A 21-year old female (A.M.) presents to the urgent care clinic with symptoms of nausea, vomiting, diarrhea, and a fever for 3 days. She states that she has Type I diabetes and has not been managing her blood sugars since she’s been ill and unable to keep any food down. She’s only tolerated sips of water and juices. Since she’s also been unable to eat, she hasn’t taken any insulin as directed. While helping A.M. from the lobby to the examining room you note that she’s unsteady, her skin is warm and flushed, and that she’s drowsy. You also note that she’s breathing rapidly and smell a slight sweet/fruity odor. A.M. has a challenge answering questions but keeps asking for water to drink.
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Diabetic ketoacidosis (DKA) most often occurs in patients with type 1 diabetes mellitus; it develops when insulin levels are too low to meet basic metabolic needs (Tran et al., 2017). In some patients with type 1 diabetes, DKA is the first manifestation of the disease. Insulin deficiency can be absolute (for example, when the subsequent injection of exogenous insulin is missed) or relative (when usual doses of insulin do not cover metabolic requirements that increase with stress). The most common physiological stresses that can cause DKA are as follows: acute infection (especially pneumonia and UTI), myocardial infarction, stroke, pancreatitis, trauma. Some drugs that can cause DKA include corticosteroids, thiazide diuretics, sympathomimetics, sodium-dependent glucose transporter type 2 (SGLT-2) inhibitors (Eledrisi & Elzouki, 2020).
The development of DKA is based on the following mechanisms: insulin deficiency (both as a result of insufficient intake and as a result of an increased need for insulin against the background of absolute insulin deficiency in patients with type 1 diabetes), as well as excessive production of counterinsular hormones (first of all, glucagon, as well as cortisol, catecholamines, growth hormone). Due to this, a decrease in glucose utilization by peripheral tissues, stimulation of gluconeogenesis as a result of increased protein breakdown and glycogenolysis, suppression of glycolysis in the liver and, ultimately, the development of severe hyperglycemia happen (Modi et al., 2017). The absolute and pronounced relative lack of insulin leads to a significant increase in the concentration of glucagon in the blood – the hormone-antagonist of insulin. Since insulin no longer inhibits the processes that glucagon stimulates in the liver, the liver’s glucose production (the net result of glycogen breakdown and gluconeogenesis) is dramatically increased.
At the same time, the utilization of glucose by the liver, muscles, and adipose tissue in the absence of insulin decreases sharply. The consequence of these processes is severe hyperglycemia, which also increases in connection with an increase in serum concentrations of other contrainsular hormones – cortisol, adrenaline, and growth hormone.
With a lack of insulin, the catabolism of body proteins increases, and the resulting amino acids are also included in gluconeogenesis in the liver, exacerbating hyperglycemia. Massive breakdown of lipids in adipose tissue, also caused by insulin deficiency, leads to a sharp increase in the concentration of free fatty acids (FFA) in the blood. In insulin deficiency, 80% of the energy is obtained by the body through the oxidation of FFA, which leads to the accumulation of by-products of their decay – ketone bodies (acetone, acetoacetic and beta-hydroxybutyric acids) (Modi et al., 2017). Gluconeogenesis and its consequence – hyperglycemia, and ketogenesis and its consequence – ketoacidosis are the results of the action of glucagon in the liver under conditions of insulin deficiency.
Symptoms and signs of diabetic ketoacidosis include hyperglycemia symptoms and nausea, vomiting, and, especially in children, abdominal pain. More severe metabolic decompensation is manifested by lethargy and drowsiness. Patients may have hypotension and tachycardia due to dehydration and acidosis. Frequent and deep breathing develops as a measure of compensation for acidemia. A fruity breath is also possible due to the presence of acetone in the exhaled air. Fever is not a sign of DKA as such and is indicative of an infectious disease. Without timely treatment, DKA leads to coma and death.
There are four directions in DKA therapy: insulin therapy, restoration of lost fluid, correction of mineral and electrolyte metabolism, treatment of coma-provoking diseases, and complications of ketoacidosis. Insulin replacement therapy is the only type of etiological treatment for DKA. To achieve an optimal active serum insulin level, a continuous infusion of 4-12 units/hour is required (Tran et al., 2017). Such a concentration of insulin in the blood inhibits the breakdown of fats and ketogenesis, promotes the synthesis of glycogen, and inhibits glucose production by the liver, thereby eliminating the two most important links in the pathogenesis of DKA. It has been proven that insulin therapy in the low dose regimen is accompanied by a significantly lower risk of complications than in the high dose regimen.
as little as 3 hours
Eledrisi, M. S., & Elzouki, A. N. (2020). Management of diabetic ketoacidosis in adults: A narrative review. Saudi journal of medicine & medical sciences, 8(3), 165-181.
Modi, A., Agrawal, A., & Morgan, F. (2017). Euglycemic diabetic ketoacidosis: a review. Current diabetes reviews, 13(3), 315-321.
Tran, T. T., Pease, A., Wood, A. J., Zajac, J. D., Mårtensson, J., Bellomo, R., & Ekinci, E. I. (2017). Review of evidence for adult diabetic ketoacidosis management protocols. Frontiers in endocrinology, 8, 106-123.