An 8-year old boy is brought to the emergency department because he has been lethargic and has had several episodes of nausea and vomiting for the past day. He has also had increased thirst over the past two months. He has lost 5.4 kg (11.9 lbs) during this time. He is otherwise healthy and has no history of serious illness. His temperature is 37.5 °C (99.5 °F), blood pressure is 95/68 mm Hg, pulse is 110/min, and respirations are 30/min. He is somnolent and slightly confused. His mucous membranes are dry. Laboratory studies show: Hemoglobin 16.2 g/dL Leukocyte count 9,500/mm3 Platelet count 380,000/mm3 Serum Na+ 130 mEq/L K+ 5.5 mEq/L Cl- 99 mEq/L HCO3- 16 mEq/L Creatinine 1.2 mg/dL Glucose 570 mg/dL Ketones positive Blood gases, arterial pH 7.25 pCO2 21 mm Hg Which of the following is the most appropriate next step in management?

Intravenous hydration with 0.9% normal saline and insulin

Intravenous hydration with 0.45% normal saline and insulin

Intravenous hydration with 5% dextrose solution and 0.45% normal saline

Intravenous hydration with 0.9% normal saline and potassium chloride

A 27-year-old man presents to the emergency department with his family because of abdominal pain, excessive urination, and drowsiness since the day before. He has had type 1 diabetes mellitus for 2 years. He ran out of insulin 2 days ago. The vital signs at admission include: temperature 36.8°C (98.2°F), blood pressure 102/69 mm Hg, and pulse 121/min. On physical examination, he is lethargic and his breathing is rapid and deep. There is a mild generalized abdominal tenderness without rebound tenderness or guarding. His serum glucose is 480 mg/dL. Arterial blood gas of this patient will most likely show which of the following?

↓ pH, ↓ bicarbonate and ↑ anion gap

↑ pH, ↑ bicarbonate, and normal pCO2

↑ pH, normal bicarbonate and ↓ pCO2

↓ pH, ↓ bicarbonate and normal anion gap

↓ pH, normal bicarbonate and ↑ pCO2

A 21-year-old man presents to the emergency room with abdominal pain and nausea for the past 5 hours. The pain is diffusely spread and of moderate intensity. The patient also says he has not felt like eating since yesterday. He has no past medical history and is not on any medications. He regularly drinks 2–4 beers per day but does not smoke or use illicit substances. Vitals show a pulse of 120/min, a respiratory rate of 26/min, a blood pressure of 110/60 mm Hg, and a temperature of 37.8°C (100.0°F). Examination reveals a soft, diffusely tender abdomen with no guarding. Bowel sounds are present. His mucous membranes are slightly dry and there is a fruity smell to his breath. Laboratory tests show: Laboratory test pH 7.31 Serum glucose (random) 450 mg/dL Serum electrolytes Sodium 149 mEq/L Potassium 5 mEq/L Chloride 99 mEq/L Bicarbonate 16 mEq/L Serum creatinine 1.0 mg/dL Blood urea nitrogen 15 mg/dL Urinalysis Proteins Negative Glucose Positive Ketones Positive Leucocytes Negative Nitrites Negative Red blood cells (RBC) Negative Casts Negative Which of the following explains this patient's presentation?

Burn out of pancreatic beta cells

Presence of gut contents in the abdominal cavity

Effects of alcohol on mitochondrial metabolic activity

A 48-year-old man presents with DKA. Initial treatment is initiated with fluids and insulin infusion. Labs show glucose 460 mg/dL, pH 7.18, bicarbonate 10 mEq/L, potassium 4.5 mEq/L, and creatinine 2.8 mg/dL (baseline 1.0). After 4 hours, glucose decreases to 380 mg/dL but pH worsens to 7.12, bicarbonate drops to 8 mEq/L, and lactate is 5.2 mmol/L (initially 1.8). Blood pressure is 85/50 mmHg. Evaluate the clinical situation and necessary intervention.

