diabetestalk.net

What Is Non Anion Gap Metabolic Acidosis?

Metabolic Acidosis; Non-gap

Metabolic Acidosis; Non-gap

Non-gap metabolic acidosis, or hyperchloremic metabolic acidosis, are a group of disorders characterized by a low bicarbonate, hyperchloremia and a normal anion gap (10-12). A non-gapped metabolic acidosis fall into three categories: 1) loss of base (bicarbonate) from the gastrointestinal (GI) tract or 2) loss of base (bicarbonate) from the kidneys, 3) intravenous administration of sodium chloride solution. Bicarbonate can be lost from the GI tract (diarrhea) or from the kidneys (renal tubular acidosis) or displaced by chloride. A. What is the differential diagnosis for this problem? Proximal renal tubular acidosis: (low K+) Distal renal tubular acidosis: (low or high K+) Prostaglandin Inhibitors, (aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors) Adrenal insufficiency (primary or secondary) (high K+) Pseudoaldosteronism, type 2 (Gordon's syndrome) B. Describe a diagnostic approach/method to the patient with this problem. Metabolic acidosis can be divided into two groups based on anion gap. If an anion gap is elevated (usually greater than 12), see gapped metabolic acidosis. Diagnosis of the cause of non-gapped metabolic acidosis is usually clinically evident - as it can be attributed to diarrhea, intravenous saline or by default, renal tubular acidosis. Occasionally, it may not be clear whether loss of base occurs due to the kidney or bowel. In such a case, one should calculate the urinary anion gap. The urinary anion gap (UAG) = sodium (Na+)+K+- chloride (Cl-). Caution if ketonuria or drug anions are in the urine as it would invalidate the calculation. As an aid, UAG is neGUTive when associated with bowel causes. Non-gapped metabolic acidosis can further be divided into two categories: 1. Historical information important in the diagnosis of 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 >>

Nonanion Gap Metabolic Acidosis In A Patient With A Pancreaticopleural Fistula | The Journal Of The American Osteopathic Association

Nonanion Gap Metabolic Acidosis In A Patient With A Pancreaticopleural Fistula | The Journal Of The American Osteopathic Association

NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula Benjamin Eovaldi, OMS IV ; Claude Zanetti, MD From the Department of Medicine at Midwestern University/Chicago College of Osteopathic Medicine in Downers Grove, Illinois, and the Department of Pulmonary Medicine at Swedish Covenant Hospital in Chicago, Illinois. Address correspondence to Benjamin Eovaldi, OMS IV, 555 31st Street, Downers Grove, IL 60615-1235.E-mail: [email protected] . NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula The Journal of the American Osteopathic Association, May 2011, Vol. 111, 344-345. doi:10.7556/jaoa.2011.111.5.344 The Journal of the American Osteopathic Association, May 2011, Vol. 111, 344-345. doi:10.7556/jaoa.2011.111.5.344 Eovaldi B, Zanetti C. NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula. J Am Osteopath Assoc 2011;111(5):344345. doi: 10.7556/jaoa.2011.111.5.344. NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account While acid-base disturbances are known to occur with chronic pancreatitis, few cases have been reported in which nonanion gap metabolic acidosis is caused by pancreaticopleural fistula, a known complication of chronic pancreatitis. The current report describes the case of a 49-year-old African American woman who presented with severe pleuritic chest pain and dyspnea at rest. The patient had a history of alcohol-induced chronic pancreatitis. Her chest radiograph was positive for a large left-sided pleural effusion. Magnetic resonance cholangiopancreatography revealed a small connection between the pancreas a Continue reading >>

Non-anion Gap Metabolic Acidosis: A Clinical Approachtoevaluation.

Non-anion Gap Metabolic Acidosis: A Clinical Approachtoevaluation.

1. Am J Kidney Dis. 2017 Feb;69(2):296-301. doi: 10.1053/j.ajkd.2016.09.013. Epub2016 Oct 28. Non-Anion Gap Metabolic Acidosis: A Clinical ApproachtoEvaluation. (1)Nephrology Section, VA Greater Los Angeles Healthcare System, David Geffen School of Medicine at UCLA, Los Angeles, CA. (2)Nephrology Section, VA Greater Los Angeles Healthcare System, David Geffen School of Medicine at UCLA, Los Angeles, CA. Electronic address: [email protected] Acid-base disturbances can result from kidney or nonkidney disorders. We present a case of high-volume ileostomy output causing large bicarbonate losses andresulting in a non-anion gap metabolic acidosis. Non-anion gap metabolic acidosiscan present as a form of either acute or chronic metabolic acidosis. A completeclinical history and physical examination are critical initial steps to begin theevaluation process, followed by measuring serum electrolytes with a focus onpotassium level, blood gas, urine pH, and either direct or indirect urineammonium concentration. The present case was selected to highlight thedifferential diagnosis of a non-anion gap metabolic acidosis and illustrate asystematic approach to this problem.Published by Elsevier Inc. Continue reading >>

Metabolic Acidosis - Endocrine And Metabolic Disorders - Merck Manuals Professional Edition

