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Dka Anion Gap

Pulmcrit – Four Dka Pearls

Pulmcrit – Four Dka Pearls

Introduction I have a confession to make: I love treating DKA. It’s satisfying to take a patient from severe acidosis, electrolytic disarray, and hypovolemia to normal physiology during an ICU shift. Although it's usually straightforward, there are some pitfalls and a few tricks that may help your patients improve faster.0 Pearl #1: Avoid normal saline A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worseningof the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient whose initial bicarbonate level is extremely low.1 A while ago I made the switch from NS to lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon when using LR. Example of the effect of normal saline resuscitation during the initial phase of DKA resuscitation. This patient received approximately 3 liters normal saline between admission labs and the next set of labs as well as an insulin infusion, all textbook management per American Diabetes Association guidelines. The anion gap decreased from 33 mEq/L to 30 mEq/L, indicating improvement of ketoacidosis. However, the bicarbonate decreased from 8 mEq/L to 5 mEq/L due to a hyperchloremic metabolic acidosis caused by the normal saline. Note the increase in chloride over four hours. Failure of the potassium to decrease significantly despite insulin infusion may reflect potassium shifting out of the cells in response to the hyperchloremic metabolic acidosis. There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl et al, 2011). These authors fou Continue reading >>

Diabetic Ketoacidosis With Normal Anion Gap To Use Or Not To Use Normal Saline?

Diabetic Ketoacidosis With Normal Anion Gap To Use Or Not To Use Normal Saline?

AG- anion gap; Cl chloride; HCO3- bicarbonate; K+ potassium; Na+ sodium; SBE standard base excess; SIG strong ion gap; *dipstick method; Normal anion gap in our laboratory is 12. Serum lactate at admission was 3.2 mmol/L. Hyperchloremic metabolic acidosis (HMA) in DKA, especially during recovery, have been reported [2] The mechanism of early HMA in our case could be gradual development of ketoacidosis and persistent urinary loss of ketoanions. A normal corrected sodium level in our patient suggested adequate oral water intake before admission to intensive care unit. HMA in children and adults during DKA management is associated with slow recovery from acidosis [3]. In a retrospective study [4], prolonged intensive care unit and hospital stay were observed in those with non-gap acidosis (secondary to hyperchloremia). Use of normal saline as a rehydration fluid is known to cause dilutional-hyperchloremic acidosis. A recent trial [5] showed extended insulin requirement and hospital stay in those who received only NS as post-bolus rehydration fluid or those who received NS but were switched to during recovery when compared with children who received only N/2 saline. Earlier resolution of acidosis was observed when Plasmalyte (containing sodium 140 mEq/L, potassium 5 mEq/L, chloride 98 mEq/L, magnesium 3 mEq/L, acetate 27 mEq/L, gluconate 23 mEq/L; osmolality: 294 mOsm/L) was used [6] instead of NS in the initial 12-hours of management of DKA. An adult trial comparing NS with Ringers lactate (RL) failed to show significant difference in time-to-resolution of DKA [7]. The only randomized trial comparing NS with balanced electrolyte solution (BES) for fluid resuscitation in children with DKA revealed that BES consistently prevented HMA [8]. The benefit of BES is attributable Continue reading >>

Anion Gap In Diabetes Ketoacidosis

Anion Gap In Diabetes Ketoacidosis

When I left the Cardiac-Surgical ICU to go to a Medical Cardiac ICU at a Level I Trauma center, it was a big change for me. It was a whole new regime of policies, protocols, and procedures. And, it was a big chance for growth for me as a nurse. I remember one of the first patients I had when I got to the new unit. I was caring for a DKA patient and the doctors continually asking me has her gap closed? I thought to myself, What the heck are they talking about? Diabetic ketoacidosis is an EMERGENCY! It must be treated as quickly as possible to prevent coma and/or death. The patients insulin needs are unable to match their insulin supply. The body metabolizes glucose for energy, so it begins to metabolize fats and acids, which in turn, create ketones. The ketones create keto acids, which create a state of acidosis. Watch this video for an in-depth conversation about DKA: Irregular pattern of deep & rapid breathing. Patients are trying to blow off CO2 to lower acid levels DKA can often be the first manifestation of Type 1 diabetes. Chronic hyperglycemia causes damage to tissues & organs over time. The body can (for the most part) tolerate and compensate while the person is young. Additionally, younger people and children burn more calories (thus, lowering their glucose levels) than adults due to: What converts the person from a state of tolerance to a state of DKA, is an injury. Injuries are not just a physical injury like a cut or something, but any type of injury which causes the body to develop a stress response to repair itself, like infection. An Anion Gap is the difference between the measured cations and anions in the serum. There are some formulas where potassium is not added to the sodium. The rational behind that is potassium is usually a small number and may not Continue reading >>

