Iatrogenic hypoglycemia causes recurrent morbidity in most people with type 1 diabetes and in many with type 2 diabetes, and it can sometimes be fatal (1). While the clinical presentation is often characteristic, particularly for the experienced individual with diabetes; the neurogenic and neuroglycopenic symptoms of hypoglycemia are nonspecific and relatively insensitive; therefore, many episodes are not recognized (1,2). Hypoglycemia can result from exogenous or endogenous insulin excess alone. In insulin-deficient diabetes (exogenous) insulin levels do not decrease as glucose levels fall, and the combination of deficient glucagon and epinephrine responses cause defective glucose counter-regulation (1,3). Furthermore reduced sympathoadrenal responses cause hypoglycemia unawareness and reduced neurogenic symptom responses to a given level of hypoglycemia. The absolute or relative insulin excess, whether from injected or from secreted insulin, is the sole determinant of risk factor of iatrogenic hypoglycemia. Although each must be considered carefully, these conventional risk factors explain only a minority of episodes of severe iatrogenic hypoglycemia (4). Obviously, one cannot solve the problem of iatrogenic hypoglycemia if it is not recognized to be a problem.

Here we report a patient presenting with hypoglycemia after an exceptional way of insulin administration. A 68-year-old woman with a history of 10 years of insulin-treated diabetes was hospitalized after an episode of disorientation. She was taking 10 units of NPH insulin at 8 AM and 6 units at 7 PM, subcutaneously. She had an 8-year history of hypertension controlled by low-salt diet and ACE inhibitor daily. She had had transient ischemic attack three years earlier. Neurologic and ophthalmologic examinations were unremarkable other than a lethargic state. Her blood pressure was 150/90 mmHg. Otherwise physical examination was normal. Laboratory studies demonstrated a blood glucose level of 25 mg/dL. ECG was normal, so glucagon of 1 mg/sc was injected. Thereafter, bolus of 100 ml 50% dextrose was given intravenously, followed by a constant infusion of 5% dextrose. During the next 30 minutes, she gradually became alert but after one hour she again became lethargic and her speech was slurred. Her blood glucose was 32 mg/dL before the administering a bolus of 50% dextrose again. Her mentation cleared immediately and neurologic signs disappeared. A control CT of the brain was normal. She constantly complained of getting worse after a visit to her physical therapist during her follow-up. When her physician was contacted; he admitted that a 300 IU NPH insulin was administered intraarticulary to her left knee in order to eliminate her gonoarthrosis symptoms. So we followed her for another 48 hours and discharged her with blood glucose level of 180 mg/dL

In conclusion, the determination of hypoglycemia etiology sometimes might be difficult. It is very important to obtain the patient's history in detail.