Insulin Dosing In Pediatric Diabetic Ketoacidosiswhere To Start?
(B) Epidural or spinal hematomas may occur in patients treated with ELIQUIS who are receiving neuraxial anesthesia or undergoing spinal puncture. These hematomas may result in long-term or permanent paralysis. Consider these risks when scheduling patients for spinal procedures. Factors that can increase the risk of developing epidural or spinal hematomas in these patients include: Increased Risk of Thrombotic Events after Premature Discontinuation: Premature discontinuation of any oral anticoagulant, including ELIQUIS, in the absence of adequate alternative anticoagulation increases the risk of thrombotic events. An increased rate of stroke was observed during the transition from ELIQUIS to warfarin in clinical trials in atrial fibrillation patients. If ELIQUIS is discontinued for a reason other than pathological bleeding or completion of a course of therapy, consider coverage with another anticoagulant. Concomitant use of drugs affecting hemostasis increases the risk of bleeding, including aspirin and other antiplatelet agents, other anticoagulants, heparin, thrombolytic agents, SSRIs, SNRIs, and NSAIDs. Spinal/Epidural Anesthesia or Puncture: Patients treated with ELIQUIS undergoing spinal/epidural anesthesia or puncture may develop an epidural or spinal hematoma which can result in long-term or permanent paralysis. The risk of these events may be increased by the postoperative use of indwelling epidural catheters or the concomitant use of medicinal products affecting hemostasis. Indwelling epidural or intrathecal catheters should not be removed earlier than 24 hours after the last administration of ELIQUIS. The next dose of ELIQUIS should not be administered earlier than 5 hours after the removal of the catheter. The risk may also be increased by traumatic or repeate Continue reading >>
Insulin Dosing In Diabetic Ketoacidosis: Less May Be More
PICO Question: Among children ≤12 years old with diabetic ketoacidosis, does low dosing of regular insulin achieve equally effective outcomes compared to standard dosing? Question type: Treatment Study design: Randomized controlled trial Investigators from the Postgraduate Institute of Medical Education and Research in India conducted a randomized controlled trial to determine if a dosing of regular insulin that is lower than the currently recommended dose could be safely and effectively used in children with diabetic ketoacidosis (DKA). Eligible participants were children ≤12 years of age who presented to the emergency department of a tertiary teaching hospital with DKA. DKA was defined as the presence of hyperglycemia (blood glucose [BG] ≥200 mg/dL), acidosis (a pH <7.3 or bicarbonate <15 mEq/L), and ketonuria (urine dipstick ≥2+). Children with … View Full Text Continue reading >>
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 >>
Why Doesn't Regular Insulin Therapy Cause Hypokalemia In Patient With Diabetes Mellitus?
Hypokalemia is low potassium. Your potassium level is maintained within a range. As part of your electrolytes that move in and out of the cells as needed. Insulin reduces serum K+ from ECF to ICF mainly because insulin increases the activity of the sodium-potassium pump. insulin is the first-line defense against hyperkalemia. a rise in plasma k+ stimulates insulin release by the pancreatic beta cell. insulin, in turn, enhances cellular potassium uptake, returning plasma k+ towards normal. the enhanced cellular uptake of k+ that results from increased insulin levels is thought to be largely due to the ability of insulin to stimulate activity of the sodium potassium atpase located in cell plasma membranes. the insulin induced cellular uptake of potassium is not dependent on the uptake of glucose caused by insulin. insulin deficiency allows a mild rise in plasma k+ chronically and makes the subject to severe hyperkalemia if a potassium load is given. conversely, potassium deficiency may cause decreased insulin release. thus plasma potassium and insulin participate in a feedback control mechanism. Continue reading >>
Management Of Diabetic Ketoacidosis In Severe Insulin Resistance
