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Which Insulin For Ketoacidosis

How To Treat Ketoacidosis

How To Treat Ketoacidosis

Immediately drink a large amount of non-caloric or low caloric fluid. Continue to drink 8 to 12 oz. every 30 minutes. Diluted Gatorade, water with Nu-Salt™ and similar fluids are good because they help restore potassium lost because of high blood sugars. Take larger-than-normal correction boluses every 3 hours until the blood sugar is below 200 mg/dl (11 mmol) and ketones are negative. It will take much more rapid insulin than normal to bring blood sugars down when ketones are present in the urine or blood. Often, one and a half to two times the normal insulin dose for a high blood sugar will be necessary. Higher insulin doses than these will be needed if there is an infection or other major stress. If nausea becomes severe or last 4 hours or more, call your physician. If vomiting starts or you can no longer drink fluids, have a friend or family member call your physician immediately, then go directly to an emergency room for treatment. Never omit your insulin, even if you cannot eat. A reduced insulin dose might be needed, but only if your blood sugar is currently low. When high blood sugars or ketoacidosis happen, it is critical that you drink lots of fluid to prevent dehydration. Take extra amounts of Humalog, Novolog or Regular insulin to bring the blood sugars down. Children with severe ketoacidosis lose 10-15 % of their previous body weight (i.e., a 60 lb. child can lose 6 to 9 lbs. of weight) due to severe dehydration. Replacement of fluids should be monitored carefully. The dehydration is caused by excess urination due to high blood sugars and is quickly worsened when vomiting starts due to the ketoacidosis. The start of vomiting requires immediate attention at an ER or hospital where IV fluid replacement can begin. If only nausea is present and it is possible 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 >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

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

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 >>

Treatment Of Insulin-resistant Diabetic Ketoacidosis With Insulin-like Growth Factor I In An Adolescent With Insulin-dependent Diabetes

Treatment Of Insulin-resistant Diabetic Ketoacidosis With Insulin-like Growth Factor I In An Adolescent With Insulin-dependent Diabetes

INSULIN plays a central part in the regulation of carbohydrate, fat, and protein metabolism. Severe insulin resistance, in which treatment with large doses of insulin does not result in adequate metabolic control, is uncommon. Such resistance occurs in the presence of circulating insulin or insulin-receptor antibodies,1 , 2 insulin-receptor abnormalities,3 and episodically in patients with previously typical insulin-dependent diabetes mellitus (IDDM).4 The therapeutic options in patients with severe insulin resistance have been limited, since insulin has been the only available hormone with insulin-like metabolic effects. Recombinant human insulin-like growth factor I (IGF-I), which shares considerable sequence homology as well as biologic properties with insulin,5 has recently become available and has been used in treating patients with Mendenhall's syndrome.6 We describe the use of IGF-I in the treatment of a 16-year-old girl with IDDM complicated by severe episodic insulin resistance. Administration of massive doses of insulin (more than 1000 U per hour) during these episodes failed to achieve glycemic control or reverse ketoacidosis. Treatment with IGF-I rapidly reversed the hyperglycemia and ketoacidosis, and subsequent weekly intravenous infusions of IGF-I markedly improved the degree of insulin sensitivity. The patient was a 16-year-old girl who had had IDDM since the age of 3. She was treated with twice-daily injections of regular and bovine or porcine isophane insulin suspension until the age of seven, at which time she began to receive human insulin. Her glycemic control subsequently improved. At the age of 13, she began to have increasingly frequent (two to three times monthly) episodes of severe hyperglycemia, usually without ketoacidosis. Her serum glucose Continue reading >>

How Can I Survive Type 1 Diabetes Without Insulin?

How Can I Survive Type 1 Diabetes Without Insulin?

This week, Wil offers some thoughts on that universal question: “How long can I really go without insulin?” Please take a read; his findings might surprise you and even bust a myth or two. Jake, type 1 from Minneapolis, writes: I’ve had diabetes for 18 years and I had someone ask me a question the other day that I didn’t really have an answer to. The question was how long I would be able to survive without any insulin. I told them 3–4 days, but I don’t know if this is true. Any info from a cinnamon whiskey swizzling T1? [email protected] D’Mine answers: If Tom Hanks’ character in Castaway had been one of us, he would’ve never lived long enough to go half-crazy and end up talking to a volleyball named Wilson. OK, so that’s a mixed blessing. But I guess the lesson there is: don’t get washed up on a deserted island if you can avoid it. To be honest, like you, I had always pegged my zero-insulin survival time in the “couple of days” zone; but once I got to thinking about your question I realized that I didn’t know how I knew that, where I learned it, or if it was even correct at all. Now, as background for you sugar-normals, type 2s, and type 3sin type 1s like Jake and me, if we run out of insulin hyperglycemia sets in. That leads to diabetic ketoacidosis (known as DKA by its friends), which then (untreated) leads to death. Well, there are a number of variables, the most critical being: Are you really out of insulin, or just low on insulin? Some type 1s use basal insulin, which has some effect for a full day or more after the last shot. Others of us PWDs use pumps, and the insulin from the pump only lasts for four hours. The bottom line here is that if two type 1s were captured by terrorists (hey, it could happen!), and if the terrorists took away their in Continue reading >>

Which Insulin For Diabetic Ketoacidosis?

