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Dka Anion Gap

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 >>

Clinical Aspects Of The Anion Gap

Clinical Aspects Of The Anion Gap

The anion gap (AG) is a calculated parameter derived from measured serum/plasma electrolyte concentrations. The clinical value of this calculated parameter is the main focus of this article. Both increased and reduced anion gap have clinical significance, but the deviation from normal that has most clinical significance is increased anion gap associated with metabolic acidosis. This reflects the main clinical utility of the anion gap, which is to help in elucidating disturbances of acid-base balance. The article begins with a discussion of the concept of the anion gap, how it is calculated and issues surrounding the anion gap reference interval. CONCEPT OF THE ANION GAP - ITS DEFINITION AND CALCULATION Blood plasma is an aqueous (water) solution containing a plethora of chemical species including some that have a net electrical charge, the result of dissociation of salts and acids in the aqueous medium. Those that have a net positive charge are called cations and those with a net negative charge are called anions; collectively these electrically charged species are called ions. The law of electrochemical neutrality demands that, in common with all solutions, blood serum/plasma is electrochemically neutral so that the sum of the concentration of cations always equals the sum of the concentration of anions [1]. This immutable law is reflected in FIGURE 1, a graphic display of the concentration of the major ions normally present in plasma/serum. It is clear from this that quantitatively the most significant cation in plasma is sodium (Na+), and the most significant anions are chloride (Cl-) and bicarbonate HCO3-. The concentration of these three plasma constituents (sodium, chloride and bicarbonate) along with the cation potassium (K+) are routinely measured in the clinica 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 >>

Anion Gap Calculator Metabolic Acidosis

Anion Gap Calculator Metabolic Acidosis

The anion gap can be used to help identify thecause of metabolic acidosis. Question: Please define the Anion Gap and its utility in diagnosis and how it relates to osmolality. The anion gap provides an estimation of the unmeasured anions in the plasma and is useful in the setting of arterial blood gas analysis. It is especially useful in helping to differentiate the cause of a metabolic acidosis, as well as following the response to therapy. Its basic premise is based on the fact that electroneutrality must exist in the body, or in other words the net charges of serum anions, which includes albumin, bicarbonate, chloride, organic acids and phosphate must equal the net charges of the serum cations, which includes calcium, magnesium, potassium and sodium.In clinical practice, the anion gap is calculated using three lab values (Na+, Cl-, and HCO3-). [Occasionally, you may see an alternative equation:Anion Gap = [Na+] + [K+] - [Cl-] - [HCO3-]. This equation is preferred by some nephrologists, because of the wide fluctuations that may occur with potassium in renal disease. ]Serum sodium represents over 90 percent of the extracellular cations, whereas chloride and bicarbonate represent approximately 85 percent of the extracellular anions. It follows then, that the anion gap in normal conditions will be a positive number since the sum of the serum anions used in the calculation represent a smaller value compared to the serum sodium concentration. The normal value for the anion gap is 12 +/-4. Side note:some newer references will list the normal anion gap as7 +/- 4. This lower level may represent a more accurate reflection of the true anion gap based on changes that have occurred in contemporary medical labs. In the past, electrolyte analysis was performed using predominantly Continue reading >>

The Anion Gap

The Anion Gap

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

Calculating The Anion Gap In Diabetic Ketoacidosis

Calculating The Anion Gap In Diabetic Ketoacidosis

Practical Pointers Discover Shortcuts Devised by Colleagues Patients with diabetic ketoacidosis (DKA) frequently have hyperglycemia. Serum sodium in these patients should not be corrected for hyperglycemia to calculate the anion gap for acidosis because extracellular fluid shifts caused by hyperglycemia will dilute serum chloride and bicarbonate. If serum sodium is corrected for hyperglycemia, it will give an erroneously high anion gap and an erroneous severity of acidosis in DKA.1,2 This is an important yet not well-known fact. Continue reading >>

