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Dka Anion Gap Range

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>

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 >>

Bun, Glucose, Creatinine

Bun, Glucose, Creatinine

Normal Values pH = 7.38 - 7.42 [H+] = 40 nM/L for a pH of 7.4 PaCO2 = 40 mm Hg [HCO3] = 24 meq/L Acid base definitions Acid base disorder is considered present when there is abnormality in HCO3 or PaCO2 or pH. Acidosis and alkalosis refer to in-vivo derangement's and not to any change in pH. Acidemia (pH < 7.38) and Alkalemia (pH >7.42) refer to derangement's of blood pH. Kidney and Respiratory system play a key roles in maintaining the acid base status. Primary Acid base disorders Metabolic acidosis loss of [HCO3] 0r addition of [H+] Metabolic alkalosis loss of [H+] or addition of [HCO3] Respiratory acidosis increase in pCO2 Respiratory alkalosis decrease in pCO2 Recquired lab values/information Arterial blood gases: pH, PaCO2,PaO2,Sat,CO BUN, Glucose, Creatinine FIO2 and Clinical history Anion and Cations ANIONS CATIONS Chloride Sodium Bicarbonate(Total CO2) Potassium Proteins Calcium Organic acids Magnesium Phosphates Sulfates Electrochemical balance means that the total anions are the same as total Cations. For practical purposes anion gap is calculated using only Sodium, Chlorides and Total CO2.((140-(104+24)) = 12. Compensatory measures Buffering---occurs immediately Respiratory regulation of pCO2 is intermediate (12-24 hours) Renal regulation of [H] and [HCO3] occurs more slowly (several days) Extracellular almost entirely through bicarbonate whose concentration highest of all buffers small contribution from phosphate Intracellular Hemoglobin can directly buffer protons H+ entry into RBC matched by exit of Na and K+ Hemoglobin can directly buffer dissolved intracellular conversion of Buffer systems Hemoglobin can directly buffer protons H+ entry into RBC matched by exit of Na and K+ Hemoglobin can directly buffer dissolved intracellular conversion of Bicarbonate Continue reading >>

Mind The Gap: Anion Gap Acidosis

Mind The Gap: Anion Gap Acidosis

A step by step approach to uncovering the cause of an elevated anion gap metabolic acidosis. We learn about the MUD PILES, the causes of anion gap acidosis, as medical students. And it gets even further drilled into us in residency. But sorting out a gap acidosis can be real challenge, even with a nifty mnemonic. To help us get smarter in understanding some of the nuance of gap acidosis, Sean Nordt, MD, PharmD. Case: Alcoholic, diabetic with a blood glucose of 295, bicarbonate of 12, and an anion gap 28. Is this alcoholic ketoacidosis (AKA), diabetic ketoacidosis (DKA), toxic alcohol, something else? What is the cognitive process for sorting out this anion gap acidosis? Nordt: Without additional history, send… -Ethanol level -VBG -UA -Serum ketones (acetone and beta hydroxybutyrate) if possible -Serum calcium- a good surrogate marker for ethylene glycol. Most hospitals have a volatile alcohol screen looking for methanol and isopropanol, but not ethylene glycol. To detect ethylene glycol, you’ll need to look at surrogate markers. -Start IV fluids Case continues: The patient has a normal mental status. Heart rhythm is sinus tachycardia in the low 100s. To treat this sinus tachycardia, he gets the sinus tachycardia antidote – 3 liters of normal saline. Since AKA (a starvation and volume depletion ketosis) is high on the differential diagnosis, he also gets a hamburger and apple juice. His labs are rechecked and few hours later and his bicarbonate is unchanged at 12 and anion gap drops slightly from 28 to 24. How fast should the anion gap and serum bicarbonate to correct in AKA? Nordt: It should start to improve in 1-2 hours and takes about 5-7 hours to reverse. If the anion gap and bicarbonate aren’t improving (or getting worse) in an hour or two, think about an al Continue reading >>

