Sugar is everything. Our cells cannot function without it. Neurons and cardiomyocytes are particularly sensitive to hypoglycemia and result in its most dramatic manifestations: seizure and cardiac arrest. Prolonged hypoglycemia can cause permanent neurological dysfunction.

Given its nonspecific effects, it is essential that we consider the possibility of hypoglycemia in every critical patient. Consider it the fifth vital sign. 

What causes our fuel gauge to be on E? Medications are the most common cause. Insulin, secretagogues, and pentamidine can cause profound hypoglycemia. Beta blocker overdose is another potential perpetrator. Organ dysfunction can also contribute – liver failure prevents effective gluconeogenesis. You must be on high alert for an infectious source, as sepsis is known to consume sugar.

Myxedema coma and adrenal insufficiency must be considered. In a young patient with no known history, consider a CT of the abdomen with contrast. Insulinomas are commonly misdiagnosed. Don’t forget that ethanol poisoning can prevent effective gluconeogenesis as well. Consider an insulin, c-peptide, and beta-hydroxybutyrate level in atypical clinical scenarios.

Once symptomatic hypoglycemia is recognized, it should be corrected. The typical initial treatment is an amp (25 g) of dextrose 50%. However, a rapid bolus of hyperosmolar fluid can spark an physiological pancreatic overcorrection, resulting in rebound hypoglycemia. If it extravasates, it can cause necrosis leading to possible limb loss. Consider a 250 mL D10 bolus wide open. Recent pre-hospital studies show no difference in time to normoglycemia or symptom resolution.

Consider this treatment algorithm for the next patient that needs a little sugar in their life. Don’t forget to check their level early and often.

References

1. Reference 1

2. Reference 2