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Clinical Features And Diagnosis Of Diabetic Ketoacidosis In Children And Adolescents

Clinical Features And Diagnosis Of Diabetic Ketoacidosis In Children And Adolescents

INTRODUCTION Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus. Less commonly, it can occur in children with type 2 diabetes mellitus. DKA is caused by absolute or relative insulin deficiency. (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The incidence and prevalence of type 2 diabetes mellitus have increased across all ethnic groups. This has been coupled with an increasing awareness that children with type 2 diabetes mellitus can present with ketosis or DKA, particularly in obese African American adolescents [1-7]. (See "Classification of diabetes mellitus and genetic diabetic syndromes", section on 'DKA in type 2 diabetes'.) The clinical features and diagnosis of DKA in children will be reviewed here. This discussion is primarily based upon the large collective experience of children with type 1 diabetes mellitus. There is limited experience in the assessment and diagnosis of DKA in children with type 2 diabetes mellitus, although the same principles should apply. The management of diabetes in children, treatment of DKA in children and the epidemiology and pathogenesis of DKA are discussed separately. (See "Management of type 1 diabetes mellitus in children and adolescents" and "Treatment and complications of diabetic ketoacidosis in children and adolescents" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) DEFINITION Diabetic ketoacidosis – A consensus statement from the International Society for Pediatric and Adolescent Diabetes (ISPAD) in 2014 defined the following biochemical criteria for the diagnosis of DKA [8]: Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Pardon Our Interruption...

Pardon Our Interruption...

As you were browsing something about your browser made us think you were a bot. There are a few reasons this might happen: You're a power user moving through this website with super-human speed. You've disabled JavaScript in your web browser. A third-party browser plugin, such as Ghostery or NoScript, is preventing JavaScript from running. Additional information is available in this support article. After completing the CAPTCHA below, you will immediately regain access to Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Clinical Features, Evaluation, And Diagnosis

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. DKA is characterized by ketoacidosis and hyperglycemia, while HHS usually has more severe hyperglycemia but no ketoacidosis (table 1). Each represents an extreme in the spectrum of hyperglycemia. The precipitating factors, clinical features, evaluation, and diagnosis of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, and treatment of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) Continue reading >>

Treatment And Complications Of Diabetic Ketoacidosis In Children And Adolescents

Treatment And Complications Of Diabetic Ketoacidosis In Children And Adolescents

INTRODUCTION Diabetic ketoacidosis (DKA) is the leading cause of morbidity and mortality in children with type 1 diabetes mellitus (T1DM), with a case fatality rate ranging from 0.15 percent to 0.31 percent [1-3]. DKA also can occur in children with type 2 DM (T2DM); this presentation is most common among youth of African-American descent [4-8]. (See "Classification of diabetes mellitus and genetic diabetic syndromes".) The management of DKA in children will be reviewed here (table 1). There is limited experience in the management and outcomes of DKA in children with T2DM, although the same principles should apply. The clinical manifestations and diagnosis of DKA in children and the pathogenesis of DKA are discussed elsewhere. (See "Clinical features and diagnosis of diabetic ketoacidosis in children and adolescents" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) DEFINITION Diabetic ketoacidosis – A consensus statement from the International Society for Pediatric and Adolescent Diabetes (ISPAD) in 2014 defined the following biochemical criteria for the diagnosis of diabetic ketoacidosis (DKA) [9]: Hyperglycemia – Blood glucose of >200 mg/dL (11 mmol/L) AND Metabolic acidosis – Venous pH <7.3 or a plasma bicarbonate <15 mEq/L (15 mmol/L) AND Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis Damian Baalmann, 2nd year EM resident A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management? Alcoholic Ketoacidosis (AKA): What is it? Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine. Alcoholic Ketoacidosis: How do I recognize it? Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folk Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

What Is It? Diabetic ketoacidosis is a potentially fatal complication of diabetes that occurs when you have much less insulin than your body needs. This problem causes the blood to become acidic and the body to become dangerously dehydrated. Diabetic ketoacidosis can occur when diabetes is not treated adequately, or it can occur during times of serious sickness. To understand this illness, you need to understand the way your body powers itself with sugar and other fuels. Foods we eat are broken down by the body, and much of what we eat becomes glucose (a type of sugar), which enters the bloodstream. Insulin helps glucose to pass from the bloodstream into body cells, where it is used for energy. Insulin normally is made by the pancreas, but people with type 1 diabetes (insulin-dependent diabetes) don't produce enough insulin and must inject it daily. Subscribe to Harvard Health Online for immediate access to health news and information from Harvard Medical School. Continue reading >>