Endocrine Emergencies

Endocrine Emergencies

This activity is intended for clinicians in primary care, notably emergency medicine, internal medicine, family medicine, diabetes and endocrinology, nurses, and medical students. The goal of this activity is to provide background and essential, practical information for healthcare providers to aid in the recognition and management of endocrine emergencies. Upon completion of this activity, participants will be able to: List common precipitating and risk factors of thyroid storm Describe diagnosis, including presentation, symptoms, and laboratory findings of thyroid storm Discuss treatment and the mortality rate of both treated and untreated thyroid storm Describe clinical presentation and findings of myxedema coma Recognize symptoms and interpret laboratory data of someone in DKA Discuss how to treat electrolyte abnormalities seen with DKA Describe how to recognize and treat adrenal crisis As an organization accredited by the ACCME, Medscape, LLC requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. Medscape, LLC encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content. Assistant Professor of Medicine, Uniformed Services University of Health Science, Bethesda, Maryland; Internal Medicine Resident, Walter Reed Army Medical Center, Washington, DC Disclosure: Anita A. Shah, DO, has disclosed no rel Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

© 1996–2017 themedicalbiochemistrypage.org, LLC | info @ themedicalbiochemistrypage.org Definition of Diabetic Ketoacidosis The most severe and life threatening complication of poorly controlled type 1 diabetes is diabetic ketoacidosis (DKA). DKA is characterized by metabolic acidosis, hyperglycemia and hyperketonemia. Diagnosis of DKA is accomplished by detection of hyperketonemia and metabolic acidosis (as measured by the anion gap) in the presence of hyperglycemia. The anion gap refers to the difference between the concentration of cations other than sodium and the concentration of anions other than chloride and bicarbonate. The anion gap therefore, represents an artificial assessment of the unmeasured ions in plasma. Calculation of the anion gap involves sodium (Na+), chloride (Cl–) and bicarbonate (HCO3–) measurements and it is defined as [Na+ – (Cl– + HCO3–)] where the sodium and chloride concentrations are measured as mEq/L and the bicarbonate concentration is mmol/L. The anion gap will increase when the concentration of plasma K+, Ca2+, or Mg2+ is decreased, when organic ions such as lactate are increased (or foreign anions accumulate), or when the concentration or charge of plasma proteins increases. Normal anion gap is between 8mEq/L and 12mEq/L and a higher number is diagnostic of metabolic acidosis. Rapid and aggressive treatment is necessary as the metabolic acidosis will result in cerebral edema and coma eventually leading to death. The hyperketonemia in DKA is the result of insulin deficiency and unregulated glucagon secretion from α-cells of the pancreas. Circulating glucagon stimulates the adipose tissue to release fatty acids stored in triglycerides. The free fatty acids enter the circulation and are taken up primarily by the liver where Continue reading >>

Calculating The Anion Gap For Patients With Acidosis And Hyperglycemia

Calculating The Anion Gap For Patients With Acidosis And Hyperglycemia

TO THE EDITOR: A frequently encountered problem in clinical practice is a patient who presents with acidosis and hyperglycemia. It has been my experience that the correct calculation of the anion gap in the face of hyperglycemia is often confusing. An example would best serve to illustrate the point. Assume a patient who is admitted with new-onset diabetes mellitus and has the following blood test results: glucose level, 700 mg/dL; sodium level, 128 mEq/L; chloride level, 97 mEq/L; and bicarbonate level, 21 mEq/L. The anion gap in this patient is [Na] ?([Bicarbonate] + [Cl]) = 128 ?(97 + 21) = 10, a value within normal limits; the patient has a mild non-anion gap acidosis. However, physicians often correct the sodium level in the face of hyperglycemia by adding 1.6 mEq/L to the sodium concentration for each 100-mg/dL increment in glucose levels above 100 mg/dL. This correction does not apply to the calculation of the anion gap in patients with acidosis and hyperglycemia because the water moving from the intracellular compartment to the extracellular compartment as a result of the hyperglycemia equally dilutes all electrolytes, including the chloride and bicarbonate. If in this case the sodium level is "corrected" for the hyperglycemia, it will be calculated as 138 mEq/L and lead to a falsely elevated calculated anion gap of 20. Thus, the patient’s condition would be erroneously diagnosed as severe anion gap acidosis, most probably diabetic ketoacidosis. Tomer, Y. Annals of Internal Medicine 129:9 p753 Continue reading >>

