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Is Lactic Acidosis?

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

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

Why Does Lactic Acid Build Up In Muscles? And Why Does It Cause Soreness?

Why Does Lactic Acid Build Up In Muscles? And Why Does It Cause Soreness?

As our bodies perform strenuous exercise, we begin to breathe faster as we attempt to shuttle more oxygen to our working muscles. The body prefers to generate most of its energy using aerobic methods, meaning with oxygen. Some circumstances, however—such as evading the historical saber tooth tiger or lifting heavy weights—require energy production faster than our bodies can adequately deliver oxygen. In those cases, the working muscles generate energy anaerobically. This energy comes from glucose through a process called glycolysis, in which glucose is broken down or metabolized into a substance called pyruvate through a series of steps. When the body has plenty of oxygen, pyruvate is shuttled to an aerobic pathway to be further broken down for more energy. But when oxygen is limited, the body temporarily converts pyruvate into a substance called lactate, which allows glucose breakdown—and thus energy production—to continue. The working muscle cells can continue this type of anaerobic energy production at high rates for one to three minutes, during which time lactate can accumulate to high levels. A side effect of high lactate levels is an increase in the acidity of the muscle cells, along with disruptions of other metabolites. The same metabolic pathways that permit the breakdown of glucose to energy perform poorly in this acidic environment. On the surface, it seems counterproductive that a working muscle would produce something that would slow its capacity for more work. In reality, this is a natural defense mechanism for the body; it prevents permanent damage during extreme exertion by slowing the key systems needed to maintain muscle contraction. Once the body slows down, oxygen becomes available and lactate reverts back to pyruvate, allowing continued aero Continue reading >>

What Is A Lactic Acid Blood Test?

What Is A Lactic Acid Blood Test?

It’s a test that measures the amount of lactic acid (also called “lactate”) in your blood. This acid is made in muscle cells and red blood cells. It forms when your body turns food into energy. Your body relies on this energy when its oxygen levels are low. Oxygen levels might drop during an intense workout or when you have an infection or disease. Once you finish your workout or recover from the illness, your lactic acid level tends to go back to normal. But sometimes, it doesn't. Higher-than-normal lactic acid levels can lead to a condition called lactic acidosis. If it’s severe enough, it can upset your body’s pH balance, which indicates the level of acid in your blood. Lactic acidosis can lead to these symptoms: It’s a simple blood test. Your doctor will draw blood from a vein or artery using a needle. In rare cases, he may take a sample of cerebrospinal fluid from your spinal column during a procedure called a spinal tap. Normally, you don’t have to adjust your routine to prepare for the test. If your lactic acid level is normal, you don’t have lactic acidosis. Your cells are making enough oxygen. It also tells your doctor that something other than lactic acidosis is causing your symptoms. He’ll likely order other tests to find out what it is. If your lactic acid level is high, it could be caused by a number of things. Most often, it’s because you have a condition that makes it hard for you to breathe in enough oxygen. Some of these conditions could include: Severe lung disease or respiratory failure Fluid build-up in your lungs Very low red blood cell count (severe anemia) A higher-than-normal lactic acid level in your blood can also be a sign of problems with your metabolism. And, your body might need more oxygen than normal because you have o 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 >>

Lactic Acidosis

Lactic Acidosis

Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's metabolism of lactic acid. Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include nausea, vomiting, rapid deep breathing, and generalised weakness. The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations, hemofiltration (purification of the blood) is temporarily required. In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as severe infections), it indicates an increased risk of death. Classification[edit] The Cohen-Woods classification categorizes causes of lactic acidosis as:[1] Type A: Decreased tissue oxygenation (e.g., from decreased blood flow) Type B B1: Underlying diseases (sometimes causing type A) B2: Medication or intoxication B3: Inborn error of metabolism Signs and symptoms[edit] Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with sepsis, the systemic inflammatory response syndrome due to another cause, severe physical trauma, or severe depletion of body fluids.[2] Symptoms in humans include all those of typical m Continue reading >>

Treatment Of Lactic Acidosis.

Treatment Of Lactic Acidosis.

