Hyperglycemia-related central pontine demyelinization after a binge-eating attack in a patient with type-2 diabetes: a case report

Abstract

BackgroundHere, we report a case of central pontine demyelinization in a type-2 diabetes patient with hyperglycemia after a binge-eating attack in the absence of a relevant hyponatremia.Case presentationA 55-year-old, male type-2 diabetic patient with liver cirrhosis stage Child-Pugh B was admitted due to dysmetria of his right arm, gait disturbance, dizziness, vertigo, and polyuria, polydipsia after a binge-eating attack of sweets (a whole fruit cake and 2 Liters of soft drinks). A recently initiated insulin therapy had been discontinued for 8 months. A serum glucose measurement obtained 5 days prior to hospitalisation was 38.5 mmol/l (694 mg/dl). The patient graved for sweets since stopping alcohol consumption 8 months earlier. On admission, venous-blood glucose was 29.1 mmol/l (523.8 mg/dl), glycated hemoglobin was 168.0 mmol/mol or 17.6%. No supplementation of sodium chloride was reported. Laboratory exams revealed an elevated serum ammonia level (127.1 μmol/l), rendering a hepatic encephalopathy very likely. After initiation of insulin therapy, capillary glucose normalized, and serum sodium rose from 133 on admission to 144 mmol/l during the hospital stay. In retrospect, the mild hyponatremia on admission was classified as pseudohyponatremia due to hyperglycemia. The patient had an insulin resistance (HOMA-IR 7.8 (normal range < 2.5)). A T2-weighted magnetic resonance imaging (MRI) of the head and a cranial computed tomography scan were obtained demonstrating a symmetric central pontine demyelinization. After 26 days in hospital, the patient was discharged with an inkretin-mimetic therapy (dulaglutide SC, 1.5 mg/week) and an intensified conventional insulin therapy (insulin aspart: 14 units/d in euglycemia, insulin glargin 20 units/d).ConclusionsCentral pontine and/or cerebellar myelinolysis can be caused by sudden, severe, and sustained hyperglycemia, especially when another risk factor (in this case, liver cirrhosis) is present. Functional neurological deficits in the context of hyperglycemia should prompt for the consideration of this differential diagnosis in all diabetes patients.

Excessive Sodium Bicarbonate Infusion May Result in Osmotic Demyelination Syndrome During Treatment of Diabetic Ketoacidosis: A Case Report

“…Several case reports have described the relationship between hyperglycemia and ODS [ 3 , 8 , 9 ]. In one such case report [ 8 ], a type 2 diabetic and cirrhotic patient presented with several neurologic symptoms following ingestion of large amounts of sugar-containing foods and was diagnosed with ODS [ 8 ]. During admission, the patient had serum sodium levels in the range of 133–144 mmol/l.…”

Hyponatremia Is Associated With Increased Osteoporosis and Bone Fractures in Patients With Diabetes With Matched Glycemic Control

“…Inarguably, hyperglycemia is directly toxic to bone, although there is recent evidence that suggests that there are additional mechanisms independent of absolute glucose level that cause increased bone resorption markers in patients with hyperglycemia [46–48]. There is also evidence that rapid changes in glucose level (with concomitant rapid changes in absolute serum sodium) can cause toxicity to the nervous system that is similar in character to the pathology seen among patients with rapidly corrected serum sodium levels in hypo-osmolar hyponatremia [49, 50]. As serum [Na + ] levels are dependent on glucose levels, the principal challenge of the current study was to demonstrate that hyponatremia among patients with diabetes mellitus could be associated with osteoporosis and fragility fracture independent of the degree of hyperglycemia.…”

A Case of Central Pontine Myelinolysis Occurred During Treatment of Hyperosmolar Hyperglycemic Syndrome

“… 2 Moreover, the rapid normalization of hyponatremia or rise in BS are the underlying mechanisms. 4 The diagnosis of either can be confirmed upon the identification of demyelinating brain lesions with magnetic resonance imaging (MRI) or computed tomography (CT); however, CT has less sensitivity than MRI. 2 We present a rarely reported incident of CPM related to HHS.…”