Hypoglycemia

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Introduction

Hypoglycemia is characterized by three things:

a blood glucose level of less than 2.5 mmol/L (45 mg/dl) in males and 2.2 mmol/L (40 mg/dl) in females
CNS symptoms such as confusion, erratic behaviour, or coma
resolution of symptoms within minutes following glucose administration

Temporary hypoglycemia can cause cerebral dysfunction, and prolonged hypoglycemia can cause death. The body thus has overlapping mechanisms to prevent or correct hypoglycemia. The most notable are elevations of glucagon and epinephrine, together with a decrease in insulin.

The Case of Sarah G.

Sarah is a 34 year-old woman who comes to the emergency department feeling anxious, tremulous, and sweaty. After a reassuring history and physical exam, lab tests reveal her blood glucose is 2.8 mmol/L.

what might be causing her low readings?
how would you investigate it?
how would you treat Sarah?

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Causes and Risk Factors

Hypoglycemia can be triggered by various factors:

hypoglycemia unawareness
blunted symptoms during sleep

Ketotic

Non-Ketotic

hyperinsulinism

starvation
emesis
hepatic dysfunction
chronic kidney disease
hypocortisolism
alcoholism
non-pancreatinc tumours

with no hyperinsulinism

endogenous - insulinoma
GDM affecting mother
exogenous - oral hypoglycemics
autoimmune (against insulin receptors)
pancreatic beta-cell tumor
metabolic disorder

Reactive

postprandial, with exaggerated insulin release
functional
undiagnosed diabetes
leucine sensitivity
fructose intolerance (genetic)
galactosemia

Insulin-Induced Hypoglycemia
Hypoglycemia frequently occurs in patients receiving insulin treatment. If patients are conscious, oral administration of carbohydrate is used. In unconsious patients, intramuscular administration of glucagon is used.

Postprandial Hypoglycemia
Exaggerated insulin release can follow a meal, triggering hypoglycemia with mild adrenergic symptoms. For this reason, it is recommended to eat frequent small meals.

Fasting Hypoglycemia
Fasting hypoglycemia tends to produce neuroglycopenic symptoms and may result from decreased liver production of glucose, ie in patients with liver damage. It may also reult from increased peripheral glucose use, often due to increased insulin levels due to a pancreatic tumour.

Hypoglycemia and Alcohol
Ethanol is oxidized first to acetaldehyde by alcohol dehydrogenase, then to acetate by aldehyde dehydrogenase. These reactions reduce NAD+, producing large amounts of NADH. This favours the reduction of pyruvate to lactate and of oxaloacetate to malate, two important intermediates in gluconeogenesis. This decreased glucose synthesis can cause hypoglycemia, especially in people who have depleted their stores of glycogen. Hypoglycemia can produce many of the symptoms of alcohol intoxication, such as agitation, impaired judgment, and surliness.

Patients who use insulin as a part of intensive therapy are at increased risk of hypoglycemia several hours after drinking alcohol.

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Pathophysiology

Glucagon and epinephrine are the most important immediate responders to hypoglycemia. Epinephrine is not normally essential, but in Type I diabetes, where glucagon secretion is impaired, epinephrine becomes critical.

Cortisol and growth hormone are less important in short-term maintenance of blood glucose but do play a role in long-term management of glucose metabolism.

3.8 mmol/L - glucagon/adrenaline released

3.2 mmol/L - symptoms begin

2.8 mmol/L - cognitive problems

1.5 mmol/L - reduced level of consciousness, convulsions, coma

One episode of hypoglycemia makes another one in the next 24 hours more likely.

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