Diabetic ketoacidosis is an endocrine emergency. A subset of diabetic patients may present with relative euglycemia with acidosis, known as euglycemic diabetic ketoacidosis (EDKA), which is often misdiagnosed due to a serum glucose <250 mg/dL. This narrative review evaluates the pathogenesis, diagnosis, and management of EDKA for emergency clinicians. EDKA is comprised of serum glucose <250 mg/dL with an anion gap metabolic acidosis and ketosis. It most commonly occurs in patients with a history of low glucose states such as starvation, chronic liver disease, pregnancy, infection, and alcohol use. Sodium-glucose cotransporter-2 (SGLT2) inhibitors, which result in increased urinary glucose excretion, are also associated with EDKA. The underlying pathophysiology involves insulin deficiency or resistance with glucagon release, poor glucose availability, ketone body production, and urinary glucose excretion. Patients typically present with nausea, vomiting, malaise, or fatigue. The physician must determine and treat the underlying etiology of EDKA. Laboratory assessment includes venous blood gas for serum pH, bicarbonate, and ketones. Management includes resuscitation with intravenous fluids, insulin, and glucose, with treatment of the underlying etiology. Clinician knowledge of this condition can improve the evaluation and management of patients with EDKA.

Three major changes have occurred in the treatment of diabetic ketoacidosis during the past decade: (1) a trend toward continuous intravenous (IV) infusion of insulin, (2) a trend toward the use of lower doses of insulin, and (3) the reintroduction of phosphate replacement. These changes are based on sound theoretical considerations, but their effects on mortality and morbidity are still being evaluated. Despite any changes, intelligent treatment of diabetic ketoacidosis still requires an understanding of the underlying pathophysiology. PATHOGENESIS OF DIABETIC KETOACIDOSIS There are two major abnormalities in diabetic ketoacidosis—metabolic acidosis and hyperglycemia. Each of these is caused by insulin deficiency. Metabolic Acidosis An understanding of fatty acid and ketone metabolism is required to understand the pathogenesis of acidosis. 1,2 Fatty acids are stored as triglycerides within fat cells. Fatty acids released by fat cells are taken up and metabolized by the liver, and ketone bodies (acetoacetic acid, β-hydroxybutyric acid,

#### What you should know Diabetic ketoacidosis (DKA) is an extreme metabolic state caused by insulin deficiency. The breakdown of fatty acids (lipolysis) produces ketone bodies (ketogenesis), which are acidic. Acidosis occurs when ketone levels exceed the body’s buffering capacity (figure⇓).1 2 Diabetic ketoacidosis may follow absolute insulin deficiency or relative insulin deficiency. Relative insulin deficiency may occur in the presence of increased levels of counter-regulatory hormones such as glucagon, cortisol, and catecholamines. Insulin deficiency results in lipolysis and ketogenesis. Ketone bodies are acidic and may initially be buffered, but when levels are high enough, will result in acidosis Data from the UK National Diabetes audit shows a crude one year incidence of 3.6% among people with type 1 diabetes.3 In the UK nearly 4% of people with type 1 diabetes experience DKA …

OBJECTIVES: To review diabetic ketoacidosis, including the "two bags system", a method of administering liquids in order to provide a smoother correction of the hyperglycemic and ketotic states. METHODS: Review of recent publications (last 7 years) from a Medline search and chapters published in pediatric textbooks that discuss the etiology, therapy, and complications of diabetic ketoacidosis. The management approach incorporates the findings of these publications as well as the clinical experience at the Childreńs Hospital of Philadelphia and Duke University Medical Center. RESULTS: The pathology of the type 1 Diabetes Mellitus involves the progressive destruction of the ss cells of the pancreas, causing insulin deficiency. Insulin is essential in the metabolism of carbohydrates, protein and fat. Insulin deficiency may lead to diabetic ketoacidosis which has three components: 1) hyperglycemia, which causes glycosuria and consequently dehydration; 2) lipolysis which, causes ketonemia/ketonuria; and 3) acidosis, that is caused by the dehydration and the high serum levels of ketones. Diabetic ketoacidosis is a serious condition and, if not treated appropriately, can cause coma and death. In children cerebral edema is the major complication of the therapy for diabetic ketoacidosis. Careful replacement of insulin, fluids, glucose and electrolytes is essential. CONCLUSIONS: The literature presents different ways to manage DKA in pediatrics, without a consensus on the cause of the

- Abstract In patients with acromegaly, glucose intolerance and diabetes mellitus are one of the frequent manifestations. And the type of diabetes in these patients is usually non-insulin dependent type secondary to insulin resistance caused by growth hormone excess. Therefore, the diabetes mellitus in these patients dose not tend to develop diabetic ketoacidosis. But we experienced and presented the case of a patient with acromegaly hospitalized due to the diabetic ketoacidosis without overt clinical manifestations of acromegaly. This case of acromegaly showed that growth hormone excess could cause diabetic ketoacidosis in the presence of relative insulin deficiency. (J Kor Diabetes Assoc 30:312～315, 2006)

Summary Diabetes in acromegaly is usually non-insulin dependent and is secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. We describe a case of acromegaly presenting with diabetic ketoacidosis. We demonstrate that growth hormone excess can cause diabetic ketoacidosis in the presence of relative, but not absolute insulin deficiency.</j

Diabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal Diabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific "fruity" or acetone smell. The onset of symptoms is usually rapid. People without a previous d Diabetic ketoacidosis (DKA) is a potentially life-threatening acute complication of diabetes mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion and occasionally loss of consciousness. A person's breath may develop a specific "fruity" or acetone smell. The onset of symptoms is usually rapid. People without a previous diagnosis of diabetes may develop DKA as the first obvious symptom. DKA happens most often in those with type 1 diabetes but can also occur in those with other types of diabetes under certain circumstances. Triggers may include infection, not taking insulin correctly, stroke and certain medications such as steroids. DKA results from a shortage of insulin; in response, the body switches to burning fatty acids, which produces acidic ketone bodies. DKA is typically diagnosed when testing finds high blood sugar, low blood pH and keto acids in either the blood or urine. The primary treatment of DKA is with intravenous fluids and insulin. Depending on the severity, insulin may be given intravenously or by injection under the skin. Usually, potassium is also needed to prevent the development of low blood potassium. Throughout treatment, blood glucose and potassium levels should be regularly checked. Underlying causes for the DKA should be identified. In those with severely low blood pH who are critically ill, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended. Rates of DKA vary around the world. Each year, about 4% of type 1 diabetics in the United Kingdom develop DKA, versus 25% of type 1 diabetics in Malaysia. DKA was first described in 1886 and continued to be a universally fatal condition until introduction of insulin therapy in the 1920s. With adequate and timely treatment, the risk of death is between <1% and 5%. DKA is common in type 1 diabetes as this form of diabetes is associated with an absolute lack of insulin production by the islets of Langerhans. In type 2 diabetes, insulin production is present but is insufficient to meet the body's requirements as a result of end-organ insulin resistance. Usually, these amounts…

chain initiation caused by the insulin deficiency of diabetes. Insulin deficiency of longer duration … Judson. MD 42. Diabetic Renal Disease 684 Eli A. Friedman, MD 43. Diabetic Neuropathy 710 … glycerol by the process of lipolysis. In starvation, since lipolysis occurs, the organism would