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Metformin Poisoning Management

Poisoning - Hypoglycaemic Agent - Kids Health Wa (pmh Ed Guidelines)

Poisoning - Hypoglycaemic Agent - Kids Health Wa (pmh Ed Guidelines)

Oral hypoglycaemic agents are used for type II diabetes mellitus (non-insulin dependent diabetes) Sulfonylurea agents increase pancreatic insulin secretion and are the most important cause of hypoglycaemic toxicity Modified-release preparations may delay onset of symptoms for up to 8-18 hours Metformin is a biguanide agent that acts by decreasing carbohydrate absorption from the gut, increasing glucose uptake in peripheral tissues in the presence of insulin, and reducing hepatic gluconeogenesis The thiazolidinedione agents act at a nuclear receptor to improve insulin sensitivity in adipose tissues, skeletal muscles and the liver. Minimal information is available regarding overdose. The sulfonylurea agents may cause prolonged and profound life-threatening hypoglycaemia after accidental paediatric ingestion or deliberate self-poisoning Large overdoses may require treatment for several days A single tablet in a toddler has the potential to cause life-threatening hypoglycaemia. The onset of hypoglycaemia may be delayed up to 18 hours after ingestion. Admission for a minimum of 12- 24 hours is indicated for blood glucose monitoring. Discharge from hospital should only occur in the daylight hours. Metformin ingestion is not associated with hypoglycaemia in normal patients, but may cause life-threatening lactic acidosis in large overdoses or in the presence of renal or cardiac failure, or when there are co-ingestants which impair renal perfusion. Haemodialysis resolves the acidosis as well as removing metformin from the blood Nausea and vomiting may occur in smaller overdoses Asymptomatic patients following accidental exposure to metformin do not require referral to hospital, decontamination or investigation Children who have taken an unintentional ingestion of up to 1700 mg Continue reading >>

Metformin Overdose: An Unusual Cause Of Severe Metabolic Acidosis Singh Y, Joshi Sc, Tayal I, Sharma N - Chrismed J Health Res

Metformin Overdose: An Unusual Cause Of Severe Metabolic Acidosis Singh Y, Joshi Sc, Tayal I, Sharma N - Chrismed J Health Res

Metformin is commonly used in the treatment of type 2 diabetes mellitus (DM). Severe lactic acidosis is a rare side effect of this drug. We present a 45-year-old man who deliberately took 30 g of metformin, presumably with suicidal intent. He had not eaten the previous night and presented with altered sensorium and recurrent seizures. He had profound metabolic acidosis at presentation with a pH of 7.06 and a low blood sugar of 44 mgs/dl. The patient was admitted in intensive care unit (ICU) with the suspicion of metformin-associated lactic acidosis. He developed irreversible renal failure, neurological deterioration and anemia. Despite of daily intensive hemodialysis and other supportive measures the patient expired 14 days later. Metformin overdose with renal failure and severe lactic acidosis have high mortality; hence, urgent medical consultation and treatment can be life saving in these patients. Keywords:Anemia, diabetes mellitus, metformin, metabolic acidosis, renal failure Singh Y, Joshi SC, Tayal I, Sharma N. Metformin overdose: An unusual cause of severe metabolic acidosis. CHRISMED J Health Res 2015;2:166-8 Singh Y, Joshi SC, Tayal I, Sharma N. Metformin overdose: An unusual cause of severe metabolic acidosis. CHRISMED J Health Res [serial online] 2015 [cited2018 Apr 1];2:166-8. Available from: Overdose with antidiabetic drugs often requires intensive care treatment and prolonged hospital stays. They can potentially contribute to increase in morbidity and mortality. [1] Metformin is considered a relatively safe oral hypoglycemic agent, although biguanides are well known to cause profound lactic acidosis. [2] However, there are only limited descriptions of metformin overdose in the literature despite its well-recognized potentially fatal side effect. [3] If ta Continue reading >>

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Metformin-related Lactic Acidosis: Case Report - Sciencedirect

