diabetestalk.net

How Much Insulin For Hyperkalemia

Updated Treatment Options In The Management Of Hyperkalemia

Updated Treatment Options In The Management Of Hyperkalemia

US Pharm. 2017;42(2):HS15-HS18. ABSTRACT: Hyperkalemia (elevated serum potassium) can become a life-threatening electrolyte abnormality due to medication use, kidney dysfunction, or alternative sources of electrolyte imbalance. Up until recently, FDA-approved therapies for the management of hyperkalemia (i.e., sodium polystyrene sulfonate) had remained unchanged for over 50 years. Other treatment options for hyperkalemia include IV calcium, insulin, sodium bicarbonate, albuterol, and diuretics. A new drug (patiromer) was recently approved for the treatment of hyperkalemia, and additional agents are also in development. Hyperkalemia is defined as a serum potassium concentration of >5.5 mEq/L in adults.1 It is a common metabolic disorder that can lead to clinical manifestations such as hemodynamic instability, neurologic sequelae, and fatal arrhythmias. Most individuals with hyperkalemia are usually asymptomatic or present with nonspecific signs and symptoms (e.g., weakness, fatigue, or gastrointestinal [GI] hypermotility). The incidence of hyperkalemia has been reported anywhere from 2.6% to 3.2% in the United States.2,3 A study in Canada showed the incidence to occur in 2.6% of emergency department visits and 3.5% of hospital admissions.4 Hyperkalemia is commonly a result of impaired urinary potassium excretion due to acute or chronic kidney disease (CKD), reduced aldosterone secretion, reduced response to aldosterone, reduced distal sodium and water delivery, effective arterial blood volume depletion, or selective impairment in potassium secretion. Hyperkalemia can also occur secondarily to metabolic acidosis, insulin deficiency, hyperglycemia, and hyperosmolar states. Medication can also lead to hyperkalemia, most notably those agents that inhibit the renin-angiotensi Continue reading >>

Clinical Research Treatment Of Hyperkalemia With A Low-dose Insulin Protocol Is Effective And Results In Reduced Hypoglycemia

Clinical Research Treatment Of Hyperkalemia With A Low-dose Insulin Protocol Is Effective And Results In Reduced Hypoglycemia

Complications associated with insulin treatment for hyperkalemia are serious and common. We hypothesize that, in chronic kidney disease (CKD) and end-stage renal disease (ESRD), giving 5 units instead of 10 units of i.v. regular insulin may reduce the risk of causing hypoglycemia when treating hyperkalemia. A retrospective quality improvement study on hyperkalemia management (K+ ≥ 6 mEq/l) from June 2013 through December 2013 was conducted at an urban emergency department center. Electronic medical records were reviewed, and data were extracted on presentation, management of hyperkalemia, incidence and timing of hypoglycemia, and whether treatment was ordered as a protocol through computerized physician order entry (CPOE). We evaluated whether an educational effort to encourage the use of a protocol through CPOE that suggests the use of 5 units might be beneficial for CKD/ESRD patients. A second audit of hyperkalemia management from July 2015 through January 2016 was conducted to assess the effects of intervention on hypoglycemia incidence. Treatments ordered using a protocol for hyperkalemia increased following the educational intervention (58 of 78 patients [74%] vs. 62 of 99 patients [62%]), and the number of CKD/ESRD patients prescribed 5 units of insulin as per protocol increased (30 of 32 patients [93%] vs. 32 of 43 [75%], P = .03). Associated with this, the incidence of hypoglycemia associated with insulin treatment was lower (7 of 63 patients [11%] vs. 22 of 76 patients [28%], P = .03), and there were no cases of severe hypoglycemia compared to the 3 cases before the intervention. Education on the use of a protocol for hyperkalemia resulted in a reduction in the number of patients with severe hypoglycemia associated with insulin treatment. Figure 2. Outline of Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Treatment And Prevention Of Hyperkalemia In Adults