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 >>

Hyperchloremic Acidosis

Hyperchloremic Acidosis

Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: Romesh Khardori, MD, PhD, FACP more... This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses , in particular the renal tubular acidoses (RTAs). [ 1 , 2 ] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [(HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG Continue reading >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment of acute non-anion gap metabolic acidosis Medical and Research Services VHAGLA Healthcare System, Division of Nephrology, VHAGLA Healthcare System Correspondence to: Jeffrey A. Kraut; E-mail: [email protected] Search for other works by this author on: Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Jeffrey A. Kraut, Ira Kurtz; Treatment of acute non-anion gap metabolic acidosis, Clinical Kidney Journal, Volume 8, Issue 1, 1 February 2015, Pages 9399, Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acidbase disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide migh 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 >>

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 >>

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 >>

Review Of The Diagnostic Evaluation Of Normal Anion Gap Metabolic Acidosis

Review Of The Diagnostic Evaluation Of Normal Anion Gap Metabolic Acidosis

Acid-Base, Electrolyte and Fluid Alterations: Review Review of the Diagnostic Evaluation of Normal Anion Gap Metabolic Acidosis I have read the Karger Terms and Conditions and agree. I have read the Karger Terms and Conditions and agree. Buy a Karger Article Bundle (KAB) and profit from a discount! If you would like to redeem your KAB credit, please log in . Save over 20% compared to the individual article price. Buy Cloud Access for unlimited viewing via different devices Access to all articles of the subscribed year(s) guaranteed for 5 years Unlimited re-access via Subscriber Login or MyKarger Unrestricted printing, no saving restrictions for personal use * The final prices may differ from the prices shown due to specifics of VAT rules. For additional information: Background: Normal anion gap metabolic acidosis is a common but often misdiagnosed clinical condition associated with diarrhea and renal tubular acidosis (RTA). Early identification of RTA remains challenging for inexperienced physicians, and diagnosis and treatment are often delayed. Summary: The presence of RTA should be considered in any patient with a high chloride level when the CL-/Na+ ratio is above 0.79, if the patient does not have diarrhea. In patients with significant hyperkalemia one should evaluate for RTA type 4, especially in diabetic patients, with a relatively conserved renal function. A still growing list of medications can produce RTA. Key Messages: This review highlights practical aspects concerning normal anion gap metabolic acidosis. Berend K, de Vries AP, Gans RO: Physiological approach to assessment of acid-base disturbances. N Engl J Med 2015;372:195. Kraut JA, Madias NE: Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol 2007;2:162-174. Roberts WL Continue reading >>

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

Differential Diagnosis Of Nongap Metabolic Acidosis: Value Of A Systematic Approach

Go to: Recognition and Pathogenesis of the Hyperchloremia and Hypobicarbonatemia of Nongap Acidosis A nongap metabolic acidosis is characterized by a serum anion gap that is unchanged from baseline, or a decrease in serum [HCO3−] that exceeds the rise in the anion gap (5,6). Whenever possible, the baseline anion gap of the patient should be used rather than the average normal value specific to a particular clinical laboratory (6) and the anion gap should be corrected for the effect of a change in serum albumin concentration (7). These steps will reduce the chance that a co-existing high anion gap acidosis will be missed if the increase in the serum anion gap does not cause the value to exceed the upper limit of the normal range (8,9). Nongap metabolic acidosis (hyperchloremic) refers a metabolic acidosis in which the fall in serum [HCO3−] is matched by an equivalent increment in serum Cl− (6,10). The serum anion gap might actually decrease slightly, because the negative charges on albumin are titrated by accumulating protons (6,11). Hyperchloremic acidosis is a descriptive term, and does not imply any primary role of chloride in the pathogenesis of the metabolic acidosis. As shown in Figure 1, a nongap metabolic acidosis can result from the direct loss of sodium bicarbonate from the gastrointestinal tract or the kidney, addition of hydrochloric acid (HCl) or substances that are metabolized to HCl, impairment of net acid excretion, marked urinary excretion of organic acid anions with replacement with endogenous or administered Cl− (12,13), or administration of Cl−-rich solutions during resuscitation (14). The development of hyperchloremic acidosis from administration of HCl is easy to visualize, with titrated HCO3− being replaced by Cl−. Similarly, gastroin 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 >>

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 >>

Acid-base Physiology

Acid-base Physiology

8.4.1 Is this the same as normal anion gap acidosis? In hyperchloraemic acidosis, the anion-gap is normal (in most cases). The anion that replaces the titrated bicarbonate is chloride and because this is accounted for in the anion gap formula, the anion gap is normal. There are TWO problems in the definition of this type of metabolic acidosis which can cause confusion. Consider the following: What is the difference between a "hyperchloraemic acidosis" and a "normal anion gap acidosis"? These terms are used here as though they were synonymous. This is mostly true, but 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'. However, you should be aware that in some cases of normal anion-gap acidosis, there will not be a hyperchloraemia if there is a significant hyponatraemia. In a disorder that typically causes a high anion gap disorder there may sometimes be a normal anion gap! The anion gap may still be within the reference range in lactic acidosis. Now this can be misleading to you when you are trying to diagnose the disorder. Once you note the presence of an anion gap within the reference range in a patient with a metabolic acidosis you naturally tend to concentrate on looking for a renal or GIT cause. 1. One possibility is the increase in anions may be too low to push the anion gap out of the reference range. In lactic acidosis, the clinical disorder can be severe but the lactate may not be grossly high (eg lactate of 6mmol/l) and the change in the anion gap may still leave it in the reference range. So the causes of high anion gap acidosis should be considered in patients with hyperchloraemic acidosis if the cause of the acidosis is otherwise not apparent. Continue reading >>

More in ketosis