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Metformin Poisoning Management

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 >>

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 Overdosage

Metformin Overdosage

Metformin is a biguanide used to treat type 2 diabetes mellitus and most commonly prescribed oral hypoglycemic agent. Metformin is now also used to treat polycystic ovary syndrome and some malignancies. Despite a good safety profile in a majority of patients with diabetes, the risk of metformin-associated lactic acidosis is genuine when safety guidelines are ignored. Overdoses with metformin are rare, but may result in serious consequences. Case reports and small case series of serious toxicity from metformin overdosage can be found in the medical literature, often with the portrayal of extracorporeal methods for the management of the subsequent severe lactic acidosis. Lactic acidosis can defined as a metabolic acidosis with a blood pH less than 7.35 and a serum lactate more than 2 mmol per liter. It can occur either with therapeutic metformin dosing (which is rare) or in overdose situations. 0.03 cases of lactic acidosis per 1000 patient-years occur within therapeutic dosing, with a majority of these cases among patients that have contraindications to metformin (such as renal insufficiency). In overdose situations, lactic acidosis is seen much more habitually, even though the precise incidence is unclear. Lactic acidosis has been observed in 1.6% of metformin exposures reported to poison control centers; nevertheless, merely 10% of these exposures were due to deliberate overdoses. The incidence of metformin-associated lactic acidosis was 12.8% in a review of poison control center inquiries from Germany. The minimum reported lethal dose was found in a 42 year-old patient who had a blood metformin level of 188 µg/ml (e.g. therapeutic range level is usually between 0.5–2.5 µg/ml). Although the intake of 35 g of metformin has shown to be lethal, the maximum reported to Continue reading >>

Metformin-associated Lactic Acidosis Following Intentional Overdose Successfully Treated With Tris-hydroxymethyl Aminomethane And Renal Replacement Therapy

Metformin-associated Lactic Acidosis Following Intentional Overdose Successfully Treated With Tris-hydroxymethyl Aminomethane And Renal Replacement Therapy

Metformin-Associated Lactic Acidosis following Intentional Overdose Successfully Treated with Tris-Hydroxymethyl Aminomethane and Renal Replacement Therapy Ngan Lam ,1,2 Gurbir Sekhon ,3and Andrew A. House 1,3 1Division of Nephrology, Department of Medicine, Western University, London, ON, Canada N6A 3K7 2London Health Sciences Centre, Kidney Clinical Research Unit, Victoria Hospital, Westminster Tower 800 Commissioners Road East, London, ON, Canada N6A 4G5 3Department of Medicine, Western University, London, ON, Canada N6A 3K7 Received 19 February 2012; Accepted 6 May 2012 Academic Editors: Y.Fujigaki, D.Packham, A.Papagianni, and H.Schiffl Copyright 2012 Ngan Lam et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 43-year-old woman was brought to the hospital with severe metabolic acidosis (pH 6.56, bicarbonate 3 mmol/L, and lactate 18.4 mmol/L) and a serum creatinine of 162 mol/L with a serum potassium of 7.8 mmol/L. A delayed diagnosis of metformin-associated lactic acidosis was made, and she was treated with tris-hydroxymethyl aminomethane (THAM) and renal replacement therapy (RRT). Following a complete recovery, she admitted to ingesting 180 tablets (90 grams) of metformin. Her peak serum metformin concentration was 170 g/mL (therapeutic range 1-2 g/mL). Our case demonstrates an intentional metformin overdose resulting in lactic acidosis in a nondiabetic patient who was successfully treated with THAM and RRT. Metformin is an oral antihyperglycemic agent that is the first-line therapy for noninsulin-dependent diabetes mellitus [ 1 ]. Although the adverse event rate is 2030%, the majority of the Continue reading >>

Hypoglycaemic Agent Poisoning

Hypoglycaemic Agent Poisoning

These guidelines have been produced to guide clinical decision making for the medical, nursing and allied health staff of Perth Childrens Hospital. They are not strict protocols, and they do not replace the judgement of a senior clinician. Clinical common-sense should be applied at all times. These clinical guidelines should never be relied on as a substitute for proper assessment with respect to the particular circumstances of each case and the needs of each patient. Clinicians should also consider the local skill level available and their local area policies before following any guideline. To guide PCH Emergency Department staff with the assessment and management of hypoglycaemic agent poisoning. This guideline is a general approach to hypoglycaemic agent poisoning. For specific details please contact 131126 or refer to the Toxicology Handbook. 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 th 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 >>

