Emergency Medicine · Year 3 · from Emergency Medicine

Case 1: Diabetic Ketoacidosis - The New-Onset Diabetic

Patient Demographics

• Age: 16 years
• Sex: Female
• Occupation: High school student

Chief Complaint

"She's been vomiting all day and is breathing really fast."

History of Present Illness

Parents bring their 16-year-old daughter for evaluation of progressive fatigue and malaise over 3 weeks, polydipsia and polyuria for 2 weeks, and today developed nausea, vomiting (x5 episodes), and abdominal pain. Parents note she has lost 15 pounds over the past month despite eating more than usual. She appears confused and is breathing rapidly.

Initial Assessment

ESI Level: 2 - High-risk metabolic emergency

First Impression:

• Appearance: Lethargic, appears dehydrated
• Work of breathing: Deep, rapid respirations (Kussmaul breathing)
• Circulation: Dry mucous membranes, pale

Vital Signs:

• Heart rate: 124 bpm
• Blood pressure: 102/58 mmHg
• Respiratory rate: 28 breaths/min, deep
• SpO2: 99% on room air
• Temperature: 37.2C
• GCS: 13 (E3V4M6)
• Weight: 52 kg (usual 67 kg per parents)

Point-of-Care Glucose: 542 mg/dL

Primary Survey

Airway: Patent Breathing: Kussmaul respirations (deep, rapid) - respiratory compensation for metabolic acidosis Circulation: Tachycardic, mild hypotension, delayed cap refill (4 seconds) Disability: Lethargic, confused (only oriented to person) Exposure: Dry skin and mucous membranes, fruity breath odor (acetone)

Classic DKA Presentation

The 3 P's of New Diabetes:

• Polyuria - frequent urination (osmotic diuresis)
• Polydipsia - excessive thirst
• Polyphagia - increased appetite (with weight loss)

DKA Triad:

1. Hyperglycemia (>250 mg/dL)
2. Ketosis (ketonemia/ketonuria)
3. Acidosis (pH <7.3, HCO3 <18)

Secondary Survey

SAMPLE History:

• Symptoms: Fatigue, polyuria, polydipsia, weight loss, nausea/vomiting, abdominal pain, confusion
• Allergies: None
• Medications: None
• PMH: Healthy, no known diabetes
• Last Meal: Attempted breakfast, vomited
• Events: Progressive symptoms over weeks, acute worsening today

Physical Examination:

• HEENT: Dry mucous membranes, sunken eyes, fruity breath
• Neck: Supple, no thyromegaly
• Cardiac: Tachycardic, no murmur
• Lungs: Clear, Kussmaul respirations
• Abdomen: Diffuse tenderness, no guarding (DKA gastroparesis)
• Skin: Dry, tenting
• Neuro: Lethargic, oriented x1, moving all extremities

Diagnostic Testing

Labs:

• Glucose: 542 mg/dL
• Na: 128 mEq/L (factitious hyponatremia - calculate corrected)
• K: 5.4 mEq/L (elevated due to acidosis despite total body depletion)
• Cl: 98 mEq/L
• HCO3: 8 mEq/L
• BUN: 32
• Cr: 1.4 (prerenal AKI from dehydration)
• Anion gap: 128 - (98 + 8) = 22 (elevated)

ABG:

• pH: 7.14
• pCO2: 22 (appropriate respiratory compensation)
• HCO3: 7

Additional Labs:

• Beta-hydroxybutyrate: 6.8 mmol/L (elevated - confirms ketosis)
• Serum osmolality: 312 mOsm/kg
• HbA1c: 13.2% (confirms prolonged hyperglycemia)
• Urinalysis: Large ketones, large glucose

Corrected Sodium Calculation:

• Corrected Na = Measured Na + 1.6 x [(Glucose - 100)/100]
• Corrected Na = 128 + 1.6 x [(542-100)/100] = 128 + 7 = 135 mEq/L

Diagnosis

Diabetic Ketoacidosis (DKA) - Severe (pH <7.1)

• New-onset Type 1 Diabetes Mellitus

Management - DKA Protocol

Hour 1:

1. IV Fluids: NS 1L bolus (20 mL/kg)
2. Insulin: Regular insulin 0.1 units/kg/hour IV infusion (5.2 units/hour)
3. Potassium: Hold initially (K >5.2); recheck in 2 hours
4. Monitoring: Hourly glucose, q2-4h BMP, continuous cardiac monitoring

Fluid Management Protocol:

• After initial bolus: NS at 250-500 mL/hour
• When glucose <200: Switch to D5 0.45% NS to prevent hypoglycemia while continuing insulin

Insulin Goals:

• Glucose decrease: 50-70 mg/dL per hour (avoid rapid correction)
• Continue insulin until anion gap closes, not based on glucose alone

Serial Monitoring

At 4 hours:

• Glucose <300: Switched to D5 0.45% NS
• K <5: Started KCl 20 mEq/L in fluids

At 12 hours:

• Anion gap closed (<12)
• Patient eating
• Transitioned to subcutaneous insulin (overlap IV for 1-2 hours)

Complications to Monitor

1. Cerebral edema (especially in children/new-onset)

• Warning signs: Headache, altered mental status, bradycardia, HTN
• This patient: Monitored closely, no signs developed

1. Hypokalemia (as acidosis corrects and insulin drives K intracellularly)

• Aggressive K replacement as needed

1. Hypoglycemia (if insulin continued without dextrose)

• Prevented by switching to dextrose-containing fluids

Disposition

• ICU admission for first 12 hours
• Transfer to floor when anion gap closed
• Diabetes education initiated
• Endocrinology consultation
• Insulin regimen: Basal-bolus with carbohydrate counting
• Discharged day 4 with extensive education

Teaching Points

1. Don't stop insulin when glucose normalizes: Continue until anion gap closes
2. Potassium shifts: Serum K may be high despite total body depletion; replace aggressively as it falls
3. Cerebral edema risk: Highest in children, new-onset diabetes, severe DKA; avoid overly rapid correction
4. Fluid before insulin: In severe dehydration, initial fluid bolus before insulin
5. Search for precipitant: Infection, medication non-compliance, new diagnosis (like this case)
6. Corrected sodium: Use formula to assess true sodium status
7. Kussmaul respirations: Deep, rapid breathing = respiratory compensation for metabolic acidosis

Clinical Image

Image Description: Illustration demonstrating Kussmaul respirations - the characteristic deep, labored breathing pattern seen in metabolic acidosis (such as DKA), representing respiratory compensation to blow off CO2 and raise pH.

Attribution: Image from Wikimedia Commons, Kussmaul breathing. Licensed under CC BY-SA 4.0. Source: https://commons.wikimedia.org/wiki/File:Kussmaul_breathing.svg

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