Diabetic ketoacidosis and hyperglycemic hyperosmolar state manifestations of poorly controlled diabetes and can coexist.
Diabetic ketoacidosis and hyperglycemic hyperosmolar state manifestations of poorly controlled diabetes and can coexist. DKA is defined by ketone production and metabolic acidosis, while hyperosmolality and minimal ketone production characterize HHS.
Poor adherence and infections are common precipitation factors of hyperglycemic crisis. Insulin deficiency and counterregulating hormones, such as glucagon and cortisosal, eventually lead to life-threatening complications. Its believed that HHS has miminal ketone production because of higher levels of endogenous circulating insulin preventing fatty acid production.
We’ll treat these hyperglycemic crisis the same. We’ll need to initiate fluid resuscitation at 1 to 1.5 ml/kg within the first hour. Supplemental electrolytes and fluid selection are patient-specific thereafter. This will increase expand intravascular volume with subsequent reduction in counter-regulatory hormones. Insulin deficiency is the underlying issue so get that insulin drip started at 0.1 units/kg/hr. For DKA, insulin shifts glucose intracellularly and breaking the ketogenesis cycle. When the BG is less than 250 mg/dL, start dextrose containing fluids to keep the insulin drip running. AG depicts resolution, not serum glucose. For HHS, we’ll target a serum osmolality less than 310 and resolution of AMS. The use of sodium bicarbonate is contraversial. Subq protocols have been utilized in mild cases.
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SLGT2-i Induced euDKA: https://www.instagram.com/p/CqjdzEegvIg/
Sulfonuyrea-induced Hypoglycemia: https://www.instagram.com/p/CqBTgpSJ6kh/
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