Diagnosis and Treatment of Hyperglycemia, Metabolic Acidosis, and Severe Infection
This patient most likely has diabetic ketoacidosis (DKA) precipitated by severe infection, requiring immediate simultaneous treatment of both the metabolic crisis and the underlying infectious process to prevent mortality.
Diagnostic Approach
The triad of hyperglycemia, metabolic acidosis, and severe infection strongly suggests DKA with sepsis as the precipitating factor. 1, 2
Essential Laboratory Evaluation
Obtain the following immediately to confirm diagnosis and guide treatment: 1
- Plasma glucose (typically >250 mg/dL in DKA, though 10% present with euglycemic DKA at <200 mg/dL) 2
- Arterial blood gas (pH <7.3 indicates DKA) 2, 3
- Serum bicarbonate (<18 mEq/L in DKA) 2, 3
- Serum ketones with β-hydroxybutyrate measurement (preferred over nitroprusside method which misses the predominant ketone body) 4, 3
- Electrolytes with calculated anion gap (elevated in DKA) 1, 4
- Blood urea nitrogen/creatinine and serum osmolality 1, 4
- Complete blood count with differential (leukocytosis may indicate infection or stress response) 1
- Blood, urine, and wound cultures before starting antibiotics 1
- HbA1c (distinguishes new-onset vs. poorly controlled diabetes) 1
Critical Clinical Assessment
Infection severity classification determines hospitalization and antibiotic approach: 1
- Patients with systemic toxicity (fever, tachycardia, hypotension, confusion, vomiting, leukocytosis, acidosis, severe hyperglycemia) have severe infection requiring immediate hospitalization 1
- Hypothermia, if present, is a poor prognostic sign 1
Treatment Protocol
Immediate Stabilization (First Hour)
Fluid resuscitation takes priority and must begin immediately: 1, 4, 2
- Administer isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour (1-1.5 liters in average adult) during the first hour 1, 4, 2
- This addresses the profound dehydration (total body water deficit ~6 liters in DKA) and restores renal perfusion 1, 3
Broad-spectrum parenteral antibiotics must be started immediately for severe infection: 1
- Cover gram-positive cocci (including MRSA if prevalent locally), gram-negative organisms, and obligate anaerobes 1
- Parenteral administration ensures adequate tissue concentrations in critically ill patients 1
Insulin Therapy
Start continuous intravenous regular insulin after initial fluid resuscitation: 4, 2, 3
- Administer 0.1 units/kg/hour continuous IV infusion (some protocols include initial 0.15 units/kg bolus) 2, 3
- Never interrupt insulin infusion when glucose falls - this is a critical error that perpetuates ketoacidosis 4, 3
- Continue insulin until complete resolution of ketoacidosis (pH >7.3, bicarbonate ≥18 mEq/L, anion gap ≤12 mEq/L), regardless of glucose level 4, 2, 3
Ongoing Fluid Management (After First Hour)
Adjust fluid composition based on corrected serum sodium: 1, 2
- 0.45% NaCl at 4-14 mL/kg/hour if corrected sodium is normal or elevated 1, 2
- 0.9% NaCl at similar rate if corrected sodium is low 1, 2
- Add 5% dextrose to fluids when glucose falls to 200-250 mg/dL to prevent hypoglycemia while continuing insulin to clear ketosis 4, 3
Electrolyte Replacement
Potassium management is critical to prevent life-threatening hypokalemia: 1, 4, 2
- Once renal function is confirmed and serum potassium <5.3-5.5 mEq/L, add 20-30 mEq/L potassium (2/3 KCl and 1/3 KPO₄) to IV fluids 1, 4, 2
- Maintain serum potassium between 4-5 mmol/L throughout treatment 4, 3
- Insulin therapy and acidosis correction drive potassium intracellularly, causing potentially fatal hypokalemia 4, 5
Bicarbonate administration is generally not recommended unless pH <6.9, as it provides no benefit in resolution of acidosis or time to discharge 1, 4, 3
Monitoring Requirements
Frequent monitoring prevents complications and guides therapy adjustments: 4, 3
- Blood glucose every 1-2 hours 4
- Serum electrolytes, glucose, BUN, creatinine, osmolality, and venous pH every 2-4 hours 4, 3
- Continuous cardiac monitoring (for potassium-related arrhythmias) 1
Infection-Specific Management
Metabolic stabilization and infection treatment must occur simultaneously: 1
- Correction of hyperglycemia, hyperosmolality, acidosis, and azotemia aids in eradicating infection 1
- Improved glycemic control enhances wound healing and immune function 1
- Surgical debridement should not be delayed >48 hours if indicated, though brief stabilization before surgery is appropriate 1
Resolution Criteria and Transition
DKA resolution requires ALL of the following: 4, 3
Transition to subcutaneous insulin requires careful timing: 1, 4, 2
- Administer basal insulin 2-4 hours before stopping IV insulin to prevent rebound ketoacidosis and hyperglycemia 1, 4, 2
- This overlap period is essential - premature discontinuation of IV insulin causes recurrence 4, 3
Critical Pitfalls to Avoid
Common errors that worsen outcomes: 4, 3, 6
- Stopping insulin when glucose normalizes before ketoacidosis resolves - glucose falls faster than ketones clear 4, 3
- Inadequate potassium replacement leading to cardiac arrhythmias 4, 2
- Delaying antibiotic administration in severe infection - infection is the precipitating factor in ~50% of DKA cases 1, 2
- Using nitroprusside method alone for ketone measurement, which doesn't detect β-hydroxybutyrate 4, 3
- Insufficient fluid resuscitation - dehydration worsens both infection and metabolic derangements 1, 6
- Premature transition to subcutaneous insulin without adequate overlap period 1, 4
Abdominal pain may be either cause or consequence of DKA - further evaluation is necessary if pain persists after metabolic improvement, as it could indicate the precipitating infection source 1