Hypokalemia (Low Potassium) - Managing Side Effects - Chemocare
There was also no correlation between glucose disposal rate and potassium (R2 Basal insulin maintains fasting plasma [K+] within the normal range (11). Normal levels of potassium are important for the maintenance of heart, and or insulin excess, especially if diabetic, can cause a shift of potassium into cells. Many factors may contribute to the onset of type 2 diabetes. This includes low potassium levels. Find out why this is and what you can do to.
When there is a breakdown or destruction of cells, the electrolyte potassium moves from inside of the cell to outside of the cell wall. This shift of potassium into the cells causes hypokalemia. Trauma or insulin excess, especially if diabetic, can cause a shift of potassium into cells hypokalemia. Potassium is excreted or "flushed out" of your system by your kidneys.
Certain drugs or conditions may cause your kidneys to excrete excess potassium. This is the most common cause of hypokalemia. Other causes of hypokalemia include: Increased excretion or loss of potassium from your body. Some medications may cause potassium loss which can lead to hypokalemia. Common medications include loop diuretics such as Furosemide.
Other drugs include steroids, licorice, sometimes aspirin, and certain antibiotics. Your kidneys will excrete too much potassium. You may have hypokalemia from a loss of body fluids due to excessive vomiting, diarrhea, or sweating.
Endocrine or hormonal problems such as increased aldosterone levels - aldosterone is a hormone that regulates potassium levels. Certain diseases of the endocrine system, such as Aldosteronism, or Cushing's syndrome, may cause potassium loss. However, some concerns have been raised regarding this approach. Endogenous insulin secretion may be unpredictable, especially in the acutely ill and in those with insulin deficiency [ 836 ]. The resultant hyperglycemia raises the plasma osmolality, which leads to movement of potassium out of the cell, worsening hyperkalemia.
Conversely, some have suggested the use of insulin alone in the setting of hyperglycemia, but this is not widely accepted or practiced due to the high likelihood of inducing hypoglycemia [ 718 ]. This is an important point since patients without DM are at risk for lack of monitoring of their blood glucose levels. Hospital staff are trained to monitor blood glucose in patients with DM and the absence of this diagnosis makes the patient more vulnerable. Also, patients without DM have greater insulin sensitivity and are more prone to develop hypoglycemia after insulin administration.
The protocol proposed by Apel et al in this study for glucose monitoring and dextrose support in the treatment of hyperkalemia with IV insulin is designed to prevent hypoglycemia. We agree that the risk of hypoglycemia can be minimized by increasing the dextrose dose. However, this recommendation has not been validated in clinical studies.
Potassium as a link between insulin and the renin-angiotensin-aldosterone system.
At our center, the patient's body weight is taken into account before insulin and dextrose are administered. The protocol at our center is to administer 25 g of dextrose with IV insulin 0. This regimen is followed by mL of D10W infused over 2 hours.
The use of a weight based insulin regimen reduces the risk of hypoglycemia in individuals with low body mass index, especially the elderly. Limited data have suggested that the administration of dextrose before insulin is effective and safe [ 37 ]. At our center, dextrose is given immediately prior to IV insulin. Blood glucose levels are obtained at baseline, 1, 2 and 3 hours post treatment.
As stated previously, beta-agonists, such as inhaled albuterol, have additive potassium-lowering effect due to a different mechanism of action. Beta-agonists, when used with insulin, may have the additional benefit of reducing the risk of hypoglycemia since they promote gluconeogenesis in the liver [ 1438 ].
In conclusion, ESRD patients are at high risk of developing severe, life-threatening hyperkalemia. When dialysis is not immediately available, non-dialytic therapies are used as temporizing measures. Treatment with insulin is effective, but can be associated with severe hypoglycemia if appropriate therapeutic guidelines are not implemented and practiced.
Education of physicians and nursing personnel, and adherence to an institution-specific treatment algorithm for hyperkalemia are extremely important in preventing this critical iatrogenic complication.
