Influence of Glucose Homeostasis Alteration on the Electrolyte and Acid-Base Balance in Patients with Diabetes Mellitus
Despite the success of the treatment of diabetes mellitus, the incidence of diabetic ketoacidosis in recent years has not decreased. Its clinical manifestations Dreshfeld first described in 1886. Insulin began to be used in 1922. Mortality of this complication was 100 %. Widespread implementation of insulin therapy into the clinical practice reduced mortality by 30 %, and with improvement of treatment, including infusion therapy, there was a further reduction. The level of mortality of patients with diabetic ketoacidosis remains high (about 5 % in specialized centers). Prediction of the disease much worsens with age, in the development of coma and hypotension. The prevalence of diabetes mellitus is growing rapidly and currently ranges from 20 to 50 % of new-onset disease in young people. Violations of electrolytes are frequent in patients with this disease and may be the result of altered distribution of electrolytes associated with hyperglycemia-induced osmotic fluid shifts or general shortages caused by osmotic diuresis. Complications from damage to the target organs and therapies used in the treatment of diabetes can also contribute to electrolyte disturbances. We highlight the ways, in which specific electrolytes may be influenced by dysregulation in glucose homeostasis. High or normal plasma sodium concentration in the presence of hyperglycemia indicates a clinically significant deficit of the total body fluid. Sodium correction in patients with glycemia helps to evaluate shortage of sodium and water, and ensure adequate assessment required for tonicity during the course of rehydration therapy. Because children with diabetic ketoacidosis are at particularly high risk of such terrible complications, as swelling of the brain, then to some extent hypernatremia is acceptable during treatment to minimize this complication. Insulin deficiency, which often occurs in type 1 diabetes mellitus, is an important factor of potassium output from the cells. Changes in potassium level, caused by metabolic acidosis, are more significant in mineral acidosis (hyperchloremic, non-anion gap acidosis) than in the organic acidosis (large anion gap acidosis), which is present in diabetic ketoacidosis. In diabetic patients receiving non-selective β-blockers, increased adrenergic activity can exacerbate hyperkalemia, because unopposed α-receptor stimulation, promotes the release of potassium from the cells. Ketoacidosis occurs when the rate, at which hepatic ketoacid is generated, exceeds peripheral utilization and the concentration of ketoacid in the blood increases. Normalization of acid-base balance is made within a few days, as the correction of bicarbonate deficit occurs through its regeneration by kidneys. Patients with primary kidney diabetic ketoacidosis are not involved (with their normal function). Kidney compensate by higher ammonia discharge. Urinary osmolarity gap is measured in order to find out whether there is a corresponding increase in the excretion of ammonia, which leads to violations in acid-base status. Low urinary osmolarity gap in patients with persistent hyperchloremic acidosis provides leads to tubular dysfunction. Despite recent advances that allowed direct assessment of the levels of β-hydroxybutyrate, determining the concentration of ketone bodies often can not fully explain the increase in anion gap and in many patients may contribute to hyperlactatemia. Lactate level may be increased in response to increased adrenergic activity, even in the absence of tissue hypoperfusion. Chronic hyperglycemia leads to the development of «carbonyl stress» and accumulation of toxic dicarbonyl compounds, such as methyl glyoxal, etc. Epidemiological studies suggest that low magnesium intake is associated with increased risk of diabetes, while higher magnesium intake is associated with lower risk of developing diabetes. In patients with diabetic ketoacidosis, osmotic diuresis due to poor glycemic control leads to renal loss of magnesium. Hypomagnesemia can cause hypocalcemia, because magnesium deficiency may lead to lower parathyroid hormone release. Randomized studies of phosphate therapy in patients with diabetic ketoacidosis did not establish that this therapy provides clinical benefit. The dysregulation of glucose homeostasis leads to many direct and indirect effects on electrolyte and acid-base balance. Since the high prevalence of diabetes ensures that clinicians of every medical specialty will interact with these patients, familiarity with related electrolyte abnormalities is important.
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