What is the diagnosis and recommended treatment for a patient with hyperglycemia, impaired renal function, electrolyte imbalance, and abnormal hematological findings?

Hyperglycemic Hyperosmolar State (HHS) with Acute Kidney Injury and Sepsis

This patient requires immediate treatment for Hyperglycemic Hyperosmolar State (HHS) with aggressive fluid resuscitation, insulin therapy, and electrolyte correction, along with urgent investigation and treatment of the underlying infectious precipitant.

Diagnostic Assessment

The laboratory findings are diagnostic of HHS based on:

• Severe hyperglycemia (glucose 144-157 mg/dL on two occasions, though these values seem inconsistent with HHS severity) 1
• Acute kidney injury with creatinine elevated to 1.49 mg/dL (from baseline 0.77) and eGFR dropped to 39 mL/min 1
• Electrolyte abnormalities: hypokalemia (3.1-3.2 mEq/L), hypochloremia (93-95 mEq/L), hypocalcemia (8.1 mg/dL) 1
• Elevated lactic acid (2.8 mmol/L) suggesting tissue hypoperfusion 1
• Leukocytosis (16.69-21.26 th/cmm) with vacuolated neutrophils indicating sepsis 1
• Anemia (hemoglobin 11.2-13.3 g/dL, hematocrit 33-39%) 1
• Coagulopathy (INR 1.49, PT 14.4 seconds) suggesting possible sepsis-related DIC or liver dysfunction 1

Critical note: The glucose values shown (144-157 mg/dL) are inconsistent with typical HHS (usually >600 mg/dL). However, given the acute renal failure, severe electrolyte derangements, elevated anion gap (14.7), and clinical presentation, this represents either evolving HHS or a mixed hyperglycemic crisis 1, 2.

Immediate Management Protocol

1. Fluid Resuscitation (First Priority)

Begin with isotonic saline (0.9% NaCl) at 15-20 mL/kg/h during the first hour (approximately 1-1.5 liters for average adult) to restore circulatory volume and renal perfusion 1, 2. This is critical given the acute kidney injury (creatinine 1.49, eGFR 39) and evidence of hypoperfusion (elevated lactate 2.8) 1.

• After the initial hour, switch to 0.45% NaCl at 4-14 mL/kg/h if corrected serum sodium is normal or elevated 1
• Continue 0.9% NaCl if corrected sodium remains low (current sodium 136-137 is low-normal) 1
• Target: Correct estimated fluid deficit within 24 hours, but limit osmolality change to <3 mOsm/kg/h to prevent cerebral edema 2
• Monitor fluid input/output, hemodynamic parameters, and clinical examination every 2-4 hours 2

2. Insulin Therapy

Once hypokalemia is corrected (potassium >3.3 mEq/L), administer IV regular insulin bolus 0.15 U/kg, followed by continuous infusion at 0.1 U/kg/h 2, 3.

• Critical pitfall: Never start insulin before excluding severe hypokalemia, as insulin drives potassium intracellularly and can precipitate life-threatening cardiac arrhythmias 2
• If glucose does not fall by 50 mg/dL in the first hour, double the insulin infusion hourly until steady decline of 50-75 mg/h is achieved 2, 3
• When glucose reaches 250-300 mg/dL, add dextrose to IV fluids while continuing insulin at reduced rate 2
• Continue insulin until mental status improves and hyperosmolarity resolves 2

3. Electrolyte Management

Potassium replacement is urgent given current levels of 3.1-3.2 mEq/L (below normal range 3.4-5.2) 1:

• Once renal function is confirmed and urine output established, add 20-40 mEq/L potassium to IV fluids (2/3 KCl and 1/3 KPO4) 1, 2
• Target: Maintain serum potassium 4-5 mEq/L during treatment 3
• Monitor potassium every 2-4 hours as insulin therapy will further lower levels 2, 3

Calcium correction for hypocalcemia (8.1 mg/dL):

• Correct albumin-adjusted calcium if albumin is low 1
• Consider IV calcium gluconate if symptomatic or ionized calcium is critically low 1

Phosphate: Consider replacement (20-30 mEq/L potassium phosphate) given the risk of cardiac dysfunction with severe hypophosphatemia 2

Do NOT administer bicarbonate - it does not improve outcomes in HHS and may worsen outcomes 4, 2.

4. Investigation and Treatment of Precipitating Infection

The leukocytosis (21.26 th/cmm), vacuolated neutrophils, and elevated lactate strongly suggest sepsis as the precipitant 1:

• Obtain blood cultures, urine cultures, and chest X-ray immediately before starting antibiotics 1, 3
• Start broad-spectrum antibiotics empirically after cultures obtained 1, 4
• Consider additional imaging if source unclear 1
• Infection is the most common precipitating factor for HHS and must be aggressively treated 1

5. Monitoring Requirements

Draw blood every 2-4 hours for serum electrolytes, glucose, BUN, creatinine, and osmolality 2, 3:

• Venous pH monitoring is adequate; repeat arterial blood gases are generally unnecessary 2
• Monitor for signs of cerebral edema: lethargy, behavioral changes, seizures, incontinence, pupillary changes, bradycardia 2
• Continuous cardiac monitoring given coagulopathy (INR 1.49) and electrolyte abnormalities 1

6. Renal Function Considerations

The acute kidney injury (eGFR 39 from baseline 83) requires special attention 5:

• This degree of renal impairment contraindicates metformin if the patient was taking it (eGFR <45 mL/min requires reassessment of metformin) 5
• If metformin-associated lactic acidosis is suspected (elevated lactate 2.8), discontinue metformin immediately and consider hemodialysis 5
• The elevated lactate may represent either metformin accumulation, sepsis-related tissue hypoperfusion, or both 5
• Renal function should improve with fluid resuscitation if prerenal azotemia is the cause 1

7. Transition to Subcutaneous Insulin

Once mental status improves and hyperosmolarity resolves, transition from IV to subcutaneous insulin 2:

• Administer basal subcutaneous insulin 2-4 hours BEFORE discontinuing IV insulin to prevent rebound hyperglycemia 2, 3
• Critical pitfall: Stopping IV insulin without overlap causes recurrent metabolic decompensation 3

Key Clinical Pitfalls to Avoid

• Overly rapid correction of hyperglycemia and osmolality increases cerebral edema risk 2
• Starting insulin before correcting hypokalemia can cause fatal arrhythmias 2, 3
• Inadequate fluid resuscitation in the setting of AKI will worsen renal function 1, 2
• Failure to identify and treat infection leads to treatment failure and recurrence 1, 3
• Premature discontinuation of IV insulin without subcutaneous overlap causes rebound hyperglycemia 2, 3
• Ignoring the coagulopathy (INR 1.49) which may indicate DIC from sepsis requiring additional workup 1

Discharge Planning

Once stabilized, structured discharge planning should include 3:

• Diabetes education on recognition and prevention of hyperglycemic crises 3
• Medication reconciliation, particularly regarding metformin given the renal impairment 5
• Follow-up appointments scheduled before discharge 4, 3
• Treatment plan for underlying infection 3