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Dka Pathophysiology

Pathophysiology Of Diabetic Ketoacidosis

Pathophysiology Of Diabetic Ketoacidosis

Diabetic ketoacidosis is one of the potentially life-threatening acute complications of diabetes mellitus. In the past, diabetic ketoacidosis was considered as the hallmark of Type I diabetes, but current data show that it can be also diagnosed in patients with type II diabetes mellitus. It is often seen among patients who are poorly compliant to insulin administration during an acute illness. It is commonly precipitated by an acute stressful event such as the development of infection leading to overt sepsis, organ infarction such as stroke and heart attack, burns, pregnancy or intake of drugs that affect carbohydrate metabolism such as corticosteroids, anti-hypertensives, loop diuretics, alcohol, cocaine, and ecstasy. The presence of these stressful conditions incite the release of counter-regulatory hormones such as glucagon, catecholamines and growth hormone. These hormones induce the mobilization of energy stores of fat, glycogen and protein. The net effect of which is the production of glucose. As a result of absent or deficient insulin release, diabetic ketoacidosis present with the following metabolic derangements: profound hyperglycemia, hyperketonemiaand metabolic acidosis. The production of ketones outweighs its excretion by the kidneys. This results in further reduction of systemic insulin, elevated concentrations of glucagon, cortisol, growth hormone and catecholamine. In peripheral tissues, such as the liver, lipolysis occurs to free fatty acids, resulting in further production of excess ketones. Thereby, causing ketosis and metabolic acidosis. Symptoms of diabetic ketoacidosis usually develop within 24 hours. Gastrointestinal symptoms such as nausea and vomiting are very prominent. If these symptoms are present in diabetics, investigation for diabetic keto Continue reading >>

Dka Pathophysiology

Dka Pathophysiology

1. Bethelhem Berhanu 2. • Two hormonal abnormalities: – Insulin deficiency and/or resistance. – Glucagon excess – required??? • increased secretion of catecholamines and cortisol Insulin Glucagon Epinephrine Cortisol Growth Hormone 3. • These will result in abnormal Metabolism of: – Carbohydrate – Fat – Protein • Inflammatory process 4. Normally… Hyperglycemia ↑Insulin ↓Glucose production ↓Gluconeogenesis ↑Glucose uptake ↓Glycogenolysis Normoglycemia 5. DKA Hyperglycemia ↑Insulin ↑Glucose production ↑ Gluconeogenesis ↓Glucose uptake ↑ Glycogenolysis Hyperglycemia 6. Carbohydrate contd. • The decrease in glucose uptake alone does not give us the degree of hyperglycemia in DKA or HHS. • Gluconeogenesis, why? – Providing the substrates (glycerol, alanine) – Increase in glucagon 7. • Glucosuria helps in reducing the serum glucose initially, but later…. Osmotic diuresis, Volume depletion ↓GFR ↓ glucose excretion 8. On fat metabolism • ↓insulin & ↑cathechilamines → Lipolysis – There will be free fatty acid mobilization to the liver – Normally, these would be converted into TGLs and VLDL, but the presence of glucagon alters the hepatic metabolism to form ketone bodies. Ketone bodies Acetone Acetoacetate β-hydroxbutyrate 9. • The acidic ketone bodies will cause metabolic acidosis. – Dehydration from osmotic diuresis also exacerbates the acidosis. • A second product of lipolysis, glycerol, will be used as a substrate for gluconeogenesis in the liver. 10. On protein metabolism • There will be increased protein breakdown and production of amino acids, which will be used in gluconeogenesis (alanine). 11. Events • Dehydration – 6 litres or more, 15-20% of their weight. Why? – Osmotic Diuresis – bl Continue reading >>

