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Difference Between Lactic Acidosis And Ketoacidosis

To Initiate Synjardy Or Synjardy Xr, Determine Appropriate Combination Of The Active Ingredient Of Jardiance And Metformin*

To Initiate Synjardy Or Synjardy Xr, Determine Appropriate Combination Of The Active Ingredient Of Jardiance And Metformin*

Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. Symptoms included malaise, myalgias, respiratory distress, somnolence, and abdominal pain. Laboratory abnormalities included elevated blood lactate levels, anion gap acidosis, increased lactate/pyruvate ratio, and metformin plasma levels generally >5 mcg/mL. Risk factors include renal impairment, concomitant use of certain drugs, age ≥65 years old, radiological studies with contrast, surgery and other procedures, hypoxic states, excessive alcohol intake, and hepatic impairment. Steps to reduce the risk of and manage metformin-associated lactic acidosis in these high risk groups are provided in the Full Prescribing Information. If lactic acidosis is suspected, discontinue SYNJARDY or SYNJARDY XR and institute general supportive measures in a hospital setting. Prompt hemodialysis is recommended. JARDIANCE is indicated to reduce the risk of cardiovascular (CV) death in adults with type 2 diabetes mellitus and established CV disease. JARDIANCE, SYNJARDY, AND SYNJARDY XR are indicated as adjuncts to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. SYNJARDY and SYNJARDY XR are indicated when both empagliflozin and metformin hydrochloride are appropriate. Empagliflozin, a component of SYNJARDY AND SYNJARDY XR, is indicated to reduce the risk of CV death in adults with type 2 diabetes mellitus and established CV disease. However, the effectiveness of SYNJARDY AND SYNJARDY XR on reducing the risk of CV death in adults with type 2 diabetes mellitus and CV disease has not been established. JARDIANCE, SYNJARDY, AND SYNJARDY XR are not recommended for patients with type 1 diabetes or for the treatment of Continue reading >>

You Don't Understand The Osm Gap - Guest Post By Rory Spiegel

You Don't Understand The Osm Gap - Guest Post By Rory Spiegel

Rory is just graduated EM Residency at Beth Israel Newark and is now pursuing advanced training in Resuscitation with Brian Wright and me at Stony Brook Hospital. He is the editor of the amazing EMNerd Blog and tweets at @EMNerd_ . This post will serve as a discussion of serum osmolarity*, its clinical utility, and the relationship between the Osm and anion gaps. The serum osmolarity has been relegated to the dark arts of medical science. Primarily, it is used to calculate the exact fluid status of patients presenting in various dysnatremic states by the physicians who happen to care for such physiological disruptions. Simply put the serum osmolarity is the number of particles present in the serum. The osmolarity does not discriminate based on a particles size or weight, but rather is concerned only with its concentration in the blood (1). As such, particles with low molecular weight that are capable of accumulating in large quantities in the serum, have the greatest potential to influence the osmolarity. In a healthy subject, the osmolarity is predominantly comprised of sodium ions and their counter anions, serum glucose, as well as blood urea nitrogen (BUN) (1). The serum osmolarity can be grossly estimated using the following formula: Briefly, this formula insures that each molecule is accounted for in its molar quantity (mmol/L) (1). The serum osmolality can also be directly measured by observing either the serums freezing point depression or boiling point elevation. If we compare this measured value to the calculated osmolarity, the difference between the two measurements is the Osm gap. Ideally this would equate to the amount of particles present in the serum that are not accounted for by the calculated formula. As such, the Osm gap should be positive in most phy Continue reading >>