Treatment And Prevention Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem that is most often a result of impaired urinary potassium excretion due to acute or chronic kidney disease (CKD) and/or disorders or drugs that inhibit the renin-angiotensin-aldosterone system (RAAS). Therapy for hyperkalemia due to potassium retention is ultimately aimed at inducing potassium loss [1,2]. In some cases, the primary problem is movement of potassium out of the cells, even though the total body potassium may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled hyperglycemia (eg, diabetic ketoacidosis or hyperosmolar hyperglycemic state). In these disorders, hyperosmolality and insulin deficiency are primarily responsible for the transcellular shift of potassium from the cells into the extracellular fluid, which can be reversed by the administration of fluids and insulin. Many of these patients have a significant deficit in whole body potassium and must be monitored carefully for the development of hypokalemia during therapy. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Potassium replacement'.) The treatment and prevention of hyperkalemia will be reviewed here. The causes, diagnosis, and clinical manifestations of hyperkalemia are discussed separately. (See "Causes and evaluation of hyperkalemia in adults" and "Clinical manifestations of hyperkalemia in adults".) DETERMINING THE URGENCY OF THERAPY The urgency of treatment of hyperkalemia varies with the presence or absence of the symptoms and signs associated with hyperkalemia, the severity of the potassium elevation, and the cause of hyperkalemia. Our approach to therapeutic urgency is as follows (algorithm 1): Continue reading >>

Hyperkalemia And Glucose / Insulin...

Hyperkalemia And Glucose / Insulin...

0 So, I'm a student. I graduate in a few weeks. I've heard that they give glucose for hyperkalemia. While researching this, I see that it is insulin and glucose that is given to push the potassium into the cells. So, I'm wondering what the mechanism is for this. Please don't respond based on assumption, I'd like to know the actual mechanism and not the assumed one. I'm thinking that glucose must be electronegative and thereby creates a complex with potassium and pulls it into the cells with it. I've only taken chemistry to organic II, but not biochemistry yet. Thanks for your informed responses! #2 2 Yup what he said.......Potassium levels are decreased by insulin. Hypokalemia suppresses insulin release leading to glucose intolerance. this was the best explanation of why it happens that I could find and seems to be tied to ATP activity: 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 liabel 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. #5 0 Quote from ImThatGuy that is correct, it is the insulin elevated serum k is cardiotoxic. insulin doe Continue reading >>

Hyperkalemia Management: Preventing Hypoglycemia From Insulin

Hyperkalemia Management: Preventing Hypoglycemia From Insulin

Insulin remains one of the cornerstones of early severe hyperkalemia management. Insulin works via a complex process to temporarily shift potassium intracellularly. Though insulin certainly lowers plasma potassium concentrations, we often underestimate the hypoglycemic potential of a 10 unit IV insulin dose in this setting. The purpose of this post is to highlight the need for proper supplemental glucose and blood glucose monitoring when treating hyperkalemia with insulin. Incidence of Hypoglycemia One of my favorite articles on the management of hyperkalemia was written by Dr. Weisberg in Critical Care Medicine.1 A 10 unit dose of IV regular insulin has an onset of action of about 5-10 minutes, peaks at 25-30 minutes, and lasts 2-3 hours (the Weisberg article actually lists subcutaneous kinetics). Herein lies the problem in that IV dextrose only lasts about an hour (at most). Allon et al reported up to 75% of hemodialysis patients with hyperkalemia developed hypoglycemia at 60 minutes after insulin administration.2 A retrospective review of 219 hyperkalemic patients reported an 8.7% incidence of hypoglycemia after insulin treatment.3 More than half of the hypoglycemic episodes occurred with the commonly used regimen of 10 units of IV insulin with 25 gm of dextrose. A more recent study of 221 end-stage renal disease patients who received insulin for treatment of hyperkalemia reported a 13% incidence of hypoglycemia.4 The overall incidence of hypoglycemia appears to be ~10%, but could be higher. Risk Factors for Developing Hypoglycemia The study by Apel et al identified three factors associated with a higher risk of developing hypoglycemia: No prior diagnosis of diabetes [odds ratio (OR) 2.3, 95% confidence interval (CI) 1.0–5.1, P = 0.05] No use of diabetes medication Continue reading >>

Why Give Glucose And Insulin For Hyperkalemia?

Why Give Glucose And Insulin For Hyperkalemia?

Hyperkalemia is a condition in which the levels of potassium in the bloodstream are abnormally high. There are many causes for hyperkalemia, mostly related to kidney disease because this organ helps control the levels of potassium in the body, and to hormonal causes. Administering glucose and insulin is one way to decrease the level of potassium in the bloodstream. Video of the Day Hyperkalemia usually results from acute or chronic kidney failure; from glomerulonephritis, in which the kidneys lose their ability to filter blood; and from rejection of a kidney transplant. According to Medline Plus, other causes include Addison’s disease, a condition in which the body fails to produce enough aldosterone, the hormone responsible for controlling the absorption of potassium from the kidneys; and from the use of diuretics, medicines used to regulate blood pressure by increasing the excretion of fluids and electrolytes in the urine. The symptoms of hyperkalemia may be mild at first, but severe hyperkalemia can cause arrhythmias, or dangerous abnormal heart rhythms, which can eventually cause the heart to stop beating. One of the reasons to give glucose and insulin to people with hyperkalemia is to decrease the chance of developing arrhythmias. Most potassium in the body resides inside the body’s cells, not in the bloodstream. Part of the treatment of hyperkalemia is driving potassium back into the cells. Insulin drives potassium into the cells by stimulating the uptake of the electrolyte by the cell membrane. This process begins within twenty to thirty minutes of the start of insulin treatment. Glucose is administered to facilitate this process and also to maintain glucose level in the bloodstream, as insulin can cause hypoglycemia, or low blood sugar. Other treatments for Continue reading >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

