are diverse, and often patients use multiple classes of medications to obtain euglycemia. Oral preparations can be divided into two categories based on their pharmacodynamics and effect or lack of an effect on insulin: hypoglycemic agents such as sulfonylureas and meglitinides; and antihyperglycemic agents such as biguanides, alpha-glucosidase inhibi Continue reading >>

Oral Hypoglycemic Agent Toxicity

Oral Hypoglycemic Agent Toxicity

Oral hypoglycemic agentssulfonylureaswhich are used to treat patients with type 2 diabetes,[1] are among the most widely prescribed medications in the world. Wide availability of these medications increases the potential for either intentional or unintentional overdose in pediatric and adult populations.[2] First-generation sulfonylurea compounds became widely available in 1955. They are acetohexamide, chlorpropamide, tolazamide, and tolbutamide. First-generation agents have long half-lives (eg, 49 hours for chlorpropamide). Second-generation sulfonylureas were introduced in 1984 and include glipizide, glyburide, and glimepiride. Second-generation sulfonylureas are more potent and have shorter half-lives than the first-generation sulfonylureas. Other agents besides sulfonylureas are used to treat type 2 diabetes, including biguanides, alpha-glucosidase inhibitors, and thiazolidinediones. Metformin (Glucophage in the United States), a biguanide, is one such agent.[3] Even in overdose, these agents do not decrease serum glucose below euglycemia; consequently, they are appropriately referred to as antihyperglycemic agents rather than hypoglycemic agents. Although overdose of antihyperglycemic agents can have dangerous adverse effects (for example, lactic acidosis from metformin[4] ), this article focuses on acute overdose of sulfonylureas. Hypoglycemia from sulfonylureas can result from small doses, can be delayed in onset, and can be persistent. Prolonged observation and intensive care to restore and maintain euglycemia may be required.[5] (See Treatment and Medication.) Sulfonylureas are sulfonamide derivatives but do not have any antibacterial activity. The exact mechanism of sulfonylureas' hypoglycemic effect remains to be elucidated. These drugs are mainly effective Continue reading >>

Systemic Effects Of Oral Glucocorticoids

Systemic Effects Of Oral Glucocorticoids

This activity is intended for physicians, nurses, respiratory therapists, and other healthcare providers caring for patients with allergies. The goal of this activity is to review new information to better understand the challenges of managing patients with asthma and allergic rhinitis. Analyze the action of corticosteroids and their formulations as they apply to a 1-airway concept in treatment for allergic diseases Review recent advances with targeted inhaled corticosteroids and their impact on systemic side effects Recognize the benefits and risks of glucocorticoids as well as the management of patients on glucocorticoid therapy As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content. Associate Professor of Clinical Medicine, Jefferson Medical College, Philadelphia, Pennsylvania; Staff Physician, Thomas Jefferson Hospital, Philadelphia, Pennsylvania Disclosure: Serge Jabbour, MD, FACP, FACE, has disclosed no relevant financial relationships. Medscape, LLC is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. Medscape, LLC designates this educational activity for a maximum of 1.0 AMA PR Continue reading >>

What Are The Possible Side Effects Of Glyburide And Metformin (glucovance)?

What Are The Possible Side Effects Of Glyburide And Metformin (glucovance)?

A A A Medications and Drugs Brand Names: Glucovance Generic Name: glyburide and metformin (Pronunciation: GLYE bure ide and met FOR min) What is the most important information I should know about glyburide and metformin (Glucovance)? What is glyburide and metformin (Glucovance)? Glyburide and metformin is a combination of two oral diabetes medicines that help control blood sugar levels. Glyburide and metformin is used to treat type 2 diabetes. This medication is not for treating type 1 diabetes. Glyburide and metformin may also be used for purposes not listed in this medication guide. This medication may cause lactic acidosis (a build-up of lactic acid in the body, which can be fatal). Lactic acidosis can start slowly and get worse over time. Get emergency medical help if you have even mild symptoms of lactic acidosis, such as: muscle pain or weakness, numb or cold feeling in your arms and legs, trouble breathing, stomach pain, nausea with vomiting, slow or uneven heart rate, dizziness, or feeling very weak or tired. Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficult breathing; swelling of your face, lips, tongue, or throat. Stop using this medicine and call your doctor at once if you have a serious side effect such as: pale or yellowed skin, dark colored urine, fever, confusion or weakness; or nausea, upper stomach pain, itching, loss of appetite, clay-colored stools, jaundice (yellowing of the skin or eyes). Less serious side effects may include: sneezing, runny nose, cough or other signs of a cold; headache, mild dizziness; or mild dizziness; or mild nausea or vomiting, diarrhea, upset stomach. This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You Continue reading >>