Jaime Moo-young, Md

Jaime Moo-young, Md

Diabetic Ketoacidosis (DKA) Pathogenesis · Insufficient insulin for a given carbohydrate load decreased cellular metabolism of glucose · Increased gluconeogenesis, glycogenolysisHyperglycemia · Increased breakdown of free fatty acids as alternative energy source ketone and ketoacid accumulation · Hyperglycemiaserum hyperosmolality osmotic diuresis dehydration and electrolyte derangements (dehydration is most lethal!) · Seen almost exclusively in Type I diabetes; rarely in Type II Definition: Triad of 1. Hyperglycemia (usually between 500 – 800 mg/dL or 27.8-44.4 mmol/L) 2. Anion Gap Metabolic Acidosis (pH usually <7.30) 3. Ketonemia: -hydroxybutyrate, acetoacetate most significant ** Urine ketones do not make the diagnosis, but they can support it** Triggers (the “I’sâ€): Don’t forget to ask about these! · Insulin deficiency: insulin non-compliance, insufficient insulin dosing, new-onset Type I diabetes · Iatrognic: glucocorticoids, atypical antipsychotics, high-dose thiazide diuretics · Infection: UTI, pneumonia, TB · Inflammation: pancreatitis, cholecystitis · Ischemia/infarction: MI, stroke, gut ischemia · Intoxication: Alcohol, cocaine, other drugs Presentation · Symptoms · Polyuria, polydipsia, weight loss · Nausea, vomiting, abdominal pain · Fatigue, malaise · Associated trigger sx (fever/chills, chest pain, etc) · Signs · Volume depletion: skin turgor, dry axillae, dry mucus membranes, HR, BP · Altered mental status: stupor, coma · Kussmaul respirations: rapid, shallow breathing = hyperventilation to counteract metabolic acidosis · Fruity, acetone odor on breath Lab workup and findings · Hyperglycemia: > 250 mg/dL in serum, + glucose on urinalysis · Acidemia (pH <7. Continue reading >>

Closing The Anion Gap: Contribution Of D-lactate To Diabetic Ketoacidosis

Closing The Anion Gap: Contribution Of D-lactate To Diabetic Ketoacidosis

Abstract A high anion gap in diabetic ketoacidosis (DKA) suggests that some unmeasured anions must contribute to the generation of the anion gap. We investigated the contribution of D-lactate to the anion gap in DKA. Diabetic patients with and without DKA and high anion gap were recruited. Plasma D-lactate was quantified by HPLC. Plasma methylglyoxal was assayed by liquid chromatography-tandem mass spectrometry. The plasma fasting glucose, β-hydroxybutyrate, and blood HbA1c levels were highly elevated in DKA. Plasma anion gap was significantly increased in DKA (20.59±6.37) compared to either the diabetic (7.50±1.88) or the control group (6.53±1.75) (p<0.001, respectively). Moreover, plasma D-lactate levels were markedly increased in DKA (3.82±2.50 mmol/l) compared to the diabetic (0.47±0.55 mmol/l) or the control group (0.25±0.35 mmol/l) (p<0.001, respectively). Regression analysis demonstrated that D-lactate was associated with acidosis and anion gap (r=0.686, p<0.001). Plasma D-lactate levels are highly elevated and associated with metabolic acidosis and the high anion gap in DKA. Laboratory monitoring of d-lactate will provide valuable information for assessment of patients with DKA. Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i 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 >>

