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Euglycemic Ketoacidosis Definition

Prolonged Ketosis In A Patient With Euglycemic Diabetic Ketoacidosis Secondary To Dapagliflozin

Prolonged Ketosis In A Patient With Euglycemic Diabetic Ketoacidosis Secondary To Dapagliflozin

Sodium-glucose cotransporter 2 inhibitors (SGLT2) are the newest class of oral agents to receive US Food and Drug Administration (FDA) approval for the treatment of type 2 diabetes (T2DM). SGLT2 inhibitors currently approved by the FDA include canagliflozin, dapagliflozin, and empagliflozin as well as various combination drugs (Table 1). The enthusiasm this class of drugs has been greeted with stems from the benefits associated with SGLT2 inhibitors. They include decrease in A1c by 0.5% to 1%, reduction in insulin doses, modest weight loss, and improved systolic and diastolic blood pressure.1 In addition, the EMPA-REG OUTCOME trial showed a reduction in all-cause and cardiovascular mortality with empagliflozin.2 Also, a post hoc analysis of a study on dapagliflozin in type 2 diabetics with moderate renal impairment showed improved albuminuria and delayed progression to severe renal failure.3 The popularity of SGLT2 inhibitors is understandable considering the paucity of oral diabetic drugs that promote both weight loss and reduction of insulin needs. Endocrinologists and internists alike have increasingly prescribed this class of drugs as to avoid initiation of insulin or escalation of insulin doses. With more patients using SGLT2 inhibitors, reports of euglycemic diabetic ketoacidosis (euDKA) have emerged. While DKA can be expected with off-label use of SGLT2 inhibitors in patients with T1DM, it has also occurred in T2DM patients. Thus, the FDA posted a drug safety communication on DKA in 2015.4 Greater understanding of how to safely use this newest tool in our arsenal against diabetes is essential. A 50-year-old African American female with T2DM since the age of 35 presented with 10 days of constipation and fatigue, as well as reduced oral intake for 3 days prior to a Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Prashanth Rawla1, Anantha R Vellipuram2, Sathyajit S Bandaru3 and Jeffrey Pradeep Raj4[1] Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA [2] Texas Tech University Health Sciences Center, El Paso, Texas, USA [3] Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA [4] Department of Pharmacology, St John’s Medical College, Bangalore, India Summary Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels. Background Diabetic ket Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Review

Euglycemic Diabetic Ketoacidosis: A Review

Euglycemic Diabetic Ketoacidosis: A Review Author(s): Anar Modi , Department of Endocrinology, Diabetes & Metabolism, Cooper University Hospital, Camden, New Jersey, United States Abhinav Agrawal* , Department of Medicine, Monmouth Medical Center, 300 Second Avenue, Long Branch, New Jersey, United States Farah Morgan . Department of Endocrinology, Diabetes & Metabolism, Cooper University Hospital, Camden, New Jersey, United States Introduction: Diabetic ketoacidosis (DKA) is one of the most serious complications of diabetes.It is characterised by the triad of hyperglycemia (blood sugar >250 mg/dl), metabolic acidosis(arterial pH <7.3 and serum bicarbonate <18 mEq/L) and ketosis. Rarely these patients can present withblood glucose (BG) levels of less than 200 mg/dl, which is defined as euglycemic DKA. The possibleetiology of euglycemic DKA includes the recent use of insulin, decreased caloric intake, heavy alcoholconsumption, chronic liver disease and glycogen storage disorders. DKA in pregnancy has also beenreported to present with euglycemia. The recent use of sodium glucose cotransporter 2 (SGLT2) inhibitorshas shed light on another possible mechanism of euglycemic DKA. Clinicians may also be misledby the presence of pseudonormoglycemia. Conclusion: Euglycemic DKA thus poses a challenge to physicians, as patients presenting with normalBG levels in ketoacidosis may be overlooked, leading to a delay in appropriate management strategies.In this article, we review all the possible etiologies and the associated pathophysiology of patients presentingwith euglycemic DKA. We also discuss the approach to diagnosis and management of suchpatients. Despite euglycemia, ketoacidosis in diabetic patients remains a medical emergency and mustbe treated in a quick and appropriate mann Continue reading >>

Euglycemic Diabetic Ketoacidosis, A Misleading Presentation Of Diabetic Ketoacidosis

Euglycemic Diabetic Ketoacidosis, A Misleading Presentation Of Diabetic Ketoacidosis

