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Lactic Acidosis

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 - Cancer Therapy Advisor

Lactic Acidosis - Cancer Therapy Advisor

Hyperlactatemia, anion gap metabolic acidosis, strong ion gap metabolic acidosis Tissue hypoperfusion, ischemia, anaerobic metabolism, shock, acid-base disorders Lactic acidosis associated with critical illness is commonly a byproduct of a much larger problem. In 1976 Cohen and Woods classified lactic acidosis based on etiology. Type A is due to clinical evidence of tissue hypoperfusion. Type B occurs in the absence of clinical evidence of tissue hypoperfusion. Type B is further divided into subgroups B1 - underlying disease/physiologic state; B2 - medication or toxin; and B3 - inborn errors of metabolism. In critically ill patients, lactic acidosis is typically associated with increased lactate production (hypoperfusion, mitochondrial dysfunction), and/or decreased metabolism/clearance. Approximately 1400 mmol of lactic acid is produced daily. The kidneys metabolize up to 30% with no significant elimination. The liver is very efficient in lactate metabolism and elimination and serum lactate levels should remain in the normal range until about 75% of hepatic function is lost. The clinical features of lactic acidosis are similar to other forms of metabolic acidoses. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Other clinical features are related to the underlying cause of lactic acidosis, such as signs of hypoperfusion. Hyperventilaton (rapid shallow or Kussmaul respirations). Seizure (generalized seizures can cause a transient lactic acidosis). Signs of hypovolemia (dry mucous membranes, decreased capillary refill, skin tenting, oliguria). Abdominal pain (especially with mesenteric ischemia). There may only be subtle clinical findings, therefore one needs to have a high suspicion in clinically relevent situations (e.g. i Continue reading >>

Hemodialysis For Lactic Acidosis

Hemodialysis For Lactic Acidosis

Department of Critical Care Medicine, Apollo First Med Hospital, Chennai, Tamil Nadu, India 1Department of Critical Care Medicine, Apollo Hospitals, Chennai, Tamil Nadu, India Address for correspondence: Dr. Ashwin K. Mani, Department of Critical Care Medicine, Apollo First Med Hospital, 154, PH Road, Chennai - 600 010, Tamil Nadu, India. E-mail: [email protected] Author information Copyright and License information Disclaimer Copyright : 2017 Indian Journal of Critical Care Medicine This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. Lactic acidosis (Type A) is common in critically ill patients and usually treated by correcting the underlying etiology. We present the case of a young female who presented with life-threatening lactic acidosis secondary to hematological malignancy. Timely initiation of hemodialysis was lifesaving. The case highlights the importance of considering Type B lactic acidosis (in this case secondary to a hematological malignancy) and also initiating renal replacement therapy when routine measures are ineffective. Keywords: Hematological malignancy, hemodialysis, hyperlactatemia, lactic acidosis, malignancy Lactic acidosis is very commonly encountered in the critical care units. Treatments are generally focused on improving oxygen delivery and restoring tissue perfusion. We present a patient with grossly elevated lactate levels associated with lymphoma which improved only after initiation of dialysis. A 21-year-old female patient was transferred from an outside hospital to our tertiary Crit 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. - Pubmed - Ncbi

Lactic Acidosis. - Pubmed - Ncbi

Division of Critical Care Medicine, Chicago Medical School, Illinois. An understanding of the pathophysiology of lactic acidosis is crucial in facilitating the optimal care of critically ill patients. The relevant biochemistry of lactic acidosis is reviewed, and the more controversial aspects relating to the genesis of the acidosis are highlighted. The current system of classification of lactic acidosis divides etiologies on the basis of the presence or absence of clinical signs of tissue hypoperfusion. Several types of lactic acidosis in which clinical evidence of tissue hypoperfusion is lacking demonstrate hemodynamic evidence of occult hypoperfusion. The diagnostic and therapeutic implications of this observation are discussed. Current diagnostic criteria for lactic acidosis include a pH less than 7.35 and blood lactate concentration greater than 5 to 6 mM/L. An important issue relates to the implications of lactate values that are greater than normal but below this diagnostic range. The use of the oxygen flux test may be valuable in the diagnosis of occult tissue hypoperfusion in patients with low-grade elevations in lactate levels. The current therapy for lactic acidosis involves addressing the primary cause and supportive management. The use of bicarbonate in the therapy for lactic acidosis is controversial due to potential adverse effects on cardiac function. The specifics of this controversy are outlined, and newer therapeutic alternatives are reviewed. The use of blood lactate concentration as a prognostic index may be more useful in patients with shock than without shock. 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 | Definition Of Lactic Acidosis By Medical Dictionary

