diabetestalk.net

Lactic Acidosis Alcohol

Alcoholism And Lactic Acidosis

Alcoholism And Lactic Acidosis

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

Survival From Profound Alcohol-related Lactic Acidosis - Sciencedirect

Survival From Profound Alcohol-related Lactic Acidosis - Sciencedirect

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

Emergent Treatment Of Alcoholic Ketoacidosis

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 >>

Lactic Acidosis And Acute Ethanol Intoxication - Sciencedirect

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 >>

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 >>

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 >>

What Is The Effect Of A Glass Of Wine After Taking Metformin?

What Is The Effect Of A Glass Of Wine After Taking Metformin?

It is generally acceptable to drink a glass of wine while taking metformin; however, it's best to be careful because of the risk of lactic acidosis. Additionally, there is a risk of hypoglycemia when a diabetes patient drinks alcohol, whether or not the patient takes metformin. Symptoms of hypoglycemia include hunger, shakiness, nervousness, sweating, dizziness, sleepiness, confusion, difficulty speaking, anxiety and weakness. Symptoms of lactic acidosis include nausea, vomiting, hyperventilation, abdominal pain, lethargy, anxiety, hypotension, rapid or irregular heart rate and metal status changes. If you take metformin or are diabetic, ask your doctor if it's safe to drink alcoholic beverages. Video of the Day Metformin is a biguanide, a type of oral medication used to treat Type 2 diabetes by helping control the amount of glucose in the blood. It primarily works to reduce gluconeogenesis, glucose production by the liver, but also aids in blood glucose control by increasing insulin sensitivity and decreasing glucose absorption in the gastrointestinal tract. The most common side effects of metformin are gastrointestinal related, but rarely, lactic acidosis can occur. Hypoglycemia is an unlikely side effect of metformin when it is used alone. The liver is largely responsible for clearing lactate from the body, and when a patient takes metformin, the rate of clearance by the liver is reduced. This is part of the reason for the correlation between taking metformin and the risk of lactic acidosis. Dr. Thomas Higgins, an endocrinologist at Boulder Medical Center, cautions against prescribing metformin to patients with conditions that predispose them to lactic acid accumulation. For example, use of metformin, which is not metabolized but cleared via tubular secretion into th Continue reading >>

Alcohol And Metformin | Alcohol With Metformin Side Effects

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 >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>

Increased Osmolal Gap In Alcoholic Ketoacidosis And Lactic Acidosis

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 >>

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

Severe Metabolic Acidosis In The Alcoholic: Differential Diagnosis And Management

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

Increased Osmolal Gap In Alcoholic Ketoacidosis And Lactic Acidosis

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 >>

Lactic Acidosis Induced By Metformin And A Large Amount Of Alcohol Drinking Into An Empty Stomach

Lactic Acidosis Induced By Metformin And A Large Amount Of Alcohol Drinking Into An Empty Stomach

Lactic acidosis induced by metformin and a large amount of alcohol drinking into an empty stomach Department of Pharmacy, the First Affiliated Hospital of Chongqing Medical UniversityChongqing 400016, China AbstractA 61-year-old male patient with type 2 diabetes received an oral metformin 850 mg about 30 minutes after drinking about 400 ml liquor containing 52% of alcohol into an empty stomach. About 4 hours later, the patient developed stuffy pain below xiphoid process and palpitation, and about 7 hous later, he developed nausea and vomiting. The laboratory examination showed that the blood pH 7.16, lactic acid 15.0 mmol/L, base excess -12.6 mmol/L, bicarbonate 15 mmol/L. He was diagnosed as diabetic lactic acidosis. Comprehensive treatments such as oxygen inhalation, acidosis correction, fluid infusion were given and metformin was changed to oral rosiglitazone 4 mg once daily. Eighteen hours later, the discomfort below xiphoid process was markedly improved, nausea and vomiting did not recur, his laboratory examination results showed the blood pH 7.41, lactic acid 1.8 mmol/L, base excess 2.3 mmol/L, and bicarbonate 27 mmol/L. Continue reading >>

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

Toxic Alcohol Ingestions: Clinical Features, Diagnosis, And Management

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

Emergent Treatment Of Alcoholic Ketoacidosis

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 >>

More in ketosis