Go to: Introduction Hyperglycemia and ketosis in diabetic ketoacidosis (DKA) are the result of insulin deficiency and an increase in the counterregulatory hormones glucagon, catecholamines, cortisol, and growth hormone. Three processes are mainly responsible for hyperglycemia: increased gluconeogenesis, accelerated glycogenolysis, and impaired glucose utilization by peripheral tissues. This might also be augmented by transient insulin resistance due to hormone imbalance, as well as elevated free fatty acids.[1] DKA is most commonly precipitated by infections. Other factors include discontinuation of or inadequate insulin therapy, pancreatitis, myocardial infarction, cerebrovascular accident, and illicit drug use. The diagnostic criteria of DKA, established by the American Diabetic Association, consists of a plasma glucose of >250 mg/dL, positive urinary or serum ketones, arterial pH of <7.3, serum bicarbonate <18 mEq/L, and a high anion gap. The key diagnostic feature of DKA is elevated circulating total blood ketone concentration. Hyperglycemia is also a key diagnostic criterion of DKA; however, a wide range of plasma glucose levels can be present on admission. Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis: A Predictable, Detectable, And Preventable Safety Concern With Sglt2 Inhibitors

The Case At Hand Recently, the U.S. Food and Drug Administration (FDA) issued a Drug Safety Communication that warns of an increased risk of diabetic ketoacidosis (DKA) with uncharacteristically mild to moderate glucose elevations (euglycemic DKA [euDKA]) associated with the use of all the approved sodium–glucose cotransporter 2 (SGLT2) inhibitors (1). This Communication was based on 20 clinical cases requiring hospitalization captured between March 2013 and June 2014 in the FDA Adverse Event Reporting System database. The scarce clinical data provided suggested that most of the DKA cases were reported in patients with type 2 diabetes (T2D), for whom this class of agents is indicated; most likely, however, they were insulin-treated patients, some with type 1 diabetes (T1D). The FDA also identified potential triggering factors such as intercurrent illness, reduced food and fluid intake, reduced insulin doses, and history of alcohol intake. The following month, at the request of the European Commission, the European Medicines Agency (EMA) announced on 12 June 2015 that the Pharmacovigilance Risk Assessment Committee has started a review of all of the three approved SGLT2 inhibitors (canagliflozin, dapagliflozin, and empagliflozin) to evaluate the risk of DKA in T2D (2). The EMA announcement claimed that as of May 2015 a total of 101 cases of DKA have been reported worldwide in EudraVigilance in T2D patients treated with SGLT2 inhibitors, with an estimated exposure over 0.5 million patient-years. No clinical details were provided except for the mention that “all cases were serious and some required hospitalisation. Although [DKA] is usually accompanied by high blood sugar levels, in a number of these reports blood sugar levels were only moderately increased” (2). Wit Continue reading >>

Euglycemic Diabetic Ketoacidosis With Acute Pancreatitis In A Patient Not Known To Have Diabetes

Euglycemic Diabetic Ketoacidosis With Acute Pancreatitis In A Patient Not Known To Have Diabetes

Diabetic ketoacidosis (DKA) is usually easily recognized and is characterized by hyperglycemia, metabolic acidosis, and increased ketones (1). Euglycemic DKA, a relatively uncommon presentation, is a less known entity and can go unrecognized at initial presentation. It can be caused by starvation of any cause in conjunction with a current illness (2) and has been described mainly in patients with type 1 diabetes (3,4) but also in subjects with type 2 and gestational diabetes (3,5). We report a case of euglycemic DKA precipitated by starvation and severe pancreatitis in a patient with history of chronic alcoholism and no known underlying diabetes. This case shows the complex interplay among severe alcohol-related pancreatic injury, ketoacidosis, and starvation physiology. It highlights the fact that euglycemic DKA should be considered in the differential diagnosis of an ill patient presenting with metabolic acidosis, even in the absence of hyperglycemia. A 36-year-old female presented to the emergency room with severe epigastric pain with radiation to her back of 3 days duration and a 1-week history of nausea and vomiting. She reported having not eaten for over 1 week and admitted to drinking 1 L of brandy daily for years; her last drink was 3 days prior to admission. She denied taking any medications. Her medical records review revealed a history of hematemesis from a Mallory-Weiss tear and rehabilitation for alcoholism in 2007 and 2008 with subsequent relapses. Her family history was significant for coronary artery disease, diabetes, and hypertension, and her mother also struggled with alcoholism. Physical examination revealed a temperature of 36.6°C, blood pressure 123/71 mm Hg, respiratory rate 24 per minute, heart rate 80 per minute, oxygen saturation 100% on room Continue reading >>

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Starvation-induced True Diabetic Euglycemic Ketoacidosis In Severe Depression