Metformin In Patients With Type 2 Diabetes And Kidney Disease

Metformin In Patients With Type 2 Diabetes And Kidney Disease

Go to: Abstract Metformin is widely viewed as the best initial pharmacological option to lower glucose concentrations in patients with type 2 diabetes mellitus. However, the drug is contraindicated in many individuals with impaired kidney function because of concerns of lactic acidosis. To assess the risk of lactic acidosis associated with metformin use in individuals with impaired kidney function. In July 2014, we searched the MEDLINE and Cochrane databases for English-language articles pertaining to metformin, kidney disease, and lactic acidosis in humans between 1950 and June 2014. We excluded reviews, letters, editorials, case reports, small case series, and manuscripts that did not directly pertain to the topic area or that met other exclusion criteria. Of an original 818 articles, 65 were included in this review, including pharmacokinetic/metabolic studies, large case series, retrospective studies, meta-analyses, and a clinical trial. Although metformin is renally cleared, drug levels generally remain within the therapeutic range and lactate concentrations are not substantially increased when used in patients with mild to moderate chronic kidney disease (estimated glomerular filtration rates, 30-60 mL/min per 1.73 m2). The overall incidence of lactic acidosis in metformin users varies across studies from approximately 3 per 100 000 person-years to 10 per 100 000 person-years and is generally indistinguishable from the background rate in the overall population with diabetes. Data suggesting an increased risk of lactic acidosis in metformin-treated patients with chronic kidney disease are limited, and no randomized controlled trials have been conducted to test the safety of metformin in patients with significantly impaired kidney function. Population-based studies d Continue reading >>

Metformin Medscape Lose

Metformin Medscape Lose

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Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Introduction A 49-year-old man presented to the emergency department complaining of dyspnea for 2 days. He had a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and a severe dilated cardiomyopathy. He had been hospitalized several times in the previous year for decompensated congestive heart failure (most recently, 1 month earlier). The plasma creatinine concentration was 1.13 mg/dl on discharge. Outpatient medications included insulin, digoxin, warfarin, spironolactone, metoprolol succinate, furosemide (80 mg two times per day; increased from 40 mg daily 1 month earlier), metolazone (2.5 mg daily; added 1 month earlier), and metformin (2500 mg in three divided doses; increased from 1000 mg 1 month earlier). Physical examination revealed an obese man in moderate respiratory distress. The temperature was 36.8°C, BP was 119/83 mmHg, and heart rate was 96 per minute. Peripheral hemoglobin oxygen saturation was 97% on room air, with a respiratory rate of 26 per minute. The heart rhythm was irregularly irregular; there was no S3 or murmur. Jugular venous pressure was about 8 cm. There was 1+ edema at the ankles. A chest radiograph showed cardiomegaly and central venous prominence. The N-terminal pro-B-type natriuretic peptide level was 5137 pg/ml (reference range = 1–138 pg/ml). The peripheral hemoglobin concentration was 12.5 g/dl, the white blood cell count was 12,500/µl (76% granulocytes), and the platelet count was 332,000/µL. Initial plasma chemistries are shown in Table 1. The impression was decompensated congestive heart failure. After administration of furosemide (160 mg intravenously), the urine output increased to 320 ml over the next 1 hour. There was no improvement in the dyspnea. Within 2 hours, the patient’s BP fell to 100/64 mmHg Continue reading >>