Lab Test

Lab Test

Initial evaluation and monitoring of diabetic ketoacidosis (DKA): Anion gap is > 10 mEQ/L in mild DKA and > 12 mEq/L in moderate to severe cases. After initial evaluation, calculate the anion gap every 2 to 4 hours to monitor resolution of acidosis. Initial evaluation of suspected hyperglycemic hyperosmolar state (HHS): About 50% of patients have an increased anion gap metabolic acidosis due to concomitant ketoacidosis and/or an increases in serum lactate levels. Suspected alcoholic ketoacidosis Suspected hypermagnesemia Suspected lactic acidosis Suspected metabolic acidosis Other conditions other than metabolic acidosis that could cause an elevated anion gap are: Dehydration, treatment with sodium salts of strong acids, treatment with sodium salts of antibiotics (e.g., penicillin, carbenicillin), alkalosis, decreased unmeasured cation (e.g., hypokalemia, hypocalcemia, hypomagnesemia), hyperalbuminemia, increased inorganic anion (e.g., phosphate, sulfate), laboratory error (e.g., falsely increased serum sodium falsely decreased serum chloride or bicarbonate). The anion gap may be lowered by one of three mechanisms: Increased unmeasured cation (e.g., hyperkalemia, hypercalcemia, hypermagnesemia, multiple myeloma, lithium intoxication, polymyxin B) By decreased unmeasured anion (e.g., hypoalbuminemia or bromide (Br-) intoxication) By laboratory error (e.g., falsely decreased serum sodium, falsely increased serum chloride or bicarbonate hyperviscosity, hyperlipidemia, dilutional studies). Calculation of the anion gap should be adjusted for albumin. The anion gap falls by approximately 2.5 mgEq/L for every 1 g/dL reduction in serum albumin concentrations. The anion gap is the measurement in the difference between the cations and the anions in the extra-cellular space. Altho Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis occurs when the body produces too much acid. It can also occur when the kidneys are not removing enough acid from the body. There are several types of metabolic acidosis. Diabetic acidosis develops when acidic substances, known as ketone bodies, build up in the body. This most often occurs with uncontrolled type 1 diabetes. It is also called diabetic ketoacidosis and DKA. Hyperchloremic acidosis results from excessive loss of sodium bicarbonate from the body. This can occur with severe diarrhea. Lactic acidosis results from a buildup of lactic acid. It can be caused by: Alcohol Cancer Exercising intensely Liver failure Medicines, such as salicylates Other causes of metabolic acidosis include: Kidney disease (distal renal tubular acidosis and proximal renal tubular acidosis) Poisoning by aspirin, ethylene glycol (found in antifreeze), or methanol Continue reading >>

Strong Ion Difference: Etiology

Strong Ion Difference: Etiology

Home / ABA Keyword Categories / 2015 Keywords (Defined) / Strong ion difference: Etiology Strong ions are cations and anions that exist as charged particles dissociated from their partner ions at physiologic pH. Thus, these ions are strong because their ionization state is independent of pH. The Strong Ion Difference (SID) is the difference between the positively- and negatively-charged strong ions in plasma. This method of evaluating acid-base disorders was developed to help determine the mechanism of the disorder rather than simply categorizing them into metabolic vs. respiratory acidosis/alkalosis as with the Henderson-Hasselbalch equation. Strong cations predominate in the plasma at physiologic pH leading to a net positive plasma charge of approximately +40-45. SID can be estimated as follows: SID = [strong cations] [strong anions] = [Na+ + K+ + Ca2+ + Mg2+] [Cl- + lactate-] Disturbances that increase the SID increase the blood pH (alkalosis) while disorders that decrease the SID lower the plasma pH (acidosis). According to the law of electroneutrality the sum of positive charges is equal to the sum of negative charges. Therefore the SID must be equal to the sum of weak anions in the body (such as bicarbonate, albumin, and phosphate). Dehydration (contraction alkalosis) due to increased Na+ Chloride loss (e.g. aggressive NG suctioning with loss of HCl) Free water excess (dilutional acidosis) due to decreased Na+ Aggressive administration of Normal Saline (NS) as the SID of Normal Saline is 0 (Na+ = 154mEq/L and Cl- = 154mEq/L SID = 154 154 = 0) Severe diarrhea due to loss of K+ and Na+ An increase in unmeasured anions such as lactate (e.g. lactic acidosis) or ketoacids (e.g. diabetic ketoacidosis) Continue reading >>

Prevalence And Significance Of Lactic Acidosis In Diabetic Ketoacidosis

Prevalence And Significance Of Lactic Acidosis In Diabetic Ketoacidosis

The publisher's final edited version of this article is available at J Crit Care See other articles in PMC that cite the published article. The prevalence and clinical significance of lactic acidosis in diabetic ketoacidosis (DKA) are understudied. The objective of this study was to determine the prevalence of lactic acidosis in DKA and its association with intensive care unit (ICU) length of stay (LOS) and mortality. Retrospective, observational study of patients with DKA presenting to the emergency department of an urban tertiary care hospital between January 2004 and June 2008. Sixty-eight patients with DKA who presented to the emergency department were included in the analysis. Of 68 patients, 46 (68%) had lactic acidosis (lactate, >2.5 mmol/L), and 27 (40%) of 68 had a high lactate (>4 mmol/L). The median lactate was 3.5 mmol/L (interquartile range, 3.324.12). There was no association between lactate and ICU LOS in a multivariable model controlling for Acute Physiology and Chronic Health Evaluation II, glucose, and creatinine. Lactate correlated negatively with blood pressure (r = 0.44; P < .001) and positively with glucose (r = 0.34; P = .004). Lactic acidosis is more common in DKA than traditionally appreciated and is not associated with increased ICU LOS or mortality. The positive correlation of lactate with glucose raises the possibility that lactic acidosis in DKA may be due not only to hypoperfusion but also to altered glucose metabolism. Keywords: Diabetic ketoacidosis, Lactic acidosis, Diabetes, Acidosis Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus that occurs when circulating insulin levels are low or absent. This state is characterized by acidosis, hyperglycemia, and the presence of serum ketones. Diabetic ketoacido Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Common Laboratory (lab) Values - Abgs

