diabetestalk.net

Alcohol Associated Lactic Acidosis

Survival From Profound Alcohol-related Lactic Acidosis - Sciencedirect

Survival From Profound Alcohol-related Lactic Acidosis - Sciencedirect

Survival from profound alcohol-related lactic acidosis Author links open overlay panel DavidLienMDa Timothy JMaderMDa Get rights and content We present the case of a patient with profound alcohol-related lactic acidosis (lactate = 16.1 mmol/L; pH = 6.67) associated with a multitude of metabolic derangements who made a remarkable recovery following aggressive management. The patient was in extremis upon arrival in the emergency department (ED), and resuscitation was begun immediately. While in the ED, the problem list generated included: acute alcohol intoxication, severe lactic acidosis, dehydration, hypothermia, hypoglycemia, acute renal insufficiency, and hepatic failure. Resuscitation continued in the intensive care unit with remarkable improvement and satisfactory outcome. In this patient, the severe lactic acidosis and associated abnormalities were all attributed to acute and chronic effects of ethanol. A brief summary of the proposed mechanism by which these metabolic derangements developed and an outline of her management follows. Continue reading >>

Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base Andelectrolyte Disorders

Metabolic Abnormalities In Alcoholic Patients: Focus On Acid Base Andelectrolyte Disorders

E-mail: [emailprotected] , [emailprotected] Received Date: December 20, 2014; Accepted Date: January 24, 2015; Published Date: January 27, 2015 Citation: Moses Elisaf MD, Rigas Kalaitzidis MD (2015) Metabolic Abnormalities in Alcoholic Patients: Focus on Acid Base and Electrolyte Disorders. J Alcohol Drug Depend 3:185. doi:10.4172/2329-6488.1000185 Copyright: 2015 Moses Elisaf MD, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Alcoholic patients commonly develop a variety of acid-base and electrolyte disturbances. The aim of this review is to describe the most commonly encountered abnormalities and their significant role in the patients morbidity and mortality. Physicians should be aware of these clinically important disturbances caused by alcohol abuse and their underlying pathophysiological mechanisms involved for their appropriate management. Alcoholic Keto Acidosis (AKA) is a medical emergency is more common than previously thought and is characterized by an increased anion gap metabolic acidosis . However, in AKA mixed acid-base disorders are commonly observed. Alcoholic patients also exhibit severe electrolyte derangements. Multifactorial origin hypomagnesaemia is the most common electrolyte abnormality observed. Hypocalcaemia is also a frequent electrolyte disturbance and is commonly associated with hypomagnesaemia. Hypokalemia is occasionally encountered in these patients, while multifactorial origin hypophosphatemia is the second common electrolyte abnormality found. Hyponatremia is also a common electrolyte derangement and may occur subsequent to several mechanisms m Continue reading >>

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic Acidosis: Symptoms, Causes, And Treatment

Lactic acidosis occurs when the body produces too much lactic acid and cannot metabolize it quickly enough. The condition can be a medical emergency. The onset of lactic acidosis might be rapid and occur within minutes or hours, or gradual, happening over a period of days. The best way to treat lactic acidosis is to find out what has caused it. Untreated lactic acidosis can result in severe and life-threatening complications. In some instances, these can escalate rapidly. It is not necessarily a medical emergency when caused by over-exercising. The prognosis for lactic acidosis will depend on its underlying cause. A blood test is used to diagnose the condition. Lactic acidosis symptoms that may indicate a medical emergency include a rapid heart rate and disorientaiton. Typically, symptoms of lactic acidosis do not stand out as distinct on their own but can be indicative of a variety of health issues. However, some symptoms known to occur in lactic acidosis indicate a medical emergency. Lactic acidosis can occur in people whose kidneys are unable to get rid of excess acid. Even when not related to just a kidney condition, some people's bodies make too much lactic acid and are unable to balance it out. Diabetes increases the risk of developing lactic acidosis. Lactic acidosis may develop in people with type 1 and 2 diabetes mellitus , especially if their diabetes is not well controlled. There have been reports of lactic acidosis in people who take metformin, which is a standard non-insulin medication for treating type 2 diabetes mellitus. However, the incidence is low, with equal to or less than 10 cases per 100,000 patient-years of using the drug, according to a 2014 report in the journal Metabolism. The incidence of lactic acidosis is higher in people with diabetes who Continue reading >>

