A 75-year-old man with type 2 diabetes mellitus is brought to the emergency department due to weakness and blurred vision. Over the last several days, the patient has had a hacking cough, sore throat, and poor appetite. Temperature is 38 C (100.5 F), blood pressure is 100/60 mm Hg, pulse is 112/min, and respirations are 18/min. On physical examination, the patient is lethargic and has dry mucous membranes. Heart sounds are regular, and the lungs are clear to auscultation. The abdomen is soft, nontender, and nondistended. No rashes are present. There is mild, generalized weakness on neurologic examination. Laboratory results are as follows: Which of the following is most likely present in this patient?

Question

A 75-year-old man with type 2 diabetes mellitus is brought to the emergency department due to weakness and blurred vision.  Over the last several days, the patient has had a hacking cough, sore throat, and poor appetite.  Temperature is 38 C (100.5 F), blood pressure is 100/60 mm Hg, pulse is 112/min, and respirations are 18/min.  On physical examination, the patient is lethargic and has dry mucous membranes.  Heart sounds are regular, and the lungs are clear to auscultation.  The abdomen is soft, nontender, and nondistended.  No rashes are present.  There is mild, generalized weakness on neurologic examination.  Laboratory results are as follows:  Which of the following is most likely present in this patient?

Quizplus · Accepted Answer

11ec25c8_d3b4_0589_bc81_57ae2bdd595b_MD0003_00 This patient's clinical features are consistent with hyperosmolar hyperglycemic state (HHS), most likely precipitated by his recent upper respiratory tract infection. Diabetic ketoacidosis (DKA) and HHS are the 2 most serious acute complications of diabetes. HHS is more common in type 2 diabetes and is characterized by severe hyperglycemia and increased serum osmolality with little or no ketonemia or acidosis (most patients have pH >7.3 and serum bicarbonate >20 mEq/L). Most patients with HHS or DKA have normal or mildly elevated serum potassium levels at initial evaluation due to the combined effects of insulin deficiency and hyperosmolality, which promote the movement of potassium out of cells into the extracellular space. However, patients frequently have a total body potassium deficit (3-6 mEq/kg) due to excessive urinary loss (caused by osmotic diuresis induced by hyperglycemia and urinary excretion of potassium ketoacid anion salts). Insulin therapy for HHS can shift potassium back into the cells, abruptly lowering circulating potassium levels, and cause severe hypokalemia. (Choice A) An increase in extracellular pH (alkalemia) promotes the binding of calcium to albumin and lowers serum ionized calcium concentration. Patients with HHS have normal to slightly acidic pH; therefore, serum ionized calcium concentration remains unchanged. (Choice B) Patients with severe hyperglycemia initially have phosphate depletion (not retention) due to phosphaturia caused by osmotic diuresis. However, relative renal phosphate retention may occur later if dehydration and prerenal acute kidney injury lead to more severe renal insufficiency (eg, glomerular filtration rate <20-25 mL/min). (Choice C) Hyperglycemia and glucosuria-induced osmotic diuresis cause free water loss that exceeds sodium loss. (Choice D) Suppression of antidiuretic hormone (ADH) secretion is seen in patients with hyponatremia due to excess free water intake. The hyponatremia in HHS is due to the osmotic shift of water from the intracellular to extracellular space. In HHS, secretion of ADH by the posterior pituitary is stimulated by the increased plasma osmolality and hypovolemia/hypotension, although patients with chronic hyperglycemia will have a lesser ADH release and antidiuretic response. Educational objective: Patients with hyperosmolar hyperglycemic state or diabetic ketoacidosis have a total body potassium deficit due to excessive urinary loss caused by glucosuria-induced osmotic diuresis. However, serum potassium levels may be normal or mildly elevated due to the shift of potassium out of cells into the extracellular space. Insulin in these patients can rapidly lower potassium levels, leading to hypokalemia. References: Hyperosmolar hyperglycemic state. (http://www.ncbi.nlm.nih.gov/pubmed/29431405) Attenuation of vasopressin-induced antidiuresis in poorly controlled type 2 diabetes. (http://www.ncbi.nlm.nih.gov/pubmed/15292031)

A 75-Year-Old Man with Type 2 Diabetes Mellitus Is Brought