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Lactic Acidosis Diagnosis

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 Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery.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 >>

Differential Diagnosis Of Elevated Serum Lactate 1,2

Differential Diagnosis Of Elevated Serum Lactate 1,2

Sinus tachycardia, LVH, secondary repolarization abnormalities No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax. No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis. Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening. There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities. Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance. The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified. Despite the patients reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patients significant lower extremity edema was more suggestive of chronic venous stasis. One notable laboratory abnormality that Continue reading >>

Lactic Acidosis And Exercise: What You Need To Know

Lactic Acidosis And Exercise: What You Need To Know

Muscle ache, burning, rapid breathing, nausea, stomach pain: If you've experienced the unpleasant feeling of lactic acidosis, you likely remember it. It's temporary. It happens when too much acid builds up in your bloodstream. The most common reason it happens is intense exercise. Symptoms The symptoms may include a burning feeling in your muscles, cramps, nausea, weakness, and feeling exhausted. It's your body's way to tell you to stop what you're doing The symptoms happen in the moment. The soreness you sometimes feel in your muscles a day or two after an intense workout isn't from lactic acidosis. It's your muscles recovering from the workout you gave them. Intense Exercise. When you exercise, your body uses oxygen to break down glucose for energy. During intense exercise, there may not be enough oxygen available to complete the process, so a substance called lactate is made. Your body can convert this lactate to energy without using oxygen. But this lactate or lactic acid can build up in your bloodstream faster than you can burn it off. The point when lactic acid starts to build up is called the "lactate threshold." Some medical conditions can also bring on lactic acidosis, including: Vitamin B deficiency Shock Some drugs, including metformin, a drug used to treat diabetes, and all nucleoside reverse transcriptase inhibitor (NRTI) drugs used to treat HIV/AIDS can cause lactic acidosis. If you are on any of these medications and have any symptoms of lactic acidosis, get medical help immediately. Preventing Lactic Acidosis Begin any exercise routine gradually. Pace yourself. Don't go from being a couch potato to trying to run a marathon in a week. Start with an aerobic exercise like running or fast walking. You can build up your pace and distance slowly. Increase the Continue reading >>

Glyburide And Metformin (oral Route)

Glyburide And Metformin (oral Route)

Precautions Drug information provided by: Micromedex It is very important that your doctor check your progress at regular visits to make sure this medicine is working properly. Blood tests may be needed to check for unwanted effects. Under certain conditions, too much metformin can cause lactic acidosis. The symptoms of lactic acidosis are severe and quick to appear. They usually occur when other health problems not related to the medicine are present and very severe, such as a heart attack or kidney failure. The symptoms of lactic acidosis include abdominal or stomach discomfort; decreased appetite; diarrhea; fast, shallow breathing; a general feeling of discomfort; muscle pain or cramping; and unusual sleepiness, tiredness, or weakness. If you have any symptoms of lactic acidosis, get emergency medical help right away. It is very important to carefully follow any instructions from your health care team about: Alcohol—Drinking alcohol may cause severe low blood sugar. Discuss this with your health care team. Other medicines—Do not take other medicines unless they have been discussed with your doctor. This especially includes nonprescription medicines such as aspirin, and medicines for appetite control, asthma, colds, cough, hay fever, or sinus problems. Counseling—Other family members need to learn how to prevent side effects or help with side effects if they occur. Also, patients with diabetes may need special counseling about diabetes medicine dosing changes that might occur because of lifestyle changes, such as changes in exercise and diet. Furthermore, counseling on contraception and pregnancy may be needed because of the problems that can occur in patients with diabetes during pregnancy. Travel—Keep your recent prescription and your medical history with yo Continue reading >>

Lactic Acidosis In Sepsis: It's Not All Anaerobic: Implications For Diagnosis Andmanagement.

Lactic Acidosis In Sepsis: It's Not All Anaerobic: Implications For Diagnosis Andmanagement.

1. Chest. 2016 Jan;149(1):252-61. doi: 10.1378/chest.15-1703. Epub 2016 Jan 6. Lactic Acidosis in Sepsis: It's Not All Anaerobic: Implications for Diagnosis andManagement. (1)Centre for Heart Lung Innovation, University of British Columbia, Vancouver, BC, Canada. (2)Centre for Heart Lung Innovation, University of British Columbia, Vancouver, BC, Canada. Electronic address: [email protected] Increased blood lactate concentration (hyperlactatemia) and lactic acidosis(hyperlactatemia and serum pH< 7.35) arecommon in patients with severe sepsisorseptic shock and are associated with significant morbidity and mortality. Insome patients, most of the lactate that is produced in shock states is due toinadequate oxygen delivery resulting in tissue hypoxia and causing anaerobicglycolysis. However, lactate formation during sepsis is not entirely related totissue hypoxia or reversible by increasing oxygen delivery. In this review,weinitially outline the metabolism of lactateand etiology of lactic acidosis;we thenaddress the pathophysiology of lacticacidosis in sepsis. We discuss the clinical implications of serum lactate measurement in diagnosis, monitoring, and prognostication in acute and intensive care settings. Finally, we exploretreatment of lactic acidosis and its impact on clinical outcome.Copyright 2016 American College of Chest Physicians. Published by Elsevier Inc.All rights reserved. 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 >>