Lactic Acidosis | Definition Of Lactic Acidosis By Medical Dictionary

Lactic acidosis | definition of lactic acidosis by Medical dictionary 1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH. 2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidotic. Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma. In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to acidosis are patients with shock, hyperthyroidism, advanced circulatory failure, renal failure, Continue reading >>

Hiv & Aids Information :: Factsheet Lactic Acidosis

Hiv & Aids Information :: Factsheet Lactic Acidosis

Please enter the email address. Separate multiple addresses with a comma. Lactic acidosis refers to a build-up of lactic acid in the blood. It is a rare but dangerous side-effect of some anti-HIV drugs most of these are no longer in regular use. Your HIV clinic will use blood tests to check your levels of lactic acid. Lacticacidosis is very rare. Nevertheless, it is an important subject to understandbecause people who develop the condition can become dangerously ill. Lacticacidosis is a serious side-effect of the nucleosidereverse transcriptaseinhibitor (NRTI)class of anti-HIV drugs. This class includes abacavir (Ziagen),didanosine (ddI, Videx), lamivudine (3TC, Epivir), stavudine (d4T,Zerit), tenofovir (Viread) andzidovudine (AZT, Retrovir). The drugsmost linked with lactic acidosis are stavudine and didanosine. However, neitherof these drugs is now used if any other treatment options are available, mainlybecause of the side-effects they can cause. Lactic acidosis is also apotential, but rare, side-effect of other drugs, including the commonlyprescribed diabetes drug, metformin. The term lactic acidosis is used to describehigh levels of a substance called lactate in the blood. Lactate is a by-productof the processing of sugar within the body. Lacticacidosis is one of several conditions which are believed to be caused by damage to mitochondria . Mitochondriaare found in all human cells and are involved in the production of energy.Other possible side-effects ofNRTIs which may also be associated withdamage to mitochondria include peripheral neuropathy (numbness or pain in the feetand hands); bone marrow suppression; pancreatitis (inflammation of thepancreas); hepatic steatosis (accumulation of fat in the liver); and myopathy(muscle damage). "Lactic acidosis may occurat a 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

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: 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 >>

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 >>

Lactic Acidosis

Lactic Acidosis

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Lactic Acidosis In Metformin-treated Patients. Prognostic Value Of Arterial Lactate Levels And Plasma Metformin Concentrations.

Lactic Acidosis In Metformin-treated Patients. Prognostic Value Of Arterial Lactate Levels And Plasma Metformin Concentrations.

Lactic acidosis in metformin-treated patients. Prognostic value of arterial lactate levels and plasma metformin concentrations. Service d'Endocrinologie-Nutrition, Hpital Universitaire, Amiens, France. [email protected] The antidiabetic drug metformin has been associated in a small number of patients with lactic acidosis, a serious condition with a poor prognosis. However, because of lack of data, the prognostic significance of hyperlactataemia in metformin-treated patients is not known. Data were collected from 49 metformin-treated patients with lactic acidosis (arterial lactate level > or = 5 mmol/L and blood pH < or = 7.35) and available plasma metformin concentration data to investigate the association of arterial lactate levels and plasma metformin concentrations with mortality. The overall mortality rate in this patients sample was 45% and the median arterial lactate level was 13.1 mmol/L. Median lactate levels were similar in patients who survived (13 mmol/L) and those who died (14.3 mmol/L), whereas the median plasma metformin concentration was 3 times higher in patients who survived (20.6 mg/L versus 6.3 mg/L). In this, the largest series of metformin-treated patients with lactic acidosis yet reported, 55% of patients survived and these patients had a median arterial lactate level of 13.1 mmol/L. Neither arterial lactate levels nor plasma metformin concentrations were of prognostic significance in relation to mortality in this sample of metformin-treated patients with lactic acidosis. Death in these patients appeared instead to be associated with other hypoxic disease or underlying ill health. These observations suggest that accumulation of metformin may not be as significant with respect to high arterial levels of lactate and their effects as has been traditio 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 >>

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