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Normal Anion Gap Metabolic Acidosis Mnemonic

The Anion Gap

The Anion Gap

The anion gap is a tool used to: Confirm that an acidosis is indeed metabolic Narrow down the cause of a metabolic acidosis Monitor the progress of treatment In a metabolic acidosis the anion gap is usually either ‘Normal’ or ‘High’. In rare cases it can be ‘low’, usually due to hypoalbuminaemia. An ABG machine will often give a print out of the anion gap, but it can also be useful to know how it is calculated. In blood, there are many cations and anions. However, the vast majority of the total number are potassium, sodium, chloride, or bicarbonate. The ‘anion’ gap is an artificial measure, which is calculated by subtracting the total number of anions (negatively charged ions – bicarbonate and chloride) from the total number of cations (sodium and potassium). Thus, the formula is: ([Na+]+ [K+]) –([Cl–]+ [HCO3–]) In reality, the concentration of potassium anions is negligible, and this often omitted. There are usually more measurable cations than anions, and thus a normal anion gap is value is positive. A normal value is usually 3-16, but may vary slightly depending on the technique used by the local laboratory. If the anion gap is <30, then there may not be ‘true’ high anion gap metabolic acidosis. In a healthy normal individual, the main unmeasured anions are albumin and phosphate. Almost all of the gap can be attributed to albumin. This means that in patients with hypoalbuminaemia and metabolic acidosis, there may be a normal anion gap. Be wary in severely unwell patients because they often have a low albumin. You can adjust for this in your calculation. Corrected anion gap: [AG] + (0.25 x (40-albumin)) In an unwell patient with a high anion gap metabolic acidosis (HAGMA) the anion gap is increased due: Accumulation of organic acids Inabili 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 >>

Metabolic Acidosis Nclex Review Notes

Metabolic Acidosis Nclex Review Notes

Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b 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 >>

Metabolic Acidosis

Metabolic Acidosis

Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis Paraldehyde, Phenformin (neither used in U.S. now) Propofol Infusion Syndrome has been proposed as a replacement in mnemonic Salicylate s (do not miss Chronic Salicylate Poisoning ) IV. Causes: Metabolic Acidosis and Normal Anion Gap (Hyperchloremia) Renal Tubular Acidosis (proximal or distal) V. Causes: Metabolic Acidosis and Elevated Osmolal Gap PaCO2 drops 1.2 mmHg per 1 meq/L bicarbonate fall Calculated PaCO2 = 1.5 x HCO3 + 8 (+/- 2) Useful in High Anion Gap Metabolic Acidosis Measured PaCO2 discrepancy: respiratory disorder Investigate normal Anion Gap Metabolic Acidosis Elevated in normal Anion Gap Metabolic Acidosis VII. Labs: Consider in Metabolic Acidosis with Increased Anion Gap Basic chemistry panel as above ( Serum Glucose , Blood Urea Nitrogen ) Rutecki (Dec 1997) Consultant, p. 3067-74 Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Metabolic Acidosis." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window A condition in which the blood is too acidic. It may be caused by severe illness or sepsis (bacteria in the bloodstream). Increased acidity in the blood secondary to acid base imbalance. Causes include diabetes, kidney failure and shock. ACIDOSIS METABOLIC, metabolic acidosis, metabolic acidosis (diagnosis), Acidosis metabolic, Metabolic acidosis NOS, Metabolic Acidoses, Acidosis, Metabolic, Acidoses, Metabolic, Metabolic Acidosis, acidosis metabolic, metabolic acidosis disorder, Acidosis, Metabolic acidosis (disorder), acidosis; metabolic, metabolic; acidosis, Metabolic acidosis, NOS, M Continue reading >>

The New Goldmark Mnemonic For Anion Gap Metabolic Acidosis From Emergency Medicine Cases

The New Goldmark Mnemonic For Anion Gap Metabolic Acidosis From Emergency Medicine Cases

