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Metabolic Acidosis Anion Gap

Metabolic Acidosis (increased Anion Gap)

Metabolic Acidosis (increased Anion Gap)

metabolic acidosis (increased anion gap) FREE subscriptions for doctors and students... click here You have 3 open access pages. Increased anion gap: diabetic ketoacidosis starvation ketoacidosis lactic acidosis (types A and B) acidosis of renal failure salicylate poisoning methanol poisoning ammonium chloride Links: diabetic ketoacidosis lactic acidosis acute renal failure (ARF) salicylate poisoning This site is intended for the use of healthcare professionals only. A licensed medical practitioner should be consulted for diagnosis and treatment of any and all medical conditions. Copyright 2016 Oxbridge Solutions Ltd®. Any distribution or duplication of the information contained herein is strictly prohibited. Oxbridge Solutions Ltd® receives funding from advertising but maintains editorial independence more... GPnotebook stores small data files on your computer called cookies so that we can recognise you and provide you with the best service. If you do not want to receive cookies please do not use GPnotebook. Continue reading >>

How Does Diabetic Ketoacidosis Develop?

How Does Diabetic Ketoacidosis Develop?

Diabetic ketoacidosis, DKA, is a serious, life-threatening condition that can cause a diabetic coma and possibly death. It develops when the body does not get enough sugar in order to produce energy because of a lack of insulin. This causes the body to start using stored fat for energy. According to WebMD, when the body cannot convert the sugar into energy, it stays inside of the bloodstream (WebMD, 2017). This causes the kidneys to filter some of the sugar from the blood into the urine. This causes ketones to be released from the breakdown of fat, making the blood’s pH level to become acidic. DKA is a condition that should not be taken lightly. It can cause several different problems inside of the body. It is very important that you take care of your body in order to prevent the development of DKA. How does DKA start? WebMD said, “Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things” (WebMD, 2017). There are things that you can control. Frequent communication with your doctor will assist you in determining how much insulin you should take and when. If you keep taking it consistently and on time, it will help immensely. It is difficult to control if you get a severe infection or illness. However, you do have control on how you will react. Do not be afraid to go to the doctor. Get the medical treatment that you need so it does not become much worse. DKA can also be caused by dehydration. Drinking water is a great way to prevent dehydration. Also, cutting out beverages like soda can also help a ton! Focusing more on water will also help you to cut out unnecessary sodium, trans fats, and sugars that you do not need. By drinking healthier, it will make yo Continue reading >>

Gold Mark: An Anion Gap Mnemonic For The 21st Century

Gold Mark: An Anion Gap Mnemonic For The 21st Century

A Lancet Editorial1 in 1977, referring to an article entitled “Clinical use of the anion gap”2 opined: “In an age when all too often plasma-electrolyte measurements are ordered without any deliberate judgment being made as to the likely usefulness of the result, it is refreshing to have a reminder of the subtleties involved in the interpretation of this commonest set of clinical-chemistry tests”. We have discovered some new twists over the past 30 years and would like to share an easily remembered mnemonic aid. The metabolic acidoses are generally separated into two categories on the basis of an anion gap calculation (Na+[Cl−HCO3−]): the high-anion-gap metabolic acidoses, and the normal-anion-gap, or hyperchloraemic, metabolic acidoses. Two popular mnemonics are often used to remember the major causes of the high-gap metabolic acidoses. The first is KUSMALE (a useful misspelling of Adolph Kussmaul's name), which represents Ketoacidosis, Uraemia, Salicylate poisoning, Methanol, Aldehyde (paraldehyde), Lactate, and Ethylene glycol. The second is MUD PILES, representing Methanol, Uraemia, Diabetes, Paraldehyde, Iron (and Isoniazid), Lactate, Ethylene glycol, and Salicylate. Metabolic acidosis due to excessive paraldehyde use has become exceedingly rare. Iron and isoniazid are just two of many drugs and toxins that cause hypotension and lactic acidosis (isoniazid can also generate a component of ketoacidosis). Three “new” organic anion-gap-generating acids and acid precursors have been recognised in recent years. They are D-lactic acid, which can occur in some patients with short bowel syndromes; 5-oxoproline (or pyroglutamic acid) associated with chronic paracetamol use, often by malnourished women; and the anion-gap acidosis generated by high-dose propylen Continue reading >>

