Physiology · Year 1 · from Physiology
Case 2: Diabetic Ketoacidosis - Glucose Homeostasis Failure
Clinical Image
Source: Wikimedia Commons - DKA symptoms - CC BY-SA 4.0
Patient Presentation
A 19-year-old college student is brought to the emergency department by her roommate after 3 days of progressive fatigue, nausea, vomiting, and abdominal pain. The roommate notes that the patient has been drinking large amounts of water and urinating frequently for the past 2 weeks. She has lost 15 pounds over the past month despite eating normally. Today she became increasingly confused and her breathing has become deep and rapid.
Demographics
- Age: 19 years
- Sex: Female
- Past Medical History: None
- Family History: Type 1 diabetes in older brother
Chief Complaint
Nausea, vomiting, abdominal pain, polyuria, polydipsia, and confusion
Physical Examination
- Blood pressure: 98/62 mmHg (supine), 78/50 mmHg (sitting)
- Heart rate: 118 bpm
- Respiratory rate: 28/min, deep (Kussmaul respirations)
- Temperature: 36.8°C
- General: Lethargic, appears dehydrated
- Mucous membranes: Dry
- Skin: Poor turgor, no rashes
- Breath: Fruity odor (acetone)
- Abdomen: Diffuse tenderness without guarding
Workup
- Blood glucose: 524 mg/dL
- Serum pH: 7.18 (metabolic acidosis)
- Serum bicarbonate: 8 mEq/L (low)
- Anion gap: 28 (elevated)
- Serum ketones: Large
- Beta-hydroxybutyrate: 6.8 mmol/L
- Serum potassium: 5.4 mEq/L (high but total body potassium depleted)
- Serum sodium: 128 mEq/L (pseudohyponatremia)
- HbA1c: 13.2%
- C-peptide: Undetectable (confirms insulin deficiency)
Diagnosis
New-onset Type 1 Diabetes Mellitus presenting with Diabetic Ketoacidosis (DKA)
Treatment
- IV fluid resuscitation: 0.9% saline initially, then 0.45% saline
- Continuous IV insulin infusion (0.1 units/kg/hour)
- Potassium replacement (added to fluids once K+ <5.3 and patient urinating)
- Dextrose added to IV fluids when glucose <200-250 mg/dL
- Frequent monitoring of glucose, electrolytes, and anion gap
- Transition to subcutaneous insulin when anion gap closed and patient eating
- Diabetes education and outpatient follow-up
Physiological Principles Demonstrated
- Counter-regulatory hormones: In the absence of insulin, counter-regulatory hormones (glucagon, cortisol, growth hormone, epinephrine) are unopposed, promoting gluconeogenesis, glycogenolysis, and lipolysis.
- Ketogenesis: Without insulin, free fatty acids are mobilized and converted to ketone bodies in the liver. Accumulation of acetoacetic acid and beta-hydroxybutyric acid causes metabolic acidosis.
- Respiratory compensation: Kussmaul respirations represent the respiratory system's attempt to compensate for metabolic acidosis by eliminating CO2, reducing the denominator in the Henderson-Hasselbalch equation.
- Feedback failure: The normal negative feedback where elevated glucose stimulates insulin release fails completely in Type 1 diabetes due to autoimmune destruction of beta cells.