Which Insulin For Diabetic Ketoacidosis?

The Lancet Choice is a new payment option that gives you the freedom and flexibility to access any 5 premium articles of your choice from across The Lancet family of journals - all for a one-off payment of $49.00 USD. Simply purchase your Lancet Choice pass from the Summary or Full Text page of an article you wish to access. This will count as the first of 5 article credits, or ‘Allowances’, and you can use your 4 remaining Allowances to access other articles from any of The Lancet journals. Continue reading >>

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

1. IV Isotonic Crystalloid Therapy • Shock fluid therapy is warranted if cardiovascular instability is present: Full shock dose of fluids is 90 mL/kg; start with ¼ to 1/3 dose and reassess until stable • Correct dehydration, provide maintenance needs, and replace ongoing losses over 6 to 24 hours: - % dehydration × body weight (kg) × 1000 plus - 20 mL/kg/day (insensible losses) plus - 20 to 40 mL/kg/day (maintenance sensible losses) plus - Account for vomiting, diarrhea, & polyuria (ongoing sensible losses) Alice Huang, VMD, & J. Catharine Scott-Moncrieff, Vet MB, MS, MA, Diplomate ACVIM & ECVIM Purdue University Canine Diabetic Ketoacidosis D i a gno s t i c Tre e / ENDOCRINOLOGY Peer Reviewed Physical Examination • Polyuria • Weight loss • Polydipsia • Vomiting • Polyphagia • Lethargy Patient may have only 1 or more of these signs. Laboratory Results • Blood glucose (BG): Hyperglycemia (> 200 mg/dL) • Blood gas (venous or arterial): Metabolic acidosis • Urine dipstick: Glucosuria; ketonuria or ketonemia Serum ketones can be measured if urine is unavailable. Diabetic Ketoacidosis Treatment 2. Electrolyte Supplementation (see Table 1, page 70) • Monitor serum potassium Q 4–6 H until within reference interval and stable; then Q 12–24 H • Monitor serum phosphorus Q 4–6 H until > 1.5; then Q 6–24 H • When supplementing potassium and phosphorus concurrently, take into account the amount of potassium contained in the potassium phosphate • Consider magnesium supplementation in instances of refractory hypokalemia 3. Regular Insulin • Continuous rate infusion (CRI) protocol:1 - Add 2.2 U/kg of regular insulin to 250 mL of 0.9% saline - Allow 50 Continue reading >>

Am I The Real Me When I Take Sertraline (zoloft) Or When I Don't Take It?

Am I The Real Me When I Take Sertraline (zoloft) Or When I Don't Take It?

There is no real you. Brain-altering drugs make it so you are not who you were before you took them. Continually using them means you are continually not who you were before you took them. Sometimes even just short term use can mean the effects last indefinitely, whether or not you continue using those drugs. But, the point here is that altered states are fundamentally different from unaltered ones. The whole purpose of taking psychotropic drugs is to change who or how you feel to be. That does not mean the unaltered you is "the real you" and the altered you is "the unreal you", though. They are different, in whatever ways, but all concepts of "you" are dynamic—not fixed. The physical "you" changes on a daily basis, even minute to minute. Antidepressants cause alterations and dysfunction which results in different physical changes than you would normally experience, but in either case there is a dynamic organic situation occurring and I would not even say the "you" is simply reduced to that physical system. I don't mean that spiritually, either...I mean our decisions and range of experiences are not solely contingent upon how our brain or body are at a given moment. Our perspectives and self-estimations and experiences of life can all be changed by drugs that alter our physical functioning, but the system drugs are acting upon is the very "you" that is being discussed. So, the "you" is a contributing factor in the outcomes of physical as well as experiential happenings. The conscious assessment of and participation in those end products is, perhaps, another kind of "you". That "you" is also quite dynamic, but even more contextual. Antidepressants cause physical and functional changes in your brain which can affect personality, brain morphology, cognition, communicatio Continue reading >>