High Anion Gap Metabolic Acidosis

High Anion Gap Metabolic Acidosis

When acidosis is present on blood tests, the first step in determining the cause is determining the anion gap. If the anion gap is high (>12 mEq/L), there are several potential causes. High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). An anion gap is usually considered to be high if it is over 12 mEq/L. High anion gap metabolic acidosis is caused generally by acid produced by the body,. More rarely, high anion gap metabolic acidosis may be caused by ingesting methanol or overdosing on aspirin.[1][2] The Delta Ratio is a formula that can be used to assess elevated anion gap metabolic acidosis and to evaluate whether mixed acid base disorder (metabolic acidosis) is present. The list of agents that cause high anion gap metabolic acidosis is similar to but broader than the list of agents that cause a serum osmolal gap. Causes[edit] Causes include: The newest mnemonic was proposed in The Lancet reflecting current causes of anion gap metabolic acidosis:[3] G — glycols (ethylene glycol & propylene glycol) O — oxoproline, a metabolite of paracetamol L — L-lactate, the chemical responsible for lactic acidosis D — D-lactate M — methanol A — aspirin R — renal failure K — ketoacidosis, ketones generated from starvation, alcohol, and diabetic ketoacidosis The mnemonic MUDPILES is commonly used to remember the causes of increased anion gap metabolic acidosis.[4][5] M — Methanol U — Uremia (chronic kidney failure) D — Diabetic ketoacidosis P — Paracetamol, Propylene glycol (used as an inactive stabilizer in many medications; historically, the "P" also stood for Paraldehyde, though this substance is not commonly used today) I — Infectio Continue reading >>

High Anion Gap Metabolic Acidosis Induced By Cumulation Of Ketones, L- And D-lactate, 5-oxoproline And Acute Renal Failure.

High Anion Gap Metabolic Acidosis Induced By Cumulation Of Ketones, L- And D-lactate, 5-oxoproline And Acute Renal Failure.

Abstract INTRODUCTION: Frequent causes of high anion gap metabolic acidosis (HAGMA) are lactic acidosis, ketoacidosis and impaired renal function. In this case report, a HAGMA caused by ketones, L- and D-lactate, acute renal failure as well as 5-oxoproline is discussed. CASE PRESENTATION: A 69-year-old woman was admitted to the emergency department with lowered consciousness, hyperventilation, diarrhoea and vomiting. The patient had suffered uncontrolled type 2 diabetes mellitus, underwent gastric bypass surgery in the past and was chronically treated with high doses of paracetamol and fosfomycin. Urosepsis was diagnosed, whilst laboratory analysis of serum bicarbonate concentration and calculation of the anion gap indicated a HAGMA. L-lactate, D-lactate, β-hydroxybutyric acid, acetone and 5-oxoproline serum levels were markedly elevated and renal function was impaired. DISCUSSION: We concluded that this case of HAGMA was induced by a variety of underlying conditions: sepsis, hyperglycaemia, prior gastric bypass surgery, decreased renal perfusion and paracetamol intake. Risk factors for 5-oxoproline intoxication present in this case are female gender, sepsis, impaired renal function and uncontrolled type 2 diabetes mellitus. Furthermore, chronic antibiotic treatment with fosfomycin might have played a role in the increased production of 5-oxoproline. CONCLUSION: Paracetamol-induced 5-oxoproline intoxication should be considered as a cause of HAGMA in patients with female gender, sepsis, impaired renal function or uncontrolled type 2 diabetes mellitus, even when other more obvious causes of HAGMA such as lactate, ketones or renal failure can be identified. Continue reading >>

