2) DKA usually occurs as a consequence of absolute or relative insulin deficiency that is accompanied by an increase in counter-regulatory hormones (ie, glucagon, cortisol, growth hormone, epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis, glycogenolysis, and lipolysis.
Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum free fatty acids. Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results in accumulation of acidic intermediate and end metabolites (ie, ketones, ketoacids).
Meanwhile, increased proteolysis and decreased protein synthesis as result …show more content…
3)
Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia, although extracellular and intracellular body buffers can limit ketonemia in its early stages, as reflected by a normal arterial pH associated with a base deficit and a mild anion gap.
When the accumulated ketones exceed the body 's capacity to extract them, they overflow into urine (ie, ketonuria). If the situation is not treated promptly, a greater accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis), with a significant drop in pH and bicarbonate serum levels. Respiratory compensation for this acidotic condition results in rapid shallow breathing (Kussmaul respirations).
Ketones/ketoacids/hydroxy acids, in particular, beta-hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA. Moreover, acetone produces the fruity breath odor that is characteristic of ketotic …show more content…
It is common to see transition from intravenous to subcutaneous insulin using sliding scale insulin only. This strategy as a sole approach should be discouraged, as it cannot provide the necessary insulin requirement in patients recovering from hyperglycemic crisis and β-cell failure. Patients should be given intermediate (neutral protamine Hagedorn) or long-acting insulin (detemir or glargine) 2 hours before termination of intravenous insulin to allow sufficient time for the injected insulin to start working . It is also feasible to begin administration of long-acting insulin while the patient continues to receive intravenous insulin therapy. The once-daily subcutaneous insulin glargine administered during intravenous insulin infusion prevents future rebound hyperglycemia without an increased risk of
Hepatic gluconeogenesis, glycogenolysis secondary to insulin deficiency, and counter-regulatory hormone excess result in severe hyperglycemia, while lipolysis increases serum free fatty acids. Hepatic metabolism of free fatty acids as an alternative energy source (ie, ketogenesis) results in accumulation of acidic intermediate and end metabolites (ie, ketones, ketoacids).
Meanwhile, increased proteolysis and decreased protein synthesis as result …show more content…
3)
Progressive rise of blood concentration of these acidic organic substances initially leads to a state of ketonemia, although extracellular and intracellular body buffers can limit ketonemia in its early stages, as reflected by a normal arterial pH associated with a base deficit and a mild anion gap.
When the accumulated ketones exceed the body 's capacity to extract them, they overflow into urine (ie, ketonuria). If the situation is not treated promptly, a greater accumulation of organic acids leads to frank clinical metabolic acidosis (ie, ketoacidosis), with a significant drop in pH and bicarbonate serum levels. Respiratory compensation for this acidotic condition results in rapid shallow breathing (Kussmaul respirations).
Ketones/ketoacids/hydroxy acids, in particular, beta-hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA. Moreover, acetone produces the fruity breath odor that is characteristic of ketotic …show more content…
It is common to see transition from intravenous to subcutaneous insulin using sliding scale insulin only. This strategy as a sole approach should be discouraged, as it cannot provide the necessary insulin requirement in patients recovering from hyperglycemic crisis and β-cell failure. Patients should be given intermediate (neutral protamine Hagedorn) or long-acting insulin (detemir or glargine) 2 hours before termination of intravenous insulin to allow sufficient time for the injected insulin to start working . It is also feasible to begin administration of long-acting insulin while the patient continues to receive intravenous insulin therapy. The once-daily subcutaneous insulin glargine administered during intravenous insulin infusion prevents future rebound hyperglycemia without an increased risk of