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 >>
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 >>
Alcoholic Ketoacidosis
Increased production of ketone bodies due to: Dehydration (nausea/vomiting, ADH inhibition) leads to increased stress hormone production leading to ketone formation Depleted glycogen stores in the liver (malnutrition/decrease carbohydrate intake) Elevated ratio of NADH/NAD due to ethanol metabolism Increased free fatty acid production Elevated NADH/NAD ratio leads to the predominate production of β–hydroxybutyrate (BHB) over acetoacetate (AcAc) Dehydration Fever absent unless there is an underlying infection Tachycardia (common) due to: Dehydration with associated orthostatic changes Concurrent alcohol withdrawal Tachypnea: Common Deep, rapid, Kussmaul respirations frequently present Nausea and vomiting Abdominal pain (nausea, vomiting, and abdominal pain are the most common symptoms): Usually diffuse with nonspecific tenderness Epigastric pain common Rebound tenderness, abdominal distension, hypoactive bowel sounds uncommon Mandates a search for an alternative, coexistent illness Decreased urinary output from hypovolemia Mental status: Minimally altered as a result of hypovolemia and possibly intoxication Altered mental status mandates a search for other associated conditions such as: Head injury, cerebrovascular accident (CVA), or intracranial hemorrhage Hypoglycemia Alcohol withdrawal Encephalopathy Toxins Visual disturbances: Reports of isolated visual disturbances with AKA common History Chronic alcohol use: Recent binge Abrupt cessation Physical Exam Findings of dehydration most common May have ketotic odor Kussmaul respirations Palmar erythema (alcoholism) Lab Acid–base disturbance: Increased anion gap metabolic acidosis hallmark Mixed acid–base disturbance common: Respiratory alkalosis Metabolic alkalosis secondary to vomiting and dehydration Hyperchlorem Continue reading >>
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 >>
Lactic Acidosis And Acute Ethanol Intoxication - Sciencedirect
Volume 12, Issue 1 , January 1994, Pages 32-35 Get rights and content Ethanol intoxication has been widely reported as a cause of lactic acidosis. To determine the frequency and severity of ethanol-induced lactic acidosis, patients who presented to an emergency department with a clinical diagnosis of acute ethanol intoxication and a serum ethanol concentration of at least 100 mg/dL were studied. Arterial blood was sampled for lactate and blood gas determinations. A total of 60 patients (mean age, 41 years) were studied. Twenty-two patients sustained minor trauma. Ethanol concentrations ranged from 100 to 667 mg/dL (mean, 287 mg/dL). Lactate concentrations were abnormal (>2.4 mmol/L) in seven patients (11.7%). In all cases, blood lactate was less than 5 mmol/L. Of the patients with elevated lactate, other potential causes for lactic acidosis, including hypoxia, seizures, and hypoperfusion, were also present. Only one case with elevated blood lactate concentration had associated acidemia. Significant elevations of blood lactate are uncommon in acute ethanol intoxication. In patients with ethanol intoxication who are found to have lactic acidosis, other etiologies for the elevated lactate level should be considered. 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 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 >>
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 >>
Emergent Treatment Of Alcoholic Ketoacidosis
Exenatide extended-release causes an increased incidence in thyroid C-cell tumors at clinically relevant exposures in rats compared to controls. It is unknown whether BYDUREON BCise causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans, as the human relevance of exenatide extended-release-induced rodent thyroid C-cell tumors has not been determined BYDUREON BCise is contraindicated in patients with a personal or family history of MTC or in patients with Multiple Endocrine Neoplasia syndrome type 2 (MEN 2). Counsel patients regarding the potential risk of MTC with the use of BYDUREON BCise and inform them of symptoms of thyroid tumors (eg, mass in the neck, dysphagia, dyspnea, persistent hoarseness). Routine monitoring of serum calcitonin or using thyroid ultrasound is of uncertain value for detection of MTC in patients treated with BYDUREON BCise Acute Pancreatitis including fatal and non-fatal hemorrhagic or necrotizing pancreatitis has been reported. After initiation, observe patients carefully for symptoms of pancreatitis. If suspected, discontinue promptly and do not restart if confirmed. Consider other antidiabetic therapies in patients with a history of pancreatitis Acute Kidney Injury and Impairment of Renal Function Altered renal function, including increased serum creatinine, renal impairment, worsened chronic renal failure, and acute renal failure, sometimes requiring hemodialysis and kidney transplantation have been reported. Not recommended in patients with severe renal impairment or end-stage renal disease. Use caution in patients with renal transplantation or moderate renal impairment Gastrointestinal Disease Because exenatide is commonly associated with gastrointestinal adverse reactions, not recommended in patients with sev Continue reading >>