Severe lactic acidosis is often associated with poor prognosis. Recognition and correction of the underlying process is the major step in the treatment of this serious condition. Intravenous administration of sodium bicarbonate has been the mainstay in the treatment of lactic acidosis. Aggressive use of this therapeutic modality, however, can lead to serious complications and should therefore be considered with caution. Peritoneal dialysis and hemodialysis provide large amounts of alkali without causing the hypernatremia or hypervolemia commonly associated with bicarbonate infusion. Peritoneal dialysis with bicarbonate-based dialysate, in particular, appears to be an ideal means of delivering physiologic buffer. Administration of methylene blue was initially thought to increase lactate metabolism by altering the cellular oxidative state. Its subsequent clinical use, however, showed little efficacy. Sodium nitroprusside has been advocated for the treatment of some forms of lactic acidosis as a method of alleviating regional hypoperfusion. Insulin therapy has been found to be quite useful in the treatment of phenformin-associated lactic acidosis and is recommended in this setting. Since dichloroacetate activates pyruvate dehydrogenase and enhances lactate metabolism, it may be a useful adjunct in the treatment of lactic acidosis. Continue reading >>

Lactic Acidosis

Lactic Acidosis

The buildup of lactic acid in the bloodstream. This medical emergency most commonly results from oxygen deprivation in the body’s tissues, impaired liver function, respiratory failure, or cardiovascular disease. It can also be caused by a class of oral diabetes drugs called biguanides, which includes metformin (brand name Glucophage). Another biguanide called phenformin was pulled from the market in the United States in 1977 because of an unacceptably high rate of lactic acidosis associated with its use. Concerns about lactic acidosis also delayed the introduction of metformin to the U.S. market until 1995, despite the fact that it had been widely used for years in other countries. There have been reports of lactic acidosis occurring in people taking metformin, and the U.S. Food and Drug Administration estimates that lactic acidosis occurs in 5 out of every 100,000 people who use metformin for any length of time. However, this risk is much lower than it was in people taking phenformin, and it is not clear whether the episodes of lactic acidosis associated with metformin have actually been due to metformin use. In fact, the lactic acidosis could have been explained by the person’s diabetes and related medical conditions. Nonetheless, diabetes experts recommend that metformin not be used in people with congestive heart failure, kidney disease, or liver disease. They also recommend that it be discontinued (at least temporarily) in people undergoing certain medical imaging tests called contrast studies. Symptoms of lactic acidosis include feeling very weak or tired or having unusual muscle pain or unusual stomach discomfort. Continue reading >>

Lactic Acidosis And Exercise

Lactic Acidosis And Exercise

Lactic acid builds up naturally in the muscles during vigorous activity. Sometimes if we've overdone it during a workout or run, the body can't clear lactic acid or lactate quickly enough, and lactic acid levels build up. Lactic acid can irritate muscles, causing discomfort and soreness. Sore muscles after exercising is called delayed onset muscle soreness or DOMS. Lactic acid is just one cause of DOMS. Because lactic acid is removed from muscles between a few hours to under a day after a workout, it can't be blamed for lasting soreness some days after working out. Cooling down or warming down after exercise can help remove the lactic acid as well as letting the heart rate slow down more gradually. Some severe medical conditions can also cause lactic acidosis, which can be dangerous. During exercise, muscles metabolise glucose (sugar) into energy. Muscles receive glucose continually through the blood, and also have their own stores of sugar (called glycogen). Every person has an upper limit of exercise ability, called the anaerobic threshold or lactate threshold. The lactate threshold is basically a measurement of how fit the heart and blood vessels are. With regular exercise training, a persons lactate threshold goes up. Exercising at an intensity level below the lactate threshold produces very little lactic acid and the body quickly clears what is produced. A person can exercise below the lactate threshold for a long time, even for hours. Once the intensity of exercise exceeds the lactate threshold, muscles begin to use glucose inefficiently, through alternative chemical reactions. Lactic acid is produced and can rapidly build up in the blood and muscles. When a person's exercise intensity crosses the lactate threshold the activity rapidly becomes much more difficult 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

