Emdocs Cases: Updates In Management Of Hyperkalemia
Authors: Brit Long, MD and Justin R. Warix, DO, FAAEM // Edited by: Alex Koyfman, MD Welcome back to emDocs Cases! Today we have case-based discussion on a core EM topic, with a look at some controversy and cutting edge treatments. A 62-year-old female with history of renal disease on dialysis, hypertension, and CAD presents with nausea and weakness. She missed todays dialysis session. Her VS are normal, and her exam is also normal. Whats your first test you obtain? The ECG! You see large, peaked T waves with absence of P waves. The VBG returns with potassium of 7.3 mmol/L, with sodium 140 mmol/L and normal lactate. You ask for your standard hyperkalemia regimen, or C BIG K DROP see more from This regimen classically consists of Calcium , Beta agonist and/or Bicarbonate , Insulin , Kayexalate , Diuretics , and Renal unit for dialysis Of Patient. Whats the literature behind this regimen? Is there anything better? Before we start, lets cover some basics. Most potassium is intracellular , with 75% found in skeletal muscle. A significant gradient between the intracellular and extracellular environment plays a vital role in generation of cellular action potentials.1-5 The renal system plays the most important role in regulation of potassium . Normal levels are 3.5-5.0 mEq/L or mmol/L.1,2 Changes iContinue reading > >
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What Causes High Potassium Levels
High blood potassium, called hyperkalemia, may be caused by kidney disease, excessive dietary potassium intake, uncontrolled diabetes, dehydration, or severe blood loss.
When blood serum potassium levels are higher than 5.2 mmol/L, this is called hyperkalemia. Hyperkalemia can lead to muscle cramps, serious heart problems, and paralysis.
Using an ACE inhibitor also puts a person at a higher risk of developing hyperkalemia.
Hyperkalemia Is The Great Ecg Imitator
These ECG findings are not specific to hyperkalemia alone. Given the broad differential for these ECG changes, hyperkalemia has been dubbed the Great ECG Imitator. It is important to consider the patients presentation, clinical complaints and trends on the ECG.
PEARL: Hyperkalemia has been known to cause almost any dysrhythmia. Pay special attention to patients in slow VT and wide-complex bradycardia and consider treating them empirically as hyperkalemia.
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What Medications Are Used To Treat Hyperkalemia
Drugs used in the treatment of hyperkalemia include the following:
- Calcium : Reduces the risk of ventricular fibrillation caused by hyperkalemia.
- Insulin administered with glucose: Facilitates the uptake of glucose into the cell, which results in an intracellular shift of potassium.
Furthermore, how do you treat hyperkalemia?
Similarly one may ask, what are the drugs that reduce potassium?
- Diuretics. Diuretics like furosemide, bumetanide, hydrochlorothiazide, and chlorthalidone are the main medication-related cause of low potassium levels.
- Risperdal and Seroquel.
What potassium level necessitates urgent treatment for hyperkalemia?
A Hyperkalemia Emergency, which we define as a serum potassium> 6.0 meq/L or a sudden increase in serum potassium 1.0 meq/L above 4.5 meq/L within 24 hours associated with cardiopulmonary arrest, evolving critical illness, AMI, or signs and symptoms of neuromuscular weakness, should be treated with agents that
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Risk Factors For Hypoglycemia
The results of the logistic regression analysis are shown in Table . In the univariable analysis, the identified risk factors for hypoglycemia were BMI, diabetes, eGFR< 60 ml/min/1.73 m2, insulin treatment, pre-treatment glucose, and location of treatment in ED. In the selection of the variables for multivariable analysis, there was weak evidence of multicollinearity between diabetes status and insulin treatment . These variables were moderately correlated and insulin treatment was not independently associated with hypoglycemia when diabetes status was included in the multivariable model. Similarly, the use of oral hypoglycemic agents was not significant after accounting for diabetes . No significant statistical interaction was noted in the final multivariable model. The c-statistic of the multivariable model was 0.76. The model calibration was satisfactory , as seen in the calibration plot .