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Abstract Alcohol-related intoxications, including methanol, ethylene glycol, diethylene glycol, and propylene glycol, and alcoholic ketoacidosis can present with a high anion gap metabolic acidosis and increased serum osmolal gap, whereas isopropanol intoxication presents with hyperosmolality alone. The effects of these substances, except for isopropanol and possibly alcoholic ketoacidosis, are due to their metabolites, which can cause metabolic acidosis and cellular dysfunction. Accumulation of the alcohols in the blood can cause an increment in the osmolality, and accumulation of their metabolites can cause an increase in the anion gap and a decrease in serum bicarbonate concentration. The presence of both laboratory abnormalities concurrently is an important diagnostic clue, although either can be absent, depending on the time after exposure when blood is sampled. In addition to metabolic acidosis, acute renal failure and neurologic disease can occur in some of the intoxications. Dialysis to remove the unmetabolized alcohol and possibly the organic acid anion can be helpful in treatment of several of the alcohol-related intoxications. Administration of fomepizole or ethanol to inhibit alcohol dehydrogenase, a critical enzyme in metabolism of the alcohols, is beneficial in treatment of ethylene glycol and methanol intoxication and possibly diethylene glycol and propylene glycol intoxication. Given the potentially high morbidity and mortality of these intoxications, it is important for the clinician to have a high degree of suspicion for these disorders in cases of high anion gap metabolic acidosis, acute renal failure, or unexplained neurologic disease so that treatment can be initiated early. Effect of Alcohols on Serum Osmolality and the Osmolal Gap The normal serum Continue reading >>

Is It Safe To Mix Metformin And Alcohol?

Is It Safe To Mix Metformin And Alcohol?

If you’re taking metformin to treat your diabetes, you may be wondering how this drug affects your ability to drink safely. Drinking alcohol can affect your diabetes symptoms directly, but there are additional risks if you drink alcohol with metformin. This article gives you information on how alcohol interacts with metformin and also how drinking alcohol can affect your diabetes. With any medicine you take, you should be aware of interactions that can happen if you use other substances. Metformin and alcohol can interact to increase your risk of harmful effects. You are at much greater risk of these effects if you frequently drink a lot of alcohol or you binge drink (drink a lot in short periods). These effects include an extremely low blood sugar level, called hypoglycemia, and a condition called lactic acidosis. Hypoglycemia Drinking alcohol while you’re taking metformin may cause extremely low blood sugar levels. Some symptoms of low blood sugar levels can be similar to symptoms of having too much alcohol. These include: drowsiness dizziness confusion Tell the people who are with you while you drink that you have diabetes. They can help you watch for these symptoms. If you or the people around you notice these symptoms, stop drinking and eat something right away to help increase your blood sugar level. If your symptoms of hypoglycemia are severe, such as losing consciousness, and you do not have a glucagon hypoglycemia rescue kit, someone with you should call 9-1-1. A glucagon hypoglycemia rescue kit includes human glucagon (a natural substance that helps balance your blood sugar level), a syringe to inject it, and instructions. You can use this kit for severe hypoglycemia when eating food will not help. If you are not familiar with this kit, talk to your doctor Continue reading >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

1 A chronic alcoholic with severe metabolic acidosis presents a difficult diagnostic problem. The most common cause is alcoholic ketoacidosis, a syndrome with a typical history but often misleading laboratory findings. This paper will focus on this important and probably underdiagnosed syndrome. 2 The disorder occurs in alcoholics who have had a heavy drinking-bout culminating in severe vomiting, with resulting dehydration, starvation, and then a β- hydroxybutyrate dominated ketoacidosis. 3 Awareness of this syndrome, thorough history-taking, physical examination and routine laboratory analyses will usually lead to a correct diagnosis. 4 The treatment is simply replacement of fluid, glucose, electrolytes and thiamine. Insulin or alkali should be avoided. 5 The most important differential diagnoses are diabetic ketoacidosis, lactic acidosis and salicylate, methanol or ethylene glycol poisoning, conditions which require quite different treatment. 6 The diagnostic management of unclear cases should always include toxicological tests, urine microscopy for calcium oxalate crystals and calculation of the serum anion and osmolal gaps. 7 It is suggested here, however, that the value of the osmolal gap should be considered against a higher reference limit than has previously been recom mended. An osmolal gap above 25 mosm/kg, in a patient with an increased anion gap acidosis, is a strong indicator of methanol or ethylene glycol intoxication. Continue reading >>

Metformin-associated Lactic Acidosis Presenting As An Ischemic Gut In A Patient Who Then Survived A Cardiac Arrest: A Case Report

Metformin-associated Lactic Acidosis Presenting As An Ischemic Gut In A Patient Who Then Survived A Cardiac Arrest: A Case Report

