Management Of Diabetic Ketoacidosis In Adults
Diabetic ketoacidosis is a potentially life-threatening complication of diabetes, making it a medical emergency. Nurses need to know how to identify and manage it and how to maintain electrolyte balance Continue reading >>
Diabetic Ketoacidosis In Dogs
My dog is diabetic. He has been doing pretty well overall, but recently he became really ill. He stopped eating well, started drinking lots of water, and got really weak. His veterinarian said that he had a condition called “ketoacidosis,” and he had to spend several days in the hospital. I’m not sure I understand this disorder. Diabetic ketoacidosis is a medical emergency that occurs when there is not enough insulin in the body to control blood sugar (glucose) levels. The body can’t use glucose properly without insulin, so blood glucose levels get very high, and the body creates ketone bodies as an emergency fuel source. When these are broken down, it creates byproducts that cause the body’s acid/base balance to shift, and the body becomes more acidic (acidosis), and it can’t maintain appropriate fluid balance. The electrolyte (mineral) balance becomes disrupted which can lead to abnormal heart rhythms and abnormal muscle function. If left untreated, diabetic ketoacidosis is fatal. How could this disorder have happened? If a diabetic dog undergoes a stress event of some kind, the body secretes stress hormones that interfere with appropriate insulin activity. Examples of stress events that can lead to diabetic ketoacidosis include infection, inflammation, and heart disease. What are the signs of diabetic ketoacidosis? The signs of diabetic ketoacidosis include: Excessive thirst/drinking Increased urination Lethargy Weakness Vomiting Increased respiratory rate Decreased appetite Weight loss (unplanned) with muscle wasting Dehydration Unkempt haircoat These same clinical signs can occur with other medical conditions, so it is important for your veterinarian to perform appropriate diagnostic tests to determine if diabetic ketoacidosis in truly the issue at hand Continue reading >>
Guidelines For Perioperative Management Of The Diabetic Patient
Surgery Research and Practice Volume 2015 (2015), Article ID 284063, 8 pages 1Texas A&M Health Science Center, 8447 State Highway 47, Bryan, TX 77807, USA 2Division of Pulmonary, Critical Care & Sleep Medicine, Texas A&M Health Science Center, Corpus Christi, 1177 West Wheeler Avenue, Suite 1, Aransas Pass, TX 78336, USA Academic Editor: Roland S. Croner Copyright © 2015 Sivakumar Sudhakaran and Salim R. Surani. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Management of glycemic levels in the perioperative setting is critical, especially in diabetic patients. The effects of surgical stress and anesthesia have unique effects on blood glucose levels, which should be taken into consideration to maintain optimum glycemic control. Each stage of surgery presents unique challenges in keeping glucose levels within target range. Additionally, there are special operative conditions that require distinctive glucose management protocols. Interestingly, the literature still does not report a consensus perioperative glucose management strategy for diabetic patients. We hope to outline the most important factors required in formulating a perioperative diabetic regimen, while still allowing for specific adjustments using prudent clinical judgment. Overall, through careful glycemic management in perioperative patients, we may reduce morbidity and mortality and improve surgical outcomes. 1. Introduction Diabetes has classically been defined as a group of metabolic diseases characterized by hyperglycemia due to defects in insulin secretion, insulin action, or a combination of both [1]. The vast majority of di Continue reading >>
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Corresponding Author:Reshad Hassannezhad, Department of Endocrinology,USA Received date:September 19, 2018; Accepted date:October 02, 2018; Published date:October 08, 2018. Citation for this Article:Reshad Hassannezhad, Hyperketonemia: Clinical features and diagnosis of Diabetic Ketoacidosis. J. Endocrinology and Disorders.Doi:10.31579/2640-1045/033 Copyright: 2018. Reshad Hassannezhad. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Diabetic ketoacidosis arises because of a lack of insulin in the body. The lack of insulin and corresponding elevation of glucagon leads to increased release of glucose by the liver (a process that is normally suppressed by insulin) from glycogen via glycogenolysis and also through gluconeogenesis. High glucose levels spill over into the urine, taking water and solutes (such as sodium and potassium) along with it in a process known as osmotic diuresis.This leads to polyuria, dehydration, and polydipsia. The absence of insulin also leads to the release of free fatty acids from adipose tissue (lipolysis), which are converted through a process called beta oxidation, again in the liver, into ketone bodies (acetoacetate and -hydroxybutyrate). -Hydroxybutyrate can serve as an energy source in the absence of insulin-mediated glucose delivery, and is a protective mechanism in case of starvation. The ketone bodies, however, have a low pKa and therefore turn the blood acidic (metabolic acidosis). The body initially buffers the change with the bicarbonate buffering system, but this system is quickly overwhelmed and other mechanisms must work to compensate for the ac Continue reading >>