This is the link to Best Case Ever 56 Anion Gap Metabolic Acidosis [link is to the podcast and shownotes] from Emergency Medicine Cases . The case discussion of a 65 yr old woman who presented to the emergency department appearing only mildly ill clinically but turned out to have complex metabolic derangements. The case discussion is approximately 21 minutes long and totally worth listening to. But this post is just about the GOLDMARK mnemonic for differential diagnosis of metabolic acidosis AND aboutthe differential diagnosis of an osmolar gap. Anion gap = [Na +] ([Cl -] + [HCO 3 ]) (normal is 12 2) from General Formulas of emedicine.medscape.com Osmolal gap = measured osmoles calculated osmoles (normal is < 10) from General Formulas of emedicine.medscape.com [Calculated] Osmoles = (2 x [Na +]) + (glucose/18) + (BUN/2.8) + (ethanol/4.6)from General Formulas of emedicine.medscape.com In addition to d-lactate, the D in GOLDMARK can stand for drugs and an 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 below is extract from the show notes that is contains a review of the new mnemonic for anion gap metabolic acidosis -GOLDMARK and a review of the osmolar gap differential diagnosis: The MUDPILES mnemonic for anion gap metabolic acidosis is out of date 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, w Continue reading >>

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

Terry W. Hensle, Erica H. Lambert, in Pediatric Urology , 2010 Nonanion gap acidosis occurs in situations in which HCO3 is lost from the kidney or the gastrointestinal tract or both. When this occurs, Cl (along with Na+) is reabsorbed to replace the HCO3; this leads to the hyperchloremia, which leaves the anion gap in normal range.10 Diarrhea causes a hyperchloremic, hypokalemic metabolic acidosis. Treatment depends on the severity of the acidosis incurred. In mild to moderate acidosis (pH >7.2), fluid and electrolyte replacement is often all that is required. Once adequate renal perfusion is restored, excess H+ can be excreted efficiently, restoring the pH to normal. In severe acidosis (pH <7.2), the addition of intravenous bicarbonate may be needed to correct the metabolic deficit. Before bicarbonate is administered, a serum potassium level should be obtained. The addition of bicarbonate can worsen hypokalemia, leading to neuromuscular complications. Hyperchloremic acidosis also occurs with renal insufficiency and renal tubular acidosis.9,20 Katherine Ahn Jin, in Comprehensive Pediatric Hospital Medicine , 2007 As in any condition, the first priority in management is stabilizing the ABCs, as necessary. Management of metabolic acidosis is directed toward treating the underlying cause. In general, treating the causes of anion gap acidosis can regenerate bicarbonate within hours; however, nonanion gap acidosis can take days to resolve and may require exogenous bicarbonate therapy. Insulin, hydration, and electrolyte repletion will correct the acidosis in diabetic ketoacidosis. In addition to treating the underlying condition, lactic acidosis can be resolved by increasing tissue oxygenation using crystalloid, blood products, afterload reduction, inotropic agents (e.g., d Continue reading >>

Hard - Up Is A Mnemonic For ,,,, - Usmle Forum

Hard - Up Is A Mnemonic For ,,,, - Usmle Forum

In renal physiology, normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap. The most common etiology of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second . The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Acetazolamide and other carbonic anhydrase inhibitors Ureteroenteric fistula - an abnormal connection (fistula) between a ureter and the gastrointestinal tract Pancreaticoduodenal fistula - an abnormal connection between the pancreas and duodenum It can be remembered with the mnemonic HARD-UP. As opposed to high anion gap acidosis (which involves increased organic acid production), normal anion gap acidosis involves either increased production of chloride (hyperchloremic acidosis) or increased excretion of bicarbonate. So NORMAL ANION GAP might involve either CHLORIDE ( Cl- )or BICARBONATE ( HCO3- ) excretion to balance H+ Continue reading >>

