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 >>
The Impact Of Hyperglycemic Emergencies On The Kidney And Liver
Copyright © 2013 Feng Bai 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. Studies on the alterations of liver and kidney function parameters in patients with diabetic ketoacidosis (DKA) and diabetic ketosis (DK) were limited. Participants with DKA, DK, non-DK, and healthy controls were enrolled in the current study. Parameters of liver and kidney function were measured and evaluated. The patients with DKA had higher levels of plasma glucose, hemoglobin A1c (HbA1c), uric acid, and creatinine but lower levels of transferases and protein compared with the other three groups ( for all). The patients with DK had higher levels of plasma glucose and HbA1c but lower levels of glutamyl transpeptidase and protein compared with the non-DK and control groups (). Prealbumin levels were significantly reduced in the severe DKA patients compared with the mild/moderate DKA patients. Serum prealbumin levels were correlated with albumin levels (, ), HCO3 (, ), and arterial pH (, ) in the DKA patients. A diagnostic analysis showed that lower prealbumin levels significantly reflected the presence of hyperglycemic emergencies (). Liver and kidney function parameters deteriorated, especially in DKA. Prealbumin levels can be of value in detecting the presence of hyperglycemic crisis. This clinical trial is registered with ChiCTR-OCH-12003077. 1. Introduction Diabetic ketoacidosis (DKA) and diabetic ketosis (DK) are common and serious complications of diabetes mellitus. DKA most often occurs in patients with type 1 diabetes (T1D). However, increasing evidence indicates that DKA and DK are also common features of ketosis-pr Continue reading >>
Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>
Diabetic Ketoacidosis
Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>
Creatinine Is Falsely Elevated In Diabetic Ketoacidosis Patients: A Comparison Of 4 Jaffe Assays With An Enzymatic Method. Asn Events
Creatinine is Falsely Elevated in Diabetic Ketoacidosis Patients: A Comparison of 4 Jaffe Assays with an Enzymatic Method. ASN Events Creatinine is Falsely Elevated in Diabetic Ketoacidosis Patients: A Comparison of 4 Jaffe Assays with an Enzymatic Method. Azni Abdul-Wahab 1 , Hanh Nguyen 2 , Mervyn Kyi 3 , Wei Ling Chiu 3 , Que Lam Lam 4 , Cherie Chiang 1 3 Pathology/ Endocrinology, Royal Melbourne Hospital, Melbourne Endocrinology, Royal Melbourne Hospital, Melbourne Endocrinology, Austin Hospital , Melbourne Falsely elevatedplasma creatinine due to glucose and ketone interference is well documented inroutine Jaffe assay (1,2). Although Jaffe assays have been recentlystandardised since the introduction of eGFR, the effect of this interference isunknown since the alignment process. Weassessed plasma creatinine in DKA patients using 4 Jaffe assays against anenzymatic method as the gold standard. Samples were collected from DKA patients presenting to the EmergencyDepartment and ten outpatients with normal glucose and bicarbonate.Aliquots were frozen, transported on dry ice, and analysed on 4 Jaffe assays (Architect,Roche, Beckman Coulter and Siemens) and the Vitros Enzymatic assay. Assay bias (Jaffecreatinine enzymatic creatinine)/ enzymatic creatinine x 100%) was correlatedwith pH, glucose, ketone and baseline creatinine. Of the 22 episodes ofDKA from 20 patients (16 M, 4 F, age 32.4 13.4 years), admission venous pHwas 7.14 0.15, bicarbonate was 9.4 5.5 mmol/L, glucose was 35.9 14.9mmol/L and capillary ketone was 5.9 1.1 mmol/L. The average enzymaticcreatinine value was 111.5 64.1 mol/L. All Jaffe creatinine results weresignificantly higher (p <0.001), in order of magnitude: Abbott (154.6 68.2mol/L), Beckman Coulter (147.1 70.5 mol/L), Roche (128.0 56.4 mol/L) andSieme Continue reading >>
Spurious Serum Creatinine Elevations In Ketoacidosis