Nebulized albuterol for acute hyperkalemia in patients on hemodialysis. Temporal profile of serum potassium concentration in nondiabetic and diabetic outpatients on chronic dialysis. Total body electrolyte composition and distribution of body water in uremia.
Ahmed J, Weisberg LS. Hyperkalemia in dialysis patients. Hyperkalemia in end-stage renal disease: J Am Soc Nephrol. Effect of single dose resin-cathartic therapy on serum potassium concentration in patients with end-stage renal disease.
Effect of prolonged bicarbonate administration on plasma potassium in terminal renal failure. Effect of hypertonic versus isotonic sodium bicarbonate on plasma potassium concentration in patients with end-stage renal disease. Hypokalemic effects of intravenous infusion or nebulization of salbutamol in patients with chronic renal failure: Am J Kidney Dis.
Intravenous infusion or nebulization of salbutamol for treatment of hyperkalemia in patients with chronic renal failure. Allon M, Copkney C.
Potassium as a link between insulin and the renin-angiotensin-aldosterone system.
Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. A critically swift response: Clin J Am Soc Nephrol.
Effect of graded doses of insulin on splanchnic and peripheral potassium metabolism in man. Non-dialytic treatment of acute hyperkalemia in the dialysis patient. Binding of insulin to receptors on such cells leads rapidly to fusion of those vesicles with the plasma membrane and insertion of the glucose transporters, thereby giving the cell an ability to efficiently take up glucose. When blood levels of insulin decrease and insulin receptors are no longer occupied, the glucose transporters are recycled back into the cytoplasm.
- What Is the Connection Between Diabetes and Potassium?
- Hypokalemia (Low Potassium)
- On the relationship between potassium and acid-base balance
It should be noted here that there are some tissues that do not require insulin for efficient uptake of glucose: This is because these cells don't use GLUT4 for importing glucose, but rather, another transporter that is not insulin-dependent. Insulin stimulates the liver to store glucose in the form of glycogen. A large fraction of glucose absorbed from the small intestine is immediately taken up by hepatocytes, which convert it into the storage polymer glycogen.
Insulin has several effects in liver which stimulate glycogen synthesis.
First, it activates the enzyme hexokinase, which phosphorylates glucose, trapping it within the cell. Coincidently, insulin acts to inhibit the activity of glucosephosphatase. Insulin also activates several of the enzymes that are directly involved in glycogen synthesis, including phosphofructokinase and glycogen synthase. The net effect is clear: A well-known effect of insulin is to decrease the concentration of glucose in blood, which should make sense considering the mechanisms described above.
Another important consideration is that, as blood glucose concentrations fall, insulin secretion ceases. In the absense of insulin, a bulk of the cells in the body become unable to take up glucose, and begin a switch to using alternative fuels like fatty acids for energy.
Neurons, however, require a constant supply of glucose, which in the short term, is provided from glycogen reserves. When insulin levels in blood fall, glycogen synthesis in the liver diminishes and enzymes responsible for breakdown of glycogen become active.
Glycogen breakdown is stimulated not only by the absense of insulin but by the presence of glucagonwhich is secreted when blood glucose levels fall below the normal range. Insulin and Lipid Metabolism The metabolic pathways for utilization of fats and carbohydrates are deeply and intricately intertwined.
Considering insulin's profound effects on carbohydrate metabolism, it stands to reason that insulin also has important effects on lipid metabolism, including the following: Insulin promotes synthesis of fatty acids in the liver.
As discussed above, insulin is stimulatory to synthesis of glycogen in the liver.
Insulin for the treatment of hyperkalemia: a double-edged sword?
When the liver is saturated with glycogen, any additional glucose taken up by hepatocytes is shunted into pathways leading to synthesis of fatty acids, which are exported from the liver as lipoproteins. The lipoproteins are ripped apart in the circulation, providing free fatty acids for use in other tissues, including adipocytes, which use them to synthesize triglyceride.
Insulin inhibits breakdown of fat in adipose tissue by inhibiting the intracellular lipase that hydrolyzes triglycerides to release fatty acids. Insulin facilitates entry of glucose into adipocytes, and within those cells, glucose can be used to synthesize glycerol.