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 >>
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 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 >>
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Drug-induced Metabolic Acidosis A Link To The Article And Some Excerpts
For an excellent brief review of acid-base disorders see Acid-Base Interpretation Updated: Oct 30, 2015 from emedicine.medscape.com In addition to d-lactate, the D in GOLDMARK * [a mnemonic for the causes of anion gap metabolic acidosis] can also stand for drugs as a cause of metabolic acidosis. * This is the link to Best Case Ever 56 Anion Gap Metabolic Acidosis [link is to the podcast and shownotes] from Emergency Medicine Cases . An excellent article that discussesdrugs causing metabolic acidosis isDrug-Induced Metabolic Acidosis[ PubMed Abstract ] [ Full Text HTML ] [ Full Text PDF ].F1000Res. 2015 Dec 16;4. pii: F1000 Faculty Rev-1460. doi: 10.12688/f1000research.7006.1. eCollection 2015. What follows are the figuresfrom the above article [See article text for details]: Metabolic acidosis could emerge from diseases disrupting acid-base equilibrium or from drugs that induce similar derangements. . . .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. 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): 2. Drugs leading to loss of bicarbonate in the gastrointestinal Continue reading >>
(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 >>
Lactic Acidosis: Background, Etiology, Epidemiology
Author: Kyle J Gunnerson, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, MCCM more... 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 Presentationand Differe Continue reading >>
Methamphetamine Overdose And Metabolic Acidosis
Begin your recovery from addiction today. Change starts with one call. (855) 837-1334 Brought to you by Elements Behavioral Health Methamphetamine Overdose and Metabolic Acidosis Posted in Stimulants by Arny Escobar Metabolic acidosis is a term used to describe the buildup of excessive amounts of acid in the bodys various fluids. In some cases, this buildup stems from excessive acid production inside the body; in other cases, it stems from the kidneys inability to eliminate sufficient amounts of acid from the bloodstream. Whatever the underlying cause, unchecked metabolic acidosis can kill an affected individual. People who use/abuse the illegal street drug methamphetamine can develop metabolic acidosis during the course of a drug overdose. The condition arises as an end result of an unsustainable methamphetamine-related increase in body temperature. Doctors refer to the relative acidity of the human body as the bodys pH level. If this level falls too low, the internal environment becomes too acidic to support good health; if the pH level rises too high, the internal environment becomes too alkaline to support good health. Relative pH is measured on a scale of 0 to 14. A pH level between 0 and 7 falls within the acidic range of this scale, while a pH level between 7 and 14 falls within the alkaline range of the scale. Under normal circumstances, the pH level of human blood falls somewhere between 7.35 and 7.45, which means it has a slightly alkaline quality. Levels that fall below 6.8 or rise above 7.8 can kill a human being. Metabolic acidosis is actually a general term that groups together several specific types of acidosis, including conditions called lactic acidosis, diabetic acidosis and hyperchloremic acidosis. Lactic acidosis occurs when the body contains too mu Continue reading >>
The kidneys and lungs maintain the balance (proper pH level) of chemicals called acids and bases in the body. Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. Acidosis is classified as either respiratory or metabolic acidosis. Respiratory acidosis develops when there is too much carbon dioxide (an acid) in the body. This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. Causes of respiratory acidosis include: Chest deformities, such as kyphosis Chest injuries Chest muscle weakness Chronic lung disease Overuse of sedative drugs Metabolic acidosis develops when too much acid is produced in the body. It can also occur when the kidneys cannot remove enough acid from the body. There are several types of metabolic acidosis: Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes. Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Lactic acidosis is a buildup of lactic acid. Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body breaks down carbohydrates to use for energy when oxygen levels are low. This can be caused by: Cancer Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar (hypoglycemia) Medications, such as salicylates MELAS (a very rare genetic mitochondrial disorder that affects energy production) Prolonged lack of oxygen from shock, heart failure, or seve Continue reading >>
Metabolic Acidosis Definition Metabolic acidosis is a pH imbalance in which the body has accumulated too much acid and does not have enough bicarbonate to effectively neutralize the effects of the acid. Description Metabolic acidosis, as a disruption of the body's acid/base balance, can be a mild symptom brought on by a lack of insulin, a starvation diet, or a gastrointestinal disorder like vomiting and diarrhea. Metabolic acidosis can indicate a more serious problem with a major organ like the liver, heart, or kidneys. It can also be one of the first signs of drug overdose or poisoning. Causes and symptoms Metabolic acidosis occurs when the body has more acid than base in it. Chemists use the term "pH" to describe how acidic or basic a substance is. Based on a scale of 14, a pH of 7.0 is neutral. A pH below 7.0 is an acid; the lower the number, the stronger the acid. A pH above 7.0 is a base; the higher the number, the stronger the base. Blood pH is slightly basic (alkaline), with a normal range of 7.36-7.44. Acid is a natural by-product of the breakdown of fats and other processes in the body; however, in some conditions, the body does not have enough bicarbonate, an acid neutralizer, to balance the acids produced. This can occur when the body uses fats for energy instead of carbohydrates. Conditions where metabolic acidosis can occur include chronic alcoholism, malnutrition, and diabetic ketoacidosis. Consuming a diet low in carbohydrates and high in fats can also produce metabolic acidosis. The disorder may also be a symptom of another condition like kidney failure, liver failure, or severe diarrhea. The build up of lactic acid in the blood due to such conditions as heart failure, shock, or cancer, induces metabolic acidosis. Some poisonings and overdoses (aspirin, Continue reading >>