Evaluate for sepsis or other concurrent illness causing lactic acidosis

Administer additional fluid bolus for persistent hypotension

Increase insulin infusion rate to accelerate ketone clearance

Add bicarbonate therapy for worsening acidosis

Continue current management as DKA takes time to resolve

A 25-year-old woman with type 1 diabetes presents with DKA. She admits to intentionally withholding insulin to lose weight. This is her fifth DKA admission in 8 months. Current pH is 7.14, glucose 520 mg/dL, bicarbonate 11 mEq/L. Medical costs exceed $150,000 for recurrent admissions. The team is frustrated. Evaluate the comprehensive management approach beyond acute DKA treatment.

Multidisciplinary approach including psychiatry, eating disorder specialist, diabetes educator, and close outpatient follow-up

Referral to ethics committee for discussion of resource allocation

Involuntary psychiatric commitment for non-compliance

Insulin pump placement to prevent future manipulation

Standard DKA treatment with discharge to outpatient endocrinology

A 55-year-old man with type 2 diabetes and end-stage renal disease on hemodialysis presents with DKA. Initial glucose is 580 mg/dL, pH 7.12, bicarbonate 10 mEq/L, and potassium 6.2 mEq/L. He is fluid overloaded with bilateral crackles and peripheral edema. His last dialysis was 3 days ago. Evaluate the optimal management strategy addressing both DKA and renal failure.

Insulin infusion with limited fluids and urgent hemodialysis

Standard DKA protocol with furosemide for fluid management

Bicarbonate therapy to correct acidosis without fluids

Subcutaneous insulin with no IV fluids due to volume overload

Standard DKA protocol with aggressive fluid resuscitation

A 38-year-old pregnant woman at 28 weeks gestation with type 1 diabetes presents with nausea and vomiting. Labs show glucose 310 mg/dL, pH 7.27, bicarbonate 15 mEq/L, and positive urine ketones. Fetal monitoring shows reactive non-stress test. She has been taking her insulin but unable to eat for 24 hours due to hyperemesis. Analyze the optimal management approach considering maternal and fetal risks.

Aggressive DKA treatment with lower glucose targets (100-150 mg/dL) and close fetal monitoring

Standard DKA protocol with standard glucose targets (200-250 mg/dL)

Immediate cesarean delivery followed by DKA treatment

Conservative management with oral intake and subcutaneous insulin

Standard DKA protocol with delivery planning after stabilization

A 42-year-old man with type 1 diabetes on insulin pump presents with DKA after pump malfunction. He is admitted and started on IV insulin infusion. After 14 hours of treatment, his glucose is 210 mg/dL on D5-0.45% saline, pH 7.36, bicarbonate 19 mEq/L, and anion gap 12. He is alert, eating, and requesting to go home. Evaluate the appropriate transition strategy.

Give subcutaneous insulin, overlap for 1-2 hours, then stop IV insulin and observe

Switch to subcutaneous insulin and discharge immediately

Stop IV insulin immediately and restart insulin pump at home

Continue IV insulin for another 6 hours to ensure stability

Discontinue IV insulin, discharge with oral medications

A 52-year-old woman with type 2 diabetes is admitted for DKA. Initial pH is 7.08, bicarbonate 8 mEq/L, and anion gap 28. She is started on standard DKA protocol. After 10 hours of treatment, her glucose is 180 mg/dL, pH is 7.28, bicarbonate is 14 mEq/L, but anion gap remains elevated at 22. Chloride is 115 mEq/L (elevated). Analyze the acid-base status.

Mixed anion gap and non-anion gap acidosis

Renal tubular acidosis unmasked by treatment

Persistent DKA requiring increased insulin rate

Non-anion gap metabolic acidosis from excessive saline administration

Resolving DKA with appropriate response to treatment

Precipitating factors identification for USMLE Step 3: High-Yield Management Lessons

The 'I' Team - DKA's Top Triggers

Identifying the underlying cause of Diabetic Ketoacidosis (DKA) is crucial for management and preventing recurrence. The most common triggers can be recalled with the "5 I's" mnemonic.