Physiology of Potassium Handling Potassium (K+) is the most abundant cation in the body. About 90% of total body potassium is intracellular and 10% is in extracellular fluid, of which less than 1% is composed of plasma. The ratio of intracellular to extracellular potassium determines neuromuscular and cardiovascular excitability, which is why serum potassium is normally regulated within a narrow range of 3.5 to 5.0 mmol/L. Dietary K+ intake is highly variable, ranging from as low as 40 mmol/day to more than 100 mmol/day.1, 2 Homeostasis is maintained by two systems. One regulates K+ excretion, or external balance through the kidneys and intestines, and the second regulates K+ shifts, or internal balance between intracellular and extracellular fluid compartments. Internal balance is mainly mediated by insulin and catecholamines. Cellular Shifts Ingested K+ is absorbed rapidly and enters the portal circulation, where it stimulates insulin secretion. Insulin increases Na+,K+-ATPase activity and facilitates potassium entry into cells, thereby averting hyperkalemia. β2-Adrenergic stimulation also promotes entry of K+ into cells through increased cyclic adenosine monophosphate (cAMP) activation of Na+,K+-ATPase. Renal Handling An increase in extracellular potassium concentration also stimulates aldosterone secretion (via angiotensin II), and aldosterone increases K+ excretion. In the steady state, K+ excretion matches intake, and approximately 90% is excreted by the kidneys and 10% in the stool. Renal K+ excretion is mediated by aldosterone and sodium (Na+) delivery (glomerular filtration rate [GFR]) in principal cells of the collecting ducts.3 K+ is freely filtered by the glomerulus, and almost all the filtered K+ is reabsorbed in the proximal tubule and loop of Henle (Fig. Continue reading >>

Hyperkalemia

Hyperkalemia

JOYCE C. HOLLANDER-RODRIGUEZ, M.D., and JAMES F. CALVERT, JR., M.D., Oregon Health & Science University, Portland, Oregon Am Fam Physician. 2006 Jan 15;73(2):283-290. Hyperkalemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors. Acute episodes of hyperkalemia commonly are triggered by the introduction of a medication affecting potassium homeostasis; illness or dehydration also can be triggers. In patients with diabetic nephropathy, hyperkalemia may be caused by the syndrome of hyporeninemic hypoaldosteronism. The presence of typical electrocardiographic changes or a rapid rise in serum potassium indicates that hyperkalemia is potentially life threatening. Urine potassium, creatinine, and osmolarity should be obtained as a first step in determining the cause of hyperkalemia, which directs long-term treatment. Intravenous calcium is effective in reversing electrocardiographic changes and reducing the risk of arrhythmias but does not lower serum potassium. Serum potassium levels can be lowered acutely by using intravenous insulin and glucose, nebulized beta2 agonists, or both. Sodium polystyrene therapy, sometimes with intravenous furosemide and saline, is then initiated to lower total body potassium levels. The prevalence of hyperkalemia in hospitalized patients is between 1 and 10 percent.1 Although the exact prevalence of hyperkalemia in community-based medical practice is unknown, potassium elevation is a common, potentially life-threatening problem most often occuring in patients with chronic renal failure or other illnesses that reduce renal potassium excretion (Table 12,3). In these patie Continue reading >>

Treating Hyperkalemia (high Blood Potassium) According To The New 2005 Cpr Guidelines

Treating Hyperkalemia (high Blood Potassium) According To The New 2005 Cpr Guidelines

