Internal Medicine · Year 3 · from Internal Medicine

Case 1: Diabetic Ketoacidosis with Anion Gap Metabolic Acidosis

Patient Demographics

  • Age: 24 years
  • Sex: Female
  • Occupation: Graduate student

Chief Complaint

"I feel terrible, I've been throwing up all day and I can't catch my breath."

History of Present Illness

The patient presents to the emergency department with a 2-day history of nausea, vomiting, and abdominal pain. She reports excessive thirst and frequent urination over the past week. Today she developed rapid, deep breathing and generalized weakness. She has a history of type 1 diabetes mellitus diagnosed at age 12, but admits to poor compliance with her insulin regimen over the past month due to stress related to graduate school examinations. Her insulin pump ran out of supplies 3 days ago and she has been using her backup insulin pen inconsistently.

Vital Signs

  • Temperature: 99.1 degrees F (37.3 degrees C)
  • Blood pressure: 98/62 mmHg
  • Heart rate: 118 bpm
  • Respiratory rate: 28/min, deep respirations (Kussmaul breathing)
  • Oxygen saturation: 99% on room air

Physical Examination

General: Ill-appearing, lethargic but arousable, fruity breath odor HEENT: Dry mucous membranes, sunken eyes Cardiovascular: Tachycardic, regular rhythm, no murmurs Pulmonary: Clear bilaterally, rapid deep breathing pattern Abdomen: Diffusely tender without guarding or rebound, hypoactive bowel sounds Extremities: Cool extremities, delayed capillary refill (4 seconds) Neurologic: Alert but slow to respond, oriented x2 (person and place)

Laboratory Findings

Arterial Blood Gas:

  • pH: 7.18 (low - acidemia)
  • PaCO2: 18 mmHg (low - respiratory compensation)
  • PaO2: 105 mmHg
  • HCO3: 6 mEq/L (low - metabolic acidosis)

Basic Metabolic Panel:

  • Sodium: 132 mEq/L
  • Potassium: 5.8 mEq/L
  • Chloride: 98 mEq/L
  • Bicarbonate: 6 mEq/L
  • BUN: 32 mg/dL
  • Creatinine: 1.8 mg/dL
  • Glucose: 486 mg/dL

Additional Studies:

  • Anion gap: 132 - (98 + 6) = 28 mEq/L (elevated, normal 8-12)
  • Beta-hydroxybutyrate: 8.2 mmol/L (markedly elevated)
  • Serum ketones: Large
  • Urinalysis: Glucose 4+, ketones 3+

Systematic ABG Interpretation

Step 1 - pH Assessment: pH 7.18 indicates acidemia

Step 2 - Primary Disorder: Low pH with low HCO3 = primary metabolic acidosis

Step 3 - Compensation Assessment:

  • Expected PaCO2 = 1.5 x HCO3 + 8 (plus/minus 2) - Winter's formula
  • Expected PaCO2 = 1.5 x 6 + 8 = 17 mmHg (range 15-19)
  • Actual PaCO2 = 18 mmHg (within expected range)
  • Interpretation: Appropriate respiratory compensation, no secondary respiratory disorder

Step 4 - Anion Gap:

  • Anion gap = 28 mEq/L (elevated)
  • Delta gap = 28 - 12 = 16
  • Delta-delta ratio = 16 / (24 - 6) = 16 / 18 = 0.89
  • Ratio between 1-2 suggests pure anion gap metabolic acidosis
  • Ratio slightly below 1 may suggest mild concurrent non-anion gap metabolic acidosis (from GI losses with vomiting)

Diagnosis

Diabetic ketoacidosis - severe, with anion gap metabolic acidosis

  • Hyperglycemia > 250 mg/dL
  • Arterial pH < 7.3
  • Serum bicarbonate < 18 mEq/L
  • Elevated anion gap
  • Ketonemia/ketonuria

Management

Fluid resuscitation:

  1. 0.9% Normal saline 1-2 L bolus over first hour
  2. Continue NS at 250-500 mL/hour based on hemodynamic status
  3. Switch to 0.45% NS once sodium normalizes

Insulin therapy:

  1. Regular insulin 0.1 units/kg IV bolus
  2. Regular insulin continuous infusion at 0.1 units/kg/hour
  3. Add dextrose to IV fluids when glucose reaches 200 mg/dL (D5 0.45% NS)
  4. Continue insulin until anion gap closes (<12)

Potassium management:

  1. Despite elevated serum potassium, total body potassium is depleted
  2. Once K < 5.3 and adequate urine output, add 20-40 mEq KCl per liter of IV fluid
  3. Hold potassium if K > 5.3, recheck every 2 hours
  4. Goal: maintain K 4.0-5.0 mEq/L

Monitoring:

  1. Basic metabolic panel every 2-4 hours
  2. Anion gap calculation with each set of labs
  3. Continuous cardiac monitoring
  4. Hourly blood glucose initially

Clinical Pearl

The anion gap in DKA is elevated due to accumulation of ketoacids (beta-hydroxybutyrate and acetoacetate). The Kussmaul breathing pattern represents maximal respiratory compensation - the body's attempt to blow off CO2 and raise the pH. Potassium management is critical: while the initial serum potassium may be normal or elevated due to transcellular shifts from acidosis and insulin deficiency, total body potassium is always depleted. Once insulin is started, potassium shifts rapidly into cells, potentially causing dangerous hypokalemia if not carefully monitored and replaced.

Clinical Image

Image Description: Clinical photograph demonstrating the deep, labored breathing pattern characteristic of diabetic ketoacidosis (Kussmaul respiration), reflecting the body's respiratory compensation for severe metabolic acidosis.

Attribution: Image from Wikimedia Commons. Licensed under CC BY-SA 3.0. Source: https://commons.wikimedia.org/wiki/File:Metabolic_acidosis.svg

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