Table 3 Logistic regression analysis.Figure 2
Calibration plot of multi-variable logistic regression model. Model diagnostics to determine how well the model fits the data. Perfect alignment along the dotted line indicates perfect correlation between predicted and observed outcomes.
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Medications In The Emergency Management Of Hyperkalemia
There are specific treatments geared at targeting each of these three main principles, which we will discuss below. Unfortunately, there is no clear evidence to guide exactly when to initiate specific treatments for hyperkalemia. Our experts recommend using two factors to guide your management:
with the following indications for immediate treatment of hyperkalemia in the ED:
Principle 1: Stabilize the cardiac membrane
There is no good literature to help guide whether calcium gluconate or calcium chloride is better for stabilizing the cardiac membrane in hyperkalemia. The most important difference to remember is that calcium chloride has 3 times more elemental calcium than calcium gluconate and has greater bioavailability. However, calcium gluconate has less risk of local tissue necrosis at the IV site. Therefore, if you decide to give calcium gluconate, ensure you are giving sufficient doses of calcium since one amp may not be enough. Three amps of calcium gluconate are often required to start to see the ECG changes of hyperkalemia resolve. Remember that calcium does not lower the potassium level.
Our experts recommend using calcium chloride through a large well-flowing peripheral IV or central line in the arrest or peri-arrest patient. Calcium gluconate is recommended for all other patients given its lower risk for local tissue necrosis.
Monitor glucose q30 minutes
How Does Insulin Work
Insulin is a hormone created by the pancreas. It allows your body to use glucose to provide the bodys cells with the necessary energy they need. Insulin production from the pancreas is based off of your blood sugar levels. If you are getting hyperglycemic, the pancreas is signaled and insulin is released into the bloodstream. Insulin then signals different cells to absorb the glucose and use it as energy or store it for later use.
When insulin facilitates glucose being pulled into a cell, a potassium cation is also pulled from extracellular fluid into the intracellular fluid. How does this affect our patients? Initially, patients in DKA have an increased extracellular potassium level due to the hyperglycemia and acidosis they are experiencing. This potassium level is quickly decreased as blood glucose is pulled into the cells.
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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.
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Association Between Hyperkalemia And Outcomes
The potassium ion is the most abundant cation in the body. There is an estimated total reserve of 30004000 mmol in adults, of which only 60 mmol are extracellular . Hyperkalemia is associated with poor outcomes in many different settings: in the general population , in patients with cardiac and renal disease and in critically ill patients . In a retrospective study of hospitalized patients, Khanagavi et al. found that acute kidney injury and prolonged hyperkalemia are independent predictors of in-hospital mortality. In acute myocardial infarction, a serum potassium above 4.5 mmol/L is associated with a higher mortality . More recently, Legrand et al. identified that a serum potassium> 4.5 mmol/L in heart failure patients admitted to the emergency department is associated with an increased risk of death.
The net effect is a U-shaped mortality curve associated with potassium abnormalities . Several observational studies have identified hypokalemia as an independent risk factor for poor outcome . This association raises concern regarding the potential for overcorrection, as may occur with some fast-acting potassium-lowering agents. However, these associations do not mean causality and thresholds for treating hyperkalemia remain debated.