Practice Essentials

Practice Essentials

Hypoglycemia is characterized by a reduction in plasma glucose concentration to a level that may induce symptoms or signs such as altered mental status and/or sympathetic nervous system stimulation. This condition typically arises from abnormalities in the mechanisms involved in glucose homeostasis. The most common cause of hypoglycemia in patients with diabetes is injecting a shot of insulin and skipping a meal or overdosing insulin. The image below depicts a diagnostic algorithm for hypoglycemia. Signs and symptoms The glucose level at which an individual becomes symptomatic is highly variable (threshold generally at < 50 mg/dL). Carefully review the patient's medication and drug history for potential causes of hypoglycemia (eg, new medications, insulin usage or ingestion of an oral hypoglycemic agent, possible toxic ingestion). The patient’s medical and/or social history may reveal the following: Diabetes mellitus, renal insufficiency/failure, alcoholism, hepatic cirrhosis/failure, other endocrine diseases, or recent surgery Central nervous system: Headache, confusion, personality changes Ethanol intake and nutritional deficiency Weight reduction, nausea and vomiting Neurogenic or neuroglycopenic symptoms of hypoglycemia may be categorized as follows: Neurogenic (adrenergic) (sympathoadrenal activation) symptoms: Sweating, shakiness, tachycardia, anxiety, and a sensation of hunger Neuroglycopenic symptoms: Weakness, tiredness, or dizziness; inappropriate behavior (sometimes mistaken for inebriation), difficulty with concentration; confusion; blurred vision; and, in extreme cases, coma and death Reactive hypoglycemic include the following features: More common in overweight and obese people who are insulin-resistant Possible higher risk in patients with a family his Continue reading >>

Lactic Acidosis, Hypotension, And Sensorineural Hearing Loss Following Intentional Metformin Overdose

Lactic Acidosis, Hypotension, And Sensorineural Hearing Loss Following Intentional Metformin Overdose

Lactic Acidosis, Hypotension, and Sensorineural Hearing Loss Following Intentional Metformin Overdose Author(s): Dale K. Miller , Amanda J. Brinson , Glenn Catalano , Maria C. Catalano . Mental Health and Behavioral Sciences Service, James A. Haley Veterans Hospital, 13000 Bruce B. Downs Boulevard tA, Tampa, Florida 33612, USA. Metformin and glyburide are antihyperglycemic agents that are widely used in the United States. There have been several cases of overdose of these medications reported in the world literature. Glyburide overdose is associated with hypoglycemia that can be severe, while metformin overdoses have been associated with lactic acidosis. In many cases of metformin overdose, lactic acidosis has led to profound hypotension and respiratory failure. In this article we will present the case of a 49-year-old man who ingested 52 grams of metformin and 350 mg of glyburide in a suicide attempt. The patient developed hypoglycemia, lactic acidosis, hypotension, respiratory failure and a profound sudden sensorineural hearing loss. We discuss prior cases of overdose with these agents, and the connection between overdose and the development of sudden sensorineural hearing loss. Keywords: Deafness, glyburide, metformin, overdose, poisoning, toxicity, hypotension, lactic acidosis Title: Lactic Acidosis, Hypotension, and Sensorineural Hearing Loss Following Intentional Metformin Overdose Author(s):Dale K. Miller, Amanda J. Brinson, Glenn Catalano and Maria C. Catalano Affiliation:Mental Health and Behavioral Sciences Service, James A. Haley Veterans Hospital, 13000 Bruce B. Downs Boulevard tA, Tampa, Florida 33612, USA. Keywords:Deafness, glyburide, metformin, overdose, poisoning, toxicity, hypotension, lactic acidosis Abstract: Metformin and glyburide are anti Continue reading >>

Toxicology Of Oral Antidiabetic Medications

Toxicology Of Oral Antidiabetic Medications

Toxicology of Oral Antidiabetic Medications Am J Health Syst Pharm.2006;63(10):929-938. In 1996, the Food and Drug Administration approved the labeling for metformin (dimethylbiguanide), the only biguanide currently available in the United States. Phenformin, the other previously available biguanide, was withdrawn from the market in 1977 because of an association with lactic acidosis. Buformin, another biguanide, is not available in the United States. The complex of mechanisms of action of metformin is multifaceted but appears to include delayed glucose absorption, increased intestinal glucose utilization, increased intestinal lactate production, inhibition of hepatic gluconeogenesis, decreased lipid oxidation, decreased free fatty acid concentration, and increased peripheral insulin-related glucose uptake.[ 70 ] Metformin absorption is incomplete, with 20-30% found in the feces. Oral bioavailability is 40-60%, depending on the dose ingested, with greater doses producing lower bioavailability.[ 71 ] The reduced bioavailability may result from the drug binding by the intestinal wall.[ 72 ] The rate of absorption is slower than the rate of elimination, which makes absorption a rate-limiting step in the elimination half-life.[ 73 , 74 ] Absorption, in therapeutic doses, is expected to be complete in 6 hours. In an overdose situation involving massive doses, absorption may be prolonged. About 90% of the absorbed metformin is eliminated through the kidneys within the first 24 hours in patients with normal renal function.[ 72 ] Metformin has no metabolites. Metformin is the second most commonly prescribed oral antidiabetic medication in both monotherapy and combination therapy.[ 11 ] In 2004, metformin had the highest number of reports to U.S. poison control centers and the Continue reading >>