Lactate And Lactic Acidosis

Lactate And Lactic Acidosis

The integrity and function of all cells depend on an adequate supply of oxygen. Severe acute illness is frequently associated with inadequate tissue perfusion and/or reduced amount of oxygen in blood (hypoxemia) leading to tissue hypoxia. If not reversed, tissue hypoxia can rapidly progress to multiorgan failure and death. For this reason a major imperative of critical care is to monitor tissue oxygenation so that timely intervention directed at restoring an adequate supply of oxygen can be implemented. Measurement of blood lactate concentration has traditionally been used to monitor tissue oxygenation, a utility based on the wisdom gleaned over 50 years ago that cells deprived of adequate oxygen produce excessive quantities of lactate. The real-time monitoring of blood lactate concentration necessary in a critical care setting was only made possible by the development of electrode-based lactate biosensors around a decade ago. These biosensors are now incorporated into modern blood gas analyzers and other point-of-care analytical instruments, allowing lactate measurement by non-laboratory staff on a drop (100 L) of blood within a minute or two. Whilst blood lactate concentration is invariably raised in those with significant tissue hypoxia, it can also be raised in a number of conditions not associated with tissue hypoxia. Very often patients with raised blood lactate concentration (hyperlactatemia) also have a reduced blood pH (acidosis). The combination of hyperlactatemia and acidosis is called lactic acidosis. This is the most common cause of metabolic acidosis. The focus of this article is the causes and clinical significance of hyperlactatemia and lactic acidosis. The article begins with a brief overview of normal lactate metabolism. Normal lactate production and Continue reading >>

Lactic Acidosis

Lactic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>

Lactic Acidosis: Diagnosis And Treatment

Lactic Acidosis: Diagnosis And Treatment

Measurements of blood lactate levels can be very useful for detecting the presence of tissue underperfusion and for guiding therapy. Increased blood lactate levels usually reflect an imbalance between the oxygen demand and the oxygen supply to the cells, but other conditions may also be responsible. The present chapter first reviews the biochemistry of blood lactate, then reviews the clinical conditions associated with hyperlactatemia and finally discusses some therapeutic implications. Septic ShockBlood LactateLactate LevelLactic AcidosisBlood Lactate Level These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Zhang H, Vincent JL (1993) Arteriovenous differences in PCO2 and pH are good indicators of critical hypoperfusion. Am Rev Respir Dis 148:867871 PubMed CrossRef Google Scholar Iberti TJ, Leibowitz AB, Papadakos PJ et al (1990) Low sensitivity of the anion gap as a screen to detect hyperlactatemia in critically ill patients. Crit Care Med 18:275277 PubMed CrossRef Google Scholar Poortmans JR, Bossche JD, Leclercq R (1978) Lactate uptake by inactive forearm during progressive leg exercise. J Appl Pysiol 45:835839 Google Scholar Freyschuss U, Strandell T (1967) Limb circulation during arm and leg exercise in supine position. J Appl Physiol 23:163170 PubMed Google Scholar Watt PW, MacLennan PA, Hundai HS et al (1988) L(+)-Lactate transport in perfused rat skeletal muscle: kinetic characteristics and sensitivity to pH and transport inhibitors. Biochem Biophys Acta 944:213222 PubMed CrossRef Google Scholar Graham TE, Barclay JK, Wilson BA (1986) Skeletal Continue reading >>

Etiology And Therapeutic Approach To Elevated Lactate

Etiology And Therapeutic Approach To Elevated Lactate

Etiology and therapeutic approach to elevated lactate aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States aResearch Center for Emergency Medicine, Aarhus University Hospital, Denmark bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States cDepartment of Medicine, Division of Pulmonary Critical Care Medicine, Beth Israel Deaconess Medical Center, Boston, MA, United States dDepartment of Anesthesia Critical Care, Beth Israel Deaconess Medical Center, Boston, MA, United States Corresponding author: Michael W. Donnino Beth Israel Deaconess Medical Center One Deaconess Road, W/CC 2 Boston, Boston, MA 02215 Phone: 617-754-2450 Fax: 617-754-2350 [email protected] The publisher's final edited version of this article is available at Mayo Clin Proc See other articles in PMC that cite the published article. Lactate levels are commonly evaluated in acutely ill patients. Although most commonly used in the context of evaluating shock, lactate can be elevated for many reasons. While tissue hypoperfusion is probably the most common cause of elevation 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 >>