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What Are Dosages Of Dextrose
Dosage Considerations Should be Given as Follows:
Acute Alcohol Intoxication
- 25-50 g administer with thiamine to prevent Wernickes encephalitis
- 10-25 g IV may require repeated boluses
- 400-600 mg of glucose/kg/hour needed for most insulin overdoses
- Alternatively, administer 25-50 g IV may repeat doses in severe cases determine glucose levels before injecting dose in emergencies, may administer promptly before obtaining glucose results
- 25-50 g plus 10 units regular insulin IV over 30-60 min
Insulin Induced Hypoglycemia
- Children under 6 months: 250-500 mg/kg/dose
- Children over 6 months: 0.5-1g/kg/dose
Hypoglycemia Following Intravenous Insulin Plus Glucose For Hyperkalemia In Patients With Impaired Renal Function
Affiliation Department of Nephrology, Hospital Clínico Universitario, Valladolid, Spain
Affiliation Department of Medicine, Dermatology and Toxicology, School of Medicine, University of Valladolid, Valladolid, Spain
Affiliations Department of Nephrology, Hospital Clínico Universitario, Valladolid, Spain, Department of Medicine, Dermatology and Toxicology, School of Medicine, University of Valladolid, Valladolid, Spain
Affiliation Department of Nephrology, RWTH University of Aachen, Aachen, Germany
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Epidemiology And Timing Of Hypoglycemia
We identified 177 episodes where an intravenous infusion of insulin and glucose was administered to treat hyperkalemia. One hundred sixty four episodes of hyperkalemia complied with the inclusion and exclusion criteria and were included in the final analysis . These episodes occurred in a total of 127 patients. All patients were Caucasians. Fifty-three of the 127 patients had diabetes. One hundred twenty-nine episodes occurred in patients with AKI while 35 episodes occurred in CKD patients. Twenty-three episodes occurred in patients with a preadmission eGFR 60 ml/min while 141 episodes occurred in patients with a preadmission eGFR < 60 ml/min. A single laboratory measurement of blood glucose and serum K+ was performed in 145 episodes , two measurements in 16 episodes and three measurements in 3 episodes . Follow-up of associated pathologies such as anemia or metabolic acidosis was the underlying cause of additional laboratory measurements. There were no significant differences in the number of laboratory measurements between patients with a blood glucose pretreatment level 120 mg/dl or lower than that value . The majority of patients experienced only a single episode of hyperkalemia . No patient who experienced more than one episode of hyperkalemia suffered multiple episodes of hypoglycemia.
Whats The Difference Between Type 1 Diabetes And Type 2 Diabetes
Type 1 diabetes is a genetic disorder that a person is born with and cannot prevent. Risk factors include having a family history of type 1 diabetes, exposure to viral illnesses, and having autoantibodies . Children and young adults are most commonly diagnosed with type 1 diabetes.
Type 2 diabetes is a disorder that develops over time and is primarily due to diet. This form of diabetes is preventable. Risk factors include living a sedentary lifestyle and being physically active fewer than three times a week, obesity, and having a family history of type 2 diabetes. Adults ages 45 and older are most commonly diagnosed with type 2 diabetes.
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Cautions With Iv Insulin
Hypoglycemia: One of the obvious labs that you must monitor very closely when administering IV insulin is the patients glucose. You would not want the patient to become hypoglycemic because too much insulin was administered. Patients may start getting sweaty, confused, feeling nauseous, begin shaking, or experiencing decreased level of consciousness when their blood sugar becomes too low.
Hypokalemia: A large cause of death in treatment of DKA patients is hypokalemia. There is an elevated serum potassium initially when patients are in a state of DKA. This quickly comes down as insulin is administered and the potassium shifts back into the cells. Hypokalemia can cause cardiac arrhythmias and death if left untreated.
Cerebral edema: Dropping a patients blood sugar too quickly can result in the development of cerebral edema. In a publication by Bohn & Daneman, they stated that the osmolar gradient caused by the high blood glucose results in water shift from the intracelluar fluid to the extracellular fluid space and contraction of cell volume. Correction with insulin and intravenous fluids can result in a rapid reduction in effective osmolarity, reversal of the fluid shift and the development of cerebral edema.
Other relevant articles include:
Insulin Dosing Evaluation In Hyperkalemia
Several studies have compared insulin dosing strategies in hyperkalemia.8-10,13,18 These studies compared patients receiving 10 units to lower doses, such as 5 units or 0.1 unit/kg, and assessed for potassium-lowering ability and incidence of hypoglycemia.8-10,13,18 Hypoglycemia was generally defined as blood glucose less than 70 mg/dL however, there were varying definitions of severe hypoglycemia and duration of monitoring for hypoglycemia after insulin administration.8-10,13,18
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Insulin For The Treatment Of Hyperkalemia: A Double
Keywords: CopyrightHypoglycemia in the treatment of hyperkalemia with insulin in patients with end-stage renal disease
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 .