Repaglinide-metformin Hcl

Repaglinide-metformin Hcl

This diabetes medication is a combination of 2 drugs ( repaglinide and metformin ). It is used along with a diet and exercise program to control high blood sugar in patients with type 2 diabetes . Repaglinide works by stimulating the release of your body's natural insulin . Metformin is a biguanide and works by decreasing the amount of sugar that your liver makes and that your stomach / intestines absorb. Both of these medications work by helping to restore your body's proper response to the insulin you naturally produce. Controlling high blood sugar helps prevent kidney damage, blindness, nerve problems, loss of limbs, and sexual function problems. Proper control of diabetes may also lessen your risk of a heart attack or stroke . Take this medication by mouth 15 minutes before a meal, usually 2-3 times a day or as directed by your doctor. Take this drug no earlier than 30 minutes before the meal. You may also take it just before the meal if necessary. Do not take a dose of medication if you are skipping a meal. Drink plenty of fluids while taking this medication unless otherwise directed by your doctor. The dosage is based on your medical condition, response to treatment, and other medications you may be taking. Be sure to tell your doctor and pharmacist about all the products you use (including prescription drugs , nonprescription drugs, and herbal products). To reduce your risk of side effects (such as upset stomach ), your doctor may direct you to start this medication at a low dose and gradually increase your dose. Follow your doctor's instructions carefully. If you are changing from a different diabetes drug (such as chlorpropamide ), follow your doctor's directions carefully for stopping the old drug and starting this combination medication. Use this medication Continue reading >>

Type 2 Diabetes Mellitus Medication

Type 2 Diabetes Mellitus Medication

Medication Summary Pharmacologic therapy of type 2 diabetes has changed dramatically in the last 10 years, with new drugs and drug classes becoming available. These drugs allow for the use of combination oral therapy, often with improvement in glycemic control that was previously beyond the reach of medical therapy. Agents used in diabetic therapy include the following: Traditionally, diet modification has been the cornerstone of diabetes management. Weight loss is more likely to control glycemia in patients with recent onset of the disease than in patients who are significantly insulinopenic. Medications that induce weight loss, such as orlistat, may be effective in highly selected patients but are not generally indicated in the treatment of the average patient with type 2 diabetes mellitus. Patients who are symptomatic at initial presentation with diabetes may require transient treatment with insulin to reduce glucose toxicity (which may reduce beta-cell insulin secretion and worsen insulin resistance) or an insulin secretagogue to rapidly relieve symptoms such as polyuria and polydipsia. Continue reading >>

Oral Hypoglycemic Agent Toxicity

Oral Hypoglycemic Agent Toxicity

Practice Essentials Oral hypoglycemic agents—sulfonylureas—which are used to treat patients with type 2 diabetes, [1] are among the most widely prescribed medications in the world. Wide availability of these medications increases the potential for either intentional or unintentional overdose in pediatric and adult populations. [2] First-generation sulfonylurea compounds became widely available in 1955. They are acetohexamide, chlorpropamide, tolazamide, and tolbutamide. First-generation agents have long half-lives (eg, 49 hours for chlorpropamide). Second-generation sulfonylureas were introduced in 1984 and include glipizide, glyburide, and glimepiride. Second-generation sulfonylureas are more potent and have shorter half-lives than the first-generation sulfonylureas. Other agents besides sulfonylureas are used to treat type 2 diabetes, including biguanides, alpha-glucosidase inhibitors, and thiazolidinediones. Metformin (Glucophage in the United States), a biguanide, is one such agent. [3] Even in overdose, these agents do not decrease serum glucose below euglycemia; consequently, they are appropriately referred to as antihyperglycemic agents rather than hypoglycemic agents. Although overdose of antihyperglycemic agents can have dangerous adverse effects (for example, lactic acidosis from metformin [4] ), this article focuses on acute overdose of sulfonylureas. Hypoglycemia from sulfonylureas can result from small doses, can be delayed in onset, and can be persistent. Prolonged observation and intensive care to restore and maintain euglycemia may be required. [5] (See Treatment and Medication.) Continue reading >>

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