Best Case Ever 56 Anion Gap Metabolic Acidosis

Best Case Ever 56 Anion Gap Metabolic Acidosis

In this month’s Best Case Ever on EM Cases Dr. Ross Claybo and Dr. Keerat Grewal tell the story of a patient with a complicated anion gap metabolic acidosis. We discuss how to sort through the differential diagnosis with a better mnemonic than MUDPILES, the controversy around administering sodium bicarbonate for metabolic acidosis, the indications for fomepizole and the value of taking time to to build a therapeutic relationship with your ED patients. Podcast production and sound design by Anton Helman. Show notes by Anton Helman, March 2017 The MUDPILES mnemonic for anion gap metabolic acidosis is out of date Why? Metabolic acidosis due to paraldehyde overdose is exceedingly rare Iron and isoniazid are just two of many drugs and toxins that cause hypotension and lactic acidosis (isoniazid can also generate a component of ketoacidosis). Three “newer” anion-gap-generating acids have been recognised recently: D-lactic acid, which can occur in some patients with short bowel syndromes. 5-oxoproline (or pyroglutamic acid) associated with chronic acetaminophen use. Propylene glycol infusions – solvent used for several IV medications including lorazepam and phenobarbital. The GOLDMARK mnemonic for anion gap metabolic acidosis is more useful GOLDMARK mnemonic for anion gap metabolic acidosis Glycols (ethylene glycol & propylene glycol) Oxoproline (metabolite of acetaminophen) L-lactate D-lactate (acetaminophen, short bowel syndrome, propylene glycol infusions for lorazepam and phenobarbital) Methanol ASA Renal Failure Ketoacidosis (starvation, alcohol and DKA) Osmolar Gap common differential diagnosis Ketoacids (DKA, AKA, starvation ketosis) Alcohols Sepsis Ischemia Sodium bicarbonate for metabolic acidosis: Still controversial The indcations for sodium bicarb for metab Continue reading >>

Approach To The Adult With Metabolic Acidosis

Approach To The Adult With Metabolic Acidosis

INTRODUCTION On a typical Western diet, approximately 15,000 mmol of carbon dioxide (which can generate carbonic acid as it combines with water) and 50 to 100 mEq of nonvolatile acid (mostly sulfuric acid derived from the metabolism of sulfur-containing amino acids) are produced each day. Acid-base balance is maintained by pulmonary and renal excretion of carbon dioxide and nonvolatile acid, respectively. Renal excretion of acid involves the combination of hydrogen ions with urinary titratable acids, particularly phosphate (HPO42- + H+ —> H2PO4-), and ammonia to form ammonium (NH3 + H+ —> NH4+) [1]. The latter is the primary adaptive response since ammonia production from the metabolism of glutamine can be appropriately increased in response to an acid load [2]. Acid-base balance is usually assessed in terms of the bicarbonate-carbon dioxide buffer system: Dissolved CO2 + H2O <—> H2CO3 <—> HCO3- + H+ The ratio between these reactants can be expressed by the Henderson-Hasselbalch equation. By convention, the pKa of 6.10 is used when the dominator is the concentration of dissolved CO2, and this is proportional to the pCO2 (the actual concentration of the acid H2CO3 is very low): TI AU Garibotto G, Sofia A, Robaudo C, Saffioti S, Sala MR, Verzola D, Vettore M, Russo R, Procopio V, Deferrari G, Tessari P To evaluate the effects of chronic metabolic acidosis on protein dynamics and amino acid oxidation in the human kidney, a combination of organ isotopic ((14)C-leucine) and mass-balance techniques in 11 subjects with normal renal function undergoing venous catheterizations was used. Five of 11 studies were performed in the presence of metabolic acidosis. In subjects with normal acid-base balance, kidney protein degradation was 35% to 130% higher than protein synthesi Continue reading >>

What Chemical Processes Or Reactions Contribute To Metabolic Acidosis?

What Chemical Processes Or Reactions Contribute To Metabolic Acidosis?