Syndromes of severe insulin resistance (IR) include mutations of or autoantibodies to the insulin receptor and lipodystrophy (1). Diabetic ketoacidosis (DKA), although rare, can occur in these patients, even in the context of hyperinsulinemia, due to impaired insulin signaling. DKA can be extremely challenging to treat, and few clinicians are experienced or comfortable in using the high doses of insulin required. We describe aggressive management of DKA in three patients with syndromic severe IR. CASE 1 An 18-year-old man with compound heterozygous mutation of the insulin receptor presented with DKA. He had poorly controlled diabetes (A1C 14% [130 mmol/mol]) treated with U-500 insulin (1,500 units/day), metreleptin (recombinant human methionyl leptin as an experimental drug), and metformin (2 g/day). Two weeks prior, he underwent a root canal for an abscessed tooth but did not take the prescribed antibiotics. Antibiotics were subsequently initiated. One day after discharge, he developed abdominal pain, nausea, vomiting, and worsening jaw pain and swelling. Two days later, he developed fatigue, malaise, and Kussmaul respirations. He presented to an outside hospital with DKA with a pH of 7.08, partial pressure CO2 of 27 mmHg, and bicarbonate of 8 mmol/L. He received fluid resuscitation for an estimated 10% dehydration. In collaboration with National Institutes of Health (NIH) physicians, an insulin drip was started at 100 units/h that was gradually increased to 1,000 units/h on the first day and 2,000 units/h on the second day, without improvement of acidosis (Fig. 1A). Because of the lack of improvement despite massive doses of insulin (>50,000 units/day) and intravenous antibiotics, bicarbonate was given and dental extraction performed. He improved thereafter on 2,000 u Continue reading >>
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 (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 >>
Ketones & Insulin Pumps
Check for ketones if you have the following: There is a higher risk for developing ketones on pump therapy. This is because long-acting insulins are not used, and rapid-acting insulin is delivered in extremely small amounts. If this basal insulin delivery is interrupted for more than an hour, check your blood sugar and ketones. If you continue to not get insulin, blood glucose and ketone levels may increase into a dangerous range. See also Acute: Diabetic ketoacidosis (DKA). Insulin pump-related ketone buildup may be caused by: Site problem Air in tubing (resulting in missed insulin) Extended pump suspension or disconnection (for more than one to two hours) Pump malfunction Insulin leakage (at insertion site or infusion set connection site) Illness or infection Vomiting or dehydration Severe emotional stress “Spoiled” insulin Ketones checklist The presence of ketones while using an insulin pump can indicate a serious medical emergency. Check for ketones if you have: An unexplained elevation in your blood sugar Persistently elevated blood sugars Symptoms of nausea or vomiting This is because you want to be sure you are not developing diabetic ketoacidosis. Remember that ketoacidosis occurs more commonly in pump users. Here’s what you should do. Use the mnemonic KISS. K – Check for Ketones I – Give Insulin by Injection (using an insulin pen or syringe – not through the pump) S – Change the infusion Set S – Check blood Sugar If ketones are positive, you need to obtain emergency medical care. Treating ketones If you have elevated ketones, insulin replacement must be delivered via an injection with an insulin pen or insulin syringe instead of the pump because the pump or infusion set may be malfunctioning and causing ketones to develop. Remember! Ketoacidosis Continue reading >>
How Dka Happens And What To Do About It
Certified Diabetes Educator Gary Scheiner offers an overview of diabetic ketoacidosis. (excerpted from Think Like A Pancreas: A Practical Guide to Managing Diabetes With Insulin by Gary Scheiner MS, CDE, DaCapo Press, 2011) Diabetic Ketoacidosis (DKA) is a condition in which the blood becomes highly acidic as a result of dehydration and excessive ketone (acid) production. When bodily fluids become acidic, some of the body’s systems stop functioning properly. It is a serious condition that will make you violently ill and it can kill you. The primary cause of DKA is a lack of working insulin in the body. Most of the body’s cells burn primarily sugar (glucose) for energy. Many cells also burn fat, but in much smaller amounts. Glucose happens to be a very “clean” form of energy—there are virtually no waste products left over when you burn it up. Fat, on the other hand, is a “dirty” source of energy. When fat is burned, there are waste products produced. These waste products are called “ketones.” Ketones are acid molecules that can pollute the bloodstream and affect the body’s delicate pH balance if produced in large quantities. Luckily, we don’t tend to burn huge amounts of fat at one time, and the ketones that are produced can be broken down during the process of glucose metabolism. Glucose and ketones can “jump into the fire” together. It is important to have an ample supply of glucose in the body’s cells. That requires two things: sugar (glucose) in the bloodstream, and insulin to shuttle the sugar into the cells. A number of things would start to go wrong if you have no insulin in the bloodstream: Without insulin, glucose cannot get into the body’s cells. As a result, the cells begin burning large amounts of fat for energy. This, of course, Continue reading >>