Hyperkalemia is a common problem that can range in severity from inconsequential to life-threatening. The treatments for hyperkalemia also vary widely and can include simply restricting dietary potassium; administering oral, intravenous or inhaled medications; and providing emergent dialysis for more extreme elevations. Given a lack of standardization, it's not surprising that different doctors treat hyperkalemia in different ways. The new 2005 CPR guidelines from the American Heart Association provide recommendations for the treatment of hyperkalemia. Unfortunately, while these new guidelines are easy to follow, there are many potential problems, and I offer some criticisms. For mild elevations (5 - 6 mEq/L), in addition to dietary and medication changes, the guidelines recommend removal of potassium from the body with Furosemide 40 - 80 mg IV. In my opinion, especially for slight elevations, in most cases intravenous diuretics are unnecessary, and oral furosemide could be just as easily substituted. Kayexalate 15 to 30 g orally in sorbitol (or by enema). While kayexalate is an important treatment for hyperkalemia, in my opinion, giving kayexalate routinely for any potassium elevation over 5 is a bad practice. It is often unnecessary and physicians frequently overlook the cramping, diarrhea, and discomfort it causes patients. Rarely, kayexalate in powdered form (which doesn't cause diarrhea) or occasionally florinef can be given to outpatients. For moderate elevations (6 to 7 mEq/L), the guidelines recommend shifting potassium intracellularly. Previously, many algorithms suggested first obtaining an ECG to look for changes due to hyperkalemia -- "peaked" t-waves and new QRS widening -- and if either of these were present, the old algorithms recommended particularly agg Continue reading >>

Treating Hyperkalemia

Treating Hyperkalemia

#6 2 Also, insulin is NOT the transport to K into a cell! Insulin is the hormone that finds to a receptor to allow glucose (carbon, which is needed in glycolysis to make ATP) to enter the cell. The resultant ATP attaches to the NA/K pump which allows 3 sodium to exit the cell and 2 potassium to enter the cell. Please research just a tiny bit before posting opinions. This is what decreases your serum or extra cellular K. Also, glucose alone would draw potassium out of the cell, so giving d50 then the vein blowing will also harm your patient.... #7 1 Klamster, I'm not sure I follow your logic. Yes, that is the mechanism by which insulin reduces extracellular K, but you are forgetting that there is already glucose in the blood to facilitate that mechanism. Whether the body uses its own glucose or the glucose from the D50, the result on K is the same. However, if it uses up it's own glucose in the reaction, hypoglycemia will result as it won't be able to produce more glucose quickly enough. In a DKA patient with hyperkalemia, you wouldn't give D50, because the patient has more than enough blood glucose. You just need insulin to draw that glucose into the cell to power the Na-K pump. Continue reading >>

Hyperkalaemia

Hyperkalaemia

Case Study of Hyperkalemia: George is a 72 year old male found collapsed at home on floor of his bedroom, incontinent of urine and faeces. He complained of significant pain in his right hip with shortening and rotation. George’s family last had contact with George 3 days prior to his collapse. Assessment: On arrival at ED he is confused and combative with a GCS 0f 13 Initial observations reveal BP 78/60; Pulse 74, RR 32, SPO2 91% (NRB 15L) ABG which shows a Potassium of 9.0, pH of 7.23 and a Blood Glucose Level of 32mmol Medical History: CCF Hypertension Type 2 DM Osteoarthritis Medication History: George is taking enlapril for hypertension; spironolactone & metoprolol for his CCF and celebrex for his osteoarthritis His diabetes is diet controlled. An ECG is performed on his arrival to the resuscitation area… You briefly review the ECG and confidently state (already knowing the ABG result) that this patient has sever hyperkalemia. Brilliant…now what? The 5 C’s of Metabolic Disturbances I use the 5 C’s approach to recognise, understand and manage metabolic disturbances in the ED. Causes – Understanding normal metabolic homeostatic mechanisms helps define potential causative events that lead to disruption of the sensitive pathophysiological milieu. Increased production; increased intake and decreased excretion are often the commonest causal factors in metabolic disruption. Clinical manifestations – evaluate, recognise and diagnose the problem Complications – what can go wrong in the short, medium and long term can define clinical manifestation, duration of illness and potentially affect management decisions Calculations – Calculate to Obviate Corrective measures – Call to action…how do you actually fix the problem! Potassium Pathophysiology Serum pot Continue reading >>

Insulin For The Treatment Of Hyperkalemia: A Double-edged Sword?

Insulin For The Treatment Of Hyperkalemia: A Double-edged Sword?