Hyperglycemia

Hyperglycemia

University of California San Francisco, Fresno, California Edited By: David A. Wald Temple University School of Medicine Philadelphia, Pennsylvania Objectives The objectives of this module will be to: Review the classic presentation of a patient with hyperglycemia, including DKA and HHS. Review the diagnostic work up of the hyperglycemic patient. Review the principles of managing a patient with hyperglycemia. Hyperglycemia complicating diabetes ranges from the asymptomatic and benign in patients with mild to moderate uncomplicated hyperglycemia to the life-threatening (i.e. diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS). DKA and HHS represent a spectrum of complications from diabetes and differ mainly in the level of hyperglycemia, extent of dehydration and presence and degree of ketoacidosis. Each condition revolves around insulin deficiency, either absolute or relative. DKA and HHS are the most serious, acute metabolic complications of diabetes. Generally DKA occurs in younger patients (<65 y/o) with Type 1 diabetes and usually evolves rapidly over 24 hours. HHS usually occurs in older patients (>65 y/o) with poorly controlled Type 2 diabetes and evolves over several days. Both disease entities originate from a reduction in insulin and an increase in counter-regulatory stress hormones. In the emergency department hyperglycemia is most often seen as a complication of diabetes (both types 1 and 2). Hyperglycemia is defined as: Fasting Blood Glucose (for 8 hrs) > 90 – 130 mg/dL Postprandial Blood Glucose > 180 mg/dL Initial Actions and Primary Survey In these patients, a thorough history and physical examination should be performed with a focus on trying to identify a precipitating cause of the hyperglycemia. In patients with an incidental findin Continue reading >>

Hyperglycemic Crises: Diabetic Ketoacidosis (dka), And Hyperglycemic Hyperosmolar State (hhs)

Hyperglycemic Crises: Diabetic Ketoacidosis (dka), And Hyperglycemic Hyperosmolar State (hhs)

Go to: Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are acute metabolic complications of diabetes mellitus that can occur in patients with both type 1 and 2 diabetes mellitus. Timely diagnosis, comprehensive clinical and biochemical evaluation, and effective management is key to the successful resolution of DKA and HHS. Critical components of the hyperglycemic crises management include coordinating fluid resuscitation, insulin therapy, and electrolyte replacement along with the continuous patient monitoring using available laboratory tools to predict the resolution of the hyperglycemic crisis. Understanding and prompt awareness of potential of special situations such as DKA or HHS presentation in comatose state, possibility of mixed acid-base disorders obscuring the diagnosis of DKA, and risk of brain edema during the therapy are important to reduce the risks of complications without affecting recovery from hyperglycemic crisis. Identification of factors that precipitated DKA or HHS during the index hospitalization should help prevent subsequent episode of hyperglycemic crisis. For extensive review of all related areas of Endocrinology, visit WWW.ENDOTEXT.ORG. Go to: INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) represent two extremes in the spectrum of decompensated diabetes. DKA and HHS remain important causes of morbidity and mortality among diabetic patients despite well developed diagnostic criteria and treatment protocols (1). The annual incidence of DKA from population-based studies is estimated to range from 4 to 8 episodes per 1,000 patient admissions with diabetes (2). The incidence of DKA continues to increase and it accounts for about 140,000 hospitalizations in the US in 2009 (Figure 1 a) (3). Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

Beste Online Kasinoer I Norge

Beste Online Kasinoer I Norge

Spilleautomater Dka Management Uptodate Pediatric diabetic ketoacidosis, uid therapy, and cerebral injury: Pediatric diabetic ketoacidosis, uid therapy, in DKA management continues to exist. Our general interest enewsletter keeps you up to date on a wide Mayo Clinic, MayoClinic. Diabetic ketoacidosis (DKA) is a common, serious, and preventable complication of type 1 diabetes, with a mortality of 35. Diabetic Ketoacidosis Abdelaziz Elamin Professor of Pediatric Endocrinology University of Khartoum, Sudan Management The management steps of DKA includes. Diabetes Management Uptodate Gestational Diabetes And Induction The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Diabetes Dka Symptoms Diabetes Type 1 Uptodate The 3 Step Trick that Reverses Diabetes medication management for diabetes type 2. Management of DKA in children the calculator, you must download it from the website to ensure that you are using the most uptodate version. Diabetes Treatment Uptodate: : We had been talking about pain management and the speaker launched a statement any. Diabetes Dka Talk to your doctor when you experience overwhelmed and work together to find a way to simplify your diabetes management. These guidelines for the management of DKA in children and young people under the age of 18 years @ Diabetes Medication Dosing Display Measure Diabetes Management Uptodate The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Diabetic ketoacidosis (DKA) is a potentially lifethreatening complication of diabetes mellitus. Signs and symptoms may include vomiting, Management Edit. Diabetes Treatment Uptodate Diabetes Management During Pregnancy The 3 Step Trick that Reverses Diabetes Permanently in As Little as 11 Days. Diabetes Type 2 Uptodate: : Diabetes Continue reading >>

Episode 63 – Pediatric Dka

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>

Dka: Critical Care Lecture Series

Dka: Critical Care Lecture Series

Results from an absolute or relative deficiency of circulating insulin Absolute deficiency occurs in previously undiagnosed type 1 or when patients on treatment do not take their insulin, purposefully or inadvertently Relative deficiency happens when counter-regulatory hormones increase due to stress:sepsis, trauma, GI illness Increases-- catecholamines, glucagon, cortisol and growth hormone Low insulin with high counter-regulatory hormones causes an accelerated catabolic state Increase glucose production by the liver and the kidney Via glycogenolysis and gluconeogenesis Impaired peripheral glucose utilization resulting in hyperosmolarity and hyperglycemia Increased lipolysis and ketogenesis resulting in metabolic acidosis and ketonemia Hyperglycemia exceeding the renal threshold and hyperketonemia cause the osmotic diuresis, dehydration and obligatory loss of electrolytes Aggravated by vomiting These mechanisms continues to increase the counter-regulatory hormones which worsen the process Without intervention, life threatening metabolic acidosis and dehydration will occur 4 Continue reading >>

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