References

References

Arterial samples: pH 7.36-7.44, HCO3 21-27, PCO2 36-44 Venous: pH 0.03 units lower, HCO3 similar, PCO2 3-8 higher Capillary: similar to arterial (assuming no prolonged tourniquet use, ischemia, etc) 1. Look at the pH. What is the primary process occurring? low pH and high PCO2: respiratory acidosis high pH and low PCO2: respiratory alkalosis high pH and high HCO3: metabolic alkalosis if the pH is near normal but PCO2 and HCO3 are significantly abnormal, there is likely a mixed disorder 2. Assess the degree/chronicity of compensation present. Acute respiratory acidosis: HCO3 increases by 1 me/L and pH decreased by 0.08 for every 10 mmHg increase in PCO2 Chronic respiratory acidosis (3-5 days for renal compensation): HCO3 increases by 4me/Lfor and pH decreased by 0.03 for every 10 mmHg increase in PCO2 Metabolic acidosis: Expected PCO2= 1.5 X HCO3 + 8 +/-2 (Winter's Formula) or the decimal digits of pH should be similar to the PCO2 (ie pH 7.25 should have a PCO2 of 25 in a metabolic acidosis). If the patient's PCO2 is higher than expected, there is a concurrent respiratory acidosis. If the patient's PCO2 is lower than expected, there is a concurrent respiratory alkalosis. If it similar to expected, the compensation is appropriate Metabolic alkalosis: PCO2 increases by 0.7 mmHg for every 1 meq/L increase in HCO3 3. If there is a metabolic acidosis, assess the anion gap. Elevated anion gap --> MUDPILES (Methanol, uremia, diabetic ketoacidosis, propylene glycol, INH, lactic acidosis, ethylene glycol, salicylates) If there is an elevated anion gap, consider calculating the / = Anion gap/ [HCO3-]. <0.4 is consistent with hyperchloremic nongap acidosis, <1 with high AG and normal AG acidosis, 1-2 pure AG acidosis, >2 concurrent metabolic alkalosis or preexisting compensated re Continue reading >>

Serum Anion Gap | Usmle Pearls

Serum Anion Gap | Usmle Pearls

Formula: SAG = (Na+ + K+) (Cl + HCO3) When Used? To differentiate between the causes of Metabolic Acidosis. Interpretation: If SAG is >12 then the metabolic acidosis is Increased Anion Gap Metabolic Acidosis. Remember the mnemonic MUDPILES for Increased Anion Gap Metabolic Acidosis: Methanol, Uremia, DKA, Propylene Glycol, Iron Poisoning/Isoniazid, Lactic Acidosis, Ethylene Glycol, Salicylates. Formula: OG = Measured Serum Osmolality Calculated Serum Osmolality When Used? To diagnose poisoning by certain alcohols. Interpretation: If >10, consider Ethanol, Methanol, Ethylene Glycol, Isopropyl Alcohol and Propylene Glycol Intoxication. (Remember Isopropyl Alcohol has Increased OG but not Increased SAG! (i.e. doesnt cause AG Metabolic Acidosis)) When Used? To differentiate between causes of Normal AG Metabolic Acidosis i.e. to differentiate between RTA vs Diarrhea as cause of the Normal AG Metabolic Acidosis Interpretation: Remember by (Na+ + K+ Cl) we are actually measuring (Urine Cations Urine Anions), the major Cation in Urine that is not usually measured is NH4+, so if UAG is negative that means Increased NH4+ (i.e. acid) excretion in the Urine which should be the case in any acidosis INCLUDING Diarrhea! But, if renal function is not normal as in RTA, NH4+ is not excreted in Urine and so UAG will be 0 or Positive. So, in Normal Anion Gap Metabolic Acidosis, if: UAG = Negative value > Diarrhea (Remember NeGUTive) Formula: Stool Osmolality (usually not measured and replaced by 290 for ease of calculation) 2 (stool Na+ + stool K+) When Used? To differentiate Secretory vs Osmotic Diarrhea SOG >100 = Osmotic Diarrhea (e.g. Lactose Intolerance) Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Acid-base Disorders - Wikem