📌 Mnemonic: The 5 I's

Infection: The most frequent cause (~40%). Pneumonia and Urinary Tract Infections (UTIs) are classic examples. Always investigate for a source.
Infarction/Ischemia: Myocardial infarction, stroke (CVA), or peripheral ischemia trigger DKA via stress hyperglycemia.
Insulin: Non-compliance, missed doses, or inadequate therapy (e.g., insulin pump failure) is a major, preventable factor.
Intoxication: Alcohol abuse, particularly binge drinking, can precipitate DKA. Other substances may also contribute.
Iatrogenic: Medications like corticosteroids, thiazide diuretics, and sympathomimetics can elevate glucose.

Other Key Triggers:

Initial presentation of Type 1 Diabetes.
Inflammation: Pancreatitis, cholecystitis.

⭐ Euglycemic DKA: Remember that SGLT2 inhibitors (e.g., canagliflozin) can trigger DKA with blood glucose levels <250 mg/dL, potentially masking the diagnosis.

Medication Mischief - The Pharma Culprits

Insulin Errors: The most common trigger. Includes non-compliance, missed doses, or insulin pump failure.
SGLT-2 Inhibitors: Canagliflozin, Dapagliflozin. Can precipitate euglycemic DKA (eDKA), where glucose may be <250 mg/dL.
Glucocorticoids: Prednisone, hydrocortisone. ↑ Insulin resistance and ↑ gluconeogenesis.
Atypical Antipsychotics: Olanzapine, clozapine. Worsen hyperglycemia and metabolic control.
Thiazide Diuretics: Hydrochlorothiazide. Can cause hyperglycemia and hypokalemia.
Sympathomimetics: Dobutamine, terbutaline, cocaine. Increase catecholamine-driven glucose production.

⭐ Exam Favorite: Always consider euglycemic DKA in patients on SGLT-2 inhibitors presenting with anion gap metabolic acidosis, even with deceptively normal blood glucose levels.

Euglycemic DKA: Risk Factors, Diagnosis, Management

Clinical Detective - Unmasking the Cause

A systematic search for the underlying trigger is crucial, as management involves treating both the DKA and its cause. The most common precipitants can be recalled with the "5 I's" mnemonic.

📌 Mnemonic: The 5 I's

Infection (~40%): The most common trigger.
- Urinary Tract Infection (UTI)
- Pneumonia
- Sepsis
- Look for fever, leukocytosis, and localized symptoms.
Infarction/Ischemia:
- Myocardial Infarction (MI): Often silent in diabetics. Always get an EKG.
- Cerebrovascular Accident (CVA) / Stroke
- Mesenteric or peripheral ischemia.
Iatrogenic:
- Medications: Corticosteroids, Thiazide diuretics, Sympathomimetics, and atypical antipsychotics.
- 💡 SGLT-2 inhibitors (e.g., canagliflozin) can cause euglycemic DKA (eDKA), where glucose may be <250 mg/dL.
Insulin Deficiency (Inadequate Insulinization):
- Non-compliance: Missed or insufficient insulin doses is a major cause, especially in known diabetics.
- New-onset Type 1 Diabetes.
- Insulin pump malfunction or catheter occlusion.
Infant (Pregnancy):
- Increased insulin resistance, particularly in the 2nd and 3rd trimesters.
- Physiological stress and hormonal changes.

⭐ Infection, particularly UTI or pneumonia, is the leading precipitant for DKA, responsible for up to 40% of cases. Always obtain urine and chest imaging if suspicious.

High‑Yield Points - ⚡ Biggest Takeaways

Infection is the most common precipitant; always rule out UTIs and pneumonia.

Insulin non-compliance or inadequate dosing is a major, preventable trigger.

Consider myocardial infarction or stroke, especially in elderly patients, even without classic symptoms.

New-onset Type 1 Diabetes frequently presents as DKA.

Iatrogenic causes like steroids or SGLT-2 inhibitors are key non-compliance triggers.

Acute pancreatitis can be both a cause and a consequence.

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