Anion Gap

Anion Gap

Pathophysiology sample values BMP/ELECTROLYTES: Na+ = 140 Cl− = 100 BUN = 20 / Glu = 150 K+ = 4 CO2 = 22 PCr = 1.0 \ ARTERIAL BLOOD GAS: HCO3− = 24 paCO2 = 40 paO2 = 95 pH = 7.40 ALVEOLAR GAS: pACO2 = 36 pAO2 = 105 A-a g = 10 OTHER: Ca = 9.5 Mg2+ = 2.0 PO4 = 1 CK = 55 BE = −0.36 AG = 16 SERUM OSMOLARITY/RENAL: PMO = 300 PCO = 295 POG = 5 BUN:Cr = 20 URINALYSIS: UNa+ = 80 UCl− = 100 UAG = 5 FENa = 0.95 UK+ = 25 USG = 1.01 UCr = 60 UO = 800 PROTEIN/GI/LIVER FUNCTION TESTS: LDH = 100 TP = 7.6 AST = 25 TBIL = 0.7 ALP = 71 Alb = 4.0 ALT = 40 BC = 0.5 AST/ALT = 0.6 BU = 0.2 AF alb = 3.0 SAAG = 1.0 SOG = 60 CSF: CSF alb = 30 CSF glu = 60 CSF/S alb = 7.5 CSF/S glu = 0.4 The anion gap[1][2] (AG or AGAP) is a value calculated from the results of multiple individual medical lab tests. It may be reported with the results of an Electrolyte Panel, which is often performed as part of a Comprehensive Metabolic Panel.[3] The anion gap is the difference between the measured cations (positively charged ions) and the measured anions (negatively charged ions) in serum, plasma, or urine. The magnitude of this difference (i.e., "gap") in the serum is often calculated in medicine when attempting to identify the cause of metabolic acidosis, a lower than normal pH in the blood. If the gap is greater than normal, then high anion gap metabolic acidosis is diagnosed. The term "anion gap" usually implies "serum anion gap", but the urine anion gap is also a clinically useful measure.[4][5][6][7] Calculation[edit] The anion gap is a calculated measure. This means that it is not directly measured by a specific lab test; rather, it is computed with a formula that uses the results of several individual lab tests, each of which measures the concentration of a specific anion or cation. The concentr Continue reading >>

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Anatomy Of A Dka Resuscitation

Anatomy Of A Dka Resuscitation

Using this formula, an elevated anion gap is above 10-12 mEq/L.1 Please don't correct for albumin, glucose, or potassium. Don't make this unnecessarily complicated.2 Many definitions of DKA may be found in the literature, most of which are antiquated. According to the Canadian DKA guidelines, there are no definitive criteria for the diagnosis of DKA.3 My preferred definition: any patient with diabetes plus a significantly elevated serum beta-hydroxybutyrate level (above 2-3 mM/L).45 DKA patients can have a normal glucose (euglycemic DKA, more on this below ). DKA patients can have a normal pH and a normal bicarbonate. This usually occurs due to a combination of ketoacidosis plus metabolic alkalosis from vomiting. That's right: DKA patients can have a totally stone-cold normal ABG. Anion gap is >>12 mEq/L with positive urinary ketones. History & physical exam are consistent with DKA (figure above) and don't suggest that anything else is going on Non-obvious DKA: In situations where the diagnosis is unclear, check lactate and beta-hydroxybutyrate levels. A significantly elevated beta-hydroxybutyrate level strongly supports the diagnosis of DKA.6 If the patient has a markedly elevated anion gap with only a mildly elevated beta-hydroxybutyrate level, consider the possibility that something else is going on (e.g. mild DKA plus toxic alcohol poisoning). ABG/VBG is neither required nor particularly helpful If you look throughout this chapter, neither pH nor pCO2 are mentioned much. These aren't required for the diagnosis or management of DKA. As explored above, DKA is diagnosed purely on the basis of venous blood chemistries (chem-7, anion gap, and if necessary beta-hydroxybutyrate). The vast majority of DKA patients can be diagnosed and managed perfectly without ever checkin Continue reading >>

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 Calculator

Anion Gap Calculator

Please enable JavaScript to view all features on this site. Enter values and press 'calculate' button. Sodium (Na) Chloride (Cl) Bicarbonate (HCO3-) Anion Gap = Na - (Cl + HCO3-) (Normal = 7 - 16) Delta Gap = Anion Gap - 12 The anion gap (AG) represents the concentration of all the unmeasured anions in the plasma. See Also : Reference Values During Pregnancy, Anion Gap Causes of a High Anion Gap : MUDPILERSO M-ethanol U-remia D-iabetic Ketoacidosis (DKA) or starvation ketosis P-araldehyde, Phenformin I-sopropyl Alcohol, Isoniazid ,Infection L-actic Acidosis E-thylene Glycol, ethyl alcohol R-habdomyolysis S-alicylates O-ther Causes: Hyperalbuminemia, administered anions All calculations must be confirmed before use. The suggested results are not a substitute for clinical judgment. Neither Perinatology.com nor any other party involved in the preparation or publication of this site shall be liable for any special, consequential, or exemplary Continue reading >>

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