Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition
(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Metabolic acidosis is acid accumulation due to Increased acid production or acid ingestion Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis ). Lactic acidosis (due to physiologic processes) Lactic acidosis (due to exogenous toxins) Toluene (initially high gap; subsequent excretion of metabolites normalizes gap) HIV nucleoside reverse transcriptase inhibitors Biguanides (rare except with acute kidney injury) Normal anion gap (hyperchloremic acidosis) Renal tubular acidosis, types 1, 2, and 4 The most common causes of a high anion gap metabolic acidosis are Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis ), but it also occurs with chronic alcoholism (see alcoholic ketoacidos Continue reading >>
Drug-induced Acid-base Disorders
Abstract The incidence of acid-base disorders (ABDs) is high, especially in hospitalized patients. ABDs are often indicators for severe systemic disorders. In everyday clinical practice, analysis of ABDs must be performed in a standardized manner. Highly sensitive diagnostic tools to distinguish the various ABDs include the anion gap and the serum osmolar gap. Drug-induced ABDs can be classified into five different categories in terms of their pathophysiology: (1) metabolic acidosis caused by acid overload, which may occur through accumulation of acids by endogenous (e.g., lactic acidosis by biguanides, propofol-related syndrome) or exogenous (e.g., glycol-dependant drugs, such as diazepam or salicylates) mechanisms or by decreased renal acid excretion (e.g., distal renal tubular acidosis by amphotericin B, nonsteroidal anti-inflammatory drugs, vitamin D); (2) base loss: proximal renal tubular acidosis by drugs (e.g., ifosfamide, aminoglycosides, carbonic anhydrase inhibitors, antiretrovirals, oxaliplatin or cisplatin) in the context of Fanconi syndrome; (3) alkalosis resulting from acid and/or chloride loss by renal (e.g., diuretics, penicillins, aminoglycosides) or extrarenal (e.g., laxative drugs) mechanisms; (4) exogenous bicarbonate loads: milk–alkali syndrome, overshoot alkalosis after bicarbonate therapy or citrate administration; and (5) respiratory acidosis or alkalosis resulting from drug-induced depression of the respiratory center or neuromuscular impairment (e.g., anesthetics, sedatives) or hyperventilation (e.g., salicylates, epinephrine, nicotine). Notes Continue reading >>
Drug-induced Metabolic Acidosis
Go to: Introduction Metabolic acidosis is defined as an excessive accumulation of non-volatile acid manifested as a primary reduction in serum bicarbonate concentration in the body associated with low plasma pH. Certain conditions may exist with other acid-base disorders such as metabolic alkalosis and respiratory acidosis/alkalosis 1. Humans possess homeostatic mechanisms that maintain acid-base balance ( Figure 1). One utilizes both bicarbonate and non-bicarbonate buffers in both the intracellular and the extracellular milieu in the immediate defense against volatile (mainly CO 2) and non-volatile (organic and inorganic) acids before excretion by the lungs and kidneys, respectively. Renal excretion of non-volatile acid is the definitive solution after temporary buffering. This is an intricate and highly efficient homeostatic system. Derangements in over-production, under-excretion, or both can potentially lead to accumulation of excess acid resulting in metabolic acidosis ( Figure 1). Drug-induced metabolic acidosis is often mild, but in rare cases it can be severe or even fatal. Not only should physicians be keenly aware of this potential iatrogenic complication but they should also be fully engaged in understanding the pathophysiological mechanisms. Metabolic acidosis resulting from drugs and/or ingestion of toxic chemicals can be grouped into four general categories ( Figure 2): Some medications cannot be placed into one single category, as they possess multiple mechanisms that can cause metabolic acidosis. In suspected drug-induced metabolic acidosis, clinicians should establish the biochemical diagnosis of metabolic acidosis along with the evaluation of respiratory compensation and whether there is presence of mixed acid-based disorders 2, then convert the bioche Continue reading >>
8drug And Chemical-induced Metabolic Acidosis
Volume 12, Issue 2 , July 1983, Pages 391-411 8Drug and chemical-induced metabolic acidosis Author links open overlay panel Robert A.Kreisberg Barry C.Wood Get rights and content Metabolic acidosis produced by drugs and/or chemicals can be convenientlydivided into those with an increase in the anion gap (anion gap = Na-(Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and -hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed. Continue reading >>
- Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA)*
- Ultraviolet Radiation Suppresses Obesity and Symptoms of Metabolic Syndrome Independently of Vitamin D in Mice Fed a High-Fat Diet
- Why Diabetes Is Dangerous: How to Recognize the Signs of this Metabolic Disease
What Is Metabolic Acidosis?
Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>
Drug-induced Hypokalemia, Hypophosphatemia, Hyperchloremic Metabolic Acidosis: Causes & Diagnoses | Symptoma.com
Secreted phosphate provides a buffer as well. [pedclerk.bsd.uchicago.edu] [] renal acid-base regulation due to impaired ability to acidify the urine and excrete acid results in net acid retention and hyperchloremic normal anion gap metabolic acidosis [lifeinthefastlane.com] induced Hypokalemia occurs with drugs that stimulate renal potassium excretion such as mineralcorticoids (mimic effects of aldosterone) and diuretics (except potassium sparing [quizlet.com] The role of dental protein in calcium and phosphate metabolism and renal function needs further research. [indianjnephrol.org] Diagnosis Hyperchloremic metabolic acidosis, normo or hypokalemia, decreased titulable acidity in urine, hypercalciuria and/or hipocitraturia. [renaltube.com] The causes of type I dRTA in adults are autoimmune disorders (Sjogren's syndrome, rheumatoid arthritis), hypercalciuria, recreational toluene sniffing and drug-induced (amphotericin [journal-ina.com] Definition (CSP) abnormally decreased amounts of phosphates in the blood; manifestations include hemolysis, lassitude, weakness, and convulsions. [fpnotebook.com] Table 1 Etiology of drug-induced hypophosphatemia 1. [qjmed.oxfordjournals.org] Deficiency of phosphorus from decreased intestinal absorption 1. [enotes.tripod.com] Missing:Hyperchloremic Metabolic Acidosis K) Specific drug therapy for Acute Pancreatitis No proven therapy for the treatment of acute pancreatitis. [epomedicine.com] E) Correct Electrolyte Abnormalities if present: Hypocalcemia: Calcium gluconate 10%: 10 mL IV over 1520 min Hypokalemia: KCl 10 mEq/h IV over 1 hr Hypomagnesemia (alcohol [epomedicine.com] Other causes of amylase: Macroamylasemia , Renal failure, Mumps parotitis , ERCP induced, Esophageal perforation, Pregnancy Imaging Studies in Acute Pancreatitis P Continue reading >>
Acid-base Physiology
8.6 Metabolic Acidosis due to Drugs and Toxins Several drugs and toxins have been implicated as direct or indirect causes of a high-anion gap metabolic acidosis (HAGMA). A consideration of these drugs needs to be included in an differential diagnosis of a HAGMA. The three most common ones to consider are methanol , ethylene glycol and salicylates . Other toxins which can cause acidosis are isopropyl alcohol and butoxyethanol. Toluene also causes an acidosis and the anion gap may be normal or elevated. The acidosis caused by these toxins may sometimes present as a normal anion-gap hyperchloraemic acidosis so don't exclude the diagnosis in such a circumstance. Co-ingestion of ethanol delays the metabolism of the more toxic methanol and ethylene glycol but can also delays the diagnosis. In this situation the osmolar gap will be even more elevated than can be explained by the measured ethanol level alone. [See also Section 11.3 : Acid-Base Disorders due to Drugs & Toxins.] Ingestion of methanol can occur accidentally, or deliberately if used as an ethanol substitute. Methanol itself is non-toxic. Onset of symptoms is delayed until the toxic metabolites are produced by theliver. Because the hepatic metabolism is slow, there is usually a considerable latent period (12-48 hours) before any toxic effects develop. Patients presenting early with a history of methanol ingestion have few symptoms due to the methanol (other than mild CNS depression), but may have symptoms due to other drugs or toxins (e.g. ethanol). Additionally co-ingestion of ethanol also contributes to the latent period by delaying metabolism of methanol. Patients presenting late are often deeply comatose and bradycardic with depressed respirations. Survivors have a high incidence of irreversible blindness. Abdo Continue reading >>
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 >>
Drug-induced Metabolic Acidosis