Ncomanzi et al.; licensee BioMed Central Ltd.2014 Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. It is recognized as a potential complication of metformin use, particularly in patients with risk factors such as renal dysfunction, liver disease, and heavy alcohol ingestion. These conditions are associated with systemic hypoxemia, which may be caused by cardiorespiratory disease, major surgery, sepsis, dehydration, old age, and overdose. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors. This case is important because it details the seriousness of metformin-associated lactic acidosis in a critically ill patient and because, to the best of our knowledge, our patient survived with minimal residual defect despite experiencing a cardiac arrest. A 66-year-old Caucasian woman presented to our hospital with profound lactic acidosis, which was initially thought to be ischemic gut. She then survived an in-hospital pulseless electrical activity arrest. Metformin-associated lactic acidosis is a diagnosis by exclusion; however, a high degree of clinical suspicion supplemented by prompt multisystem organ support can significantly influence the outcome in critically ill patients. Cardiac arrestGutIschemiaLactic acidosisMetformin Metformin is an oral biguanide anti-diabetic agent. It is a small, non-plasma-protein-bound molecule, and 90% of metformin is excreted unchanged by the kidneys through glomerular filtration and possibly through tubular secretion. In addition to being relatively safe, its use has been advocated in the treatment of type 2 diabetes in patients who are obese and has been shown to slow cardiovascular complications associated with diabetes. By decreasing ex Continue reading >>

Causes Of Lactic Acidosis

Causes Of Lactic Acidosis

INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>

Lactic Acidosis: What You Need To Know

Lactic Acidosis: What You Need To Know

Lactic acidosis is a form of metabolic acidosis that begins in the kidneys. People with lactic acidosis have kidneys that are unable to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike. This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis. Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism. There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate. Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening. The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause. Several symptoms of lactic acidosis represent a medical emergency: fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis) confusion jaundice (yellowing of the skin or the whites of the eyes) trouble breathing or shallow, rapid breathing If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away. Other lactic acidosis symptoms include: exhaustion or extreme fatigue muscle cramps or pain body weakness overall feelings of physical discomfort abdominal pain or discomfort diarrhea decrease in appetite headache rapid heart rate Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoni Continue reading >>

Alcoholism And Lactic Acidosis

Alcoholism And Lactic Acidosis

Learn more about the SDN Exhibition Forums for exclusive discounts and contests. So the way I understood this is that both alcohol metabolism and latcate to pyrvuate conversion require NAD, and with too much alcohol consumption the body uses up all the NAD for alcohol metabolism right? The part that I'm a bit troubled with this mechanism is that unless we are doing extreme exercise, we don't really generate lactic acid. In most cases, the body uses oxidative phosphorylation, right? So lactic acidosis will most likely occur when you drink alcohol and then do extreme exercise, correct? SDN Members don't see this ad. About the ads. My understanding is that high NADH levels from EtOH metab drives the pyruvate -> lactate conversion. So you don't need to be exercising +drinking, either will do it on their own. I actually enjoy your questions, though some things are really easily looked up. The several different causes of lactic acidosis: I actually enjoy your questions, though some things are really easily looked up. The several different causes of lactic acidosis: But the reasons behind why lactic acidosis occurs for these is significantly different.... For example, in exercise- lactic acidosis- due to depletion of ATP such that the ability to generate ATP via oxidation is overwhelmed. This leads to high levels of ADP> than the O2 intake from respiration. When the ADP/ATP ratio are elevated but O2 is no longer sufficient the body switches to anaerobic metabolism to quickly generate ATP= leading to lactic acidosis. In alcoholism, the NADH levels are elevated. Why does this take place? because degeneration of alcohol to acetic acid (the final state) is via transferring electrons from ETOH to aldehyde DEHYDROGENASE and alcohol DEHYDROGENASE to NAD- the elevation to NADH forces Continue reading >>

Metformin-associated Lactic Acidosis

Metformin-associated Lactic Acidosis

OVERVIEW metformin use is associated with lactic acidosis, but it remians controversial as a disease entity MECHANISM the mechanism of lactic acidosis is uncertain Metabolic effects of metformin include: decreased gluconeogenesis increased peripheral glucose uptake decreased fatty acid oxidation CLINICAL FEATURES presence of risk factors abdominal pain nausea and vomiting fatigue myalgias altered mental status myocardial insufficiency multi-organ failure RISK FACTORS advanced age high dose renal failure (metformin is excreted unchanged in the urine) hypoxia active alcohol intake sepsis dehydration shock acidosis INVESTIGATIONS high anion gap metabolic acidosis (HAGMA) high lactate MANAGEMENT rule out other causes of lactic acidosis (sepsis, cardiogenic shock, hypoperfusion, ischaemic bowel) withdrawal of metformin RRT RRT remove metformin and correct acidosis best performed early due to large volume of distribution of metformin use hemodialysis use HCO3 buffer CONTROVERSY Some argue that metformin itself does not cause lactic acidosis, that it is actually due to the underlying conditions such as renal failure and diabetes mellitus. However, there are definite cases of lactic acidosis from acute metformin overdose with no other underlying risk factors. References and Links Journal articles Orban JC, Fontaine E, Ichai C. Metformin overdose: time to move on. Crit Care. 2012 Oct 25;16(5):164. [Epub ahead of print] PubMed PMID: 23110819; PubMed Central PMCID: PMC3682282. Salpeter SR, Greyber E, Pasternak GA, Salpeter EE. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010 Apr 14;(4):CD002967. doi: 10.1002/14651858.CD002967.pub4. Review. PubMed PMID: 20393934. FOAM and web resources Continue reading >>

