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Dka Pathophysiology

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 >>

Chapter 220. Diabetic Ketoacidosis

Chapter 220. Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. The incidence and prevalence of diabetes are rising; as of 2005, an estimated 7% of the U.S. population had diabetes. In patients age 60 or older, the prevalence is estimated to be 20.9%.1 DKA occurs predominately in patients with type 1 (insulin-dependent) diabetes mellitus, but unprovoked DKA can occur in newly diagnosed type 2 (non–insulin-dependent) diabetes mellitus, especially in blacks and Hispanics.2 Between 1993 and 2003, the yearly rate of ED visits for DKA per 10,000 U.S. population with diabetes was 64, with a trend toward an increased rate of visits among the black population compared with the white population.3 Europe has a comparable incidence. A better understanding of pathophysiology and an aggressive, uniform approach to diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers.4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (Figure 220-1). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion gap metabolic acidosis.4 Insulin deficiency. Patho Continue reading >>

Diabetic Ketoacidosis: Pathophysiology, Management And Complications

Diabetic Ketoacidosis: Pathophysiology, Management And Complications

Abstract 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 In Type 2 Diabetes Mellitus—pathophysiology And Clinical Presentation

Diabetic Ketoacidosis In Type 2 Diabetes Mellitus—pathophysiology And Clinical Presentation

SN Davis is supported by research grants from the NIH. GE Umpierrez is supported by research grants from the NIH, the American Diabetes Association, and the American Heart Association. The authors declare no competing financial interests. 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 >>

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 >>

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 >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab 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 - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

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 >>

Childhood Ketoacidosis

Childhood 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 one of our health articles more useful. Diabetic ketoacidosis (DKA) is the leading cause of mortality in childhood diabetes.[1]The primary cause of DKA is absolute or relative insulin deficiency: Absolute - eg, previously undiagnosed type 1 diabetes mellitus or a patient with known type 1 diabetes who does not take their insulin. Relative - stress causes a rise in counter-regulatory hormones with relative insulin deficiency. DKA can be fatal The usual causes of death are: Cerebral oedema - associated with 25% mortality (see 'Cerebral odedema', below). Hypokalaemia - which is preventable with good monitoring. Aspiration pneumonia - thus, use of a nasogastric tube in the semi-conscious or unconscious is advised. Deficiency of insulin. Rise in counter-regulatory hormones, including glucagon, cortisol, growth hormone, and catecholamines. Thus, inappropriate gluconeogenesis and liver glycogenolysis occur compounding the hyperglycaemia, which causes hyperosmolarity and ensuing polyuria, dehydration and loss of electrolytes. Accelerated catabolism from lipolysis of adipose tissue leads to increased free fatty acid circulation, which on hepatic oxidation produces the ketone bodies (acetoacetic acid and beta-hydroxybutyric acid) that cause the metabolic acidosis. A vicious circle is usually set up as vomiting usually occurs compounding the stress and dehydration; the cycle can only be broken by providing insulin and fluids; otherwise, severe acidosis occurs and can be fatal. Biochemical criteria The biochemical criteria required for a diagnosis of DKA to be made are 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 >>

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: A Current Appraisal Of Pathophysiology And Management

Diabetic Ketoacidosis: A Current Appraisal Of Pathophysiology And Management

This is a current appraisal of new insights into the pathophysiology and management of diabetic ketoacidosis (DKA), including laboratory work-up, monitoring of insulin, and fluid management. This article also discussed the complications of DKA and its treatment, focusing on cerebral edema (CE). The author recommends that fluid deficits be replaced at an even rate over 48 h, not to exceed 4/L/m2/24 h. Regular insulin should be started at 0.1 units/kg/h (no bolus). In general, it is recommended that bicarbonate not be administered unless correction of a pH < 6.9 is necessary. To access this article, please choose from the options below Continue reading >>

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