> Hyperglycemia And Diabetic Ketoacidosis

> Hyperglycemia And Diabetic Ketoacidosis

When blood glucose levels (also called blood sugar levels) are too high, it's called hyperglycemia. Glucose is a sugar that comes from foods, and is formed and stored inside the body. It's the main source of energy for the body's cells and is carried to each through the bloodstream. But even though we need glucose for energy, too much glucose in the blood can be unhealthy. Hyperglycemia is the hallmark of diabetes — it happens when the body either can't make insulin (type 1 diabetes) or can't respond to insulin properly (type 2 diabetes). The body needs insulin so glucose in the blood can enter the cells to be used for energy. In people who have developed diabetes, glucose builds up in the blood, resulting in hyperglycemia. If it's not treated, hyperglycemia can cause serious health problems. Too much sugar in the bloodstream for long periods of time can damage the vessels that supply blood to vital organs. And, too much sugar in the bloodstream can cause other types of damage to body tissues, which can increase the risk of heart disease and stroke, kidney disease, vision problems, and nerve problems in people with diabetes. These problems don't usually show up in kids or teens with diabetes who have had the disease for only a few years. However, they can happen in adulthood in some people, particularly if they haven't managed or controlled their diabetes properly. Blood sugar levels are considered high when they're above someone's target range. The diabetes health care team will let you know what your child's target blood sugar levels are, which will vary based on factors like your child's age. A major goal in controlling diabetes is to keep blood sugar levels as close to the desired range as possible. It's a three-way balancing act of: diabetes medicines (such as in Continue reading >>

Diabetes: What Is Ketoacidosis And How Can Be Avoided & Treated?

Diabetes: What Is Ketoacidosis And How Can Be Avoided & Treated?

Good question! According to Wikipedia: Diabetic ketoacidosis is a potentially life-threatening complication in patients with diabetes mellitus. In order to define ketoacidosis a little better, let's go back to the source: diabetes. Someone who is diabetic is unable to produce insulin, a hormone necessary for the transfer of sugar from the bloodstream to the cells, which in turn produce energy. If this progression is disrupted, through lack of insulin for example, the body has to try to compensate by creating energy elsewhere. And so the body starts to burn fat and muscle to meet its energy needs. Unfortunately, this chemical reaction produces molecules known as ketone bodies. In small quantities, these are fine, and it is in fact normal to have traces of them in your blood (approximately 1mg/dl). However, if the quantity of ketones surpasses this threshold by too much, it starts to affect the pH of your blood (which becomes progressively more acidic). Even the slightest drop in pH can have dangerous effects: as the quantity of the ketones in your blood increases, and the blood pH diminishes, your kidneys start having problems. Eventually, if the ketoacidosis is left untreated, your kidneys can fail and you can die from dehydration, tachycardia and hypotension. A number of other symptoms can appear in extreme cases. Fortunately for us, the quantity of ketones has to be consequential, and it usually takes a while before individuals start manifesting symptoms. In my case, my diabetes went undiagnosed for a month and a half before it was discovered, and even then my ketone levels were relatively normal. If you're a diabetic, ketoacidosis can be easily avoided by controlling your blood sugar levels and maintaining a healthy lifestyle. Some doctors, preferring to stay on the Continue reading >>

Were There Any American Citizens Living On Us Soil Who Died Because They Couldn't Afford Healthcare?

Were There Any American Citizens Living On Us Soil Who Died Because They Couldn't Afford Healthcare?

Various answers to answers (I guess coming from incredulous non-Americans) have asked why the American people would put up with such a system, or why anyone could think it is better than the “socialist” model. Some have mentioned the stigma associated with the word socialism which Americans have been indoctrinated with since the Cold War. While that is true, it’s important to consider where that message originated, and why it was spread. “Single payer” healthcare is paid for by tax revenue. Healthcare is expensive in any country compared to other parts of the federal budget like public building maintenance, forestry etc., so a significant percentage of all taxes collected go to pay for socialist healthcare. That applies to the taxes of a poor American who doesn’t pay any taxes (20% of zero is zero), just as it does to a wealthy “1%er”, or an ultra-wealthy billionaire like Trump or Koch. In the American private health insurance system, if your insurance for a family costs $20k per year, that’s your liability for private health insurance regardless of your income. Joe the Plummer or Mitt Romney or Bill Gates - That same insurance costs each of them $20k more or less. This is from the Fraser Institute (Conservative Canadian “think tank”): “The 10% of Canadian families with the lowest incomes will pay an average of about $477 for public health care insurance in 2015. The 10% of Canadian families who earn an average income of $59,666 will pay an average of $5,684 for public health care insurance and the families among the top 10% of income earners in Canada will pay $37,180.” For extremely high-income wealthy Americans like Koch or Trump, that number would be a lot higher. If 20% of tax revenue goes to pay for healthcare, and George Soros pays $100 Continue reading >>