Potassium plays a critical role in cellular metabolism and normal neuromuscular function. Tightly regulated homeostatic mechanisms have developed in the process of evolution to provide primary defense against the threats of hyper- and hypokalemia. The kidney plays a primary role in potassium balance, by increasing or decreasing the rate of potassium excretion. Distribution of potassium between the intracellular and the extracellular fluid compartments is regulated by physiologic factors such as insulin and catecholamines which stimulate the activity of the Na+-K+ ATPase. Only about 10% of the ingested potassium is excreted via the gut under normal physiologic conditions [1]. End stage renal disease (ESRD) patients rely largely on extra-renal mechanisms and dialysis to maintain potassium homeostasis. Despite the availability of dialysis and the adaptive increase in colonic excretion of potassium in renal insufficiency, severe hyperkalemia (defined as serum potassium level > 6 mEq/L [6 mmol/L]) is observed in 5-10% of maintenance dialysis patients and is responsible for 0.7% of deaths in the dialysis population in the United States [2–4]. Several factors can explain the high incidence of hyperkalemia in this population. Tolerance for a rapid potassium load is impaired in ESRD, not only because of lack of renal excretion, but also as a result of impaired cellular distribution of potassium [5]. The latter may result from defect in the Na+-K+ ATPase and possibly elevated glucagon levels in uremia [5, 6]. High dietary potassium intake and missed dialysis treatments are common contributors to hyperkalemia in ESRD patients. Other factors such as constipation (decreased colonic excretion) and fasting state (relative lack of insulin) may also predispose ESRD patients to hyperka Continue reading >>

Misadministration Of Iv Insulin Associated With Dose Measurement And Hyperkalemia Treatment

Misadministration Of Iv Insulin Associated With Dose Measurement And Hyperkalemia Treatment

Problem: We are aware of numerous reports of serious errors associated with the misadministration of insulin. These events have involved various types of practitioners, including physician house officers (HO), nurses, and a pharmacist. Human error (e.g., mental slips, lapses, forgetfulness) associated with insulin dose measurement and hyperkalemia treatment was the predominant proximate cause of these events; most of the human errors were associated with knowledge deficits regarding insulin concentration (specifically that “U-100” means the concentration is 100 units per mL), the differences between insulin syringes and other parenteral syringes, and a perceived urgency with treating hyperkalemia. In the most recent event, a physician ordered IV dextrose 50% injection (50 mL) along with 4 units of regular insulin IV (U-100) for a patient with renal failure and severe hyperkalemia. However, a nurse drew 4 mL (400 units) of insulin into a 10 mL syringe and administered the dose IV. The patient became severely hypoglycemic and had to be transferred to a critical care unit for treatment and monitoring. In another case, a nurse accidentally added 50 units of regular insulin to an existing IV infusion instead of 5 units. A physician had asked the nurse to add 5 units to the IV bag. The nurse felt the ½ inch insulin needle on an insulin syringe was not long enough to insert into the IV bag. Thus, the nurse drew the insulin into a 3 mL syringe with a longer needle. However, she accidentally withdrew 0.5 mL (50 units) of insulin instead of the correct volume of 0.05 mL (5 units). She quickly showed the prepared dose to another nurse, who also failed to pick up the error. Later, the nurse recognized her error while preparing a subcutaneous insulin dose for another patient us Continue reading >>

Optimal Dose And Method Of Administration Of Intravenous Insulin In The Management Of Emergency Hyperkalemia: A Systematic Review

Optimal Dose And Method Of Administration Of Intravenous Insulin In The Management Of Emergency Hyperkalemia: A Systematic Review

Abstract Background and Objectives Hyperkalemia is a common electrolyte disorder that can result in fatal cardiac arrhythmias. Despite the importance of insulin as a lifesaving intervention in the treatment of hyperkalemia in an emergency setting, there is no consensus on the dose or the method (bolus or infusion) of its administration. Our aim was to review data in the literature to determine the optimal dose and route of administration of insulin in the management of emergency hyperkalemia. Design, Setting, Participants, & Measurements We searched several databases from their date of inception through February 2015 for eligible articles published in any language. We included any study that reported on the use of insulin in the management of hyperkalemia. Results We identified eleven studies. In seven studies, 10 units of regular insulin was administered (bolus in five studies, infusion in two studies), in one study 12 units of regular insulin was infused over 30 minutes, and in three studies 20 units of regular insulin was infused over 60 minutes. The majority of included studies were biased. There was no statistically significant difference in mean decrease in serum potassium (K+) concentration at 60 minutes between studies in which insulin was administered as an infusion of 20 units over 60 minutes and studies in which 10 units of insulin was administered as a bolus (0.79±0.25 mmol/L versus 0.78±0.25 mmol/L, P = 0.98) or studies in which 10 units of insulin was administered as an infusion (0.79±0.25 mmol/L versus 0.39±0.09 mmol/L, P = 0.1). Almost one fifth of the study population experienced an episode of hypoglycemia. Conclusion The limited data available in the literature shows no statistically significant difference between the different regimens of insulin Continue reading >>

More in insulin