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 >>
Metformin-induced Lactic Acidosis: No One Left Behind
Abstract Metformin is a safe drug when correctly used in properly selected patients. In real life, however, associated lactic acidosis has been repeatedly, although rarely, reported. The term metformin-induced lactic acidosis refers to cases that cannot be explained by any major risk factor other than drug accumulation, usually due to renal failure. Treatment consists of vital function support and drug removal, mainly achieved by renal replacement therapy. Despite dramatic clinical presentation, the prognosis of metformin-induced lactic acidosis is usually surprisingly good. In the previous issue of Critical Care, Friesecke and colleagues demonstrate that the survival rate of patients with severe lactic acidosis due to metformin accumulation can be strikingly higher than expected based on the initial clinical evaluation . Metformin is nowadays the first-line drug of choice for the treatment of adults with type 2 diabetes . This drug is the sixth most frequently prescribed in the USA (> 50 million prescriptions in 2009) and is taken by almost 1.5% of the Italian population [3, 4]. Metformin is a safe drug when correctly used in properly selected patients. In particular, no cases of lactic acidosis (a relatively common side effect of other biguanide compounds) were reported in 347 trials with 70,490 patient-years of metformin use . Real life can differ from research settings, however, and lactic acidosis has been repeatedly, although rarely, observed in patients treated with metformin. The number of inquiries to the Swedish Poison Information Centre for metformin intoxication has increased 10 times during the past decade, with 25 cases of severe lactic acidosis reported in 2007 and 2008 . According to the American Association of Poison Control Centers, metform Continue reading >>
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2018 Icd-10-cm Diagnosis Code
A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). A disorder characterized by abnormally high acidity (high hydrogen-ion concentration) of the blood and other body tissues. A pathologic condition of acid accumulation or depletion of base in the body. The two main types are respiratory acidosis and metabolic acidosis, due to metabolic acid build up. A state due to excess retention of carbon dioxide in the body. Acid base imbalance resulting from an accumulation of carbon dioxide secondary to hypoventilation. Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized. It may occur spontaneously or in association with diseases such as diabetes mellitus, leukemia, or liver failure. Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized; may occur spontaneously or in association with diseases such as diabetes mellitus, leukemia, or liver failure. An abnormal increase in the acidity of the body's fluids An abnormally high acidity (excess hydrogen-ion concentration) of the blood and other body tissues. An abnormally high acidity of the blood and other body tissues. Acidosis can be either respiratory or metabolic. Excess retention of carbon dioxide in the body resulting from ventilatory impairment. Increased acidity in the blood secondary to acid base imbalance. Causes include diabetes, kidney failure and shock. Metabolic acidosis characterized by the accumulation of lactate in the body. It is caused by tissue hypoxia. Pathologic condition resulting from accumulation of acid or depletion of the alkaline reserve (bicarbonate) content of the blood and body tissues, and characterized by an increase in hydrogen ion concentration (decrease in ph). Respi Continue reading >>
Exercise-induced Metabolic Acidosis
The scientific method involves stringent criteria for the evaluation of knowledge, but the method is not perfect. Research findings and their interpretations can be raised prematurely to the status of a fact. Some of these facts can even become a pivotal component of a knowledge base, termed a construct. Consequently, continual re-evaluation of the content of any academic discipline or profession is essential to ensure that knowledge and practice is based on fact. In recent years I have come to question a construct that has been accepted by a wide range of academic, research and professional entities: that the increasing free proton concentration within contracting skeletal muscle is caused by the increased production of lactic acid. One only has to read any of the textbooks in exercise physiology or pure biochemistry to be informed that when pyruvic acid is converted to lactic acid, the pK of lactic acid results in an immediate, near complete dissociation of the proton from the carboxylic acid functional group. This interpretation results in the logical belief that the net result in vivo is the production of lactate ions and the release of a proton. A generic chemical equation used to support this explanation is as follows: Pyruvic acid + NADH + H+ lactic acid + NAD+ lactate-Na+ + NAD+ + H+ This equation is typically extended to illustrate the bicarbonate buffering of the proton from lactate, resulting in the non-metabolic production of carbon dioxide (Brooks et al., 2000). Physiology is then extended to provide a cause-effect association between lactate production, the development of acidosis, the added free H+ and CO2 stimulation of ventilation, and the temporal alignment of the lactate and ventilatory thresholds. The above physiological and biochemical interpretati 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 >>
Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>