Open Access funded by Sociedad Colombiana de Anestesiologa y Reanimacin Lactic acidosis is defined as the presence of pH <7.35, blood lactate >2.0mmol/L and PaCO2 <42mmHg. However, the definition of severe lactic acidosis is controversial. The primary cause of severe lactic acidosis is shock. Although rare, metformin-related lactic acidosis is associated with a mortality as high as 50%. The treatment for metabolic acidosis, including lactic acidosis, may be specific or general, using sodium bicarbonate, trihydroxyaminomethane, carbicarb or continuous haemodiafiltration. The successful treatment of lactic acidosis depends on the control of the aetiological source. Intermittent or continuous renal replacement therapy is perfectly justified, shock being the argument for deciding which modality to use. We report a case of a male patient presenting with metformin poisoning as a result of attempted suicide, who developed lactic acidosis and multiple organ failure. The critical success factor was treatment with continuous haemodiafiltration. Definimos acidosis lctica en presencia de pH <7.35, lactato en sangre >2.0mmol/L y PaCO2 <42mmHg. Por otro lado, la definicin de acidosis lctica grave es controvertida. La causa principal de acidosis lctica grave es el estado de choque. La acidosis lctica por metformina es rara pero alcanza mortalidad del 50%. La acidosis metablica incluyendo a la acidosis lctica puede recibir tratamiento especfico o tratamiento general con bicarbonato de sodio, trihidroxiaminometano, carbicarb o hemodiafiltracin continua. El xito del tratamiento de la acidosis lctica yace en el control de la fuente etiolgica; la terapia de reemplazo renal intermitente o continua est perfectamente justificada, donde el argumento para decidir cul utilizar ser el estado de Continue reading >>

Metformin Intoxication

Metformin Intoxication

Can we love Metformin? Need we to fear it? Or perhaps we must give it Machiavellis ultimate accolade, and love and fear the drug with equal weight? Why to love Metformin? It is endorsed in the US, UK and Europe as the initial drug treatment for adults with type 2 diabetes. It treats diabetes, does not cause weight gain, does not increase risk of hypoglycaemia, and might reduce heart attacks and strokes. One tablet costs about 0.20 ($0.29/0.26) and the drug has been widely used for upwards of 60 years. So, must the love be tempered by fear? Metformin inhibits the mitochondrial respiratory chain, driving anaerobic metabolism and increasing lactic acid production. The drug is excreted almost entirely unchanged in urine so reduced kidney function may lead to accumulation of both metformin and lactate and therefore, a metformin-associated lactic acidosis (MALA). Where ingestion of overdose doses of metformin is seen, acutely or intentionally, this may be termed metformin-induced lactic acidosis (MILA). Notoriously, a similar drug, Phenformin, was withdrawn in the late 1970s after catastrophic lactic acidosis occurred in patients. The fear of metformin has lingered ever since, despite the overall incidence of lactic acidosis in metformin users being somewhere between 3 and 10 cases per 100,000 patient years and generally indistinguishable from the base rate in diabetics. Admittedly, reliable data specifically in patients with CKD is hard to come by and UK and US recommendations are to review the dose and not start the drug at an eGFR <45ml/min and stop the drug at <30ml/min. If youve seen a case of MALA, it might have extinguished any love you had for metformin; mortality is 30-50%, serum lactate is often over 20mmol/l and pH can fall below 7. Those are frightening numbers. Continue reading >>

Severe Metformin Poisoning Successfully Treated With Simultaneous Venovenous Hemofiltration And Prolonged Intermittent Hemodialysis

Severe Metformin Poisoning Successfully Treated With Simultaneous Venovenous Hemofiltration And Prolonged Intermittent Hemodialysis

Volume 2018 |Article ID 3868051 | 4 pages | Severe Metformin Poisoning Successfully Treated with Simultaneous Venovenous Hemofiltration and Prolonged Intermittent Hemodialysis ,1 Bo Madsen,2 Anne Schmedes,3 Niels H. Buus,2 and Bodil S. Rasmussen1,4 1Department of Anaesthesiology and Intensive Care Medicine, Aalborg University Hospital, Aalborg, Denmark 2Department of Nephrology, Aalborg University Hospital, Aalborg, Denmark 3Department of Biochemistry and Immunology, Lillebaelt Hospital, Vejle, Denmark 4Department of Clinical Medicine, Aalborg University, Aalborg, Denmark Metformin poisoning is a life-threatening condition with a high mortality rate. We present a patient case of metformin poisoning following intake of 80 g metformin resulting in severe lactate acidosis with a nadir pH of 6.73 and circulatory collapse, successfully treated with addition of prolonged intermittent hemodialysis (HD) to continuous venovenous hemofiltration (CVVH). The patients pH became normal 48 hours after metformin ingestion during simultaneous CVVH and addition of 22 hours of intermittent HD in the ICU. The highest metformin level was found to be 991 mol/L (therapeutic range 3.923.2 mol/L). We conclude that in cases of severe metformin poisoning with circulatory shock and extreme lactic acidosis, the usual CVVH modality might not efficiently clear metformin. Therefore, additional prolonged HD should be considered even in the state of cardiovascular collapse with vasopressor requirement. Metformin is widely used and is the most frequently prescribed oral antidiabetic drug of the biguanide family [ 1 ]. Metformin inhibits hepatic gluconeogenesis and glycogenolysis and enhances peripheral glucose utilisation in patients with non-insulin-dependent diabetes [ 2 , 3 ]. Metformin use is genera Continue reading >>

