An 83-year-old obtunded woman is evaluated in the emergency department. She has a history of type 2 diabetes mellitus treated with insulin glargine. The patient developed nausea, vomiting, and diarrhea 2 days ago. Her oral intake was limited, and she did not receive her insulin. Today, the patient was found minimally responsive.
On physical examination, the patient responds only to noxious stimuli with groaning. Temperature is 35.9°C (96.7°F), blood pressure is 90/50 mm Hg, pulse rate is 120/min, and respiration rate is 14/min. She has dry mucous membranes, and her skin demonstrates prolonged tenting. Other than obtundation, the neurologic examination is normal.
||976 mg/dL (54.2 mmol/L)
|Blood urea nitrogen
||46 mg/dL ( 16.4 mmol/L)
||2.1 mg/dL ( 185.6 mmol/L)
||132 meq/L (132 mmol/L)
||4.8 meq/L (4.8 mmol/L)
||98 meq/L (98 mmol/L)
||22 meq/L (22 mmol/L)
||335 mosm/kg H2O
The next management step for this patient is rapid infusion of intravenous fluids. This patient has hyperglycemic hyperosmolar syndrome. Diagnostic criteria include plasma glucose level greater than 600 mg/dL (33.3 mmol/L), arterial pH greater than 7.30, serum bicarbonate greater than 15 mg/dL (15 mmol/L), serum osmolality greater than 320 mosm/kg H2O, and absent urine or serum ketones. Patients with this disorder usually have a precipitating factor, such as severe infection, myocardial infarction, or new kidney insufficiency. Management of hyperglycemic hyperosmolar syndrome mainly involves identifying the underlying precipitating illness and restoring a markedly contracted plasma volume. Normal saline, which is already comparatively hypotonic in such patients, is usually chosen first to replenish the extracellular space. If the patient has hypotension, fluids should be administered as rapidly as tolerated to restore plasma (intravascular) volume. When blood pressure is restored and urine output is established, administration rates should be slowed and hypotonic solutions should be administered. The total body water deficit can be calculated by using standard formulas, with the goal of replacing one-half the deficit during the first 24 hours and the remainder during the next 2 to 3 days.
Insulin reduces glucose levels but should be administered only after expansion of the intravascular space has begun. If given earlier, movement of glucose into cells theoretically can reduce circulating volume further, which threatens cerebral, kidney, and coronary perfusion.
Electrolytes should be monitored, especially potassium, because the potassium level may fall as urine output is restored and kidney function improves with intravenous fluid therapy; in addition, potassium is shifted intracellularly by the administration of insulin therapy. Potassium should not be administered until urine output is verified, because these patients are prone to acute kidney injury. Mild metabolic acidosis does not require bicarbonate therapy, because normalization of circulating volume will quickly correct this defect. Antibiotics are not required unless a bacterial infection is identified.
- Management of hyperglycemic hyperosmolar syndrome involves identifying the underlying precipitating illness and restoring plasma volume with intravenous fluids.