1. Hypoglycemia Paolo Aquino 29 January 2003

2. Overview of hypoglycemia  What is it?  Why do we care about it?  What causes it?  How do we diagnose it?  What do we do about it?  How do we prevent it?

3. What is it?  Strictly, hypoglycemia refers to a low level of serum glucose  It occurs when a mismatch of endogenous glucose need with exogenous and endogenous glucose availability derails the metabolic engine of normal glucose homeostasis  Often defined as a plasma glucose level < 2.5-2.8 mmol/L (< 45-50 mg/dL)

4. Why do we care about it?  Because hypoglycemia can kill

5. Why do we care about it?  Physiology –Glucose is an obligate metabolic fuel for the brain under physiologic conditions, while other organs can use other forms of fuel (i.e. fatty acids) –The brain can not synthesize its own glucose; it requires a continuous supply via arterial blood

6. Why do we care about it?  Physiology –As the plasma glucose concentration falls below the physiologic range, blood- to-brain glucose transport becomes insufficient for adequate brain energy metabolism and functioning

7. Why do we care about it?  Maintenance of glucose homeostasis –Narrow plasma glucose range is normally maintained despite fluctuations in food intake and activity levels –Maintenance through diet, glycogen breakdown (liver) and gluconeogenesis (liver and kidney)

8. Glucose metabolism

9.  Glycogen stores can last 8-12 hours  Precursors for gluconeogenesis coordinated amongst liver, muscle and adipose tissue –Muscle: lactate, pyruvate, amino acids –Adipose: glycerol, fatty acids

10. Hormonal control  Insulin- inhibits glycogenolysis and gluconeogenesis  decreased serum glucose  Glucagon- promotes glycogenolysis and gluconeogenesis  Epinephrine- limits utilization of glucose by insulin-sensistive tissues  Growth hormone and cortisol have a role during prolonged hypoglycemia

11. What causes it?  Two major etiological classes –Increased insulin levels  Over-medicating  Insulinoma  Sepsis –Underproduction of glucose  Medications- alcohol, salicylates, -blockers  Adrenal insufficiency  Liver disease  Malnutrition, dehydration

12. Hypoglycemia in diabetes

14. Whipple’s Triad  Symptoms of hypoglycemia  Low plasma glucose levels  Resolution of symptoms with administration of glucose

15. Symptoms  Adrenergic: diaphoresis, tachycardia, anxiety, hunger  Neuroglycopenic: dizziness, confusion, slurred speech, seizure

16. Diagnosis  History –Drug use, infection, illness (hepatic, renal, cardiac), surgeries  Laboratory tests- serum glucose, CBC, lytes, BUN/Cr, UA  Other tests: ECG, CXR

17. Diagnosis  Differential –Neurologic: CVA/TIA, seizure disorder –Drug/alcohol intoxication –Psychosis, depression

18. Treatment  Glucose –Oral glucose –IV dextrose: 5-20% solutions, 50% ampules –IM glucagon  Monitor glucose q 2-4 hours  If adrenal insufficiency, administer 100 mg hydrocortisone & 1 mg glucagon  If resistant hypoglycemia secondary to sulfonylureas, administer diazoxide 300 mg over 30 minutes IV q 4 hours PRN

19. Prevention  Treatment of underlying problem –Eliminate/reduce offending drug –Resection of insulinoma –Treat infection –Frequent feedings, avoidance of fasting