Metformin

Metformin

Metformin, marketed under the trade name Glucophage among others, is the first-line medication for the treatment of type 2 diabetes,[4][5] particularly in people who are overweight.[6] It is also used in the treatment of polycystic ovary syndrome.[4] Limited evidence suggests metformin may prevent the cardiovascular disease and cancer complications of diabetes.[7][8] It is not associated with weight gain.[8] It is taken by mouth.[4] Metformin is generally well tolerated.[9] Common side effects include diarrhea, nausea and abdominal pain.[4] It has a low risk of causing low blood sugar.[4] High blood lactic acid level is a concern if the medication is prescribed inappropriately and in overly large doses.[10] It should not be used in those with significant liver disease or kidney problems.[4] While no clear harm comes from use during pregnancy, insulin is generally preferred for gestational diabetes.[4][11] Metformin is in the biguanide class.[4] It works by decreasing glucose production by the liver and increasing the insulin sensitivity of body tissues.[4] Metformin was discovered in 1922.[12] French physician Jean Sterne began study in humans in the 1950s.[12] It was introduced as a medication in France in 1957 and the United States in 1995.[4][13] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[14] Metformin is believed to be the most widely used medication for diabetes which is taken by mouth.[12] It is available as a generic medication.[4] The wholesale price in the developed world is between 0.21 and 5.55 USD per month as of 2014.[15] In the United States, it costs 5 to 25 USD per month.[4] Medical uses[edit] Metformin is primarily used for type 2 diabetes, but is increasingly be Continue reading >>

Treatment Of Metformin Intoxication Complicated By Lactic Acidosis And Acute Kidney Injury: The Role Of Prolonged Intermittent Hemodialysis

Treatment Of Metformin Intoxication Complicated By Lactic Acidosis And Acute Kidney Injury: The Role Of Prolonged Intermittent Hemodialysis

Intoduction: Acute kidney injury (AKI) is a seriously complication of cardiopulmonary bypass (CPB) and represents a persistent problem in clinical medicine. The diagnosis of AKI is usually based on changes in serum creatinine, but such measurements are poor early marker of acute deterioration in kidney function. The lack of early biomarkers has resulted in an unacceptable delay in initiating ... [Show full abstract] therapies. Several biomarkers of AKI have been identified over the past few years that are elevated in ischemic renal injury. One of them is Neutrofil Gelatinase-Associated Lipocain (NGAL) which rapidly released by renal tubules in response to injury. Aim: Perioperative monitoring of Neutrofil Gelatinase-Associated Lipocain measured in plasma (pNGAL) in adult patients after cardiac surgery and association between increases in pNGAL and acute kidney injury (AKI). Materials and methods: This study included 70 (49 male and 21 female) adult patients after cardiac surgery. All patients admitted to the hospital were without any kidney disease. Diagnosis of AKI was based on the RIFLE (risk, injury, failure, loss, and end- stage) criteria. NGAL, serum creatinine and creatinine clearance (CrCl) was measured the preoperatively and 2, 6 and 24 hours after CPB. The NGAL was measured with a particle-enhanced turbidimetric immunoassay in human plasma. Results: Only three patients had AKI defined by the RIFLE on the 2-nd hour after CPB. At the 6-th hour eight patients had Risk for AKI and on the 24-th hour fifteen developed Injury witch required renal replacement therapy. Plasma NGAL raised three- to five folds from the baseline in patients who developed AKI postoperatively. In patients without AKI plasma NGAL levels at the 2-nd postoperative hour was higher too (about tw Continue reading >>