> 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 >>
Case Report Severe Allergic Reaction To Human Insulin In The Patient With Diabetic Ketoacidosis
1. Introduction Diabetic ketoacidosis (DKA) is a potentially fatal crisis of diabetes mellitus (DM). In the treatment of DKA, fluid resuscitation, insulin therapy, and electrolyte replacement are important. Rarely, insulin allergies can be developed in the patient treated with insulin. The most common symptoms of insulin allergies are localized and limited. Life-threatening allergic reactions are rarely reported. Insulin allergies can be managed safely and successfully by desensitization treatment.1,2 We present treatment of a patient with DKA who developed an insulin allergy. In this case report, we aimed to discuss DKA treatment options in patient with insulin allergies. 2. Case report A 45-year-old male was brought to our emergency department with chest pain and hyperglycemia. He had a history of type 2 DM and had been using an oral antidiabetic drug for two years, but he had been stopped using for a month. HIs past medical history did not show any drug allergies. His vitals were measured: 1.) blood pressure of 166/98 mmHg; 2.) pulse 100/min; 3.) respiration number 24/min; 4.) O2 saturation 98%; and 5.) temperature 36.0 °C. His electrocardiograms (ECG's) were normal. His blood glucose level was 405 mg/dL, urinary ketones 15 mmol/L, pH was 6.8, HCO3 4.7 mmol/L, and lactate 3.6 mmol/L. Regular insulin (0.1unit/kg IV bolus) was initiated in addition to 2000 mL of intravenous saline, and a 0.1 unit/kg/hour infusion was started. He developed a generalized skin rash, hoarseness, and uvular edema at the 30th minute of treatment, which then expanded to the soft palate. The vital findings were normal except for the presence of tachycardia. At that moment his vitals were measured: 1.) blood pressure 126/75 mmHg; 2.) pulse 104/min; 3.) respiration number 24/min; 4.) O2 saturat Continue reading >>
Diabetic Ketoacidosis: Should Current Management Include Subcutaneous Insulin Injections?
Rocio Gavidia Quezada MD, Hawa Edriss MD Corresponding author: Rocio Gavidia Contact Information: [email protected] DOI: 10.12746/swrccc.v5i19.389 ABSTRACT Diabetic ketoacidosis is a well-known acute complication in patients with both type 1 and type 2 diabetes mellitus. Although mortality has decreased considerably, it remains an important cause for admission to intensive care units. Medical management includes intravenous fluid therapy, insulin, correction of electrolyte abnormalities, and addressing the precipitating factor which in most cases is infection or non-compliance with insulin therapy. Usually patients with diabetic ketoacidosis are admitted to the intensive care unit for continuous infusion of insulin; however, the development of rapid acting insulin analogues has made it possible to treat mild to moderate diabetic ketoacidosis with subcutaneous insulin. Although studies using subcutaneous insulin include only a small number of patients, this approach seems as effective as intravenous insulin infusions in patients with mild to moderate diabetic ketoacidosis. Diabetic education and close follow-up for patients admitted for diabetic ketoacidosis remain essential to avoid recurrence and readmissions. Keywords: Diabetic ketoacidosis, acute complication in diabetes, rapid acting insulin analogues, subcutaneous insulin in diabetic ketoacidosis INTRODUCTION Diabetic ketoacidosis (DKA) is a well-known acute complication in patients with both type 1 and type 2 diabetes. This condition results from a relative or absolute insulin deficiency combined with counter-regulatory hormone excess: glucagon, catecholamines, cortisol, and growth hormone.1 Diabetic ketoacidosis can be life threatening, but mortality rates have fallen since 1980, according to the National Continue reading >>
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
- Do Simvastatin Side Effects Include Diabetes and Joint Pain?
- CMS Urged to Include mHealth in Diabetes Prevention Program
Is There Any Benefit To An Initial Insulin Bolus In Diabetic Ketoacidosis?