Background In basic terms, lactic acid is the normal endpoint of the anaerobic breakdown of glucose in the tissues. The lactate exits the cells and is transported to the liver, where it is oxidized back to pyruvate and ultimately converted to glucose via the Cori cycle. In the setting of decreased tissue oxygenation, lactic acid is produced as the anaerobic cycle is utilized for energy production. With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from chronic dysfunction or excessive production), lactic acidosis ensues. [1, 2] (See Etiology.) Lactic acid exists in 2 optical isomeric forms, L-lactate and D-lactate. L-lactate is the most commonly measured level, as it is the only form produced in human metabolism. Its excess represents increased anaerobic metabolism due to tissue hypoperfusion. (See Workup.) D-lactate is a byproduct of bacterial metabolism and may accumulate in patients with short-gut syndrome or in those with a history of gastric bypass or small-bowel resection. [3] By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. In their classic 1976 monograph, Cohen and Woods classified the causes of lactic acidosis according to the presence or absence of adequate tissue oxygenation. (See Presentation and Differentials.) The causes of lactic acidosis are listed in the chart below. Go to Acute Lactic Ac Continue reading >>

Lactic Acidosis

Lactic Acidosis

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A Side Effect You Should Know About

A Side Effect You Should Know About

The glucose-lowering medication metformin (Glucophage) could cause lactic acidosis if your kidneys and liver are not working efficiently. Lactic acidosis is when high levels build up in the blood of a substance called lactic acid — a chemical that is normally produced by your body in small amounts and removed by your liver and kidneys. The risk of lactic acidosis goes up if you: have heart failure or a lung ailment have kidney or liver problems drink alcohol heavily In these cases, you might not be able to take metformin. If you don't have one of these problems, you are at a very low risk for developing lactic acidosis from metformin. You should, however, contact your doctor immediately if you suddenly develop any of these symptoms of lactic acidosis: diarrhea fast and shallow breathing muscle pain or cramping weakness tiredness or unusual sleepiness You should also let your doctor know if you get the flu or any illness that results in severe vomiting, diarrhea, and/or fever, or if your intake of fluids becomes significantly reduced. Severe dehydration can affect your kidney or liver function and increase your risk of lactic acidosis from metformin. Continue reading >>

Severe Lactic Acidosis Reversed By Thiamine Within 24 Hours

Severe Lactic Acidosis Reversed By Thiamine Within 24 Hours

Severe lactic acidosis reversed by thiamine within 24 hours 1Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, A-8036 Graz, Austria Karin Amrein: [email protected] ; Werner Ribitsch: [email protected] ; Ronald Otto: [email protected] ; Harald C Worm: [email protected] ; Rudolf E Stauber: [email protected] This article has been cited by other articles in PMC. Thiamine is a water-soluble vitamin that plays a pivotal role in carbohydrate metabolism. In acute deficiency, pyruvate accumulates and is metabolized to lactate, and chronic deficiency may cause polyneuropathy and Wernicke encephalopathy. Classic symptoms include mental status change, ophthalmoplegia, and ataxia but are present in only a few patients [ 1 ]. Critically ill patients are prone to thiamine deficiency because of preexistent malnutrition, increased consumption in high-carbohydrate nutrition, and accelerated clearance in renal replacement. In retrospective [ 2 ] and prospective [ 3 , 4 ] studies, a substantial prevalence of thiamine deficiency has been described in both adult (10% to 20%) and pediatric (28%) patients. Thiamine deficiency may become clinically evident in any type of malnutrition that outlasts thiamine body stores (2 to 3 weeks), including alcoholism, bariatric surgery, or hyperemesis gravidarum, and results in high morbidity and mortality if untreated [ 1 ]. We report the case of a 56-year-old man with profound lactic acidosis that resolved rapidly after thiamine infusion. He was admitted because of a decreased level of consciousness (Glasgow Coma Scale score of 6). Vital signs, including blood pressure, heart rate, and oxygen saturation, were normal. Besides reporting regular alcohol consumption, relatives reported recen Continue reading >>

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