Metformin Poisoning: A Complex Presentation

Metformin Poisoning: A Complex Presentation

Metformin poisoning: A complex presentation We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Metformin poisoning: A complex presentation Manish Jagia, Salah Taqi, and Mahmud Hanafi The objective of this case report is to highlight presentation, complications and treatment of metformin poisoning. Patient after ingestion of 45gms of metformin developed colicky abdominal pain, severe tachypnea and vomiting. He developed severe lactic acidosis, cardiac arrest, pancreatitis and hemolytic anemia which was treated with charcoal, sodium bicarbonate, early initiation of high volume continuous veno-venous hemofiltration and supportive therapy. Metformin poisoning is a rare presentation and we discuss course of events in the management of metformin poisoning and its associated complications. Keywords: Cardiac arrest, haemolytic anemia, lactic acidosis, metformin poisoning, pancreatitis Metformin is a biguanide oral hypoglycemic agent used for non-insulin dependent diabetes mellitus (NIDDM). Metformin poisoning can cause fatal complications like severe lactic acidosis, haemolytic anemia and pancreatitis. Early diagnosis can result in successful outcome. Here, we report a case having good recovery despite metformin induced complications and cardiac arrest. A 36-year-old man presented in the Emergency Department after ingestion of 45 g metformin. He presented with colicky abdominal pain, severe tachypnoea and vomiting. He had history of NIDDM Continue reading >>

Lactic Acidosis Secondary To Metformin Overdose: A Case Report

Lactic Acidosis Secondary To Metformin Overdose: A Case Report

Timbrell et al.; licensee BioMed Central Ltd.2012 Metformin is a commonly used treatment modality in type 2 diabetes mellitus, with a well documented side effect of lactic acidosis. In the intensive care setting lactate and pH levels are regularly used as a useful predictor of poor prognosis. In this article we highlight how high lactate levels are not an accurate predictor of mortality in deliberate metformin overdose. We present the case of a 70-year-old Caucasian man who took a deliberate metformin overdose of unknown quantity. He had a profound lactic acidosis at presentation with a pH of 6.93 and a lactate level of more than 20mmol/L. These figures would normally correspond with a mortality of more than 80%; however, with appropriate management this patients condition improved. We provide evidence that the decision to treat severe lactic acidosis in deliberate metformin overdose should not be based on arterial lactate and pH levels, as would be the case in other overdoses. We also demonstrate that appropriate treatment with hemodiafiltration and 8.4% sodium bicarbonate, even in patients with a very high lactate and low pH, can be successful. MetforminLactate LevelLactic AcidosisArterial LactateCritical Care Patient Metformin is a biguanide typically used as a first line drug for the treatment of type 2 diabetes mellitus. Its chief modes of action are reduced absorption of glucose from the gastrointestinal tract, decreased hepatic gluconeogenesis and increased peripheral utilization of glucose[ 1 ]. All of these actions lower plasma levels of glucose. Commonly reported side effects are predominantly gastrointestinal and include: nausea, vomiting and abdominal pain. Lactic acidosis is a well-recognized consequence of toxicity and is often associated with concurrent Continue reading >>

Pharmacology And Toxicology: Treatment Of Poisons - Metformin Intoxication

Pharmacology And Toxicology: Treatment Of Poisons - Metformin Intoxication

Pharmacology and Toxicology: Treatment of Poisons - Metformin Intoxication Pharmacology and Toxicology: Treatment of Poisons - Metformin Intoxication Does this patient have metformin intoxication? Since its introduction to the US market in 1995, the biguinide, metformin has become one of the most prescribed oral hypoglycemics. It is now considered the first line agent to treat type 2 diabetes. Because of its similarity to the drug another biguinide, phenformin, there was concern that it might increase the risk of lactic acidosis as was seen in phenformin. This delayed its release in the United States and led to a number of safety studies in the 1990s. One such study compared the incidence of lactic acidosis in patients treated with metformin and found that among the 7,227 patients followed on metformin, there were no incidents of lactic acidosis reported. Following its introduction, there have been a number of comparative studies with other oral agents for diabetes showing that metformin has a superior safety profile and excellent efficacy. As per the manufacturer, metformin is contraindicated in patients with chronic kidney disease. This is defined as a creatinine 1.4 mg/dL in women and 1.5 mg/dL in men. There have been a number of studies in patients with diabetes and chronic kidney disease that show that metformin remains a very safe medication and a number of authors have argued that its use should no longer be restricted in chronic kidney disease. Other authors have argued that for consistency sake alone, metformin should be restricted by a creatinine clearance estimate as it is with most medications whose clearance depends on renal function rather than a serum creatinine. For the time being, this author recommends following the restricted use of metformin as desc Continue reading >>