Increased Osmolal Gap In Alcoholic Ketoacidosis And Lactic Acidosis
Increased Osmolal Gap in Alcoholic Ketoacidosis and Lactic Acidosis Jeffrey R. Schelling, MD; Randy L. Howard, MD; Sara D. Winter, MD; Stuart L. Linas, MD Objective: To determine whether an elevated osmolal gap is specific for toxic alcohol ingestion. Setting: Emergency room and medical and surgical inpatient wards at a university-affiliated hospital. Patients: Twenty-three patients with lactic acidosis, 19 with alcoholic ketoacidosis, and 10 randomly selected controls. Measurements and Main Results: Calculated and measured serum osmolality was determined in all study participants. The osmolal gap was increased in patients with lactic acidosis (17.4 5.4 mmol/kg) and alcoholic ketoacidosis (26.9 7.6 mmol/kg) when compared with controls (- 1.7 1.7 mmol/kg, P < 0.05 for both comparisons). When ethanol was included in the calculation, the osmolal gap remained elevated in the lactic acidosis (10.3 2.0 mmol/kg) and alcoholic ketoacidosis (11.1 3.2 mmol/kg) groups (P < 0.05 for both comparisons). Conclusions: The osmolal gap is often used as a screen for toxic alcohol ingestion. When calculating the osmolal gap, the contribution of ethanol should be considered. An elevated osmolal gap is not specific for toxic alcohol ingestion, as the osmolal gap was elevated in patients with lactic acidosis and alcoholic ketoacidosis. These two conditions should be considered when using the osmolal gap to design therapy (for example, hemodialysis) in the setting of anion gap metabolic acidosis and suspected toxic alcohol ingestion. Continue reading >>
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 >>
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Lactic Acidosis And Acute Ethanol Intoxication.
Lactic acidosis and acute ethanol intoxication. MacDonald L(1), Kruse JA, Levy DB, Marulendra S, Sweeny PJ. (1)Division of Critical Care Medicine, Wayne State University School of Medicine, Detroit, MI. Ethanol intoxication has been widely reported as a cause of lactic acidosis. Todetermine the frequency and severity of ethanol-induced lactic acidosis, patientswho presented to an emergency department with a clinical diagnosis of acuteethanol intoxication and a serum ethanol concentration of at least 100 mg/dL werestudied. Arterial blood was sampled for lactate and blood gas determinations. Atotal of 60 patients (mean age, 41 years) were studied. Twenty-two patientssustained minor trauma. Ethanol concentrations ranged from 100 to 667 mg/dL(mean, 287 mg/dL). Lactate concentrations were abnormal (> 2.4 mmol/L) in sevenpatients (11.7%). In all cases, blood lactate was less than 5 mmol/L. Of thepatients with elevated lactate, other potential causes for lactic acidosis,including hypoxia, seizures, and hypoperfusion, were also present. Only one case with elevated blood lactate concentration had associated acidemia. Significantelevations of blood lactate are uncommon in acute ethanol intoxication. Inpatients with ethanol intoxication who are found to have lactic acidosis, otheretiologies for the elevated lactate level should be considered. Continue reading >>
Emergent Treatment Of Alcoholic Ketoacidosis
Emergent Treatment of Alcoholic Ketoacidosis Author: Adam Blumenberg, MD, MA; Chief Editor: Erik D Schraga, MD more... Alcoholic ketoacidosis (AKA) is an acute metabolic acidosis seen in persons with a recent history of binge drinking and little or no nutritional intake. Alcoholic ketoacidosis is characterized by high serum ketone levels and an elevated anion gap (see the Anion Gap calculator). A concomitant metabolic alkalosis is also common, resulting from vomiting and volume depletion. Although AKA most commonly occurs in adults with alcoholism, alcoholic ketoacidosis has been reported in less-experienced drinkers of all ages. [ 1 , 2 ] Go to Alcoholic Ketoacidosis , Metabolic Alkalosis , and Pediatric Metabolic Alkalosis for complete