D-lactic Acidosis: An Underrecognized Complication Of Short Bowel Syndrome

D-lactic Acidosis: An Underrecognized Complication Of Short Bowel Syndrome

D-Lactic Acidosis: An Underrecognized Complication of Short Bowel Syndrome Department of Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT 06102, USA Received 26 November 2014; Revised 28 March 2015; Accepted 8 April 2015 Copyright 2015 N. Gurukripa Kowlgi and Lovely Chhabra. 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. D-lactic acidosis or D-lactate encephalopathy is a rare condition that occurs primarily in individuals who have a history of short bowel syndrome. The unabsorbed carbohydrates act as a substrate for colonic bacteria to form D-lactic acid among other organic acids. The acidic pH generated as a result of D-lactate production further propagates production of D-lactic acid, hence giving rise to a vicious cycle. D-lactic acid accumulation in the blood can cause neurologic symptoms such as delirium, ataxia, and slurred speech. Diagnosis is made by a combination of clinical and laboratory data including special assays for D-lactate. Treatment includes correcting the acidosis and decreasing substrate for D-lactate such as carbohydrates in meals. In addition, antibiotics can be used to clear colonic flora. Although newer techniques for diagnosis and treatment are being developed, clinical diagnosis still holds paramount importance, as there can be many confounders in the diagnosis as will be discussed subsequently. D-lactic acidosis (D-la) is a rare form of lactic acidosis seen mostly in patients with short bowel syndrome (SBS). Other conditions implicated are toxic ingestions of chemicals such as propylene glycol and rarely in patients with severe diabetic Continue reading >>

Life Threatening Lactic Acidosis

Life Threatening Lactic Acidosis

M Lemyze, specialist registrar in critical care medicine 1 , J F Baudry, specialist registrar in critical care medicine 2 , F Collet, specialist registrar in critical care medicine 2 , N Guinard, specialist registrar in critical care medicine 2 1Department of Critical Care Medicine, Schaffner Hospital, 62300 Lens, France 2Department of Critical Care Medicine, Broussais Hospital, 35400 Saint Malo, France Correspondence to: M Lemyze malcolmlemyze{at}yahoo.fr An 83 year old woman with diabetes presented to the emergency department with progressive shortness of breath and a two week history of diarrhoea. Her drugs included aspirin, 75 mg four times a day; a combination of irbesartan with hydrochlorothiazide, 300/25 mg four times a day; and metformin, 1000 mg three times a day. She had no previously known renal insufficiency, but on arrival she was oliguric, disoriented, and confused. Her respiratory rate was 32 breaths/min, blood pressure was 76/46 mm Hg, heart rate was 125 beats/min, and rectal temperature reached 36.8C. She had cool and clammy extremities and a persistent skinfoldadditional evidence of severe dehydration. Arterial blood gases showed a profound lactic acidosis, with pH 6.72, partial pressure of carbon dioxide (PCO2) 14 mm Hg, partial pressure of oxygen (PO2) 106 mm Hg, bicarbonate 12 mmol/l, and a high lactate concentration of 17.4 mmol/l. Laboratory results showed a normal blood glucose concentration of 9 mmol/l, a serum urea of 22 mmol/l, a serum creatinine of 779 mol/l, an increased serum potassium concentration of 6.8 mmol/l, and a decreased prothrombin activity of 43% (prothrombin time of 21 seconds). Chest and abdominal examination, chest radiography, urine dipstick, plasma C reactive protein (<5 mg/l), and procalcitonin (<0.5 g/l) concentrations sh Continue reading >>

Acute Lactic Acidosis - General Practice Notebook

Acute Lactic Acidosis - General Practice Notebook

Lactic acid is the end product of anaerobic glycolysis. Lactate is in equilibrium with pyruvate, anaerobic conditions increasing the normal 10:1 lactate:pyruvate ratio. The concentration of lactate in the blood is usually less than 1 mM, but rise physiologically after severe exercise to as high as 10 mM. Lactic acidosis should be suspected in patients with a high anion gap metabolic acidosis, when uraemia and ketoacidosis have be excluded. Home| About us| Facebook| Contact us| Authors| Help| FAQ This site is intended for the use of healthcare professionals only. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions. Copyright 2016 Oxbridge Solutions Ltd. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions Ltd receives funding from advertising but maintains editorial independence more... GPnotebook stores small data files on your computer called cookies so that we can recognise you and provide you with the best service. If you do not want to receive cookies please do not use GPnotebook. 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 >>

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