Spurious Serum Creatinine Elevations in Ketoacidosis MARK E. MOLITCH, M.D.; ELISE RODMAN, M.D.; CARL A. HIRSCH, M.D.; ELI DUBINSKY, M.D. Article, Author, and Disclosure Information Author, Article, and Disclosure Information Dr. Molitch is a Clinical Associate of the General Clinical Research Centers program, U.S. Public Health Service (grant RR0054-7). Diabetic ketoacidosis is usually accompanied by dehydration resulting in prerenal azotemia, in which the levels of blood urea nitrogen are elevated out of proportion to those of the serum creatinine (1). In contrast, one patient who had been admitted to our hospital in diabetic ketoacidosis a number of times consistently displayed serum creatinine levels repeatedly elevated out of proportion to her blood urea nitrogen levels but had normal renal function between episodes of ketoacidosis. Investigation showed the elevated creatinine levels to be due to the artifactual interference of acetoacetate in the automated measurement of serum creatinine, a fact not widely Continue reading >>
Measure Electrolyte And Ketone Levels And Determine Anion Gap In Patients With Diabetes And Normal Sugar Levels
DIABETIC KETOACIDOSIS DX: Diabetic Ketoacidosis (DKA) when the blood glucose is >=250 mg/dL, arterial pH <=7.30, serum bicarbonate <=15 mEq/L, and positive serum ketones. (Hyperglycemia, ketonemia, ketonuria, metabolic acidosis) Screening for Diabetic Ketoacidosis - Consider DKA if hyperglycemia, acidosis, or ketonemia are present. Screen all patients with moderate to severely elevated blood sugars (glucose >350 mg/dL). Measure electrolytes, glucose, ketones, and blood gases to determine whether anion gap metabolic acidosis is present in patients with positive ketones, constitutional symptoms, or suspicion of DKA. in patients with an anion gap metabolic acidosis. Measure serum glucose in patients with metabolic acidosis. in diabetes patients with infection, CVA, MI, or other illness. Measure serum glucose and if glucose >250 mg/dL, check the patient's electrolyte and ketone levels and anion gap. in diabetic patients with symptoms of nausea and vomiting (with polyuria, polydipsia), even if blood glucose is <250 mg/dL. if symptoms suggest DKA despite normal blood sugar levels. in patients on atypical antipsychotics who present with hyperglycemia. Measure anion gap and ketones in patients on atypical antipsychotics who present with moderate to severe hyperglycemia. SX: Dehydration with hypotension, hyperventilation with fruity "acetone" odor, polyphagia, polydipsia, polyuria, altered mental status, N&V. History and Physical Examination Elements for Diabetic Ketoacidosis History Type 1 diabetes - DKA is a frequent complication of type 1 diabetes Constitutional symptoms - DKA may show vague symptoms of lethargy, diminished appetite, and headache Polyuria, polydipsia - May precede the development of DKA by 1 or 2 days, especially if intercurrent illness (infection) is present Continue reading >>
Falsely-elevated Serum Creatinine Values In Diabetic Ketoacidosis -- Clinical Implications.
Falsely-elevated serum creatinine values in diabetic ketoacidosis -- clinical implications. Unusual elevations of serum creatinine (S-CR) out proportion to increases in serum urea nitrogen (S-UN) are frequently observed in patients with diabetic ketoacidosis when S-CR is measured by the Jaffe end-point reaction. This has been ascribed to interference from acetoacetate but this is not however observed with kinetic DuPont ACA methodology. Eighteen patients with diabetic ketoacidosis were studied: SCR measurements were done using the end point Technicon SMA 6/60 method (Group a, 10 patients) or the kinetic DuPont ACA method (Group B, 8 patients). The values for S-CR in Group A patients (mean value and S-D were 3.3 +/- 1.1 mg/dl) were significantly different from Group B patients (1.6 +/- 0.24 mg/dl) (P less than 0.01). A significant positive correlation was obtained between the "excess anion gap" and S-CR in Group A patients (r = + 0.81, p less than 0.01). The results from two patients in whom serial measurements of S-UN, S-CR and the anion gap were carried out further demonstrate the analytical interference. The study demonstrates that in diabetic ketoacidosis elevated creatinine values measured by an end-point method should not necessarily be interpreted as evidence of significant renal impairment and if possible should be verified by a kinetic method which is free of "ketone" interference. Continue reading >>
Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome
In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>
Severe Hyperkalaemia In Association With Diabetic Ketoacidosis In A Patient Presenting With Severe Generalized Muscle Weakness
Diabetic ketoacidosis (DKA) is an acute, life‐threatening metabolic complication of diabetes mellitus. Hyperglycaemia, ketosis (ketonaemia or ketonuria) and acidosis are the cardinal features of DKA [1]. Other features that indicate the severity of DKA include volume depletion, acidosis and concurrent electrolyte disturbances, especially abnormalities of potassium homeostasis [1,2]. We describe a type 2 diabetic patient presenting with severe generalized muscle weakness and electrocardiographic evidence of severe hyperkalaemia in association with DKA and discuss the related pathophysiology. A 65‐year‐old male was admitted because of impaired mental status. He was a known insulin‐treated diabetic on quinapril (20 mg once daily) and was taking oral ampicillin 500 mg/day because of dysuria which had started 5 days prior to admission. He was disoriented in place and time with severe generalized muscle weakness; he was apyrexial (temperature 36.4°C), tachycardic (120 beats/min) and tachypneic (25 respirations/min) with cold extremities (supine blood pressure was 100/60 mmHg). An electrocardiogram (ECG) showed absent P waves, widening of QRS (‘sine wave’ in leads I, II, V5 and V6), depression of ST segments and tall peaked symmetrical T waves in leads V3–V6 (Figure 1). Blood glucose was 485 mg/dl, plasma creatinine 5.1 mg/dl (reference range (r.r.) 0.6–1.2 mg/dl, measured by the Jaffe method), urea 270 mg/dl (r.r. 11–54 mg/dl), albumin 4.2 g/dl (r.r. 3.4–4.7 g/dl), sodium 136 mmol/l (r.r. 135–145 mmol/l), chloride 102 mmol/l (r.r. 98–107 mmol/l), potassium 8.3 mmol/l (r.r. 3.5–5.4 mmol/l), phosphorus 1.6 mmol/l (r.r. 0.8–1.45 mmol/l) and magnesium 0.62 mmol/l (r.r. 0.75–1.25 mmol/l). A complete blood count revealed leukocytosis (12 090/µl with Continue reading >>
Diabetic Ketoacidosis
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 the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>
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
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 >>
The Influence Of Ketoacids On Plasma Creatinine Assays In Diabetic Ketoacidosis.
The influence of ketoacids on plasma creatinine assays in diabetic ketoacidosis. Kemperman FA(1), Weber JA, Gorgels J, van Zanten AP, Krediet RT, Arisz L. (1)Department of Internal Medicine, Academic Medical Centre, University of Amsterdam, The Netherlands. [email protected] OBJECTIVE: Analysis of the interference of ketoacids on various routine plasmacreatinine assays during a clinical episode of diabetic ketoacidosis (DKA).DESIGN: Observational study. Blood samples were drawn before, during and afterstandard in-hospital treatment. Plasma creatinine was measured with twodissimilar enzymatic assays (creatininase PAP + and creatinine iminohydrolaseSerapak), a kinetic alkaline picrate method (Jaff) and a high-performance liquidchromatography (HPLC) procedure. Acetoacetate and beta-hydroxybutyrate wereanalysed by enzymatic methods.SETTING: Department of Medicine, University Hospital.SUBJECTS: Nine patients who experienced 10 episodes of DKA.MAIN OUTCOME MEASURES: Agreement of the routine plasma creatinine assays withHPLC and analysis of possible interferents.RESULTS: At presentation, the Jaff assay gave falsely high values of plasmacreatinine (median 99 micromol L(-1)), in contrast to the PAP+ (median 60.5micromol L(-1)) and HPLC assays (median 67.5 micromol L(-1)). This positive errordecreased during treatment. This was due to a decrease in acetoacetate, as thepositive error by the Jaff method correlated with the acetoacetate concentration(r = 0.79, P < 0.0001). In the multiple regression analysis, beta-hydroxybutyratecaused no additional interference by the Jaff assay, confirmed by in vitroexperiments. Analysis of agreement showed that the difference between PAP+ andHPLC creatinine was -4.6 +/- 3.0 micromol L(-1) (mean +/- SD), and 2.0 +/- 5.3micromol L(-1) between Continue reading >>
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 >>