Extracorporeal Treatment For Metformin Poisoning

Extracorporeal Treatment For Metformin Poisoning

Extracorporeal Treatment for Metformin Poisoning Systematic Review and Recommendations From the Extracorporeal Treatments in Poisoning Workgroup Calello, Diane P. MD1; Liu, Kathleen D. MD, PhD2; Wiegand, Timothy J. MD3; Roberts, Darren M. PhD, FRACP4; Lavergne, Valry MD5; Gosselin, Sophie MD6; Hoffman, Robert S. MD7; Nolin, Thomas D. PharmD, PhD8; Ghannoum, Marc MDCM9on behalf of the Extracorporeal Treatments in Poisoning Workgroup 1Department of Emergency Medicine, Medical Toxicology Service, Morristown Medical Center, Morristown, NJ. 2Division of Nephrology, Department of Medicine, University of California, San Francisco, CA. 3The University of Rochester Medical Center and Strong Memorial Hospital, Rochester, NY. 4Burns, Trauma and Critical Care Research Centre, School of Medicine, Royal Brisbane and Womens Hospital, Herston, QLD, Australia. 5Department of Medical Biology, Sacr-Coeur Hospital, University of Montreal, Montreal, QC, Canada. 6Department of Emergency Medicine, Medical Toxicology Consultation Service, McGill University Health Centre, Montreal, QC, Canada. 7Division of Medical Toxicology, Ronald O. Perelman Department of Emergency Medicine, New York University School of Medicine, New York, NY. 8Department of Pharmacy and Therapeutics, Center for Clinical Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, PA. 9Department of Nephrology, Verdun Hospital, University of Montreal, Verdun, QC, Canada. The Extracorporeal Treatments in Poisoning workgroup also includes the following members: Kurt Anseeuw, Ashish Bhalla, Emmanuel A. Burdmann, Paul I. Dargan, Brian S. Decker, David S. Goldfarb, Tais Galvo, Lotte C. Hoegberg, David Juurlink, Jan T. Kielstein, Martin Lalibert, Yi Li, Robert MacLaren, Robert Mactier, Bruno Mgarbane, James Continue reading >>

Extracorporeal Treatment For Metformin Poisoning: Systematic Review And Recommendations From The Extracorporeal Treatments In Poisoning Workgroup

Extracorporeal Treatment For Metformin Poisoning: Systematic Review And Recommendations From The Extracorporeal Treatments In Poisoning Workgroup

Background:Metformin toxicity, a challenging clinical entity, is associated with a mortality of 30%. The role of extracorporeal treatments such as hemodialysis is poorly defined at present. Here, the Extracorporeal Treatments In Poisoning workgroup, comprising international experts representing diverse professions, presents its systematic review and clinical recommendations for extracorporeal treatment in metformin poisoning. Methods:A systematic literature search was performed, data extracted, findings summarized, and structured voting statements developed. A two-round modified Delphi method was used to achieve consensus on voting statements and RAND/UCLA Appropriateness Method to quantify disagreement. Anonymized votes and opinions were compiled and discussed. A second vote determined the final recommendations. Results:One hundred seventy-five articles were identified, including 63 deaths: one observational study, 160 case reports or series, 11 studies of descriptive cohorts, and three pharmacokinetic studies in end-stage renal disease, yielding a very low quality of evidence for all recommendations. The workgroup concluded that metformin is moderately dialyzable (level of evidence C) and made the following recommendations: extracorporeal treatment is recommended in severe metformin poisoning (1D). Indications for extracorporeal treatment include lactate concentration greater than 20 mmol/L (1D), pH less than or equal to 7.0 (1D), shock (1D), failure of standard supportive measures (1D), and decreased level of consciousness (2D). Extracorporeal treatment should be continued until the lactate concentration is less than 3 mmol/L (1D) and pH greater than 7.35 (1D), at which time close monitoring is warranted to determine the need for additional courses of extracorporeal Continue reading >>