Renal Fellow Network: Mnemonic For Non-anion Gap Metabolic Acidosis

Renal Fellow Network: Mnemonic For Non-anion Gap Metabolic Acidosis

Mnemonic for NON-Anion Gap Metabolic Acidosis As I've mentioned previously on this blog, the "MUDPALES" mnemonic for anion gap metabolic acidosis is one of the most successful medical mnemonic's of all time. A less successful (and admittedly less useful) mnemonic exists for non-anion gap metabolic acidoses (NAGMA), which I learned as a resident. It's "HARDUP", which stands for the following: H = hyperalimentation (e.g., starting TPN). R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism. U = uretosigmoid fistula (because the colon will waste bicarbonate). P = pancreatic fistula (because of alkali loss--the pancreas secretes a bicarbonate-rich fluid). Practically speaking however, the two main causes you really have to remember for NAGMA are DIARRHEA or RENAL TUBULAR ACIDOSIS, which 90% of the time you can distinguish between based on the history alone. Another way to think about the differential diagnosis of NAGMA is to ask whether or not there is GI LOSS or RENAL LOSS of bicarbonate. If the history does not provide an obvious explanation, one can distinguish between GI versus renal bicarbonate losses by determining the urine anion gap (urine AG = urine Na + urine K - urine Cl), where a positive value indicates renal bicarbonate loss whereas a largely negative value indicates extra-renal bicarbonate loss. Continue reading >>

Causes Of Metabolic Acidosis

Causes Of Metabolic Acidosis

In practically every CICM exam paper, the candidates are presented with an ABG (sometimes several) which expect the diagnosis of a metabolic acidosis of some sort. It is therefore essential to develop some sort of mnemonic aid to recall the differential diagnosis of metabolic acidosis. In spite of its many obvious disadvantages, the anion gap classification of metabolic acid-base disorders is useful tool. Causes of Metabolic Acidosis High anion gap Normal anion gap MUD PILES Methanol and other toxic alcohols Uraemia Diabetic (or other) ketoacidosis Pyroglutamic acidosis Iron overdose Lactic acidosis Ethylene glycol Salicylates PANDA RUSH Pancreatic secretion loss Acetazolamide Normal saline intoxication Diarrhoea Aldosterone antagonists Renal tubular acidosis Type 1 (distal) Ureteric diversion Small bowel fistula Hyperalimentation (TPN) The MUDPILES mnemonic is showing its age. Nowhere is there space for citrate, for instance. This is a problem, as several SAQs (eg. Question 3.3 from the second paper of 2013) present the candidate with a citrate-based acidosis. The "P" in PILES used to be "Paraldehyde", but paraldehyde has fallen out of favour since the 1980s, and so "Pyroglutamic acidosis" is probably a better substitute. Iron is not a cause of a high anion gap on its own (in fact, ionised iron is cationic) but it can cause the anion gap to increase when it is removed from solution by its conversion to ferric hydroxide. Also, methanol and ethylene glycol are insufficiently distinct to merit their own individual places in the mnemonic (both are toxic alcohols). In spite of these concerns, the MUDPILES meme is still propagated throughout the medical school curricula, as the educators cynically expect their graduates to never have to seriously think about acidosis. It's s Continue reading >>

Normal Anion Gap Acidosis

Normal Anion Gap Acidosis

In renal physiology , normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap . The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second. The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Diarrhea : due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringers solution are used instead of normal saline to replace GI losses. [2] Continue reading >>

Normal Anion Gap Metabolic Acidosis

Normal Anion Gap Metabolic Acidosis

Home | Critical Care Compendium | Normal Anion Gap Metabolic Acidosis Normal Anion Gap Metabolic Acidosis (NAGMA) HCO3 loss and replaced with Cl- -> anion gap normal if hyponatraemia is present the plasma [Cl-] may be normal despite the presence of a normal anion gap acidosis -> this could be considered a ‘relative hyperchloraemia’. Extras – RTA, ingestion of oral acidifying salts, recovery phase of DKA loss of bicarbonate with chloride replacement -> hyperchloraemic acidosis secretions into the large and small bowel are mostly alkaline with a bicarbonate level higher than that in plasma. some typical at risk clinical situations are: external drainage of pancreatic or biliary secretions (eg fistulas) this should be easily established by history normally 85% of filtered bicarbonate is reabsorbed in the proximal tubule and the remaining 15% is reabsorbed in the rest of the tubule in patients receiving acetazolamide (or other carbonic anhydrase inhibitors), proximal reabsorption of bicarbonate is decreased resulting in increased distal delivery and HCO3- appears in urine this results in a hyperchloraemic metabolic acidosis and is essentially a form of proximal renal tubular acidosis but is usually not classified as such. hyperchloraemic metabolic acidosis commonly develops during therapy of diabetic ketoacidosis with normal saline oral administration of CaCl2 or NH4Cl is equivalent to giving an acid load both of these salts are used in acid loading tests for the diagnosis of renal tubular acidosis CaCl2 reacts with bicarbonate in the small bowel resulting in the production of insoluble CaCO3 and H+ the hepatic metabolism of NH4+ to urea results in an equivalent production of H+ REASONS WHY ANION GAP MAY BE NORMAL DESPITE A ‘HIGH ANION GAP METABOLIC ACIDOSIS’ 1. 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 >>

