Severe Diabetic Ketoacidosis with Life-Threatening Acidosis
This patient requires immediate aggressive resuscitation with isotonic saline at 15-20 mL/kg/hour, continuous IV regular insulin infusion at 0.1 units/kg/hour, potassium replacement (if K+ >3.3 mEq/L), and consideration of sodium bicarbonate therapy given the pH of 6.99, along with intensive monitoring in an ICU setting. 1, 2
Immediate Fluid Resuscitation
Begin isotonic saline (0.9% NaCl) at 15-20 mL/kg/hour immediately to restore circulatory volume and tissue perfusion, which is critical given the severe dehydration indicated by the hyperosmolality (314 mOsm/kg) and tachycardia. 1, 2, 3
The typical adult will receive 1-1.5 liters in the first hour, with subsequent fluid choice depending on corrected serum sodium (add 1.6 mEq to measured sodium for every 100 mg/dL glucose above 100 mg/dL). 1
Total fluid replacement should aim to correct estimated deficits (typically 6-9 liters in severe DKA) within 24 hours. 1, 2
Insulin Therapy Protocol
Check serum potassium before starting insulin - if K+ <3.3 mEq/L, delay insulin and aggressively replace potassium first to prevent fatal cardiac arrhythmias. 2
Start continuous IV regular insulin infusion at 0.1 units/kg/hour (typically 5-7 units/hour in adults) without an initial bolus, targeting glucose decline of 50-75 mg/dL per hour. 1, 2, 3
Continue IV insulin until DKA resolution criteria are met: glucose <200 mg/dL, venous pH >7.3, serum bicarbonate ≥18 mEq/L, and anion gap ≤12 mEq/L. 1, 2
Bicarbonate Therapy for Severe Acidosis
Given the pH of 6.99, bicarbonate therapy is indicated. 1, 4
The American Diabetes Association recommends bicarbonate may be beneficial in patients with pH <6.9, though not necessary if pH is ≥7.0. 1
Administer 1-2 vials (44.6-100 mEq) of sodium bicarbonate IV initially, which can be repeated every 5-10 minutes as indicated by arterial pH and blood gas monitoring. 4
For pH <7.0 after initial hydration, administer 1-2 mEq/kg sodium bicarbonate over 1 hour, added to NaCl with required potassium to produce a solution not exceeding 155 mEq/L sodium. 1
Caution: Bicarbonate solutions are hypertonic and may produce undesirable rise in plasma sodium, but in severe acidosis with pH 6.99, the risks from acidosis exceed those of hypernatremia. 4
Potassium Replacement
Despite total body potassium depletion (typical deficit 3-5 mEq/kg), initial serum potassium may be normal or elevated due to acidosis-induced transcellular shifts. 1
Once renal function is assured and K+ >3.3 mEq/L, add 20-30 mEq potassium to each liter of IV fluid to maintain serum potassium between 4-5 mEq/L. 1
If initial K+ <3.3 mEq/L, hold insulin and give potassium replacement at 20-30 mEq/hour until K+ >3.3 mEq/L. 2
Phosphate Considerations
Despite whole-body phosphate deficits averaging 1.0 mmol/kg, prospective randomized studies have failed to show beneficial effect of phosphate replacement on clinical outcomes in DKA. 1
Consider careful phosphate replacement only in patients with cardiac dysfunction, anemia, respiratory depression, or serum phosphate <1.0 mg/dL to avoid cardiac and skeletal muscle weakness. 1
Overzealous phosphate therapy can cause severe hypocalcemia. 1
Intensive Monitoring Requirements
Check blood glucose, electrolytes, BUN, creatinine, venous pH, and β-hydroxybutyrate every 2-4 hours. 2, 3
Venous pH adequately monitors acidosis resolution, making repeated arterial blood gases unnecessary. 2
Monitor for cerebral edema (especially in younger patients), which is the most serious complication of DKA treatment. 1
Continuous cardiac monitoring is essential given the tachycardia (132 bpm) and risk of arrhythmias from electrolyte shifts. 1
Identifying and Treating Precipitating Causes
Obtain cultures (blood, urine, throat) and chest X-ray if infection is suspected, as infection is the most common precipitating cause. 1, 2
Consider myocardial infarction, stroke, pancreatitis, or medication non-adherence as potential triggers. 2, 5
Administer appropriate antibiotics if infection is identified. 1
Critical Pitfalls to Avoid
Do not attempt full correction of bicarbonate to normal in the first 24 hours - achieving total CO2 of ~20 mEq/L by end of day 1 is appropriate, as overly rapid correction can cause rebound alkalosis due to delayed ventilatory readjustment. 4
Never abruptly discontinue IV insulin - when transitioning to subcutaneous insulin, continue IV insulin for 1-2 hours after subcutaneous dose to prevent rebound hyperglycemia and ketoacidosis. 1, 3
The altered mental status (drowsiness/confusion) with this degree of acidosis requires ICU-level care with frequent neurological assessments. 1
The elevated β-hydroxybutyrate (6.51-6.77 mmol/L) confirms severe ketoacidosis and should be monitored as a marker of treatment response. 2, 6