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 Toxicity Litfl Toxicology Library Toxicant

Metformin Toxicity Litfl Toxicology Library Toxicant

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 >>

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 >>

Mala: Metformin-associated Lactic Acidosis

Mala: Metformin-associated Lactic Acidosis

By Charles W. O’Connell, MD Introduction Metformin is a first-line agent for type 2 diabetes mellitus often used as monotherapy or in combination with oral diabetic medications. It is a member of the biguanide class and its main intended effect is expressed by the inhibition of hepatic gluconeogenesis. In addition, metformin increases insulin sensitivity, enhances peripheral glucose utilization and decreases glucose uptake in the gastrointestinal tract. Phenformin, a previously used biguanide, as withdrawn from the market in the 1970’s due its association with numerous cases of lactic acidosis. Metformin is currently used extensively in the management of diabetes and is the most commonly prescribed biguanide worldwide. The therapeutic dosage of metformin ranges from 850 mg to a maximum of 3000 mg daily and is typically divided into twice daily dosing. It is primarily used in the treatment of diabetes but has been used in other conditions associated with insulin resistance such as polycystic ovarian syndrome. MALA is a rare but well reported event that occurs with both therapeutic use and overdose states. Case presentation A 22-year-old female presents to the Emergency Department after being found alongside a suicide note by her family. She was thought to have taken an unknown, but large amount of her husband’s metformin. She arrives at the ED nearly 10 hours after ingestion. She was agitated, but conversant. She reports having nausea and vague feelings of being unwell and is very distraught over the state of her critically ill husband. She has some self-inflicted superficial lacerations over her left anterior forearm. Her vital assigns upon arrival were: T 98.9 degrees Fahrenheit, HR initially 140 bpm which improved to 110 bpm soon after arrival, BP 100/50, RR 22, Continue reading >>

Prolonged Hemodialysis For Severe Metformin Intoxication

Prolonged Hemodialysis For Severe Metformin Intoxication

Prolonged Hemodialysis for Severe Metformin Intoxication Lactic acidosis is a rare and often lethal complication of metformin therapy. We describe a patient who ingested at least 52 g, and possibly more, of metformin and presented with severe lactic acidosis and acute renal failure. He was treated with prolonged hemodialysis: a 3.5 h treatment that did not result in significant clinical improvement, followed by an additional 31 h treatment. With this treatment regimen, his lactate levels gradually decreased and his clinical status improved. A metformin level drawn approximately 25 h after the initiation of the second hemodialysis treatment was still elevated at about five times the upper therapeutic limit. It is suggested that prolonged dialysis is indicated in patients with severe metformin overdose, particularly those with renal failure. In patients whose cardiovascular status permits, prolonged hemodialysis should be strongly considered. Keywords: Metformin , hemodialysis , diabetes mellitus , intoxication , renal failure Metformin is a biguanide oral antihyperglycemic agent that has been used for over three decades worldwide and the United States since 1995 for the treatment of type 2 diabetes mellitus. Its primary mechanisms of action appear to be suppression of gluconeogenesis and enhancement of peripheral glucose utilization. It was the most prescribed antidiabetic medication in the United States in the year 2000. 1 Barrueto F, Meggs WJ, Barchman MJ. Clearance of metformin by hemofiltration in overdose. J Toxicol Clin Toxicol. 2002;40:177180. [Taylor & Francis Online] , [Google Scholar] It has been recommended as the drug of first choice in patients diagnosed with type 2 diabetes in a consensus document issued by the American Diabetic Association and the Europea Continue reading >>

Management Of Metformin-associated Lactic Acidosis By Continuous Renal Replacement Therapy

Management Of Metformin-associated Lactic Acidosis By Continuous Renal Replacement Therapy