Pharmacologically-Induced Metabolic Acidosis. Liamis G et al. Drug Saf 2010 May 1; 33:371-391. This somewhat wordy article is a complete review of drug-induced metabolic acidosis, and well worth reading for those interested in expanding their knowledge beyond the mnemonic MUDPILES or reviewing the 4 types of renal tubular acidosis. There is so much detail here that the paper is impossible to summarize, but here are some of its clinical pearls: Most of the patients who develop metformin-associated lactic acidosis had been taking the drug despite have a contraindication to its use, such as renal insufficiency or severe underlying disease. Antiviral therapy, especially nucleotide reverse transcriptase inhibitors, have been associated with life-threatening metabolic acidosis. Drugs implicated most often include didanosine, stavudine, and zidovudine. Linezolid impairs mitochondrial function and can cause metabolic acidosis, usually after prolonged therapy. The occurrence of metabolic acidosis in patients on propofol may herald onset of propofol infusion syndrome , which has a mortality rate of greater than 80%. Occult laxative abuse is on the differential diagnosis for a patient with unexplained hyperchloremic metabolic acidosis. Continue reading >>
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 >>
Topiramate And Metabolic Acidosis: An Evolving Story
Get access/doi/full/10.1080/21548331.2017.1370969?needAccess=true Topiramate is an anticonvulsant that is being increasingly used for a number of different off-label indications. Its inhibition of carbonic anhydrase isoenzymes can lead to metabolic acidosis, elevated urine pH, reduced urine citrate, and hypercalciuria, thereby creating a milieu that is ripe for calcium phosphate stone formation. In this review, we describe a case of topiramate-induced metabolic acidosis. We review the frequency of metabolic acidosis among children and adults, as well as the mechanism of hyperchloremic metabolic acidosis and renal tubular acidosis in topiramate users. Finally, we describe the long-term effects of topiramate-induced metabolic acidosis, including nephrolithiasis, nephrocalcinosis, and bone degradation. Patients who are prescribed topiramate should be carefully monitored for metabolic derangements, and they may benefit from alkali supplementation, or in extreme cases, discontinuation of the drug altogether. Continue reading >>
Drug-induced Metabolic Acidosis
Moe, Orson W. ; Pham, Amy Quynh Trang ; Xu, Li Hao Richie. / Drug-Induced Metabolic Acidosis . In: F1000Research . 2015 ; Vol. 4. @article{4757cc9a0238471c8ee7bd9f0136f127, title = "Drug-Induced Metabolic Acidosis", abstract = "Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is imperative that clinicians not only are fully aware of the list of drugs that may lead to metabolic acidosis but also understand the underlying pathogenic mechanisms. In this review, we categorized drug-induced metabolic acidosis in terms of pathophysiological mechanisms, as well as individual drugs' characteristics.", author = "Moe, {Orson W.} and Pham, {Amy Quynh Trang} and Xu, {Li Hao Richie}", N2 - Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is imperative that clinicians not only are fully aware of the list of drugs that may lead to metabolic acidosis but also understand the underlying pathogenic mechanisms. In this review, we categorized drug-induced metabolic acidosis in terms of pathophysiological mechanisms, as well as individual drugs' characteristics. AB - Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. Occurrences are usually accompanied by comorbid conditions of drug-induced metabolic acidosis, and clinical outcomes may range from mild to fatal. It is i Continue reading >>
Toxin-induced Metabolic Acidosis
