Acute complications of diabetes (hypoglycemia, ketoacidosis, hyperosmolar state) Hypoglycemia
Definition
Blood glucose <70 mg/dL, severe if patient requires help to correct it.
Etiology
- Exogenous insulin overdose (most common in insulin-treated DM).
- Sulfonylurea overdose.
- Skipping meals or delayed eating after insulin.
- Strenuous exercise (↑ glucose uptake).
- Alcohol (blocks gluconeogenesis).
Pathogenesis
- Excess insulin → rapid glucose uptake into muscle and fat → decreased plasma glucose.
- Reduced hepatic glucose production (especially when alcohol impairs gluconeogenesis).
- Decreased glucose supply to brain (neuroglycopenia).
Symptoms
Autonomic (adrenergic) symptoms
- Tremor, palpitations, sweating, anxiety, hunger.
- Due to sympathetic and adrenal medullary activation.
Neuroglycopenic symptoms
- Difficulty concentrating, dizziness, weakness, confusion.
- Visual disturbances.
- Seizures, loss of consciousness → coma if severe.
Complications
- Permanent neurological damage if prolonged.
- Repeated episodes → "hypoglycemia unawareness" (blunted adrenergic warning symptoms).
Diabetic Ketoacidosis (DKA)
Definition
- Severe metabolic state characterized by:
- Hyperglycemia (>250 mg/dL).
- Metabolic acidosis (pH <7.3, bicarbonate <15 mEq/L).
- Ketonemia or ketonuria.
Etiology
- Most common in type 1 DM, can rarely occur in advanced type 2 (e.g., under stress).
- Precipitating factors:
- Infection (UTI, pneumonia).
- Trauma, surgery.
- Myocardial infarction.
- Insulin omission.
Pathogenesis
- Absolute insulin deficiency + elevated counter-regulatory hormones (glucagon, cortisol, catecholamines, growth hormone).
- Increased hepatic glucose output (gluconeogenesis & glycogenolysis) → severe hyperglycemia.
- Lipolysis → free fatty acids → liver ketogenesis → ketone bodies (acetoacetate, β-hydroxybutyrate).
- Metabolic acidosis from excess ketones.
- Osmotic diuresis → dehydration, electrolyte depletion (Na, K, phosphate).
Electrolyte disturbances
- Total body potassium depleted (due to osmotic diuresis), even though initial serum K may appear normal or high (shift from cells due to acidosis).
- Hyponatremia (due to osmotic effect of hyperglycemia drawing water into extracellular space).
Clinical manifestations
- Polyuria, polydipsia.
- Dehydration (hypotension, tachycardia).
- Abdominal pain, nausea, vomiting (from acidosis and gastric stasis).
- Kussmaul respiration (deep, rapid breathing to blow off CO₂ and compensate for acidosis).
Fruity odor on breath (acetone).
Mental status changes → stupor, coma.