Anion Gap

Anion Gap

SEEBRI NEOHALER should not be initiated in patients with acutely deteriorating or potentially life-threatening episodes of COPD or used as rescue therapy for acute episodes of bronchospasm. Acute symptoms should be treated with an inhaled short-acting beta2-agonist. As with other inhaled medicines, SEEBRI NEOHALER can produce paradoxical bronchospasm that may be life threatening. If paradoxical bronchospasm occurs following dosing with SEEBRI NEOHALER, it should be treated immediately with an inhaled, short-acting bronchodilator; SEEBRI NEOHALER should be discontinued immediately and alternative therapy instituted. Immediate hypersensitivity reactions have been reported with SEEBRI NEOHALER. If signs occur, discontinue immediately and institute alternative therapy. SEEBRI NEOHALER should be used with caution in patients with severe hypersensitivity to milk proteins. SEEBRI NEOHALER should be used with caution in patients with narrow-angle glaucoma and in patients with urinary retention. Prescribers and patients should be alert for signs and symptoms of acute narrow-angle glaucoma (e.g., eye pain or discomfort, blurred vision, visual halos or colored images in association with red eyes from conjunctival congestion and corneal edema) and of urinary retention (e.g., difficulty passing urine, painful urination), especially in patients with prostatic hyperplasia or bladder-neck obstruction. Patients should be instructed to consult a physician immediately should any of these signs or symptoms develop. The most common adverse events reported in ≥1% of patients taking SEEBRI NEOHALER, and occurring more frequently than in patients taking placebo, were upper respiratory tract infection (3.4% vs 2.3%), nasopharyngitis (2.1% vs 1.9%), oropharyngeal pain (1.8% vs 1.2%), urinary t 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 >>

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 >>

Get Unlimited Access On Medscape.

Get Unlimited Access On Medscape.

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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 >>

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 >>

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 >>

Closing Anion Gap Without Insulin In Euglycaemic Diabetic Ketoacidosis Poudel Rr, Kafle Nk - J Diabetol

Closing Anion Gap Without Insulin In Euglycaemic Diabetic Ketoacidosis Poudel Rr, Kafle Nk - J Diabetol

Euglycaemic diabetic ketoacidosis (euDKA) occurs in patients with poor carbohydrate intake who continue to take insulin. For these patients are not truly in the insulin-deficient state, intravenous fluid resuscitation alone can correct the ketoacidosis without any risk of hypoglycaemia. Diagnosis of euDKA can be missed in inexperienced settings; therefore, calculating anion gap and measuring ketone levels should be practiced in every sick diabetic patient regardless of glucose levels. Keywords: Anion gap, euglycaemic diabetic ketoacidosis, insulin Poudel RR, Kafle NK. Closing anion gap without insulin in euglycaemic diabetic ketoacidosis. J Diabetol 2017;8:92-3 Poudel RR, Kafle NK. Closing anion gap without insulin in euglycaemic diabetic ketoacidosis. J Diabetol [serial online] 2017 [cited 2018 Mar 22];8:92-3. Available from:  Euglycaemic diabetic ketoacidosis (euDKA) (blood glucose <250 mg/dL) represents initial spectrum of DKA, which requires similar management with intravenous (IV) fluids and insulin. euDKA was first described by Munro in 1973. [1] We report a case of euDKA in type 2 diabetes mellitus (DM) precipitated by poor food intake while continuing insulin use which was treated without Insulin. A 65-year-old female with a history of type 2 DM on insulin, hypertension, poorly controlled depression and anxiety disorder presented with nausea, vomiting, polyuria, weakness and confusion for 3 days. She had no fever, abdominal pain or burning urination. She had decreased appetite and was eating poorly for more than a week; however, she was taking all her medications including insulin regularly. On examination, she was obese (body mass index 31 kg/m 2), somewhat confused and had mild bilateral pedal oedema. Blood pressure was 135/67 mmHg. Chemistries revealed: g Continue reading >>

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Treatment Of Acute Non-anion Gap Metabolic Acidosis

Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid–base 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 might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidence-based guidelines for therapy of this important and increasingly common acid–base disorder. Introduction Acute metabolic acidosis (defined temporally as lasting minutes to a few days) has traditionally been divided into two major categories based on the level Continue reading >>

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