Acid-base disorders, poisoning, toxic, toxins, overdose, metabolic acidosis, acidosis, anion gap metabolic acidosis, strong ion gap acidosis Metabolic acidosis is a common and serious presentation of several toxins. Toxin-induced metabolic acidosis can be due to multiple diverse pathways and can become become evident at various stages and time-frames of the poisoning. These include organic acid production through metabolic pathways, exogenous acid addition, tissue hypoperfusion, renal impairment and cytopathic pathways. These variable pathways and presentations make the diagnosis and treatment challenging, and when a poisoning is suspected, consultation with a regional poison center and toxicologist is hightly recommended. There are numerous toxins that produce acid-base disturbances; however, we will only discuss the most common and serious toxins that result in a metabolic acidosis. The clinical features of metabolic acidosis are similar regardless of the etiology. Depending on the toxin, type and amount of exposure, there may be other specific clinical features. These may include respiratory compensatory signs such as tachypnea and Kussmaul respirations. Hyperventilation (rapid shallow or Kussmaul respirations). Chest pain, cardiac dysrhythmias, palpations. Many poisoned patients are unable to provide a reliable history; therefore, laboratory and other ancillary testing is essential. Some patients will present with classic toxidromes (e.g. opioid, anticholinergic, cholinergic or sympathomimetic), others will have family or friends relay important information regarding recent activity and possible exposure. To adequately assess these patients, it is essential to use a systematic approach, as many different poisons will have subtle overlapping signs and symptoms. Mana Continue reading >>
Drug And Chemical-induced Metabolic Acidosis.
Abstract Metabolic acidosis produced by drugs and/or chemicals can be conveniently divided into those with an increase in the anion gap (anion gap = Na- (Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and beta-hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed. Continue reading >>
- Diabetes drug and aspirin boosts cancer drug effectiveness | Daily Mail Online
- Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA)*
- Ultraviolet Radiation Suppresses Obesity and Symptoms of Metabolic Syndrome Independently of Vitamin D in Mice Fed a High-Fat Diet
(pdf) Drug-induced Metabolic Acidosis
Background: Tigecycline (TGC) is a last resort antibiotic having broad spectrum antibacterial activity againstgram-negative bacteria. Beyond its standard dosing regimen, a double dosing regimen has been practicing forlast couple of years to achieve adequate drug concentration in the targeted body tissues. TGC interferes with themitochondrial protein translation process and may lead to non-anion gap acute metabolic acidosis (NAGAMA) withlow blood-pH level. The main objective of this retrospective study was to evaluate the frequency of high dose TGCinducedNAGAMA events in the South Asian critically ill patients.Methods: The retrospective data of 24 critically ill patients of an intensive care unit (ICU) were considered forthis study. Patients of this study received high dose of TGC. Including all necessary laboratory data, patients aniongap, blood-pH level data in pre and post-TGC therapy were also recorded from the ICUs clinical-record archive. Allthe data were analyzed to find out the significance of NAGAMA event with high dose TGC therapy.Results: Among the patients administered with high dose TGC, 45.83% (11; n=24) of patients were experiencedwith NAGAMA event and in every 2.18 patients, 1 patient developed this event. Among those 11 patients, 63.64%of patients were recovered within 24 hours after stopping the TGC therapy and the rest of the patients (36.36%)were recovered within 48 hours, where 4 patients required therapeutic intervention to overcome the NAGAMA event.Conclusion: High dose TGC-induced NAGAMA event is an unusual event, globally. Mitochondrial toxicity isa TGC-associated adverse event and the related NAGAMA is a detrimental clinical consequence. However, thecomplete mechanism of this event is even not fully clear but, caution should be taken in the use Continue reading >>