There are three primary states metabolic acidosis. Their underlying physiological causes are from diabetes (ketoacidosis), normal anion gap acidosis from ailments such as kidney malfunction (renal tubular acidosis or more specifically hyperchloremic acidosis), and rare congenital mitochondrial disorders (lactic acidosis). More common causes of metabolic acidosis may come from liver disease or damage or from the ingestion of certain anti-retroviral drugs and poisons such as arsenic. In ketoacidosis, the body does not have enough insulin which allows glucose to be transported across the cell membranes. The body's response is to try to compensate for the supposed lack of energy source (starvation defense, even though there is plenty in the blood) by digesting fat which is converted by the liver into alternative energy sources, i.e. ketones such as acetoacetate and the carboxylic acid β-hydroxybutyrate. These byproducts are acidic and lower the pH of the blood. In renal tubular acidosis (RTA) the kidneys are not acidifying the urine as efficiently as they should which allows acid in the blood to accumulate. RTA is a normal anion gap acidosis during which the alpha intercalated cells fail to secret acid. This can be caused by toxin damage from toluene or lithium carbonate among others, or by mutations. Two well known genetic causes of RTA are a mutation in the anion exchanger AE1 (Band 3) transport protein that controls chloride and bicarbonate exchange across the plasma membrane, and mutations to the apical proton pump vH+-ATPase. A reduction in plasma bicarb concentration and increased chloride prevents pH buffering and reduces the pH. Lesser known mutations that have the same effect are in the family of serine-threonine protein kinases WNK1 or WNK4, specifically, the min Continue reading >>

Serum Anion Gap In The Differential Diagnosis Of Metabolic Acidosis In Critically Ill Newborns.

Serum Anion Gap In The Differential Diagnosis Of Metabolic Acidosis In Critically Ill Newborns.

Abstract OBJECTIVES: To determine in critically ill newborn infants (1) the range of the serum anion gap without metabolic acidosis and (2) whether the serum anion gap can be used to distinguish newborns with lactic acidosis from those with hyperchloremic metabolic acidosis. STUDY DESIGN: Umbilical arterial blood gases and serum electrolyte and lactate concentrations were measured simultaneously in 210 samples from 63 infants over the first week of life. Metabolic acidosis was defined as a blood base deficit (BD) >4 mmol/L. The anion gap was calculated as [Na(+)] - [C1(-)] - [TCO (2)]. Lactic acidosis was defined as a serum lactate concentration >2 SD above the mean serum lactate concentration in samples without metabolic acidosis. RESULTS: In 89 blood samples with BD <4 mmol/L, serum lactate concentration decreased with postnatal age (r = 0.51). The upper limit of serum lactate concentration was 3.8 mmol/L at less than 48 hours, 2.4 mmol/L between 48 and 96 hours, and 1.5 mmol/L for infants greater than 96 hours of age. The mean serum anion gap +/- 2 SD in 174 samples without lactic acidosis was 8 +/- 4 mmol/L; in 36 samples with lactic acidosis it was 16 +/- 9 mmol/L (P <.0001). Serum anion gap and lactate concentration were poorly correlated for samples without lactic acidosis (r = 0.04) but highly correlated in those with lactic acidosis (r = 0.81, P <.0001). None of the 85 samples with metabolic acidosis but without lactic acidosis had an anion gap >16 mmol/L; only 4 of 36 samples with lactic acidosis had an anion gap <8 meq/L. However, 25 of 36 samples with lactic acidosis had serum anion gaps of 8 to 16 mmol/L. CONCLUSION: In the presence of metabolic acidosis, a serum anion gap >16 mmol/L is highly predictive of lactic acidosis; a serum anion gap <8 is highly pr Continue reading >>

High Anion Gap Metabolic Acidosis

High Anion Gap Metabolic Acidosis

Go to: Introduction High anion gap metabolic acidosis (HAGMA) is a subcategory of acidosis of metabolic (i.e., non-respiratory) etiology. Differentiation of acidosis into a particular subtype, whether high anion gap metabolic acidosis or non-anion gap metabolic acidosis (NAGMA), aids in the determination of the etiology and hence appropriate treatment. Go to: Etiology Although there have been many broadly inclusive mnemonic devices for high anion gap metabolic acidosis, the use of "GOLD MARK" has gained popularity for its focus on causes common to the 21st century. Glycols (ethylene glycol, propylene glycol) Oxoproline (pyroglutamic acid, the toxic metabolite of excessive acetaminophen or paracetamol) L-Lactate (standard lactic acid seen in lactic acidosis) D-Lactate (exogenous lactic acid produced by gut bacteria) Methanol (this is inclusive of alcohols in general) Aspirin (salicylic acid) Ketones (diabetic, alcoholic and starvation ketosis) Of note, metformin has been omitted from this list due to a lack of evidence for metformin-induced lactic acidosis. In fact, a Cochrane review found substantial evidence that metformin was not a cause of lactic acidosis. The same could not be said of the older biguanide, phenformin, which does increase the incidence of lactic acidosis by approximately tenfold. Furthermore, the addition of massive rhabdomyolysis would be appropriate given the potentially large amounts of hydrogen ions released by muscle breakdown. Go to: Epidemiology High anion gap metabolic acidosis is one of the most common metabolic derangements seen in critical care patients. Exact numbers are not readily available. Go to: Pathophysiology The most common method of evaluation of metabolic acidosis involves the Henderson-Hasselbalch equation and the Lewis model in Continue reading >>

