Hypoglycemia

last authored:
last reviewed:

 

 

Introduction

 

Hypoglycemia is characterized by three things:

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.

return to top

 

 

 

Causes and Risk Factors

Hypoglycemia can be triggered by various factors:

 

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.

 

return to top

 

 

 

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.

return to top

 

 

 

Signs and Symptoms

  • history
  • physical exam

History

Symptoms of hypoglycemia can be divided into two categories:

 

Adrenergic Symptoms
Adrenergic symptoms are mediated by epinephrine release due to hypoglycemia sensing of the hypothalamus. These include

  • anxiety
  • palpitations
  • tremors
  • sweating

These symptoms usually occur when blood glucose levels fall abruptly.

 

 

Neuroglycopenic Symptoms
Neuroglycopenia is the impaired delivery of glucose to the brain, and results in:

  • headache
  • confusion
  • slurred speech
  • seizures
  • coma
  • death

These symptoms often result from a gradual decline in blood glucose which does not trigger an epinephrine response.

Physical Exam

 

return to top

 

 

 

Investigations

  • lab investigations
  • diagnostic imaging

Lab Investigations

Tests to consider include:

  • serum blood glucose
  • electrolytes
  • BUN and creatinine
  • blood gases
  • cortisol
  • glucagon
  • epinephrine
  • insulin, proinsulin, and C-peptide
  • growth hormone
  • ketones (beta-hydroxybutyrate, acetate)
  • urinalysis

Diagnostic Imaging

 

return to top

 

 

 

Differential Diagnosis

 

return to top

 

 

 

Treatments

ABCs and vitals

 

Mild-moderate

BG <4 mmol/L: 15g carbohydrate

BG<2.2 mmol/L: 20g carbohydrate

severe and unconscious: unable to drink

 

return to top

 

 

 

Consequences and Course

Decrease glucose delivery to the brain can ultimately result in seizures, coma, and death. These can have many other effects as well.

 

return to top

 

 

 

Resources and References

 

return to top

 

 

Topic Development

authors:

reviewers:

 

return to top