Acid-base Disorders - Wikem

We need you! See something you could improve? Make an edit and help improve WikEM for everyone. If albumin goes up more acidotic (since albumin is an acid) If difference shrinks (i.e. more Cl) more acidotic Principle of electrical neutrality requires more H+ to offset the additional Cl If difference increases (i.e. more Na) more alkalotic Principle of electrical neutrality requires more bicarb to offset the additional Na Strong ions include Na, Cl, lactate, ketoacid, toxic alcohols Eliminates the respiratory component of acidosis so only left with the metabolic component Is equivalent to the amount of base (or acid) you would have to add to get to pH 7.4 If base deficit is normal but patient is acidotic must all be from CO2 If base deficit is abnormal must explain by SID, weak acids, or unmeasured strong ions If no BD is available 24.2 serum bicarb can be used as okay substitute a pre-existing compensated respiratory acidosis The purpose of this calculation is to assess the bodys ability to change HCO3 in response to a metabolic acid. In cases with a pure anion gap metabolic acidosis, the rise in anion gap from 12 should equal the fall in HCO3 from from 24 Will allow for identification of a secondary process Respiratory acidosis and alkalosis (acute acid-base changes based on PCO2 and HCO3): For every or of PCO2 by 1 the pH changes by 0.008 For every or of HCO3 by 1 the pH changes by 0.015 Estimate of baseline PCO2 in patients with Acute Respiratory Acidosis: Estimated baseline PCO2 = 2.4 (admission measured HCO3 22) HCO3 increases by 4 for every 10 mmHg in pCO2 above 40 Continue reading >>

Lab Test Interpretation

Lab Test Interpretation

The various multiparameter blood chemistry and hematology profilesoffered by most labs represent an economical way by which alarge amount of information concerning a patient's physiologic statuscan be made available to the physician. The purpose of this monograph isto serve as a reference for the interpretation of abnormalities of eachof the parameters. Because reference ranges (except for some lipid studies)are typically defined as the range of values of the median 95% of thehealthy population, it is unlikely that a given specimen, even from ahealthy patient, will show "normal" values for all the tests ina lengthy profile. Therefore, caution should be exercised to preventoverreaction to miscellaneous, mild abnormalities without clinicalcorrelate. Units of measurement: America against the world American labs use a different version of the metric system than doesmost of the rest of the world, which uses the SystmeInternationale (SI). In some cases translation between the twosystems is easy, but the difference between the two is most pronouncedin measurement of chemical concentration. The American system generallyuses mass per unit volume, while SI uses moles per unit volume. Sincemass per mole varies with the molecular weight of the analyte,conversion between American and SI units requires many differentconversion factors. Where appropriate, in this paper SI units are givenafter American units. Dennis Jay, PhD, has kindly made available anonline converter between SI and conventional units: Increase in serum sodium is seenin conditions with water loss in excessof salt loss, as in profuse sweating, severe diarrhea or vomiting,polyuria (as in diabetes mellitus or insipidus), hypergluco- ormineralocorticoidism, and inadequate water intake. Drugs causingelevated sodium inclu Continue reading >>