Causes Of Non-anion Gap Metabolic Acidosis

Causes Of Non-anion Gap Metabolic Acidosis

Bicarbonate-rich fluid excreted into the intestines where it is lost (GI loss of HCO3). There is an additional mechanism by which NH4Cl causes a non-AG metabolic acidosis. It is similar to the mechanism by which TPN causes a non-AG metabolic acidosis. Either the NH4Cl or the amino acids in TPN are meatbolized to HCl which causes a transient non-AG metabolic acidosis. The decreased pH and decreased HCO3 stimulate renal tubular reabsorption and generation of HCO3 (secretion of H+). You only end up with a metabolic acidosis if the addition of acid overrides the ability of the renal tubules to secrete H+ and generate NH3+ for excretion in the urine, usually a short-lived process. In prolonged hypercapnia renal tubular cells compensate for a prolonged respiratory alkalosis by decreasing reclaimation and generation of HCO3 (which takes 12-24 hrs for full affect). If the respiratory alkalosis resolves rapidly, reclaimation and generation of HCO3 will return to normal over 1-2 days. During this period you can get a (resolving) non-AG metabolic acidosis. The two main causes you for non-anion gap metabolic acidosis are diarrhea and RTA . Most of the time you can distinguish between these two based on the history alone.Another way to think about the differential diagnosis of non-anion gap metabolic acidosisis to ask whether or not there is GI loss or Renal loss of bicarbonate. If the history does not provide an obvious explanation, you can distinguish between GI vsrenal bicarbonate losses by determining the urine anion gap(urine AG = urine Na + urine K - urine Cl), where a positive value indicates renalbicarbonate loss and a largely negative value indicates extra-renal bicarbonate loss. Why is that? Because if a large amount of HCO3 is lost, a large amount ofNH+ is excreted in th Continue reading >>

Why Renal Tubular Acidosis Is Normal Gap Metabolic Acidosis? - Usmle Forums

Why Renal Tubular Acidosis Is Normal Gap Metabolic Acidosis? - Usmle Forums

Therefore, in any metabolic acidosis you'll have increased anion gap unless the chloride compensates for the depressed bicarb. Therefore, any normal anion gap metabolic acidosis is essentially hyperchloremic metabolic acidosis. See normal anion gap mnemonic thread In proximal renal tubular acidosis you have failure of bicarbonate reabsorption and this will be compensated by chloride reabsorption to maintain neutrality across the renal tubule membrane. See this thread for a similar issue Abdulaziz (02-21-2012), anoop_1198 (05-21-2010), dr.burhan (01-12-2010), lichen70 (06-17-2015), Linc (02-20-2016), rigbbm (09-04-2017), Seetal (03-12-2010), Thrax_usmle (03-12-2013), usmleguy (04-26-2010), wahaha007 (01-13-2010) Therefore, in any metabolic acidosis you'll have increased anion gap unless the chloride compensates for the depressed bicarb. Therefore, any normal anion gap metabolic acidosis is essentially hyperchloremic metabolic acidosis. See normal anion gap mnemonic thread In proximal renal tubular acidosis you have failure of bicarbonate reabsorption and this will be compensated by chloride reabsorption to maintain neutrality across the renal tubule membrane. See this thread for a similar issue thank you. what i really want to know is what is the mechanism for hyperchloremia. in rta. is an ion pump involved? Continue reading >>

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