Intravenous Fluids
Learn more about Intravenous fluids Deborah C. Silverstein DVM, DACVECC, Kari Santoro-Beer DVM, DACVECC, in Small Animal Critical Care Medicine (Second Edition), 2015 Intravenous fluid therapy is vital for the management of cardiovascular shock, interstitial dehydration, and daily maintenance fluid needs in critically ill animals (see Chapters 58, 60, and 193 to 195Chapter 4Chapter 58Chapter 60Chapter 193Chapter 194Chapter 195). This chapter focuses primarily on the distribution of total body water, patient assessment, and the delivery of synthetic intravenous fluids to maintain normal water, electrolyte, and acid-base status in critically ill dogs and cats that are hemodynamically stable. Because critically ill animals often have fluid and electrolyte balance derangements, overall recovery often depends on recognition and appropriate treatment of these disorders, in addition to diagnosing and treating the primary disease process. Intravenous fluid therapy is vital for the management of shock, dehydration, and maintenance in animals that require parenteral fluid therapy (see Chapters 61, 62, and 63Chapter 61Chapter 62Chapter 63, Peripheral Venous Catheterization, Intraosseous Catheterization, and Central Venous Catheterization, respectively, and Chapter 65 and 66, Shock Fluids and Fluid Challenge and Transfusion Medicine, respectively). This chapter focuses primarily on the distribution of total body water, patient assessment, and the delivery of synthetic intravenous fluids to maintain normal water, electrolyte, and acid-base status in critically ill dogs and cats that are hemodynamically stable. Because critically ill animals often have fluid and electrolyte balance derangements, overall recovery often depends on recognition and appropriate treatment of these disorder Continue reading >>
Hyperosmolar Hyperglycaemic State
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 the Type 2 Diabetes article more useful, or one of our other health articles. Synonyms: hyperosmolar hyperglycaemic nonketotic coma (HONK), diabetic nonketotic coma, hyperosmolar nonketotic state, hyperosmolar nonketotic hyperglycaemia (HNKH) See also separate articles Coma, Diabetes and Intercurrent Illness, Management of Type 2 Diabetes Mellitus, Diabetic Ketoacidosis and Childhood Ketoacidosis. Hyperosmolar hyperglycaemic state (HHS) occurs in people with type 2 diabetes. Very high blood glucose levels (often over 40 mmol/L) develop as a result of a combination of illness, dehydration and an inability to take normal diabetes medication due to the effect of illness. HHS is characterised by severe hyperglycaemia with marked serum hyperosmolarity, without evidence of significant ketosis. HHS is a potentially life-threatening emergency. Hyperglycaemia causes an osmotic diuresis with hyperosmolarity leading to an osmotic shift of water into the intravascular compartment, resulting in severe intracellular dehydration. Ketosis does not occur due to the presence of basal insulin secretion sufficient to prevent ketogenesis but insufficient to reduce blood glucose. A mixed picture of HHS and diabetic ketoacidosis (DKA) may occur. There is no precise definition of HHS but there are characteristic features that differentiate it from other hyperglycaemic states such as DKA. These are:[1] Hypovolaemia. Marked hyperglycaemia (30 mmol/L or more) without significant hyperketonaemia (<3 mmol/L) or acidosis (pH>7.3, bicarbonate >15 mmol/L). Osmolality usually 320 mosmol/kg or more. Causative conditions Continue reading >>
Diabetic Ketoacidosistreatment & Management
Diabetic KetoacidosisTreatment & Management Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... 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: Correction of fluid loss with intravenous fluids Correction of electrolyte disturbances, particularly potassium loss Treatment of concurrent infection, if present 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 ultrashort-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 Continue reading >>
Like This Study Set?