Anion Gap Calculator

Anion Gap Calculator

This anion gap calculator allows you to compute the AG value and delta gap for the sodium, chloride and bicarbonate values you input in the Na Cl and HCO3 fields. You can discover more on the implications of the anion gap below the form. This is a health tool that can prove useful when analyzing the result of certain medical tests. It helps anyone quickly calculate the anion gap in mEq/L based on the Na (Sodium), Cl (Chloride) and HCO3 (Bicarbonate) values. The first two should be no lower than 80mEq/L for Na and 60mEq/L for Cl. The reference range for AG is 3-11 mEq/L. This anion gap calculator is based on the following formulas that allow to identify the cause of metabolic acidosis: - Anion gap (mEq/L) = [Na] ([Cl] + [HCO3]) - Delta gap (mEq/L) = Anion Gap Baseline gap (here 12) - Delta ratio = Delta gap / (24 [HCO3]) - milliequivalents/liter abbreviated as mEq/L; Lets take into account that we are presented with the following data: Na = 145 mEq/L; Cl = 104 mEq/L; HCO3 = 26 mEq/L Anion gap = 145 (104 +26) => AG = 15 mEq/L Delta ratio = 3 / (24 26) => Delta ratio = -1.5 This is an indicator allowing us to give measure to the undetermined ions in plasma or serum. Anion gap is basically the difference between primary measured cations and anions in serum. What results is the unmeasured concentration of anions in the plasma. Then the result is then defined as low, normal or high. While the serum anion gap complete formula is (Na + K) - (Cl + HCO3), the simpler version, presented above, which excludes K is commonly used. - Representative for the presence of metabolic acidosis - Differentiation between the causes of metabolic acidosis A low result, under 6 mEq/L is suggestive for hypoalbuminemia, albumin being the most relevant unmeasured anion. A normal value in the range Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Increases 0.3-0.7 mEq/l [0.3-0.7 mmol/L] per 0.1 decr pH Difference between measured plasma cation (ie, Na+) and anions (ie, chloride (Cl-), HCO3-) concentrations Lactic acidosis (mild LA may have normal AG) Also called hyperchloremic acidosis (decreased HCO3, increased Cl) Renal tubular acidosis: impairment in renal acidification Type III (term no longer used) Formerly used to define distal RTA with bicarbonate wasting in children Bicarbonaturia resolves with age and is not truly part of a pathologic process Type IV: common in obstructive nephropathy, DM, hyporenin/hypoaldosteronehyper K+, acidosis Intestinal loss of bicarbonate (diarrhea, pancreatic fistula) Carbonic anhydrase inhibitors (e.g. acetazolamide) Dilutional acidosis (due to rapid infusion of bicarbonate-free isotonic saline) Ingestion of exogenous acids (ammonium chloride, methionine, cystine, calcium chloride) Drugs: amiloride, triamterine, Bactrim, chemotherapy, pentamidines As diagnostic aid, is not absolute "Delta gap" = calculated anion gap:nl anion gap In anion gap acidosis, "delta gap" should equal "delta HCO3" If HCO3 higher than predictedsuperimposed metabolic alkalosis If HCO3 lower than predictedsuperimposed non-anion gap metabolic acidosis Allows diagnosisof mixed metabolic disturbance Mixed metabolic disturbance plus respiratory disturbance Check urine pH before initializing therapy NaHCO3 therapy for pH < 7.1 - 7.2 Only used emergently to raise pH to > 7.1 or 7.2 Controversial, depends on disorder and symptoms i.e. NaHCO3 not beneficial in DKA treatment with pH under 7.0) DO NOT give this entire amount 2 ampulesof 8.4% NaHCO3 in 1 Liter of 1/4 NS OR 3-4 ampulesof 8.4% NaHCO3 in 1 Liter D5W Overaggressive NaHCO3"overshoot alkalosis" Bicarbonate level should be corrected only to 15 mEq/L [15 m Continue reading >>

Acid-base Disorders

Acid-base Disorders

Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diagnosis of DKA: � Initial STAT labs include • CBC with diff • Serum electrolytes • BUN • Creatinine • Glucose • Arterial blood gases • Bicarbonate • Urinalysis • Lactate • Serum ketones • Calculation of the Anion Gap � serum anion gap = serum sodium – (serum chloride + bicarbonate) • Electrocardiogram Treatment Protocol for Diabetic Ketoacidosis Reviewed 5/2/2017 2 Updated 05/02/17 DKA Diagnostic Criteria: � Blood glucose >250 mg/dl � Arterial pH <7.3 � Bicarbonate ≤18 mEq/l � Anion Gap Acidosis � Moderate ketonuria or ketonemia 1. Start IV fluids (1 L of 0.9% NaCl per hr initially) 2. If serum K+ is <3.3 mEq/L hold insulin � Give 40 mEq/h until K ≥ 3.3 mEq/L 3. Initiate DKA Order Set Phase I (*In PREGNANCY utilize OB DKA order set) 4. Start insulin 0.14 units/kg/hr IV infusion (calculate dose) RN will titrate per DKA protocol Insulin Potassium Bicarbonate IVF Look for the Cause - Infection/Inflammation (PNA, UTI, pancreatitis, cholecystitis) - Ischemia/Infarction (myocardial, cerebral, gut) - Intoxication (EtOH, drugs) - Iatrogenic (drugs, lack of insulin) - Insulin deficiency - Pregnancy DKA/HHS Pathway Phase 1 (Adult) Approved by Diabetes Steering Committee, MMC, 2015, Revised DKA Workgroup 1_2016 Initiate and continue insulin gtt until serum glucose reaches 250 mg/dl. RN will titrate per protocol to achieve target. When sugar < 250 mg/dl proceed to DKA Phase II *In PREGNANCY when sugar <200 proceed to OB DKA Phase II *PREGNANCY � Utilize OB DKA order set Phase 1 � When glucose reaches 200mg/dL, Initiate OB DKA Phase 2 � Glucose goals 100-150mg/dL OB DKA Phase 2 Determine hydration status Hypovolemic shock Mild hypotensio Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

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