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What Electrolytes Are Monitored In The Acute Stage Of Dka Why?

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 >>

Dka-practice

Dka-practice

DKA is caused when the body has little or no insulin to use. The blood glucose level keepsinfection. Hormonal changes lead to increased liver and renal glucose production andacidosis. DKA most commonly occurs in a person with type 1 diabetes. The lack of insulin The outcome of insulin therapy is to lower serum glucose by about 75 to 150 mg/dL/hr.the start of the infusion. An initial IV bolus dose of 0.1 unit/kg is followed by an IV drip of 0.1 treatment is effective), may be taken from a normal blood test taken from a vein, as there is Please download to get full document. View again Cytochrome Ally Financial Survey Research Irish Poetry Mythology Books Georgetown (Washington Republican National Committee Theater (Warfare) Communalism Culture Of Hong Kong 2-0-fokus-kajian -> 2-b-spo-pemeriksa 2-b1if-installati -> 2-konsep-compleme 2-konsep-dasar -> 2-sk-visi-misi-fi 2002-jonathan-g-m -> 2008-h1-cs-q2 2014-cra -> 2016-kak-pos-gizi 20170310-jouw-eig -> 21-pilapil-vs-iba 242050626-geologi -> 252 252-1236-1-pb -> 264398587-rancang 26440557-role-of- -> 280-1978-pdf 29379540-pelan-st -> 2zz-ge-electrical 2nd Millennium Conflicts 2nd Millennium Books 2nd Millennium Bc Conflicts 2nd Millennium Bc 24 Hours Of Le Mans 221 B Baker Street 21st Century Fox 20th Century Fox Franchises 2016 Democratic National Committee Email Leak 2012 Phenomenon 2010–11 Israeli–Palestinian Peace Talks 2009 United Nations Climate Change Conference 2009 Flu Pandemic 2007–08 World Food Price Crisis 2003 Invasion Of Iraq 2000s Energy Crisis 2000 Camp David Summit 2 D Computer Graphics Continue reading >>

Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 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 >>

Diabetic Ketoacidosis

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 >>

Diabetic Ketoacidosis | Management In Adults | Nursing Times

Diabetic Ketoacidosis | Management In Adults | Nursing Times

Scroll down to read the article or download a print-friendly PDF, including any tables and figures Diabetic ketoacidosis (DKA) is a serious and potentially life-threatening complication of diabetes (Joint British Diabetes Societies, 2013). It is a complex disordered metabolic state characterised by hyperglycaemia (elevated blood glucose), acidosis (pH imbalance) and ketonaemia (excess ketones in the blood). Although the majority of patients presenting with DKA have type 1 diabetes, those with type 2 diabetes can also develop the condition, especially during acute illness (Umpierrez et al, 2002). People from non-Caucasian ethnic groups are more likely to develop DKA in the presence of type 2 diabetes (Yehia et al, 2008). While the incidence of DKA is difficult to establish, population-based studies suggest an annual incidence of 4.6-8.0 episodes per 1,000 patients with diabetes (Faich et al, 1983); the worldwide mortality rate is 2-10% (Yehia et al, 2008). Over the past 20 years, mortality rates in developed countries have fallen from 7.96% to 0.67% (Lin, 2005) due to a better understanding of the pathophysiology of DKA and advances in the clinical management. Many cases could be prevented by better access to medical care, education and effective communication between patients and health professionals during concurrent illness (Kitabchi et al, 2004). DKA results from a dysregulation of carbohydrates, protein and lipid metabolism (Yehia et al, 2008) and usually occurs as a consequence of absolute or relative insulin deficiency accompanied by an increase in counter-regulatory hormones (glucagon, catecholamine, cortisol, growth hormones and epinephrine), which contribute to increased blood glucose levels and insulin resistance. The combination of insulin deficiency and inc 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 >>

Intravenous Fluids

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 >>

Hyperglycemic Crises In Patients With Diabetes Mellitus

Hyperglycemic Crises In Patients With Diabetes Mellitus

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are inadequate to f Continue reading >>

Like This Study Set?

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 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 >>

Guidelines For Perioperative Management Of The Diabetic Patient

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 >>

Pathophysiologic Changes In Dka

Pathophysiologic Changes In Dka

1. Describe the pathophysiologic changes in DKA. The lack of available insulin results in a disorder in the metabolism of carbs, protein, and fat. Because they are attempting to rid the body of excess glucose, the kidneys excrete the glucose along with water and electrolytes (esp. sodium and potassium). The fatty acids are converted into ketone bodies by the liver. Ketone bodies are acidic; their accumulation in the circulation due to lack of insulin leads to metabolic acidosis. 2. What are the commonly seen blood glucose levels? 300-800 mg/dL but some can get as high as 1,000 mg/dL 3. What fluid and electrolyte disturbances commonly occur and why? Soidum and potassium due to the amount of water loss 4. What acid-base disturbances commonly occur and why? Metabolic acidosis due to low serum bicarbonate and low pH from the bodys metabolic process 5. Describe the medical management and nursing management of a patient in DKA: a. How is fluid status monitored in the acute stage of DKA? Assessed for presence of edema, I & Os, lab values of sodium and potassium, vital signs performed q hour, breath sounds assessed, cardiac monitoring. b. How is hypovolemia corrected? How rapidly is fluid volume replaced? Why? .09% NS is infused at 500 ml/hr for 2-3 hours, then .45% NS administered in order to increase the fluid volume back within normal range c. How are the complications of fluid replacement prevented? By monitoring I&Os, vitals, orthostatic blood pressure, heart rate, ECGs, d. How are blood glucose levels monitored? How often? e. How are elevated blood glucose levels corrected? A regular insulin IV drip of 5 u/hr is given until back within normal range of 140-180 f. How quickly is blood glucose corrected? Why? Within 1-1.5 hours because regular insulin is the only type that Continue reading >>

Diabetic Ketoacidosis In Dogs

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 >>

Diabetic Ketoacidosistreatment & Management

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 >>

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