A client with a diagnosis of diabetic ketoacidosis (DKA) is being treated in the emergency department. Which findings would the nurse expect to note as confirming this diagnosis? Select all that apply. 1. Increase in pH 2. Comatose state 3. Deep, rapid breathing 4. Decreased urine output 5. Elevated blood glucose level 6. Low plasma bicarbonate level 3,5,6 Rationale: In DKA, the arterial pH is lower than 7.35, plasma bicarbonate is lower than 15 mEq/L, the blood glucose level is higher than 250 mg/dL, and ketones are present in the blood and urine. The client would be experiencing polyuria, and Kussmaul's respirations (deep and rapid breathing pattern) would be present. A comatose state may occur if DKA is not treated, but coma would not confirm the diagnosis. The nurse teaches a client with diabetes mellitus about differentiating between hypoglycemia and ketoacidosis. The client demonstrates an understanding of the teaching by stating that a form of glucose should be taken if which symptoms develop? Select all that apply. 1. Polyuria 2. Shakiness 3. Palpitations 4. Blurred vision 5. Lightheadedness 6. Fruity breath odor 2,3,5 A client is admitted to a hospital with a diagnosis of diabetic ketoacidosis (DKA). The initial blood glucose level was 950 mg/dL. A continuous intravenous infusion of short-acting insulin is initiated, along with intravenous rehydration with normal saline. The serum glucose level is now 240 mg/dL. The nurse would next prepare to administer which item? 1. Ampule of 50% dextrose 2. NPH insulin subcutaneously 3. Intravenous fluids containing dextrose 4. Phenytoin (Dilantin) for the prevention of seizures 3 Rationale: During management of DKA, when the blood glucose level falls to 250 to 300 mg/dL, the infusion rate is reduced and a dextrose solution Continue reading >>
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 >>
Questions To Prepare For Osce
1. Describe the pathophysiologic changes in DKA. a. Why do blood glucose levels increase? - Without insulin, the amount of glucose entering the cells is reduced, so then the liver increases glucose production The patient lacks insulin which is required to breakdown sugar for energy. This results in an increase in glucose levels. b. What are commonly seen blood glucose levels? - Blood glucose levels may vary from 16.6 to 44.4 mmol/L. Some may have lower, and others may have values of 55.5mmol/L c. What fluid and electrolyte disturbances commonly occur? -Water, sodium, potassium, and chloride d. What causes the fluid and electrolyte disturbances? -In an attempt to rid the body of the excess glucose, the kidneys excrete the glucose along with water and electrolytes. Patients with DKA may lose up to 6.5 litres of water and up o 400 to 500 mmol/L each of sodium, potassium, and chloride. Due to the lack of insulin, cells are not receiving an adequate fuel source to produce energy. Even though the blood is loaded with glucose, the cells go into a starvation mode. This triggers the release of glucagon and other counter-regulatory hormones that promote the breakdown of triglycerides into free fatty acids and initiate gluconeogenesis to produce more glucose for the starving cells. This further elevates the blood glucose level as the body begins to metabolize protein and fat to produce a source of energy. Due to the insulin deficiency and release of large amounts of glucagon, free fatty acids circulate in abundance in the blood and are metabolized into acetoacetic acid and B-hydroxybutric acid — both of which are strong organic acids and are referred to as ketones. As acetoacetic acid is metabolized it produces acetone, which begins to accumulate in the blood. Small amounts Continue reading >>
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Exam Shows Diffuse Abdominal Tenderness With Guarding.
