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How Much Insulin For Hyperkalemia

Hyperkalemia

Hyperkalemia

Definition Physiologic antagonists: 500 mg calcium chloride, or 1 gm calcium gluconate is enough to temporarily stabilize the heart from the effects of hyperkalemia Shift K+ from plasma back into the cell: intravenous glucose (25 to 50 g dextrose, or 1-2 amps D50) plus 5-10 U regular insulin will reduce serum potassium levels within 10 to 20 minutes, and the effects last 4 to 6 hours, hyperventilation, β-agonists. In the past, bicarbonate (1 mEq/kg, or 1-2 amps in a typical adult) was recommended, however keep in mind that bicarbonate rarely helps, and furthermore binds Ca++, which may be counterproductive. Note that in the setting of liver tranplantation, prophylactic insulin and glucose has been suggested. Increase renal excretion: diuretics (furosemide, 20-40 mg IV), resin exchange, dialysis, aldosterone agonists (fludrocortisone) Acute Hyperkalemia Treatment Membrane Stabilization: CaCl2 K+ Shift: glucose/insulin, induce alkalosis (bicarbonate, hyperventilation), β-agonists K+ Excretion: furosemide, resins, fludrocortisone, dialysis Causes of acute hyperkalemia: drugs (succinylcholine, ACE/ARB’s, mannitol, spironolactone, digitalis, non-selective beta blockers) that cause decreased renal K+ excretion, reperfusion of an organ/vascular bed after ischemia (usually greater than 4 hours), adrenal inhibition or decreased aldosterone levels, transcellular shifts (intracellular to extracellular), often caused by acidosis, acute renal failure Symptoms: mild elevation (6-7 mEq/L) can cause peaked T-waves on EKG tracing, 10-12 mEq/L can cause prolonged PR interval, widened QRS, VFib, Asystole. Clinical symptoms are muscle weakness and paralysis. Subspecialty Keyword history See Also: Sources PubMed M Allon, A Takeshian, N Shanklin Effect of insulin-plus-glucose infusion wi 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 >>

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 >>

Insulin And Potassium

Insulin And Potassium

Insulin has a number of actions on the body besides lowering your blood glucose levels. Insulin suppresses the breakdown and buildup of glycogen, which is the storage form of glucose, it blocks fat metabolism and the release of fatty acids, and it puts potassium into the cells by activating the sodium-potassium cellular channels. Insulin stimulates the uptake of glucose and potassium in all cells of the body but primarily fuels the muscle cells as well as some of the fat cells. In type 2 diabetes or metabolic syndrome (a form of metabolic disease), insulin is not functioning up to its normal level. The cells of the body become resistant to insulin and the blood sugar levels are elevated. The serum potassium (K+) level is a reflection of the total body stores of potassium, although it can be inaccurate in some conditions that affect the distribution of potassium in the body’s cells. The plasma potassium level determines the resting potential of the cells of the body. A person can have low potassium (hypokalemia) or high potassium (hyperkalemia), both of which are asymptomatic conditions that can be serious as they both cause heart arrhythmias. The Relationship between Insulin and Potassium Shortly after insulin was discovered, scientists revealed that insulin had something to do with the potassium levels in both the cells and in the blood. The insulin is the hormone in the body that keeps the potassium level in the blood within the normal range. When insulin is decreased, the potassium level rises and can rise even further if you eat something high in potassium, such as salt substitutes and bananas. When the potassium level is high, it causes the pancreas to release insulin in order to counteract the effects of high potassium levels. When you eat something that is high Continue reading >>

Microsoft Word - Urgent Reduction In Hyperkalaemia.doc

Microsoft Word - Urgent Reduction In Hyperkalaemia.doc

The following guideline is approved only for use at University College London Hospitals NHS Foundation Trust. It is provided as supporting information for the UCLH Injectable Medicines Administration Guide. Neither UCLH nor Wiley accept liability for errors or omissions within the guideline. Wherever possible, users of the Guide should refer to locally produced practice guidelines. UCLH’s guidelines represent the expert opinion of the clinicians within the hospital and may not be applicable to patients outside the Trust. Guideline for the urgent reduction in hyperkalaemia (K+ > 6.5 mmol/L) in adults Adapted from the Renal Emergencies chapter of UCLH Guidelines for the management of common medical emergencies and for the use of antimicrobial drugs Hyperkalaemia requires immediate action with the following measures: 1. Stop potassium supplements and/or potassium sparing diuretics. Consider other medications that may conserve potassium, eg. ACE inhibitors, salt substitutes and non-steroidal anti-inflammatory drugs. Restrict dietary administration of products high in potassium, eg. fruit juice, fresh fruit, and vegetables. 2. Perform a baseline blood glucose measurement on the ward. Add 10 units of neutral soluble insulin (Human Actrapid) to 50ml of glucose 50% and infuse over 15 minutes, preferably via a large vein (monitoring for signs of thrombophlebitis). This should lower plasma K + after 30 minutes by approximately 1 mmol/L, for approximately 2 hours. Continue 50% glucose at a rate of 50ml/hr for one hour via large vein, unless glucose >10mmol/L (NB. Very irritant; alternatives are 10% glucose 250ml or 5% glucose 500ml over 1 hour, depending on fluid status). Monitor blood glucose every thirty minutes for 2 hours. Re-check K+ levels, 2 hours after insulin and g 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 >>

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 >>

Hyperkalemia In Emergency Medicine

Hyperkalemia In Emergency Medicine

Practice Essentials Hyperkalemia can be difficult to diagnose clinically because symptoms may be vague or absent. The fact, however, that hyperkalemia can lead to sudden death from cardiac arrhythmias requires that physicians be quick to consider hyperkalemia in patients who are at risk for it. See the electrocardiogram below. See also Can't-Miss ECG Findings, Life-Threatening Conditions: Slideshow, a Critical Images slideshow, to help recognize the conditions shown in various tracings. Signs and symptoms Patients with hyperkalemia may be asymptomatic, or they may report the following symptoms (cardiac and neurologic symptoms predominate): Evaluation of vital signs is essential for determining the patient’s hemodynamic stability and the presence of cardiac arrhythmias related to hyperkalemia. [1] Additional important components of the physical exam may include the following: Signs of renal failure, such as edema, skin changes, and dialysis sites, may be present Signs of trauma may indicate that the patient has rhabdomyolysis, which is one cause of hyperkalemia See Clinical Presentation for more detail. Diagnosis Laboratory studies The following lab studies can be used in the diagnosis of hyperkalemia: Potassium level: The relationship between serum potassium level and symptoms is not consistent; for example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients; the rapidity of change in the potassium level influences the symptoms observed at various potassium levels Calcium level: If the patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances) Urinalysis: To look for evidence of glomerulonephritis if signs of renal insufficiency without a known cause are present Cortisol a 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

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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

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