Go to: A 34-year-old man with a 19-year history of type 1 diabetes presented as an emergency with a 4-day history of nausea, vomiting, and flu-like symptoms. He was on a basal bolus insulin regime comprising 8 units of bolus insulin lispro injected at mealtimes and 12 units of basal isophane insulin at bedtime, but did not monitor capillary blood glucose levels. He did however empirically increase his insulin doses during times of illness and had increased his isophane insulin to 15 units during the 3 days prior to presentation. He had only one prior hospital admission, which occurred 6 years previously and was due to an episode of DKA precipitated by gastroenteritis. He was single, unemployed, did not drink alcohol, had no previous psychiatric history, no family history of diabetes or other medical conditions, and lived in a hostel. He had a record of poor clinic attendances and a history of long-term cannabis use. He denied any salicylate consumption, but admitted to some weight loss; however, he was unable to quantify this. His body mass index (BMI) was 19 kg/m2, and he looked unkempt. Physical examination revealed a temperature of 36.4°C (97.5°F), heart rate of 106 beats per minute, supine blood pressure of 131/85 mmHg, and sitting blood pressure of 122/80 mmHg. He had a respiratory rate of 30 breaths per minute, and his oxygen saturation using a pulsoximeter was 99% on room air. He appeared clinically dehydrated with dry oral mucosa, but cardiovascular, respiratory, abdominal, and neurological examinations were otherwise normal. Diabetic ketoacidosis (DKA) was suspected; metabolic acidosis was confirmed with a pH of 7.3, bicarbonate concentration of 10 mEq/l, and an elevated anion gap of 29 mEq/l [sodium = 134 mEq/l, potassium = 5.7 mEq/l, chloride = 101 mEq/l, b Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With SodiumGlucose Cotransporter 2 Inhibition We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With SodiumGlucose Cotransporter 2 Inhibition Anne L. Peters, Elizabeth O. Buschur, [...], and Irl B. Hirsch Sodiumglucose cotransporter 2 (SGLT-2) inhibitors are the most recently approved antihyperglycemic medications. We sought to describe their association with euglycemic diabetic ketoacidosis (euDKA) in hopes that it will enhance recognition of this potentially life-threatening complication. Cases identified incidentally are described. We identified 13 episodes of SGLT-2 inhibitorassociated euDKA or ketosis in nine individuals, seven with type 1 diabetes and two with type 2 diabetes, from various practices across the U.S. The absence of significant hyperglycemia in these patients delayed recognition of the emergent nature of the problem by patients and providers. SGLT-2 inhibitors seem to be associated with euglycemic DKA and ketosis, perhaps as a consequence of their noninsulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. Patients with type 1 or type 2 diabetes who experience nausea, vomiting, or malaise or develop a metabolic acidosis in the setting of SGLT-2 inhibitor therapy should be promptly evaluated for the presence of urine and/or serum ketones. SGLT-2 inhi Continue reading >>

Euglycemic Ketoacidosis

Euglycemic Ketoacidosis

The purpose of this ariticle is to highlight the importance of not relying exclusively on blood glucose measurements when assessing sick type I diabetics. Urinary ketones and venous bicarbonate are essential in making the diagnosis of relatively low blood glucose plus ketoacidosis, that we call euglycaemic ketoacidosis. Pak J Med Sci January - March 2008 Vol. 24 No. 1 161-162 1. Dr. Muhammad Shahzad Rauf, MBBS, MRCP, Core Medical Training Aberdeen Royal Infirmary, * Received for Publication: October 31, 2007 The condition is defined as diabetic ketoacidosis with a bicarbonate level of less than 10mEq/L and a glucose level of less than 16.7mmol/l or 300mg% along with ketonemia or ketonuria, Euglycemic ketoacidosis occurred in 30% of patients admitted to the hospital on account of diabetic ketoacidosis. 1 True euglycaemic ketoacidosis (initial blood glucose 10mmol/l (180mg%) or less) is rare, occurring in 0.81.1% of all episodes depending on the defining plasma bicarbonate concentration.2 Clinically Euglycaemic ketoacidosis is usually manifested by vomiting. In addition some patient can present with, abdominal pain dysuria, productive cough, thirst, nausea. The cause of preserved "euglycemia" could be greater urinary loss of glucose triggered by counter-regulatory hormones or decreased rate of hepatic glucose production observed during a fast. It has also been demonstrated that the key path physiologic determinant is the quantity of food ingested prior to development of diabetic ketoacidosis: When patients are well fed, their liver contains large amounts of glycogen, which primes it to make glucose and to suppress ketogenesis. However, when patients have been vomiting and unable to eat, the liver is depleted of glycogen and primed to produce ketones. Thus, patients with Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>

Diabetic Ketoacidosis

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 >>

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodium–glucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodium–glucose Cotransporter 2 Inhibition

