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This is a clinician-written, evidence-based summary aligned to the USMLE Step 2 CK Content Outline. It is intended for medical students preparing for USMLE Step 2 CK. Management reflects current ACC/AHA, USPSTF, and APA guidelines. Always cross-reference with UpToDate, institutional protocols, and clinical judgment.
The Bottom Line
- DKA = hyperglycemia + ketosis + anion gap metabolic acidosis, most common in type 1 diabetes
- Diagnostic pattern: glucose usually >250 mg/dL, pH <7.30, bicarbonate <18, positive beta-hydroxybutyrate, elevated anion gap
- Initial therapy: isotonic IV fluids first, then IV regular insulin once potassium is known
- Do NOT start insulin if K+ <3.3 mEq/L — replace potassium first to avoid fatal arrhythmia
- DKA is resolved when anion gap closes, bicarbonate improves, pH normalizes, and patient can eat
Overview
Diabetic ketoacidosis is an acute metabolic emergency caused by insulin deficiency and counterregulatory hormone excess. Without enough insulin, hepatic gluconeogenesis and glycogenolysis cause hyperglycemia, while lipolysis generates free fatty acids that are converted into ketone bodies, especially beta-hydroxybutyrate. The result is osmotic diuresis, dehydration, electrolyte depletion, and anion gap metabolic acidosis. DKA is classically associated with type 1 diabetes, but it can also occur in type 2 diabetes during severe physiologic stress or in ketosis-prone diabetes.
Epidemiology
DKA is one of the most common endocrine emergencies in the United States and is a frequent reason for hospitalization in children, adolescents, and adults with type 1 diabetes. Common precipitants include infection, missed insulin, new-onset type 1 diabetes, myocardial infarction, stroke, pancreatitis, pregnancy, trauma, corticosteroids, sympathomimetics, atypical antipsychotics, and SGLT2 inhibitors. Euglycemic DKA is increasingly tested because glucose may be <250 mg/dL, especially with SGLT2 inhibitor use, pregnancy, starvation, or partial insulin treatment.
Clinical Features
Symptoms
Polyuria, polydipsia, and marked thirst from osmotic diuresis
Nausea, vomiting, and abdominal pain that may mimic a surgical abdomen
Weight loss, fatigue, and weakness
Altered mental status ranging from lethargy to coma in severe DKA
Recent infection symptoms, missed insulin, or new diabetes symptoms
Signs
Tachycardia, dry mucous membranes, poor skin turgor, orthostatic hypotension
Kussmaul respirations from metabolic acidosis
Fruity or acetone breath odor
Hypothermia or fever depending on precipitating infection
Hypotension or shock in severe dehydration
Cerebral edema signs: headache, bradycardia, hypertension, declining mental status — especially in children
Investigations
First-line
Basic metabolic panelGlucose, sodium, potassium, bicarbonate, BUN/Cr. Calculate anion gap: Na - (Cl + HCO3). Correct sodium for hyperglycemia by adding ~1.6 mEq/L for each 100 mg/dL glucose above 100
Venous blood gaspH <7.30 supports DKA. Venous pH is usually adequate and avoids arterial sampling
Serum beta-hydroxybutyratePreferred ketone test; urine nitroprusside can underestimate early DKA because it detects acetoacetate more than beta-hydroxybutyrate
Serum osmolalityAssesses hyperosmolarity and overlap with HHS
Second-line
CBC, urinalysis, blood cultures if febrileSearch for infection trigger; leukocytosis may occur from stress even without infection
ECGEvaluate potassium effects and screen for MI in adults or patients with chest symptoms
HbA1cHelps distinguish chronic poor control from acute presentation
Specialist
Chest X-ray or targeted imagingIf pneumonia, sepsis, abdominal pathology, or another precipitant is suspected
Frequent bedside glucose and electrolytesGlucose hourly; BMP every 2-4 hours during insulin infusion
1
Initial stabilization
- Assess airway, breathing, circulation; place on cardiac monitoring if moderate/severe DKA or potassium abnormality
- Start 0.9% saline or balanced crystalloid 15-20 mL/kg in first hour unless contraindicated
- Identify and treat precipitating cause: infection, missed insulin, MI, stroke, pancreatitis, pregnancy, medication trigger
2
Potassium-first decision
- K+ <3.3 mEq/L: hold insulin; give potassium 20-30 mEq/h until K+ >3.3
- K+ 3.3-5.2: give 20-30 mEq K+ in each liter IV fluid
- K+ >5.2: do not give potassium initially; recheck every 2 hours
3
Insulin therapy
- Start IV regular insulin 0.1 units/kg/h after potassium is confirmed >=3.3 mEq/L
- Expected glucose fall: 50-75 mg/dL per hour
- When glucose reaches ~200 mg/dL, add dextrose to IV fluids and continue insulin until anion gap closes
- Do not stop insulin just because glucose normalizes — ketogenesis stops only when insulin is continued
4
Bicarbonate and phosphate
- Bicarbonate generally not indicated unless pH <6.9
- Replace phosphate only if severe hypophosphatemia, respiratory depression, cardiac dysfunction, or anemia
5
Transition to subcutaneous insulin
- DKA resolution: anion gap closed, bicarbonate >=15-18, pH >7.3, patient clinically improved and able to eat
- Overlap IV insulin with basal subcutaneous insulin by 2-4 hours to prevent rebound DKA
- Provide sick-day education, insulin access review, and follow-up plan before discharge
Complications
- Cerebral edema: Rare in adults but feared in children; presents with headache, altered mental status, bradycardia, hypertension
- Hypokalemia: Total body potassium depleted even if initial serum K+ is normal or high; insulin shifts K+ intracellularly
- Hypoglycemia: Occurs if insulin continues without dextrose once glucose falls
- Non-anion gap acidosis: Can appear during recovery due to chloride-rich fluids and urinary ketoanion loss
- ARDS, thrombosis, shock: Severe dehydration and systemic inflammation increase risk
USMLE Step 2 CK Exam Tips
- 1DKA labs: glucose >250, positive ketones, pH <7.30, bicarbonate <18, elevated anion gap
- 2First step is IV fluids, not insulin, because patients are profoundly volume depleted
- 3Always check potassium before insulin. K+ <3.3 = potassium first, insulin later
- 4Euglycemic DKA with SGLT2 inhibitors: acidosis + ketones with glucose <250 — do not be reassured by a modest glucose
- 5Continue insulin until the anion gap closes, even after glucose reaches 200 mg/dL; add dextrose instead of stopping insulin
- 6Abdominal pain in DKA can mimic appendicitis; reassess after metabolic correction unless peritoneal signs persist
- 7Cerebral edema after treatment in a child with headache/bradycardia/declining mental status = mannitol or hypertonic saline
- 8Bicarbonate is almost never the answer unless pH <6.9
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