Common Laboratory (lab) Values - Abgs

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z Laboratory VALUES Home Page Arterial Blood Gases Arterial blood gas analysis provides information on the following: 1] Oxygenation of blood through gas exchange in the lungs. 2] Carbon dioxide (CO2) elimination through respiration. 3] Acid-base balance or imbalance in extra-cellular fluid (ECF). Normal Blood Gases Arterial Venous pH 7.35 - 7.45 7.32 - 7.42 Not a gas, but a measurement of acidity or alkalinity, based on the hydrogen (H+) ions present. The pH of a solution is equal to the negative log of the hydrogen ion concentration in that solution: pH = - log [H+]. PaO2 80 to 100 mm Hg. 28 - 48 mm Hg The partial pressure of oxygen that is dissolved in arterial blood. New Born – Acceptable range 40-70 mm Hg. Elderly: Subtract 1 mm Hg from the minimal 80 mm Hg level for every year over 60 years of age: 80 - (age- 60) (Note: up to age 90) HCO3 22 to 26 mEq/liter (21–28 mEq/L) 19 to 25 mEq/liter The calculated value of the amount of bicarbonate in the bloodstream. Not a blood gas but the anion of carbonic acid. PaCO2 35-45 mm Hg 38-52 mm Hg The amount of carbon dioxide dissolved in arterial blood. Measured. Partial pressure of arterial CO2. (Note: Large A= alveolor CO2). CO2 is called a “volatile acid” because it can combine reversibly with H2O to yield a strongly acidic H+ ion and a weak basic bicarbonate ion (HCO3 -) according to the following equation: CO2 + H2O <--- --> H+ + HCO3 B.E. –2 to +2 mEq/liter Other sources: normal reference range is between -5 to +3. The base excess indicates the amount of excess or insufficient level of bicarbonate in the system. (A negative base excess indicates a base deficit in the blood.) A negative base excess is equivalent to an acid excess. A value outside of the normal r Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis is a state of insulin deficiency, characterised by rapid onset, extreme metabolic acidosis, a generally intact sensorium, and only mild hyperglycaemia. DKA comes up frequently in the CICM SAQs, but usually as an ABG interpretation exercise. This chapter focuses on the medical side of DKA, including its causes, manifestations, complications, and management strategies. Questions which have required such thinking have included the following: Question 1 from the second paper of 2016 (differences between HONK and DKA) Question 17 from the first paper of 2014 (differences between HONK and DKA) Question 2 from the second paper of 2009 (general approach to management) Question 15 from the second paper of 2000 (whether or not saline is appropriate) Definition of diabetic ketoacidosis How does one discriminate between DKA and HONK even when in about 30% of instances the two disorders coexist? Arbitrary definitions exist, proposed by the American Diabetes Association. In summary: DKA presents with acidosis as the major feature HONK presents with hyperglycaemia as the major feature Discriminating Between HONK and DKA Domain Features suggestive of DKA Features suggestive of HONK Demographic Young Known Type 1 diabetic Elderly Known Type 2 diabetic History Rapid clinical course History of noncompliance with insulin Abdominal pain Shortness of breath Prolonged course History of noncompliance with oral antihyperglycaemic agents and insulin Polydipsia, polyuria, weight loss Neurological symptoms Examination Tachypnoea Normal level of consciousness, or only slightly decreased Coma Seizures Biochemistry Severe acidosis Severe ketosis Mild hyperglycaemia Renal function normalises rapidly Mild acidosis Little ketosis; mainly lactate is raised Severe hyperglycaemia Esta Continue reading >>

Alcoholic Ketoacidosis And Lactic Acidosis

Alcoholic Ketoacidosis And Lactic Acidosis

The clinical picture of 33 patients with life-threatening generalized infections is characterized by some of the following symptoms: tachycardia, hypotension, disturbances of mental state, tachypnea, and oliguria or anurai. The haemodynamic findings are lowered peripheral resistance, normal or increased cardiac output, more or less pronounced hypotension and normal or decreased AVDO2. In spite of ... [Show full abstract] normal oxygen supply, the arterial lactate concentration is often elevated. In order to evaluate the causes, the oxygen consumption of rat liver mitochondria was measured before and after application of Coli-endotoxinin vivo andin vitro. A decreased coupling of respiration and phosphorylation was found. During the early phase of life-threatening infections a respiratory alkalosis can often be seen. Lactic acidosis ofliquor cerebrospinalis is not the cause of this hypoventilation, nor is diminished cerebral blood flow the cause of somnolence. The patients are threatened by impaired function of various organs. The decisive therapeutic measure are surgery and/or broad spectrum antibiotic therapy. Horses competing in 3-day, combined-training events develop a metabolic acidosis that is partially compensated for by a respiratory alkalosis immediately after phases B and D. By the end of phase C and 30 minutes to 2 hours after phase D, the acidosis is resolved by the oxidation of lactate, and a metabolic alkalosis prevails. A reduction in TBW and cation content occurs, which often is not ... [Show full abstract] replenished 12 to 24 hours after the event, even though the serum or plasma concentration of various constituents may be within normal limits. Hypochloremia and hypocalcemia, however, may persist 12 or more hours after the speed and endurance test. All Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Copyright © 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>

