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Diabetic Emergencies: Diagnosis and Clinical Management: Hypoglycemia Caused by Insulin Secretagogues, Part 3, Case Studies

Nikolaos Tentolouris, Nikolaos Katsilambros
Diabetic_Emergencies

 

 

 

 

Case study 5.1

A 76-year-old female patient was admitted to the orthopedic unit for right hip replacement.

She had been treated with glibenclamide (glyburide) 5 mg twice daily and metformin 1 g/day. In the morning of the admission day and after she had taken her diabetes medications at home, she complained of nausea, vomiting, and diarrhea and refused any food intake. In the afternoon the patient was found in bed in coma. Computed tomography of the brain was normal. Blood was sent to the laboratory for biochemical analysis; after about 2 hours the laboratory informed the unit that the patient’s blood glucose was 20 mg/dl (1.1 mmol/L).

What was wrong with this patient?
 
Glibenclamide (glyburide) is a well-known sulfonylurea that may cause severe hypoglycemia more often than other sulfonylureas due to the prolonged duration of action of the medication and its metabolites. The relatives should have been informed about the risk of hypoglycemia with glibenclamide (glyburide) and they should have informed the personnel of the unit that the patient had taken her medications before admission.

Blood glucose should have been closely monitored in the hospital and, if it was low, intravenous glucose infusion should have begun.

In addition, every unconscious patient should be considered as hypoglycemic, especially if the patient has diabetes, until immediate estimation of the blood glucose levels rules out hypoglycemia. Thus the patient should have been managed as having been in hypoglycemic coma until the results of the blood test were available.

How will you manage this patient?

The patient was unconscious, thus a bolus of 20-50 ml of 50% glucose solution or 50 ml of 35% glucose solution, followed by infusion of 10-20% glucose solution should begin with frequent monitoring of blood glucose.

What was the outcome? 

Despite the increase in blood glucose levels after intravenous infusion of glucose solution 10%, the patient’s brain function never recovered. Severe and prolonged hypoglycemia may cause neuronal death, resulting in permanent impairment of brain function. If hypoglycemia is treated early and effectively, apparent full recovery is the rule, even after severe episodes of hypoglycemia.

Case study 5.2 

An 82-year-old male patient was taken to the emergency room in the afternoon for loss of consciousness in the previous hour. The patient had hypertension, chronic ischemic heart disease, and mild diabetes treated with 30 mg gliclazide MR daily. On examination the patient had coma (Glasgow scale 5) and right hemiplegia.

How will you manage this patient?

An immediate blood glucose determination in the emergency room using a portable glucose meter was 30 mg/dl (1.7 mmol/L). A bolus injection of 50 ml 35% glucose solution was given followed by infusion of 10% glucose solution. The patient recovered fully and no neurological deficits were detected 30 minutes after correction of hypoglycemia. The results of the blood tests from the laboratory 1 hour later confirmed hypoglycemia.

What was the cause of hypoglycemia?

The patient was living alone and his relatives took care of him once daily, usually in the afternoon. Although the risk of hypoglycemia with gliclazide is lower than with other long-acting sulfonylureas, it may still occur under certain circumstances. The patient did not remember if he had eaten his breakfast and lunch. The relatives noticed that the patient had eaten a small amount of his breakfast and no lunch. Thus, the cause of hypoglycemia was reduced food intake together with treatment with gliclazide.

When will you discharge this patient?

Every patient with hypoglycemia caused by insulin secretagogues should be hospitalized for 24-72 hours, managed with intravenous glucose infusion, and have frequent blood glucose monitoring. In case of early discharge, hypoglycemia may recur, especially in patients taking long-lasting sulfonylureas.

Case study 5.3

A 71-year-old male patient with type 2 diabetes complained of frequent episodes of symptomatic hypoglycemia in the previous week manifesting as excess sweating, feeling of hunger, and tremor. His diabetes control was excellent (HbA1c 6.5%) with glimepiride 4 mg daily and metformin 2 g daily. His renal function was normal and he did not have microalbuminuria. No changes in dietary habits and exercise program were reported. The patient noticed that the hypoglycemic episodes commenced after initiation of propranolol for supraventricular tachycardia. 

What is the cause of hypoglycemia?

Non-selective β-adrenergic blockers such as propranolol have been associated with hypoglycemia in patients treated with insulin or sulfonylureas. Data from the literature suggest that it is difficult to prove a cause and effect relationship between therapy with β-adrenergic blockers and hypoglycemia. However, β-adrenergic blockers can increase glucose uptake in skeletal muscle by antagonizing the effects of catecholamines on glucose uptake and lipolysis.

In addition, suppression of lipolysis and reduction in non-esterified fatty acids in plasma improve insulin sensitivity and indirectly reduce gluconeogenesis. On the other hand, β-adrenergic blockers decrease insulin secretion. Thus, the effect of these medications on diabetes may be towards low or high blood glucose levels. β-adrenergic blockers were not associated with higher risk for hypoglycemia in the UKPDS. 32 In addition, β-adrenergic blockers can block the adrenergic response to hypoglycemia and delay recovery because of inhibition of catecholamine-mediated glucose counter-regulation. In this patient no other apparent cause of hypoglycemia could be found and it was attributed to propranolol.

How will you manage this patient?

Propranolol was discontinued and a selective β-adrenergic blocker was initiated. Hypoglycemic episodes stopped and no recurrences were observed. Drug interactions from concomitant treatments can cause severe episodes of hypoglycemia in people with type 2 diabetes treated with insulin secretagogues. Physicians should be aware of these drug interactions and they should inform patients of the need for frequent self-monitoring when additional treatments are necessary.

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Nikolaos Katsilambros, MD, PhD, FACP
SCOPE Founding Fellow
Professor of Internal Medicine
Athens University Medical School
Evgenideion Hospital and Research Laboratory ‘Christeas Hall’
Athens, Greece
Christina Kanaka-Gantenbein, MD, PhD
Associate Professor of Pediatric Endocrinology and Diabetology
First Department of Pediatrics, University of Athens
Agia Sofia Children’s Hospital
Athens, Greece
Stavros Liatis, MD
Consultant in Internal Medicine and Diabetology
Laiko General Hospital
Konstantinos Makrilakis, MD, MPH, PhD
Assistant Professor of Internal Medicine and Diabetology
Athens University Medical School
Laiko General Hospital
Athens, Greece
Nikolaos Tentolouris, MD, PhD
Assistant Professor of Internal Medicine and Diabetology
University of Athens
Laiko General Hospital
Athens, Greece
A John Wiley & Sons, Ltd., Publication This edition first published 2011 © 2011 by John Wiley & Sons, Ltd.
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Diabetic Emergencies: Diagnosis and Clinical Management provides emergency room staff, diabetes specialists and endocrinologists with highly practical, clear-cut clinical guidance on both the presentation of serious diabetic emergencies like ketoacidosis, hyperosmolar coma and severe hyper- and hypoglycemia, and the best methods of both managing the emergencies and administering appropriate follow-up care.
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