OBJECTIVE Sodium–glucose cotransporter 2 (SGLT-2) inhibitors are the most recently approved antihyperglycemic medications. We sought to describe their association with euglycemic diabetic ketoacidosis (euDKA) in hopes that it will enhance recognition of this potentially life-threatening complication. RESEARCH DESIGN AND METHODS Cases identified incidentally are described. RESULTS We identified 13 episodes of SGLT-2 inhibitor–associated euDKA or ketosis in nine individuals, seven with type 1 diabetes and two with type 2 diabetes, from various practices across the U.S. The absence of significant hyperglycemia in these patients delayed recognition of the emergent nature of the problem by patients and providers. CONCLUSIONS SGLT-2 inhibitors seem to be associated with euglycemic DKA and ketosis, perhaps as a consequence of their noninsulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. Patients with type 1 or type 2 diabetes who experience nausea, vomiting, or malaise or develop a metabolic acidosis in the setting of SGLT-2 inhibitor therapy should be promptly evaluated for the presence of urine and/or serum ketones. SGLT-2 inhibitors should only be used with great caution, extensive counseling, and close monitoring in the setting of type 1 diabetes. Sodium–glucose cotransporter 2 (SGLT-2) inhibitors are the newest class of antihyperglycemic medications, first marketed in 2013 for the treatment of type 2 diabetes (1). Limited studies suggest that SGLT-2 inhibitors may be effective in addressing many of the unmet needs of people with type 1 diabetes, including improving average glycemia, while reducing glycemic variability and postprandial hyperglycemia, without increasing hypoglycemia, as well as promoting weight loss while reducing insulin dose Continue reading >>

Euglycemic Dka: It’s Not A Myth

Euglycemic Dka: It’s Not A Myth

Background: Diabetic ketoacidosis (DKA) is traditionally defined as a triad of hyperglycemia (>250mg/dL), anion gap acidosis, and increased plasma ketones. There is another entity that providers must be aware of known as euglycemic DKA (euDKA), which is essentially DKA without the hyperglycemia (Serum glucose <200 mg/dL). Euglycemic DKA is a rare entity that mostly occurs in patients with type 1 diabetes, but can possibly occur in type 2 diabetes as well. The exact mechanism of euDKA is not entirely known, but has been associated with partial treatment of diabetes, carbohydrate food restriction, alcohol intake, and inhibition of gluconeogenesis. euDKA, can also be associated with sodium-glucose cotransporter 2 (SGLT-2) inhibitor medications. These medications first came onto the market in 2013 and are FDA approved for the treatment of type 2 diabetes, however many physicians use them off-label for type I diabetes due to their ability to improve average glucose levels, reduce glycemic variability without increasing hypoglycemia, and finally promote weight loss. Does euDKA Exist even in Patients not Using SGLT-2 Inhibitors? The short answer is YES. Munro JF et al [5] reviewed a case series of 37 episodes of euDKA in a publication from 1973. Although, dated and not robust evidence some take home messages can be derived: All but one episode was in insulin dependent diabetics Vomiting was the most frequent symptom of euDKA in 32% of patients Management in most cases consisted of: Intravenous fluids and electrolyte replacement. No deaths occurred in this case series What are the Names of the SGLT-2 Inhibitors? Ipragliflozin (Suglat) – Approved in Japan Dapagliflozin (Farxiga) – 1st SGLT2 Inhibitor Approved; Approved in US Luseogliflozin (Lusefi) – Approved in Japan Tofo Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Objective Sodiumglucose cotransporter 2 (SGLT-2) inhibitors are the most recently approved antihyperglycemic medications. We sought to describe their association with euglycemic diabetic ketoacidosis (euDKA) in hopes that it will enhance recognition of this potentially life-threatening complication. Research Design and Methods Cases identified incidentally are described. Results We identified 13 episodes of SGLT-2 inhibitorassociated euDKA or ketosis in nine individuals, seven with type 1 diabetes and two with type 2 diabetes, from various practices across the U.S. The absence of significant hyperglycemia in these patients delayed recognition of the emergent nature of the problem by patients and providers. Conclusions SGLT-2 inhibitors seem to be associated with euglycemic DKA and ketosis, perhaps as a consequence of their noninsulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. Patients with type 1 or type 2 diabetes who experience nausea, vomiting, or malaise or develop a metabolic acidosis in the setting of SGLT-2 inhibitor therapy should be promptly evaluated for the presence of urine and/or serum ketones. SGLT-2 inhibitors should only be used with great caution, extensive counseling, and close monitoring in the setting of type 1 diabetes. Sodiumglucose cotransporter 2 (SGLT-2) inhibitors are the newest class of antihyperglycemic medications, first marketed in 2013 for the treatment of type 2 diabetes.[ 1 ] Limited studies suggest that SGLT-2 inhibitors may be effective in addressing many of the unmet needs of people with type 1 diabetes, including improving average glycemia, while reducing glycemic variability and postprandial hyperglycemia, without increasing hypoglycemia, as well as promoting weight loss while reducing insulin doses.[ 28 Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma 1Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA, 2Texas Tech University Health Sciences Center, El Paso, Texas, USA, 3Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA, 4Department of Pharmacology, St Johns Medical College, Bangalore, India, Received 2017 Jul 18; Accepted 2017 Aug 4. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License . Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine Continue reading >>

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