The definition of hypoglycemia has been a topic of debate. The workgroup of the American Diabetes Association and the Endocrine Society defines iatrogenic hypoglycemia in patients with diabetes mellitus as all episodes of an abnormally low plasma glucose concentration that expose the individual to potential harm. A plasma glucose concentration of 70 mg/dL is recommended as the alert value even though symptoms of hypoglycemia usually develop at a level below this threshold . This value allows time for close monitoring of the patient to prevent symptomatic hypoglycemia and has been used to define hypoglycemia in numerous clinical trials.
Disclosures. None declared.
What About Using Dextrose Only
Theoretically, administering dextrose should stimulate insulin release and thereby lower serum potassium concentrations. Early reports recommend against this technique for 2 reasons.9
On the flip side, a randomized, crossover study was conducted in 10 chronic hemodialysis patients who were prone to hyperkalemia.10 Administration of 10 units of insulin with 100 mL of 50% glucose was compared with the administration of 100 mL of 50% glucose only. Infusion of a glucose-only bolus caused a clinically significant decrease in serum potassium by 0.5 mEq/L without any episodes of hypoglycemia. The insulin/glucose group saw a drop in potassium of 0.83 mEq/L at 60 minutes.
Bottom Line: Based on conflicting data, and considering that many patients have ESRD plus diabetes, this approach has potential but may not be ready for mainstream use. Also, hyperglycemia may be undesirable in some patients.
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Strategies For Avoiding Hypoglycemia
Preventing hypoglycemia is important. Some clinicians use up to 20 units of IV regular insulin as the hypokalemic effect is dose-dependent.8 Here is a suggested strategy for administering enough dextrose to counter the initial insulin bolus of 10 or 20 units. It is loosely based on the Rush University protocol.4 Other strategies include q30 minute glucose checks for the first 3 hours with as needed supplemental glucose orders or lower insulin doses.
|50 gm of D50* OR25 gm of D50 + D10 infusion 250 mL/hr for first hour||25 gm of D50 if blood glucose < 70 mg/dL||q 30 minutes for first hour, then hourly up to 3 hours|
|D50 = dextrose 50% D10 = dextrose 10%
* There are drawbacks to administering 100 mL of D50. Adam Spaulding, PharmD discusses D50 vs. D10 for severe hypoglycemia in the ED. 50 mL of D50 + infusion of D10 might prevent rebound hypoglycemia and hypertonicity issues with an initial 100 mL dose of D50.
** A supplemental D10 infusion may be needed beyond one hour depending on blood glucose concentrations.
When Do You Recheck Potassium After Hyperkalemia Treatment
After initial interventions, potassium should be rechecked within one to two hours, to ensure effectiveness of the intervention, following which the frequency of monitoring could be reduced. Subsequent monitoring depends on the potassium level and the potential reversibility of the underlying cause.
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Causes Of Hyperkalemia In Acutely Ill Patients
Factors associated with the development of hyperkalemia can be classified into three categories, and include altered renal clearance of potassium , release from the intracellular space and altered transfer to the intracellular space . Hyperkalemia in the patient with normal renal function is unusual and should prompt evaluation for pseudo-hyperkalemia if no ECG abnormalities consistent with hyperkalemia are identified . While concomitant medications are often a contributor to hyperkalemia, in our experience they are rarely the only cause in acute settings.
Table 1 Mechanisms contributing to the development of hyperkalemia
A special warning should be made with regards to the use of succinylcholine, classically used to induce paralysis in acutely ill patients for rapid sequence intubation. Succinylcholine induces skeletal muscle cell depolarization with an efflux of intracellular potassium by nicotinic receptor activation. In a population of critically ill patients, succinylcholine increased serum potassium on average 0.4 mmol/L . It should be avoided in patients with hyperkalemia and in patients with up-regulation of nicotinic receptors, as they are at risk of greater potassium elevation. This includes those with anatomical denervation, prolonged administration of neuromuscular blocking drugs, burn injury, and prolonged immobilization . Alternative to succinylcholine are available in patients at risk of hyperkalemia .