Pathophysiology And Treatment

Pathophysiology And Treatment

The Kabod Volume 2 Issue 1 Fall 2015 Article 3 Diabetic Ketoacidosis: Pathophysiology and Treatment Laura E. Mumme Liberty University, [email protected] Follow this and additional works at: Part of the Medical Biochemistry Commons, and the Medical Physiology Commons Recommended Citations MLA: Mumme, Laura E. "Diabetic Ketoacidosis: Pathophysiology and Treatment," The Kabod 2. 1 (2015) Article 3. Liberty University Digital Commons. Web. [xx Month xxxx]. APA: Mumme, Laura E. (2015) "Diabetic Ketoacidosis: Pathophysiology and Treatment" The Kabod 2( 1 (2015)), Article 3. Retrieved from Turabian: Mumme, Laura E. "Diabetic Ketoacidosis: Pathophysiology and Treatment" The Kabod 2 , no. 1 2015 (2015) Accessed [Month x, xxxx]. Liberty University Digital Commons. Running head: DIABETIC KETOACIDOSIS 1 Diabetic Ketoacidosis Pathophysiology and Treatment Liberty University 1 Mumme: Diabetic Ketoacidosis Published by [email protected] University, 2015 DIABETIC KETOACIDOSIS 2 Diabetic Ketoacidosis: Pathophysiology and Treatment Diabetic ketoacidosis (DKA), also known as diabetic acidosis or diabetic coma, is a severe complication of diabetes mellitus (DM; Michel, 2011). More commonly seen in patients with type 1 diabetes (T1D), DKA results when lipid breakdown generates a surplus of acidic ketone bodies (Guven, Matfin, & Kuenzi, 2009). According to Dods (2013), DKA can be defined as a condition with “blood glucose greater than 250 mg/dL, blood bicarbonate less than 15 mEq/L, pH less than 7.35, ketonemia, and increased anion gap†(p. 266). The pathophysiology of DKA in patients with T1D will first be addressed, followed by a discussion of proper emergency treatment for this life-threatening condition. The three main abnormalities of DKA patients include hyperglycemia, Continue reading >>

Confidential And Proprietary Any Use Of This Material Without Specific Permission Is Strictly Prohibited.

Confidential And Proprietary Any Use Of This Material Without Specific Permission Is Strictly Prohibited.

State of Ohio Overview of the diabetic ketoacidosis (DKA)/ hyperglycemic hyperosmolar state (HHS) episode of care CONFIDENTIAL AND PROPRIETARY Any use of this material without specific permission is strictly prohibited. CONFIDENTIAL AND PROPRIETARY Any use of this material without specific permission is strictly prohibited. December 23, 2016 | 1 Overview of the diabetic ketoacidosis (DKA)/hyperglycemic hyperosmolar state (HHS) episode of care 1. CLINICAL OVERVIEW AND RATIONALE FOR DEVELOPMENT OF THE DKA/HHS EPISODE 1.1 Rationale for development of the DKA/HHS episode of care DKA and HHS are among the most serious acute complications of diabetes. Clinically, DKA and HHS differ only by the degree of dehydration and the severity of metabolic acidosis. Both require prompt diagnosis and treatment. According to the American Diabetes Association, DKA accounts for more than $1 of every $4 spent on direct care for adult patients with Type I diabetes, and $1 of every $2 spent on patients experiencing multiple morbidities.1 In the United States, approximately 145,000 hospitalizations occur for DKA each year with an average cost of $17,500 per patient.2 The direct and indirect total annual cost of hospitalizations is estimated to be $2.4 billion.3 While the hospitalization rate for HHS is less than one percent of all diabetes-related admissions, death occurs in an estimated 5-16 percent of these patients, a rate 10 times higher than that of DKA.4 The complex pathophysiology of both DKA and HHS requires careful selection of approaches to restore glycemic control and deficiencies in intravascular volume and electrolytes. Appropriate treatment also includes the diagnosis and management of the underlying precipitating event. Death in patients with DKA/HHS is typically caused by the und Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Course Summary Diabetic ketoacidosis is an acute complication of diabetes mellitus, which requires prompt, aggressive, treatment. Complications of diabetic ketoacidosis throughout the age spectrum and during pregnancy require a close evaluation of symptoms, testing, treatment and outcomes to treatment. Anyone with diabetes, regardless of age or gender, can develop ketoacidosis. Guidelines exist that guide diabetes health teams and clinical care of the diabetic patient. Appropriate and timely treatment can reduce diabetic ketoacidosis complications and patients can recover to full health. Course Format Homestudy Course Syllabus Introduction Epidemiology Glucose, Insulin, And Diabetes: A Brief Review Glucose and Energy Type 1 and Type 2 Diabetes Classification System: Out of Date? Pathophysiology Of DKA - Pathophysiology, Signs and Symptoms of DKA Precipitating Causes Of DKA Clinical Signs And Symptoms Of DKA Diagnosis Of DKA Laboratory Tests Hyperkalemia Hyponatremia Other Electrolytes Amylase and Lipase Hepatic Transaminases Leukocytosis Serum Osmolality Renal Function Studies Troponin Levels Euglycemic DKA Gestational Diabetes And DKA Atypical Antipsychotics And DKA Complications Of DKA - Children, DKA and Cerebral Edema XI. Treatment For Diabetic Ketoacidosis Laboratory Tests Fluid Replacement Electrolyte Imbalances Insulin Therapy Acid-Base Disturbances and Bicarbonate Therapy Continuing Care and Monitoring for Complications Treatment Of Cerebral Edema Clinical Care, Prevention and Education Poor Access to Medical Care Lack of Information Emotional Acceptance and Non-compliance Summary Continue reading >>

