1) What’s the difference? HHS patients, as opposed to DKA patients, usually have some residual circulating insulin that prevents secretion of glucagon and glucocorticoids. These hormones are responsible for the breakdown of free fatty acids and the formation of ketone bodies seen in DKA.


2) What about this patients labs? NA: 118 K: 7.8 Cl: 89 HcO3: 18 BUN: 51 Cr: 3 Gluc: 1200


This patient’s hyperkalemia is not from acidosis as is seen commonly in DKA. This patient’s hyperkalemia and acidosis is secondary to renal failure from the dehydration caused by HHS.


3) Do I manage them differently? Yes! HHS is a state of profound dehydration from osmotic diuresis. Fluids are the initial treatment. Lowering the glucose too fast with aggressive insulin regimens can cause cerebral edema


4) Look for an underlying etiology: HHS is often the result of an underlying event such as sepsis or ischemia.


Managing hyperglycaemic emergencies: an illustrative case and review of recent British guidelines. Clinical Medicine 2013, Vol 13, No 2: 160–2





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