Author gratefully acknowledges Monash University for providing fully funded Ph. Diabetic ketoacidosis: risk factors and management strategies. Treat Endocrinol 2 2 — Savage MW, Kilvert A. ABCD guidelines for the management of hyperglycaemic emergencies in adults. Pract Diab Int 23 5 — Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association.
Diabetes Care 29 12 — Hormone-sensitive lipase: control of intracellular tri- di- acylglycerol and cholesteryl ester hydrolysis. J Lipid Res 43 10 — Profiles of diabetic ketoacidosis in multiethnic diabetic population of Malaysia.
Trop J Pharm Res 14 1 — Can J Diabetes 40 3 —9. Determinants of plasma potassium levels in diabetic ketoacidosis. Medicine Baltimore 65 3 — Plasma acid-base patterns in diabetic-ketoacidosis.
N Engl J Med 26 — Changes in plasma potassium concentration during acute acid-base disturbances. Am J Med 71 3 — Kes P. Hyperkalemia: a potentially lethal clinical condition. Acta Clin Croat — Google Scholar. Acid-Base, Electrolyte, and Metabolic Abnormalities. Critical Care Medicine.
Philadelphia: Elsevier Spurious electrolyte disorders: a diagnostic challenge for clinicians. Am J Nephrol 38 1 —7. Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state.
Endocrinol Metab Clin North Am 35 4 —51,viii. Disorders of potassium. Emerg Med Clin North Am 23 3 —47,viii—ix. Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabet Med 28 5 — Malaysia MoH. Importance of potassium in cardiovascular disease. J Clin Hypertens Greenwich 4 3 — Shargel L. Baker TW. A clinical survey of one hundred and eight consecutive cases of diabetic coma.
Arch Intern Med 58 3 — Holler JW. Potassium deficiency occurring during the treatment of diabetic acidosis. J Am Med Assoc 15 —9. Low serum potassium level during recovery from diabetic coma with special reference to its cardiovascular manifestations.
Arch Intern Med Chic 80 6 — Martin HE, Wertman M. Electrolyte changes and the electrocardiogram in diabetic acidosis. Am Heart J 34 5 — Death, probably due to potassium deficiency, following control of diabetic coma.
J Clin Endocrinol Metab 8 8 — Studies in diabetic acidosis and coma, with particular emphasis on the retention of administered potassium. J Clin Invest 28 1 :1—9. Keywords: diabetic ketoacidosis, hypokalemia, potassium replacement, treatment outcome, cardiovascular diseases, mortality.
The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. However, due to their late onset of action at least two hours , questionable efficacy, and possible toxicities such as colonic necrosis, cation exchange resins are not the recommended first-line therapy in acute hyperkalemia [ 9 ].
The use of intravenous bicarbonate therapy has also been discouraged due to the lack of benefit [ 10 , 11 ].
Other measures that result in the shift of potassium from the extracellular to intracellular space, such as albuterol and insulin, have been proven to be effective in patients with chronic kidney disease CKD and are more rapid in onset, usually over 30—60 minutes [ 2 , 12—14 ]. However, for unclear reasons, a subset of ESRD patients is resistant to the actions of albuterol [ 8 ]. Intravenous IV insulin is therefore often the first-line therapy for acute hyperkalemia in hospitalized ESRD patients.
It is typically used in conjunction with dextrose to prevent hypoglycemia, and is often combined with other therapies such as nebulized albuterol. Even though insulin-mediated glucose uptake is impaired in uremia, the potassium-lowering effect of insulin is unaffected [ 7 ]. This is thought to be due to the independent pathways for potassium and glucose transport across cell membrane [ 15 ]. IV insulin leads to a dose-dependent decline in serum potassium levels [ 16 ]. However, this therapy may be associated with significant hypoglycemia [ 14 , 18—21 ].
In one study of hospitalized patients treated with IV insulin for hyperkalemia, 8. The definition of hypoglycemia has been a topic of debate. 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.
Hypoglycemia in the inpatient setting is a common problem, with incidences ranging from 3. The symptoms of hypoglycemia can include irritability, impaired cognitive function, seizures, coma, ventricular arrhythmias, and even death [ 22 , 24 , 25 ].
There are multiple risk factors for hypoglycemia. These include medications, drug-to-drug interaction, endogenous insulin deficiency with concomitant abnormal glucagon response , critical illness, poor nutritional intake, low body weight, older age, history of recurrent hypoglycemia, liver failure, and renal failure [ 20 , 23 , 24 ]. In this issue of Clinical Kidney Journal, Apel et al [ 26 ] reports the incidence and timing of hypoglycemia, as well as associated risk factors in inpatient ESRD patients after treatment of hyperkalemia with 10 units of IV insulin and 25 g of dextrose.
Risk factors for hypoglycemia were: no prior diagnosis of DM, no use of DM medication prior to admission, and a lower pre-treatment glucose level. Hypoglycemia occurred at a median of 2 hours after insulin and persisted for a median of 2 hours. In the setting of normal kidney function, the kidney contributes to nearly half of overall gluconeogenesis, and is therefore as important as the liver in carbohydrate metabolism [ 29 , 30 ].
The kidney also plays a critical role in insulin metabolism. Even though evidence implies that CKD creates an insulin-resistant state, hypoglycemia can ensue due to decreased gluconeogenesis and insulin degradation [ 31 ]. Other factors such as altered drug metabolism, malnutrition, decreased hepatic gluconeogenesis, and infection also increase the risk of hypoglycemia in this population [ 27 , 32 ].
In hemodialysis patients, the use of glucose-free dialysis solution increases the risk of hypoglycemia due to transfer of plasma glucose to the dialyzate.
Addition of glucose to dialysis solution significantly decreases this risk [ 33 , 34 ]. Apel et al do not specify in their study whether there is a difference between hemodialysis and peritoneal dialysis patients. Theoretically, the incidence of hypoglycemia is lower in peritoneal dialysis due to the presence of dextrose in the dialysis solution.
The results from Apel's study emphasize the importance of intense blood glucose monitoring after insulin administration. Since IV insulin is a commonly used therapy for severe hyperkalemia in ESRD patients in the hospital setting, we agree with Apel et al that a protocol-driven approach may be able to decrease the incidence of hypoglycemia.
Published literature indicates that the insulin and dextrose regimen varies from center to center. Dose of insulin ranges from 5—10 units and amount of glucose ranges from 25 to 60 g [ 35 ]. Others have recommended additional dextrose infusion after intravenous push of dextrose and insulin to prevent hypoglycemia [ 17 , 20 ].
Due to risks of hypoglycemia, some have advocated the use of glucose alone in the treatment of hyperkalemia. The rationale is based on the theory that exogenous glucose stimulates insulin secretion which shifts potassium into the cell. In a randomized, crossover study of 10 non-diabetic, ESRD patients on hemodialysis with hyperkalemia, dextrose alone led to a clinically significant decrease in serum potassium level.
The rates of hyperglycemia were not reported [ 36 ]. 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 [ 8 , 36 ]. 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 [ 7 , 18 ].
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. 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 [ 14 , 38 ]. 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.
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Volume 7.
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