Diabetic ketoacidosis (DKA) is a common endocrine emergency encountered in the emergency department. DKA associated mortality is relatively low in adults, but in children with type 1 diabetes, the elderly, and adults with concomitant illnesses have a mortality rate is > 5% (19564476). Guidelines for the management of hyperglycemic crisis in adults provide recommendations for intravenous fluid administration, correction of electrolyte abnormalities, insulin and bicarbonate therapy. While the recommendations made in the American Diabetes Association (ADA) consensus statement are intended to be evidence based, there are two recommendations which have less than optimal supporting evidence which results in controversy in the emergency department: 1. Use of regular insulin boluses of 0.1 units/kg and 2. patients with a pH < 6.9 should receive sodium bicarbonate therapy. Today we will attempt to answer the question, is there any benefit to an initial insulin bolus in DKA? Is there a benefit to an initial insulin bolus in diabetic ketoacidosis? Many prospective randomized trials have laid bare the use of low-dose insulin infusion leading to the successful recovery of patients with DKA. However, the data supporting an initial insulin bolus prior to the initiation of insulin infusions is not nearly as robust. The rationale for such a bolus is to overcome the relative insulin deficiency seen in DKA in order to suppress lypolysis and hepatic gluconeogenesis and limit further acidosis (more on that next time). However, insulin boluses may lead to harm including hypoglycemia, hypokalemia, and if glucose levels are too rapidly corrected, cerebral edema (18514472). Since the publication of the ADA consensus statement, two investigations have attempted to answer the question of what aff Continue reading >>
Extreme Insulin Resistance In A Patient With Diabetes Ketoacidosis And Acute Myocardial Infarction
Case Reports in Endocrinology Volume 2013 (2013), Article ID 520904, 7 pages 1Division of Endocrinology, SUNY Downstate Medical Center, Brooklyn, NY 11203, USA 2Division of Endocrinology, Maimonides Medical Center, Brooklyn, NY 11219, USA Academic Editors: O. Isozaki, W. V. Moore, and R. Murray Copyright © 2013 Yin H. Oo et al. 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 Hyperglycemia is common in hospitalized patients and associated with adverse clinical outcomes. In hospitalized patients, multiple factors contribute to hyperglycemia, such as underlying medical conditions, pathophysiological stress, and medications. The development of transient insulin resistance is a known cause of hyperglycemia in both diabetic and nondiabetic patients. Though physicians are familiar with common diseases that are known to be associated with insulin resistance, the majority of us rarely come across a case of extreme insulin resistance. Here, we report a case of prolonged course of extreme insulin resistance in a patient admitted with diabetic ketoacidosis (DKA) and acute myocardial infarction (MI). The main purpose of this paper is to review the literature to identify the underlying mechanisms of extreme insulin resistance in a patient with DKA and MI. We will also briefly discuss the different clinical conditions that are associated with insulin resistance and a general approach to a patient with severe insulin resistance. 1. Introduction In hospitalized patients, the development of transient insulin resistance related to different medical conditions such as acute myocardial infarction (MI), sepsis, and Continue reading >>
What Are The Short-term Consequences Of Not Controlling Type 1 Diabetes?
Death. Well, that depends on just how poorly controlled you're talking, but if you mean not treating at all, then you can progress through some serious consequences ending in death over the course of a day or so. Unlike the more common Type 2 Diabetes Mellitus, people with Diabetes mellitus type 1 do not produce insulin on their own, and need an external source of insulin to survive. That is because cells cannot take in sugar from the bloodstream to fuel themselves without insulin, so once the sugar in there is used up the cells have to start breaking down fatty acids to stay alive, but that produces ketones, which are toxic. At the same time, all the sugar that's stuck, unusable, in the bloodstream interferes with kidney function, causing dehydration. Its a combination that leads to Diabetic ketoacidosis, which can kill a person within 24 hours of their first symptoms. Ok, so now lets consider a person who is still taking some insulin, but not really paying attention to their blood sugar. It is still possible for them to undertreat themselves, which can potentially still lead to diabetic ketoacidosis. Or, they can overtreat themselves, causing hypoglycaemia, which if only slight might just make them a little woozy, but if severe can lead to unconsciousness and death if they are not found and treated. Easing up a little more, we can imagine a person who's a bit more careful. They still take their insulin, they check their blood sugars relatively often, but they can be a little forgetful about just how many helpings of dessert they had. Their sugars will run high, but there should be enough getting into the cells to prevent DKA. Most of the consequences of that are going to be long-term, like peripheral vascular disease, kidney damage and retinopathy. In the short term, Continue reading >>