Atypical Presentation of Silent Nocturnal Hypoglycemia in an Older Person

To the Editor: We report a case of nocturnal falls secondary to the Somogyi phenomenon in an older diabetic. To our knowledge, this is the first case report describing the Somogyi phenomenon as a cause of falls. The patient was an 81-year-old woman with a 3-year history of episodic falls whose fall frequency had increased in the last 6 months during the night. These nighttime falls were unwitnessed, and she had no recollection of the circumstances around them. Apparently, when she would wake up in the morning, she would be on the floor with bruises, and there would be disarray in her apartment suggesting that she had fallen. She denied chest pain, palpitations, seizure-like symptoms, or dizziness on standing up. She had had diabetes mellitus type II for 30 years and had been on insulin for the past 25 years. Her past medical history included hypertension, gastroesophageal reflux disease, osteoarthritis, and hypothyroidism. The patient also had decreased visual acuity due to diabetic retinopathy and had received laser treatment in the previous 2 years. She had been living in a seniors' apartment and was independent in all activities of daily living. Although home care was helping with insulin management, her chemstrips ranged widely, from 2 to 26. Aside from decreased visual acuity and mild cognitive impairment, physical examination was essentially normal. There was no postural drop in blood pressure. Electroencephalogram was normal and Ambulatory Cardiac Holter Monitoring did not show any evidence of arrhythmias. Her HBA1C 0.084 (8.4%) was elevated, whereas her blood urea and serum creatinine were normal. Her chemstrips in the hospital consistently showed early-morning (3 a.m.) hypoglycemia with normal to slightly increased fasting blood sugars (7 a.m.). Initially, her evening intermediate-acting insulin was moved to bedtime along with a snack at that time. Even with that adjustment, the patient continued to have early-morning hypoglycemia. Subsequently, the bedtime dose of intermediate-acting insulin was decreased, but the problem persisted. The renal parameters were within normal limits. The creatinine clearance calculated with the Cockroft Gault formula was decreased, at 45 ml/min. Because insulin is mainly excreted via the kidneys, it was speculated that the morning intermediate insulin's action was prolonged because of her decreased renal function. The morning insulin dose was subsequently reduced and the patient's early-morning (3 a.m.) hypoglycemia resolved; her nocturnal falls did not recur. Older people may not have the same sense of hypoglycemia as do young people.1 Hypoglycemic unawareness can be defined as the inability to perceive consciously or to discern the onset of acute hypoglycemia. The Somogyi phenomenon is hyperglycemia caused by the release of counterregulatory hormones following unrecognized nocturnal hypoglycemia.2 The Somogyi phenomenon is an unusual cause of fasting hyperglycemia. Literature suggests that unrecognized nocturnal hypoglycemia is common in diabetic patients requiring insulin.3,4 Silent nocturnal hypoglycemia should be considered in any subject taking more than 1 unit of insulin per kilogram of body weight.5 The intensification of insulin regimens for tighter blood glucose control often provokes a significant increase in the incidence of nocturnal hypoglycemias. Patients are particularly vulnerable to hypoglycemia during sleep because of their inability to detect early warning symptoms of autonomic activation. Sleep itself suppresses the hypoglycemic sympathoadrenal response.6 The subtle clinical manifestations of nocturnal hypoglycemia include night sweats, nightmares, vivid dreams, restless behavior during sleep, and morning headache. Nocturnal hypoglycemia can also cause neuroglycopenia during sleep, manifested as restlessness and abnormal movements of the sleeping patient. Prolonged severe nocturnal hypoglycemia may result in convulsions and/or coma. Nocturnal hypoglycemia may be a cause of sudden death in insulin-treated diabetic patients.7 Gale et al. reported nocturnal hypoglycemia in 22 of 39 (56%) poorly controlled adult diabetic patients on conventional insulin therapy.8 Dornan et al. reported a prevalence of nocturnal hypoglycemia (blood glucose <2.0 mmol/l or 40 mg /dL) in 29% of 82 diabetic adults treated conventionally with twice daily insulin.9 Blood glucose concentrations at 10:00 p.m. have been shown to be predictive of nocturnal hypoglycemia. Pramming et al. reported that if blood glucose was <6.0 mmol/l (110 mg /dL) at 10:00 p.m., then the risk of nocturnal hypoglycemia was 80%, whereas if it was> 6.0 mmol/l (110 mg /dL) the likelihood of nocturnal hypoglycemia was 12%.10 High titers of insulin antibodies may alter insulin pharmacokinetics and encourage recurrent hypoglycemia, possibly in association with altered awareness.11 Despite these numerous reports of nocturnal hypoglycemia, falls in this setting have not been described. In older patients, the avoidance of hypoglycemia is of much greater immediate importance than the long-term risk of developing microvascular complications associated with hyperglycemia. The timing of insulin injection and estimation of renal clearance are important in preventing nocturnal hypoglycemias. Delaying the evening injection to 10:00 p.m. and understanding that the decrease in creatinine clearance may prolong the duration of extended insulin may help to prevent nocturnal hypoglycemias. Regular self-monitoring by diabetic patients of blood glucose at 10:00 p.m., and eating a snack containing 10 g to 20 g of carbohydrate if the blood glucose is <6.0 mmol (110 mg /dL) may effectively prevent nocturnal hypoglycemia. With aging, there is a decline in the rate of insulin removal from plasma.12 There is also variability of absorption of extended-release preparations and their renal clearance in older people, which may be a significant obstacle in their use in intensified insulin regimens. This variability may be as high as 50% between individuals for the same dose and 25% between days in the same individual. In practice, it may result in hyperglycemia on one day and hypoglycemia on another day. Although the cause of variation is poorly understood, some clinical factors, such as the depth of injection (muscle or adipose tissue), may have a significant impact on the subsequent rate of insulin delivery in the circulation. Additional factors such as increased skin temperature (blankets) and nocturnal exercise, such as sexual intercourse, might also have a significant influence on the rate of insulin delivery during the night. Switching the intermediate-acting insulin to bedtime will avoid the danger of nocturnal hypoglycemia and may help to reduce fasting hyperglycemia. If the patient is currently receiving intermediate-acting insulin at bedtime, there are three options available. To reduce the risk of severe hypoglycemia, therapeutic goals of treatment should be modified to permit suboptimal glycemic control, accepting that this may have detrimental effects on the progression of vascular complications. Checking the renal function and creatinine clearance and modifying the dose of the morning intermediate-acting insulin, as done in our patient may be helpful. The final option is to place the patient on an insulin infusion pump to ensure more even insulin absorption, although this usually is not the practice consideration. This case is reported to heighten awareness that nocturnal hypoglycemia and Somogyi phenomenon should be considered in the differential diagnosis of nocturnal falls in diabetics, especially those requiring insulin. It also stresses the importance of calculating renal function in all patients on insulin and adjusting the dose and timing of insulin accordingly to prevent nocturnal hypoglycemias and the falls associated with it.

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