A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. 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. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>
Diabetes Simulation (dka) Preparation Questions
Submitted By thecarrot Words 549 Pages 3 Diabetes Simulation (DKA) Fall 2015 Preparation Questions 1. Describe the pathophysiologic changes in DKA. In DKA, insulin deficiency causes the body to metabolize amino acids and triglycerides for energy instead of glucose. This leads to the production of ketones which are acidic and cause metabolic acidosis. Hyperglycemia in DKA causes osmotic diuresis in kiidneys and ketones, water, Na, and K are excreted. 2. What are the commonly seen blood glucose levels? 70-130 is for normal non DKA, In DKA levels are 250-600+. 3. What fluid and electrolyte disturbances commonly occur and why? Hyperglycemia due to insulin deficiency causes an osmotic diuresis that leads to marked urinary losses of water and electrolytes. Urinary excretion of ketones causes additional losses of Na and K. If serum K is not monitored and replaced as needed, life-threatening hypokalemia may develop. 4. What acid-base disturbances commonly occur and why? Insulin deficiency causes the body to metabolize amino acids and triglycerides for energy instead of glucose. This leads to the production of ketones which are acidic and cause metabolic acidosis. 5. Describe the medical management and nursing management of a patient in DKA. Hydration – fluid replacement initially rapid 0.9% NS to restore fluid balance Insulin – rapid or short acting insulin IV to bring blood glucose below 250. Electrolytes – Na deficiency treated with 0.9% NS. Once fluid balance restored may switch to lactated ringers to restore potassium levels or supplement per provider order. 6. How is fluid status monitored in the acute stage of DKA? Close monitoring of I&O. Serum electrolytes. 7. How is hypovolemia corrected? How rapidly is fluid volume replaced? Why? IV NS 0.9% rapid infusion, then Continue reading >>
Diabetic Ketoacidosis
Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>
Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications
Diabetic ketoacidosis definition and facts Diabetic ketoacidosis is a life-threatening complication of type 1 diabetes (though rare, it can occur in people with type 2 diabetes) that occurs when the body produces high levels of ketones due to lack of insulin. Diabetic ketoacidosis occurs when the body cannot produce enough insulin. The signs and symptoms of diabetic ketoacidosis include Risk factors for diabetic ketoacidosis are type 1 diabetes, and missing insulin doses frequently, or being exposed to a stressor requiring higher insulin doses (infection, etc). Diabetic ketoacidosis is diagnosed by an elevated blood sugar (glucose) level, elevated blood ketones and acidity of the blood (acidosis). The treatment for diabetic ketoacidosis is insulin, fluids and electrolyte therapy. Diabetic ketoacidosis can be prevented by taking insulin as prescribed and monitoring glucose and ketone levels. The prognosis for a person with diabetic ketoacidosis depends on the severity of the disease and the other underlying medical conditions. Diabetic ketoacidosis (DKA) is a severe and life-threatening complication of diabetes. Diabetic ketoacidosis occurs when the cells in our body do not receive the sugar (glucose) they need for energy. This happens while there is plenty of glucose in the bloodstream, but not enough insulin to help convert glucose for use in the cells. The body recognizes this and starts breaking down muscle and fat for energy. This breakdown produces ketones (also called fatty acids), which cause an imbalance in our electrolyte system leading to the ketoacidosis (a metabolic acidosis). The sugar that cannot be used because of the lack of insulin stays in the bloodstream (rather than going into the cell and provide energy). The kidneys filter some of the glucose (suga Continue reading >>
Diabetic Ketoacidosis
Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>