Long-acting Insulin On The Road To Recovery With Diabetic Ketoacidosis

Long-acting Insulin On The Road To Recovery With Diabetic Ketoacidosis

Diabetes mellitus, caused by a deficiency of the pancreatic hormone insulin, affects millions of individuals every year. In the United States, 29.1 million people had a diagnosis of diabetes in 2012 (9.3% of the US population). Worldwide, the World Health Organization reported 415 million adults with diabetes.1 As the seventh leading cause of death in the United States, diabetes claimed 69 071 lives in 2012.2 Many complications and comorbid conditions are associated with diabetes including myocardial infarction (1.8 times higher risk), stroke (1.5 times higher risk), and cardiovascular deaths (1.7 times higher risk). In adults, diabetes is the most common cause of nontraumatic lower-limb amputations, kidney failure that results in the need for chronic dialysis or kidney transplant, and vision loss/impairment.3 Diabetic ketoacidosis (DKA) is the most serious acute metabolic complication of diabetes. Hospitalizations for DKA in the United States are on the rise. According to epidemiological studies, DKA increased 35% from 1996 to 2006, with primary diagnoses of DKA totaling 136 500 in 2006. Two-thirds of DKA patients are type 1 diabetics, with the majority either between 18 and 44 years old or more than 65 years old. Although overall mortality is low (< 1%), higher mortality is seen in older adults and those with life-threatening conditions.4,5 In addition, the direct and indirect costs incurred for the acute management of DKA exceed $2 billion annually.6,7 Successful treatment of DKA requires correction of dehydration, hyperglycemia, and electrolyte imbalances. Hyperglycemia during acute illness results from increased hepatic glucose production and impaired glucose use in peripheral tissues. Excess counter-regulatory hormones such as glucagon, cortisol, and catecholamine Continue reading >>

Diabetic Ketoacidosis Explained

Diabetic Ketoacidosis Explained

Twitter Summary: DKA - a major complication of #diabetes – we describe what it is, symptoms, who’s at risk, prevention + treatment! One of the most notorious complications of diabetes is diabetic ketoacidosis, or DKA. First described in the late 19th century, DKA represented something close to the ultimate diabetes emergency: In just 24 hours, people can experience an onset of severe symptoms, all leading to coma or death. But DKA also represents one of the great triumphs of the revolution in diabetes care over the last century. Before the discovery of insulin in 1920, DKA was almost invariably fatal, but the mortality rate for DKA dropped to below 30 percent within 10 years, and now fewer than 1 percent of those who develop DKA die from it, provided they get adequate care in time. Don’t skip over that last phrase, because it’s crucial: DKA is very treatable, but only as long as it’s diagnosed promptly and patients understand the risk. Table of Contents: What are the symptoms of DKA? Does DKA occur in both type 1 and type 2 diabetes? What Can Patients do to Prevent DKA? What is DKA? Insulin plays a critical role in the body’s functioning: it tells cells to absorb the glucose in the blood so that the body can use it for energy. When there’s no insulin to take that glucose out of the blood, high blood sugar (hyperglycemia) results. The body will also start burning fatty acids for energy, since it can’t get that energy from glucose. To make fatty acids usable for energy, the liver has to convert them into compounds known as ketones, and these ketones make the blood more acidic. DKA results when acid levels get too high in the blood. There are other issues too, as DKA also often leads to the overproduction and release of hormones like glucagon and adrenaline Continue reading >>

Original Contribution Utility Of Initial Bolus Insulin In The Treatment Of Diabetic Ketoacidosis

Original Contribution Utility Of Initial Bolus Insulin In The Treatment Of Diabetic Ketoacidosis

Abstract Current guidelines for treatment of diabetic ketoacidosis (DKA) recommend administration of an intravenous bolus dose of insulin followed by a continuous infusion. This study was designed to investigate whether the initial bolus dose is of significant benefit to adult patients with DKA and if it is associated with increased complications. This was a non-concurrent, prospective observational cohort study of adult patients who presented with DKA in a 12-month period. Charts were divided into two groups depending on whether they received an initial bolus dose of insulin. Data on glucose levels, anion gap (AG), intravenous fluid administration (IVF), and length of stay (LOS) were collected. Primary outcome was hypoglycemia (need for administration of 50% dextrose). Of 157 charts, 78 received a bolus of insulin and were designated the treatment group, the remaining 79 formed the control group. Groups were similar at baseline and received equivalent IVF and insulin drips. There were no statistically significant differences in the incidence of hypoglycemia (6% vs. 1%, respectively, p = 0.12), rate of change of glucose (60 vs. 56 mg/dL/h, respectively, p = 0.54) or AG (1.9 vs. 1.9 mEq/L/h, respectively, p = 0.66), LOS in the Emergency Department (8 vs. 7 h, respectively, p = 0.37) or hospital (5.6 vs. 5.9 days, p = 0.81). Equivalence testing revealed no clinically relevant differences in IVF change, rate of change of glucose, or AG. Administration of an initial bolus dose of insulin was not associated with significant benefit to patients with DKA and demonstrated equivalent changes in clinically relevant endpoints when compared to patients not administered the bolus. Continue reading >>

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