Metformin Litfl Life In The Fast Lane Medical Blog

Metformin Litfl Life In The Fast Lane Medical Blog

Metformin rarely causes hypoglycaemia but it can cause a profound lactic acidosis in overdose and in patients with renal failure. Used therapeutically to inhibit glucogenogenesis and stimulate peripheral glucose uptake, in toxic doses it causes a profound lactaemia. All the mechanisms are unclear but it is in part due to the inhibition of gluconeogenesis (which lactate is required). Therefore in healthy individuals there is some build up of lactate, this is normally excreted in the urine but at impaired renal function or an acute overdose there is excess lactate. It is not metabolised and excretion relies solely on renal excretion A lactic acidosis in the context of therapeutic metformin has a high mortality rate and an underlying cause (sepsis) needs to be managed Metformin overdose is usually benign but doses > 10 grams are concerning Lactic acidosis will occur in these individuals who are susceptible (renal, cardiac, respiratory failure) or in patients who have ingested co-ingestants or are on medications that impair cardiac and renal function Severe lactic acidosis usually manifests with non-specific symptoms several hours later but can progress to coma, shock and death Children: Unintentional ingestion of up to 1700mg is benign. Hypoglycaemia, if present can be managed with dextrose . Severe acidosis and hyperkalaemia may require the administration of sodium bicarbonate (1 2 mmol/kg). However, it is likely the patient is already hyperventilating to compensate for the metabolic acidosis, haemodialysis is the ultimate priority. If in a patient on therapeutic metformin, stop further administration and seek the underlying cause for their deterioration (sepsis, acute kidney injury) Screening: 12 lead ECG, BSL, Paracetamol level 50 grams of charcoal to the co-operative Continue reading >>

Survival Following A Metformin Overdose Of 63 G: A Case Report

Survival Following A Metformin Overdose Of 63 G: A Case Report

Survival Following a Metformin Overdose of 63 g: A Case Report Department of Clinical Pharmacology, Aarhus University Hospital, Aarhus Amtssygehus, DK8000 Aarhus C, Denmark Author for correspondence: Jrgen Rungby, Department of Endocrinology C, Aarhus University Hospital, Tage Hansensgade, DK8000 Aarhus C, Denmark (fax +45 8949 7659, Department of Clinical Pharmacology, Aarhus University Hospital, Aarhus Amtssygehus, DK8000 Aarhus C, Denmark Author for correspondence: Jrgen Rungby, Department of Endocrinology C, Aarhus University Hospital, Tage Hansensgade, DK8000 Aarhus C, Denmark (fax +45 8949 7659, Please review our Terms and Conditions of Use and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Use the link below to share a full-text version of this article with your friends and colleagues. Learn more. Metformin is a biguanide used in the treatment of type 2 diabetes mellitus. It lowers hepatic glucose production and peripheral insulin resistance. Hypoglycaemia is seen only after intake of toxic doses or in combination with other antidiabetic drugs or after prolonged fasting. As metformin is excreted by the kidneys, care must be taken in renal insufficiency or liver disease because of risk of lactic acidosis. Large overdoses of metformin can lead to lactic acidosis as well. Suicide with metformin is rare. Intake of 35 g of metformin has been shown to be lethal ( Teale et al. 1998 ). In the present paper we report on the treatment and outcome of a 70 year old man after ingestion of 63 g of metformin. Previously, survival after intake of up to 50 g has been described. A 70 year old man with type 2 diabetes mellitus who was being treated with metformin 850 mg twice daily and glimepiride Continue reading >>

Ph 6.68surviving Severe Metformin Intoxication

Ph 6.68surviving Severe Metformin Intoxication

Metformin, a widely used anti-diabetic agent of the biguanide family, although generally safe, 1 , 2 , 3 , 4 holds the risk of developing a potentially lethal acidosis. 5 , 6 The association between lactic acidosis and metformin is well-established but rarely seen in patients taking this medication. 7 Its elimination relies solely on kidneys excretion, 8 so its accumulation is feasible in just two circumstances: renal failure (RF) and acute overdosage. At normal dosage, a toxic accumulation of drug requires time after the development of RF, due to metformin high clearance. About 90% of the drug is eliminated by glomerular filtration and tubular secretion (serum half-life of 1.55 h). Moreover, RF is itself associated with acidosis as it impairs kidneys ability to excrete protons. Acute intoxication on the other hand is a viable option in those cases where renal function is normal and can correlate with a psychiatric disorder. The mechanism thought to be responsible for lactic acidosis is suppression of gluconeogenesis forming lactate, pyruvate, glycerol and amino acids leading to lactate accumulation, 9 a risk that is increased by either chronic or acute RF (ARF). Usually hyperlactatemia is the most common finding leaving lactic acidosis for the most severe intoxications. A 47-year-old, apparently previously fit, non-insulin-dependent diabetic male was brought to the Emergency Department for hypoglycemia, agitation and hyperventilation. Ambulance crew found blood glucose level at 1.33 mmol/l (24 mg/dl) and administered 20 ml of 33% glucose solution followed by other 250 ml at 5%. At the arrival in the Emergency Room, the patient was confused and agitated with no signs of respiratory distress or shock. Arterial blood gases (ABG) and laboratory tests are summarized in Tab Continue reading >>

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