Metformin And Fatal Lactic Acidosis

Metformin And Fatal Lactic Acidosis

Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major Continue reading >>

Metformin‐associated Lactic Acidosis In A Patient With Liver Disease

Metformin‐associated Lactic Acidosis In A Patient With Liver Disease

Sir, Metformin is an orally active biguanide, and was found to reduce mortality and complications in obese diabetic patients in the UK Prospective Diabetes Study.1 As a result, the drug is widely used as first‐line therapy for patients with obesity and type 2 diabetes. We would like to remind prescribers of a rare, but commonly fatal complication of metformin therapy in patients with liver or renal disease. A 40‐year‐old Gujerati man was admitted through accident and emergency. On admission, little history was available from the patient, and no corroborative history was available, apart from the fact that he was diabetic and on metformin. He was short of breath at rest, with oxygen saturation of 84% on air, and had a Glasgow Coma Score of 13/15. Capillary blood glucose was 1.7 mmol/l. Arterial blood gas analysis on 60% oxygen revealed severe metabolic acidosis: pH 6.62, pCO2 8.3 kPa, pO2 47.8 kPa, base excess −31.2, bicarbonate 6.4 mmol/l, anion gap 37 mmol/l. Serum lactate was extremely high at >20 mmol/l. He had a low urea of 2.4 mmol/l, normal creatinine of 63 µmol/l, a raised aspartate transaminase (110 IU/l, NR 10–50), bilirubin (64 µmol/l, NR 2–17) and alkaline phosphatase (323 IU/l, NR 40–135). He had a macrocytic anaemia (haemoglobin 9.7 g/dl, NR 13.0–17.0; MCV 99.0 fl, NR 76.0–96.0), and deranged clotting (PT 30 s, control 12 s; KPTT 65 s, control 35 s), but normal platelet count (152×109/l, NR 135–450). Hypoglycaemia was confirmed by a venous plasma glucose of 1.9 mmol/l. On review of his medical notes, he had been diagnosed with type 2 diabetes 3 years prior to admission. He had not been seen at diabetic clinic for over 2 years, when his diabetes was well controlled with metformin 850 mg twice daily. Eighteen months previously, he was a Continue reading >>

Prognosis Of Alcohol-associated Lactic Acidosis In Critically Ill Patients: An 8-year Study

Prognosis Of Alcohol-associated Lactic Acidosis In Critically Ill Patients: An 8-year Study

Prognosis of alcohol-associated lactic acidosis in critically ill patients: an 8-year study 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. Prognosis of alcohol-associated lactic acidosis in critically ill patients: an 8-year study Chun-Chieh Yang, Khee-Siang Chan, [...], and Shih-Feng Weng Lactic acidosis is common in critical care; by contrast, a subtype called alcohol-associated lactic acidosis (AALA) is rarely encountered. The primary purpose of this study was to determine the prognosis of AALA in critically ill patients and the second aim was to determine whether the survival was associated to the peak blood lactate concentration. An 8-year retrospective analysis of adult patients admitted to the intensive care unit (ICU) with AALA between January 2007 and December 2014 was considered in a tertiary care hospital. In total, 23 patients were analyzed and the median peak blood lactate level was 15.9 mmol/L. Only 2 patients (8.7%) presented peak blood lactate levels <10 mmol/L. In this study, 21 patients survived from ICU and hospital, the mortality rate was 8.7%. The result indicted the survival of AALA was not associated with peak blood lactate concentration although survivors still had a better lactate clearance rate per hour than non-survivors. Moreover, AALA patients with coexisting sepsis presenting higher lactate clearance rate and shorter lactate clearance time than those of AALA patients with solely sepsis-related lact Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Background In 1940, Dillon and colleagues first described alcoholic ketoacidosis (AKA) as a distinct syndrome. AKA is characterized by metabolic acidosis with an elevated anion gap, elevated serum ketone levels, and a normal or low glucose concentration. [1, 2] Although AKA most commonly occurs in adults with alcoholism, it has been reported in less-experienced drinkers of all ages. Patients typically have a recent history of binge drinking, little or no food intake, and persistent vomiting. [3, 4, 5] A concomitant metabolic alkalosis is common, secondary to vomiting and volume depletion (see Workup). [6] Treatment of AKA is directed toward reversing the 3 major pathophysiologic causes of the syndrome, which are: This goal can usually be achieved through the administration of dextrose and saline solutions (see Treatment). Continue reading >>

More in ketosis