Abstract Metformin-associated lactic acidosis (MALA) is a severe metabolic failure with high related mortality. Although its use is controversial, intermittent hemodialysis is reported to be the most frequently used treatment in conjunction with nonspecific supportive measures. Our aim was to report the evolution and outcome of cases managed by continuous renal replacement therapy (CRRT). Methodology and Principal Findings Over a 3-year period, we retrospectively identified patients admitted to the intensive care unit for severe lactic acidosis caused by metformin. We included patients in our study who were treated with CRRT because of shock. We describe their clinical and biological features at admission and during renal support, as well as their evolution. We enrolled six patients with severe lactic acidosis; the mean pH and mean lactate was 6.92±0.20 and 14.4±5.1 mmol/l, respectively. Patients had high illness severity scores, including the Simplified Acute Physiology Score II (SAPS II) (average score 63±12 points). Early CRRT comprised either venovenous hemofiltration (n = 3) or hemodiafiltration (n = 3) with a mean effluent flow rate of 34±6 ml/kg/h. Metabolic acidosis control and metformin elimination was rapid and there was no rebound. Outcome was favorable in all cases. Continue reading >>

Metformin Overdose

Metformin Overdose

Tweet Save As with any medication, it is possible to overdose on metformin. Some of the effects of a metformin overdose may include low blood sugar or lactic acidosis. Symptoms of low blood sugar include blurred vision, shakiness, and extreme hunger. Some symptoms of lactic acidosis can include an irregular heartbeat, trouble breathing, and feeling tired. There are some treatment options for a metformin overdose, including dialysis or using a sugar solution to increase blood sugar levels. Metformin Overdose: An Overview Metformin (Glucophage®) is a prescription medication that has been licensed to treat type 2 diabetes. As with all medicines, it is possible to take too much metformin. Effects of a metformin overdose will vary depending on a number of factors, including how much metformin was taken and whether it was taken with any other medicines, alcohol, and/or drugs. If you happen to overdose on metformin, seek medical attention immediately. Symptoms of a Metformin Overdose The effects of a metformin overdose may include: Possible symptoms of low blood sugar include: Sweating Shakiness Extreme hunger Dizziness Cold sweats Blurry vision. More severe low blood sugar symptoms include: Changes in behavior, such as irritability Loss of coordination Difficulty speaking Confusion Loss of consciousness Coma Lactic acidosis symptoms include: Feeling tired or weak Muscle pain Trouble breathing Abdominal pain (or stomach pain) Feeling cold Dizziness or lightheadedness A slow or irregular heartbeat Loss of life. Tweet Our free DiscountRx savings card can help you and your family save money on your prescriptions. This card is accepted at all major chain pharmacies, nationwide. Enter your name and email address to receive your free savings card. Treatment for a Metformin Overdose Continue reading >>

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 Toxicity

Metformin Toxicity

Summarized from DellAglio D, Perino L, Kazzi Z et al. Acute metformin overdose: Examining serum pH lactate Levels and metformin concentrations in survivors versus nonsurvivors: A systematic review of the literature. Annals of Emerg Med 2009; 54: 818-23 Metformin, a blood-glucose-lowering drug widely used for treatment of type 2 diabetes, is associated with risk of potentially fatal metabolic (lactic) acidosis. This can occur not only following overdose but also at therapeutic dose in patients with pre-existing renal or liver disease. Results of arterial blood gas analysis reflect metabolic acidosis (reduced blood pH, reduced bicarbonate compensatory increase in pCO2) and increased plasma lactate. Is it possible, as might be intuitively expected, to predict survival in such cases from the severity of the acidosis and/or severity of the hyperlactatemia? That is the question addressed by a recent study. Investigators conducted a systematic review of the literature and identified 22 well-documented case histories of metformin overdose, five of which had a fatal outcome. For each of these cases, investigators abstracted lowest (nadir) pH, highest (peak) plasma lactate concentration and highest (peak) plasma metformin concentration. The median nadir pH among non-survivors was 6.71 (interquartile IQ range 6.71-6.73), this compared with median pH 7.30 (IQ range 7.22-7.36) for survivors. The median peak plasma lactate among non-survivors was 35 mmol/L (IQ range 33.3-39.0) and among survivors 10.8 mmol/L (IQ range 4.2-12.9). Results allowed the conclusion that patients who died following metformin overdose had much lower nadir blood pH and much higher peak plasma lactate concentration than those who survived. No patients with pH > 6.9 and plasma lactate < 25 mmol/L died. Intuiti Continue reading >>

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