information on these topics. Assess the patient's airway and manage as clinically indicated. Administer oxygen as indicated. Obtain intravenous access and administer fluid resuscitation for volume depletion and/or hypotension. Consider and treat hypoglycemia. [ 3 ] If the patient's mental status is diminished, consider administration of naloxone and thiamine . Note information about the patient's social situation and the presence of intoxicating agents besides alcohol. Suspect alcoholic ketoacidosis in any patient with recent binge drinking and an elevated anion gap. A history of alcoholism is not necessary for the development of alcoholic ketoacidosis. One episode of heavy alcohol intake combined with inadequate carbohydrate intake is sufficient to generate this disease state. Presenting symptoms may include nausea & vomiting, malaise, abdominal pain, dizziness, tremulousness, tachypnea, tachycardia, and hypotension. [ 4 ] Urine tests for ketones may be falsely negative or only trace positive in alcoholic ketoacidosis. This is because Continue reading >>
Increased Osmolal Gap In Alcoholic Ketoacidosis And Lactic Acidosis
Increased Osmolal Gap in Alcoholic Ketoacidosis and Lactic Acidosis Jeffrey R. Schelling, MD; Randy L. Howard, MD; Sara D. Winter, MD; Stuart L. Linas, MD Objective: To determine whether an elevated osmolal gap is specific for toxic alcohol ingestion. Setting: Emergency room and medical and surgical inpatient wards at a university-affiliated hospital. Patients: Twenty-three patients with lactic acidosis, 19 with alcoholic ketoacidosis, and 10 randomly selected controls. Measurements and Main Results: Calculated and measured serum osmolality was determined in all study participants. The osmolal gap was increased in patients with lactic acidosis (17.4 5.4 mmol/kg) and alcoholic ketoacidosis (26.9 7.6 mmol/kg) when compared with controls (- 1.7 1.7 mmol/kg, P < 0.05 for both comparisons). When ethanol was included in the calculation, the osmolal gap remained elevated in the lactic acidosis (10.3 2.0 mmol/kg) and alcoholic ketoacidosis (11.1 3.2 mmol/kg) groups (P < 0.05 for both comparisons). Conclusions: The osmolal gap is often used as a screen for toxic alcohol ingestion. When calculating the osmolal gap, the contribution of ethanol should be considered. An elevated osmolal gap is not specific for toxic alcohol ingestion, as the osmolal gap was elevated in patients with lactic acidosis and alcoholic ketoacidosis. These two conditions should be considered when using the osmolal gap to design therapy (for example, hemodialysis) in the setting of anion gap metabolic acidosis and suspected toxic alcohol ingestion. Continue reading >>
Alcohol And Metformin | Alcohol With Metformin Side Effects
What are the possible interactions of alcohol and metformin? What should you know about alcohol with metformin side effects? These are common questions people about metformin, which is a diabetic drug. Below what should be known about alcohol and metformin will be covered, including the possible alcohol with metformin side effects. Metformin is a drug that’s used to treat type 2 diabetes, and it can be used alone or with other medicines, and in adults and children. For people who are at risk of developing diabetes it can also be used as a way to prevent that, and it can be used as a treatment option for polycystic ovaries and weight gain due to the use of certain medicines. Metformin helps control high blood sugar levels, and this can in turn help prevent serious complications like kidney damage, nerve problems, and blindness. When your diabetes is well-controlled, it can also help lower the risk of a stroke or heart attack. The way metformin works is by restoring the way your body responds to the insulin you produce, and it decreases the amount of sugar made by your liver, and thereby absorbed by your stomach and intestines. Side effects of metformin can include nausea, vomiting, general upset stomach, diarrhea, weakness or a metallic taste in your mouth. In some cases, if metformin is taken with other diabetic medications, it can cause low blood sugar, but this isn’t usually a symptom of this medicine on its own. Understanding drug interactions is important with any medicine you’re prescribed, which is why you should tell your doctor about all other medicines you’re taking, your medical history, and even supplements and vitamins you take. Some of the medicines that can interact with metformin include beta-blockers and any medicine that affects your blood sugar Continue reading >>
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 >>
