What is the appropriate management for a patient presenting to the emergency department with persistent nausea, recurrent vomiting, progressive shortness of breath, diffuse abdominal pain, increasing fatigue, history of polyuria (excessive urine production) and polydipsia (excessive thirst), and recent poor oral intake?

Diabetic Ketoacidosis (DKA) Management

This patient is presenting with diabetic ketoacidosis (DKA) and requires immediate emergency treatment with intravenous insulin, aggressive fluid resuscitation, and electrolyte replacement, particularly potassium monitoring. 1

Recognition of DKA

The clinical presentation is classic for DKA with the constellation of:

• Polyuria and polydipsia (early hyperglycemia symptoms that have now lessened due to dehydration) 1
• Nausea, vomiting, and diffuse abdominal pain (present in up to 25% of DKA patients) 1
• Progressive shortness of breath (representing Kussmaul respirations—compensatory tachypnea for metabolic acidosis) 1
• "Deep breathing" sensation and lightheadedness (further evidence of respiratory compensation and altered mental status) 1
• Poor oral intake leading to dehydration 1

The evolution typically occurs within 24 hours in type 1 diabetes, though it can develop over several days in type 2 diabetes. 1 The fact that polyuria/polydipsia have "lessened" is concerning—this indicates progression to severe dehydration where the patient can no longer maintain osmotic diuresis. 1

Immediate Diagnostic Workup

Order the following laboratory tests immediately upon ED arrival:

• Serum glucose to confirm hyperglycemia 2
• Serum electrolytes including sodium, potassium, chloride, and bicarbonate to assess metabolic acidosis and electrolyte derangements 1, 2
• Arterial or venous blood gas to quantify acidosis 1
• Serum ketones (β-hydroxybutyrate preferred) or urine ketones to confirm ketonemia/ketonuria 1
• Complete blood count to assess for infection as precipitating factor 2
• Lipase to exclude pancreatitis 2
• Urinalysis to assess for ketones and rule out urinary tract infection 2
• HbA1c to determine if this is new-onset diabetes 3

Critical Initial Management

Fluid Resuscitation

Begin aggressive intravenous fluid replacement immediately with 0.9% normal saline at 15-20 mL/kg/hour (approximately 1-1.5 L) in the first hour. 1 DKA causes profound osmotic diuresis leading to severe dehydration with loss of water, sodium, potassium, and other electrolytes. 1

Insulin Therapy

Start continuous intravenous regular insulin infusion at 0.1 units/kg/hour after initial fluid bolus. 1, 4 Intravenous insulin has rapid onset of action and is essential for DKA management. 4 The insulin will suppress lipolysis, halt ketone body production, and facilitate glucose utilization. 1

Potassium Replacement—Critical Pitfall

Monitor serum potassium closely and replace aggressively. 1, 4 This is the most dangerous aspect of DKA management:

• Insulin stimulates potassium movement into cells, potentially causing life-threatening hypokalemia 4
• Hypokalemia can cause respiratory paralysis, ventricular arrhythmia, and death 4
• Do not start insulin if serum potassium is <3.3 mEq/L—replace potassium first 1
• Add potassium to IV fluids once urine output is established and serum potassium is <5.3 mEq/L 1
• Intravenously administered insulin requires increased attention to hypokalemia monitoring 4

Identify Precipitating Factors

Search for the trigger while initiating treatment:

• Infection is the most common precipitating factor 1
• New-onset type 1 diabetes or insulin omission in known diabetes 1
• Other triggers include myocardial infarction, stroke, pancreatitis, trauma, or medications (corticosteroids, thiazides, sympathomimetics) 1

Common Pitfalls to Avoid

Never dismiss the abdominal pain as purely metabolic. While abdominal pain occurs in DKA itself, up to 25% have hemorrhagic gastritis with coffee-ground emesis. 1 If abdominal pain is severe or persistent after initial treatment, consider pancreatitis (check lipase) or other intra-abdominal pathology. 2

Never use antiemetics if mechanical obstruction is suspected, as this masks progressive ileus. 2 However, in confirmed DKA without obstruction, antiemetics may be appropriate for symptom relief.

Hypothermia is a poor prognostic sign. 1 Patients with DKA can be normothermic or hypothermic despite infection due to peripheral vasodilation. 1

Monitor mental status closely. Altered consciousness can range from full alertness to profound lethargy or coma, with the latter more common in hyperosmolar hyperglycemic state (HHS). 1 However, significant mental status changes can occur in DKA and indicate severity.

Disposition

This patient requires ICU-level monitoring for continuous insulin infusion, hourly glucose and electrolyte monitoring (especially potassium), and close observation for complications including cerebral edema, hypokalemia, and hypoglycemia. 1, 4