Diabetic Ketoacidosis: Pathophysiology, Management And Complications

Diabetic Ketoacidosis: Pathophysiology, Management And Complications

Diabetic ketoacidosis (DKA) is a common and potentially life-threatening complication of diabetes mellitus, the second most common chronic childhood disease [1]. Prior to the introduction of insulin to clinical medicine by Banting and Best in 1922, DKA had a mortality rate greater than 60% [2]. As insulin was introduced into clinical practice, there was a gradual decrease in mortality associated with DKA over the subsequent 30 years. Recent epidemiological data reveal current mortality varies from 0 to 19% [3,4]. DKA continues to be the most common cause of death in patients younger than 24 years of age; it accounts for as many as 50% of deaths of young diabetic patients [5–7]. In elderly diabetics who have coexisting diseases, DKA carries a high mortality [8]. Despite many advances in the care of diabetic patients, the prevalence of DKA is not declining; it accounts for 14% of all diabetes-related hospital admissions [3, 4, 9]. The incidence of insulin-dependent diabetes mellitus continues to increase worldwide and has roughly doubled in each recent decade [10–13]. Because insulin-dependent diabetes mellitus is increasing, and preventative measures to avoid DKA in diabetic patients have not been successful, the incidence of DKA can also be expected to increase in coming years. Prevention of DKA is the ultimate goal (80% of hospital admissions for DKA occur in treated diabetics) [3,8]. It is necessary for clinicians to understand the pathophysiology and treatment of DKA to care for this increasing diabetic population. We discuss the pathophysiology of diabetic ketoacidosis, its management, and its complications. Continue reading >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea 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 >>

Endocrine Pathophysiology Diabetes, Dka, Hhs

Endocrine Pathophysiology Diabetes, Dka, Hhs

Sort Life-threatening problem that affects people w/diabetes, occurs when body cannot use sugar for fuel because there is no insulin or not enough insulin. Fat is used for fuel instead. Waste products called ketones build up in blood/urine, levels are poisonous. Diabetic Ketoacidosis Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Advanced Diabetic Ketoacidosis

Advanced Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a dangerous condition characterized by a severe rise in blood sugar or hyperglycemia, depleted bodily fluids, shock, and in some cases unconsciousness. Coma and even death may occur if DKA is left untreated or if it becomes more severe due to excessive vomiting. Symptoms of DKA In the early stages of DKA, the affected individual appears flushed and breathes rapidly and deeply. This is called hyperventilation. As the condition progresses, the skin may turn pale, cool and clammy, dehydration may begin to set in and the heart rate may become rapid and breathing shallow. Nausea, vomiting and severe abdominal cramps. Blurred vision Fruity or pungent smelling breath due to the presence of acetone and ketones in the breath. Pathophysiology Although DKA can occur in patients with type 2 diabetes, it mainly develops in people with type 1 diabetes who need to take insulin for their condition. If individuals do not receive insulin, they will develop DKA. If there is a shortage of insulin, the body fails to use glucose in the blood for energy and instead fats are broken down in the liver. When these fats are broken down, acidic compounds called ketones are produced as a by-product. These ketones build up in the body and eventually cause ketoacidosis. Aside from missed or inadequate doses of insulin, another common cause of DKA is infection or illness as this can raise the level of hormones that counteract the effects of insulin. In addition, the dehydration caused by major injury or surgery can raise levels of these hormones. Diagnosis and treatment Blood tests are performed to check the sugar levels and blood pH, which is classified as acidic if it is below the usual 7.3. Unlike non-ketotic hyperosmolar coma, in DKA the blood and urine levels of keto 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 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 >>

25-40% Of Newly Diagnosed Cases Present In Dka

25-40% Of Newly Diagnosed Cases Present In Dka

Case Scenario #1 What is your assessment? DKA exists when: Venous pH < 7.3 Serum bicarbonate < 15 mEq/dL Blood glucose > 300 mg/dL Presence of ketonemia/ketonuria How much fluid would you administer as a bolus? Would you administer bicarbonate? How much insulin would you administer? What IVF would you start? At what rate? * 10 - 20 cc/kg bolus of NS would be adequate. Though the patient is dehydrated (dry lips), his hemodynamics are good, with acceptable vitals and good perfusion. There would be no reason to administer more than 20 cc/kg fluids. While this patient is clearly acidemic, he is NOT in impending cardiovascular collapse and therefore there is no justification for the administration of bicarbonate. In fact, administration of bicarbonate has been associated with the development of cerebral edema. The “true†serum sodium is 143 133 + 0.016[700-100] Insulin is generally started at 0.1 u/kg/hr. Therefore, in this 30 kg patient, an insulin infusion of 3 u/hr of regular insulin should be initiated. IVF of NS should be started at ~ 2400 cc/m2/day, which is approximately 1.5 x maintenance 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 >>

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