Recurrent Severe Anion Gap Metabolic Acidosis Secondary To Episodic Ethylene Glycol Intoxication.

Recurrent Severe Anion Gap Metabolic Acidosis Secondary To Episodic Ethylene Glycol Intoxication.

Abstract Acute ethylene glycol toxicity and its attendant metabolic derangement is a well described clinical entity. Recurrent severe anion gap metabolic acidosis consequent to episodic ingestion of ethylene glycol has not been previously reported. We present a patient who developed severe anion gap metabolic acidosis with no osmolar gap and hypokalemia, consequent to episodic ethylene glycol ingestion. Modest artifactual elevation of the serum lactic acid level and rapid response to intravenous bicarbonate infusion may serve as diagnostic clues. Consideration of these aberrant features should be included in the clinical assessment of severe anion gap metabolic acidosis. Continue reading >>

High Anion Gap Metabolic Acidosis

High Anion Gap Metabolic Acidosis

Abstract In the previous chapter, we presented various causes of high anion gap (AG) metabolic acidosis. For discussion purpose, these causes can be conveniently divided into the following categories: 3. 5-Oxoproline (pyroglutamic acid) Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

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. 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). High anion gap acidosis Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis), but it also occurs with chronic alcoholism (see alcoholic ketoacidosis), undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulation results from a combination of excess formation and decreased utilization of lactate. Excess lactate production occurs during states of anaerobic metabolism. The most serious form occurs during the various types o Continue reading >>

Medical Mnemonics: Causes Of Anion Gap Metabolic Acidosis – “gold Mark”

Medical Mnemonics: Causes Of Anion Gap Metabolic Acidosis – “gold Mark”

The classic mnemonic often used to remember the causes of anion gap metabolic acidosis is “MUDPILES” M – Methanol U – Uremia D – Diabetic ketoacidosis P – Propylene Glycol I – Isoniazid L – Lactic Acidosis E – Ethylene Glycol S – Salicylates More recently a new mnemonic has been suggested to update new our understanding of anion-gap generating acids. The updated mnemonic “GOLD MARK” was proposed in a 2008 article in The Lancet. G – Glycols (ethylene glycol and propylene glycol) O – Oxoproline L – L-Lactate D – D-Lactate M – Methanol A – Aspirin R – Renal Failure K – Ketoacidosis As medicine evolves, so do our Mnemonics. This is the fifth medical mnemonic in our series of Monday Mnemonics. Continue reading >>

Anion Gap

Anion Gap

The anion gap is the difference between primary measured cations (sodium Na+ and potassium K+) and the primary measured anions (chloride Cl- and bicarbonate HCO3-) in serum. This test is most commonly performed in patients who present with altered mental status, unknown exposures, acute renal failure, and acute illnesses. [1] See the Anion Gap calculator. The reference range of the anion gap is 3-11 mEq/L The normal value for the serum anion gap is 8-16 mEq/L. However, there are always unmeasurable anions, so an anion gap of less than 11 mEq/L using any of the equations listed in Description is considered normal. For the urine anion gap, the most prominently unmeasured anion is ammonia. Healthy subjects typically have a gap of 0 to slightly normal (< 10 mEq/L). A urine anion gap of more than 20 mEq/L is seen in metabolic acidosis when the kidneys are unable to excrete ammonia (such as in renal tubular acidosis). If the urine anion gap is zero or negative but the serum AG is positive, the source is most likely gastrointestinal (diarrhea or vomiting). [2] Continue reading >>

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