What is the emergency management of a diabetic patient presenting with hyperglycemia, weakness, and poor appetite?

Why Diabetics Present to the ER with Elevated Blood Sugar Despite Poor Appetite

Diabetics with poor appetite develop hyperglycemia and weakness because reduced oral intake triggers a stress response that increases counterregulatory hormones (glucagon, catecholamines, cortisol), which raise blood glucose even without food consumption, while concurrent dehydration from osmotic diuresis and potential insulin deficiency or omission create a hyperglycemic crisis. 1

Pathophysiological Mechanism

The paradox of hyperglycemia without eating occurs through several interconnected mechanisms:

• Counterregulatory hormone surge: Poor appetite often accompanies illness or stress, which triggers elevation of glucagon, catecholamines, cortisol, and growth hormone that promote hepatic glucose production (gluconeogenesis and glycogenolysis) independent of food intake 2

• Insulin deficiency compounds the problem: Patients may reduce or omit insulin doses when not eating (a critical error), or the underlying illness increases insulin resistance, creating relative or absolute insulin deficiency 1, 3

• Progressive dehydration creates a vicious cycle: Hyperglycemia causes osmotic diuresis leading to polyuria, which combined with poor oral intake from decreased appetite, results in severe volume depletion that concentrates blood glucose further and impairs insulin delivery to tissues 4, 5

Clinical Presentation Pattern

These patients typically present with one of two hyperglycemic crises:

Diabetic Ketoacidosis (DKA)

• Develops over hours to days 1
• Usually alert initially 1
• Presents with polyuria, polydipsia, weight loss, dehydration, nausea, vomiting, abdominal pain 1
• May have Kussmaul respirations 1

Hyperosmolar Hyperglycemic State (HHS)

• Develops over days to a week 1
• Change in cognitive state is common 1
• Often copresenting with other acute illness 1
• Associated with greater volume depletion 1

Important caveat: Approximately one-third of hyperglycemic emergencies present with hybrid DKA-HHS features, making the clinical picture less clear-cut 1

Emergency Management Algorithm

Step 1: Immediate Assessment (First 15 minutes)

• Obtain arterial blood gases to determine pH: DKA (pH <7.3) versus HHS (pH >7.3) 6
• Calculate effective serum osmolality: 2[measured Na (mEq/L)] + glucose (mg/dL)/18 6, 7
• Calculate corrected sodium: Add 1.6 mEq/L for each 100 mg/dL glucose above 100 mg/dL 6
• Check potassium level immediately before any insulin administration 6, 7

Step 2: Aggressive Fluid Resuscitation (First Hour)

• Initiate isotonic saline (0.9% NaCl) at 15-20 mL/kg/h to restore intravascular volume and tissue perfusion 6
• This addresses the primary pathophysiology of volume depletion that perpetuates hyperglycemia 4

Step 3: Insulin Therapy (After Confirming K⁺ >3.3 mEq/L)

• Verify potassium >3.3 mEq/L before starting insulin to prevent life-threatening hypokalemia 6, 3
• Administer 0.15 units/kg IV bolus of regular insulin 6
• Start continuous IV infusion at 0.1 units/kg/h 6
• Critical error to avoid: Never stop basal insulin even when patients are not eating—this is a common precipitating factor for these crises 1, 3

Step 4: Electrolyte Management

• Add potassium (20-30 mEq/L) to IV fluids when K⁺ <5.5 mEq/L with adequate renal function 7
• Use 2/3 KCl and 1/3 KPO₄ 7
• Monitor potassium closely: Approximately 50% of patients develop hypokalemia during treatment as insulin drives potassium intracellularly 7, 3

Step 5: Ongoing Monitoring

• Monitor blood glucose, electrolytes, BUN, creatinine, and effective osmolality every 2-4 hours 6, 7
• When glucose reaches 250-300 mg/dL, add dextrose 5% to IV fluids to prevent hypoglycemia while continuing insulin to clear ketones 6, 7

Step 6: Transition to Subcutaneous Insulin

• Administer subcutaneous basal insulin 2-4 hours BEFORE stopping IV insulin to prevent rebound hyperglycemia and recurrent crisis 6, 7
• Maintain IV insulin infusion for 1-2 hours after starting subcutaneous regimen 7

Critical Pitfalls to Avoid

• Never advise patients to stop basal insulin when not eating—this is a primary precipitating factor for hyperglycemic crises 1, 3
• Do not start insulin if potassium <3.3 mEq/L—this can cause respiratory paralysis, ventricular arrhythmia, and death 3
• Do not stop IV insulin prematurely—this is the most common management error leading to recurrent hyperglycemia 8
• Do not use hypotonic fluids initially in hemodynamically unstable patients—restore intravascular volume with isotonic saline first 6, 4

Why This Matters for Morbidity and Mortality

• DKA mortality remains 3.4-4.6% despite advances in care 2
• HHS mortality is even higher at approximately 15% 2
• Prognosis is substantially worse in patients >65 years and those presenting with coma or hypotension 2
• The key to reducing mortality is aggressive early fluid resuscitation combined with appropriate insulin therapy and meticulous electrolyte monitoring 6, 8