Hyperchloremic Acidosis During The Recovery Phase Of Diabetic Ketosis

Hyperchloremic Acidosis During The Recovery Phase Of Diabetic Ketosis

Hyperchloremic Acidosis During the Recovery Phase of Diabetic Ketosis MAN S. OH, M.D.; HUGH J. CARROLL, M.D.; DAVID A. GOLDSTEIN, M.D.; I. ALAN FEIN, M.D. Author, Article, and Disclosure Information Requests for reprints should be addressed to Man S. Oh, M.D.; Box 21, Downstate Medical Center, 450 Clarkson Ave.; Brooklyn, NY 11203. We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine. Continue reading >>

Ketosis & Acidosis

Ketosis & Acidosis

Ketosis occurs when the fat in your body does not break down completely, producing ketones. It's a condition that can occur when you go on a low-carb diet and glycogen stores in your liver are depleted. When you have too much acid in your system, you can develop acidosis. The acid build-up can take place in your kidneys or lungs for a variety of reasons. The build-up of ketones can cause an imbalance that leads to excessive acid production. Video of the Day Diabetics may be prone to ketosis or acidosis when insulin levels drop below healthy levels or when ketones build up in the body due to uncontrolled insulin levels. Ketones are the byproduct produced when the body relies primarily on fat stores for energy. While short-term ketosis can help you lose weight, ketones that continue to build up in your blood and urine are poisonous and lead to diabetic ketoacidosis, also referred to as diabetic acidosis. The condition is a more common complication of Type 1 diabetes. In addition to low insulin levels, trauma, severe infection, a heart attack or surgery can lead to diabetic ketoacidosis. Diabetic acidosis requires immediate medical attention. As insulin levels drop, your body produces blood sugar by uncontrollably burning fat. Your body turns acidic as glucose begins to appear in your urine. As your body tries to find a balance, your breathing becomes deeper and quicker, leading to a temporary balance as you blow off excess carbon dioxide. Symptoms may start with confusion, thirst, fatigue and increased urination. You may become unconscious. As acidosis progresses, you can smell acetone on your breath. Symptoms usually appear quickly, so you should seek emergency treatment. A high fat and high protein diet that's low in carbohydrates can lead to ketosis. At the same time, Continue reading >>

Acid-base Imbalance, Abnormal Blood Ph

Acid-base Imbalance, Abnormal Blood Ph

Metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis, mixed acid-base disorders Derangements in blood pH result from increased intake, altered production or impaired/excessive excretion of acid or base. With time, respiratory and renal adjustments correct the pH towards normal by altering the plasma levels of pCO2 or strong ions (Na+,Cl- ), and result in predictable changes in bicarbonate concentration that can also be used to characterize the disorder (see = [(pCO2 -40)/10] +24= [(pCO2 -40)/3] +24 Acidosis: A physiologic process leading to acidemia Alkalosis: A physiologic process leading to alkalemi. Respiratory: The primary disorder results from an abnormal pCO2 --increased = acidosis; decreased = alkalosis Metabolic: The primary disorder does not result from abnormal pCO2 Mixed (Complex): More than one disorder is present Compensation: Changes in pCO2 or strong ions (Na+,Cl- ) resulting from normal physiologic mechanisms to restore acid-base balance Standard base excess (SBE): Quantity of metabolic acid-base disturbance where a positive value indicates alkalosis and a negative value (also referred to as a base deficit) indicates an acidosis Strong ion difference: The difference in charge between "strong" (completely dissociated) cations (positive) and anions (negative). (See pathophysiology section.) Anion gap: The difference in charge between commonly measured electrolytes (See laboratory findings section.) Acidosis: chloride administration (e.g. saline), aspirin overdose Alkalosis: NaHCO3 administration, antacid abuse, buffered replacement fluid (hemofiltration) Increased acid production: lactic acidosis, diabetic ketoacidosis Hypercapnic respiratory failure, permissive hypercapnia Alkalosis: vomiting, large gastric aspirates, diur Continue reading >>

What Is Metabolic Acidosis?

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 >>

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