A 42-year-old woman with severe sepsis from urosepsis is admitted to the ICU. She has been oliguric (urine output 0.3 mL/kg/hr) for 18 hours despite aggressive fluid resuscitation. Serum creatinine has risen from 1.2 to 4.1 mg/dL. Urinalysis shows muddy brown casts, and fractional excretion of sodium (FENa) is 3.2%. Serum potassium is 6.8 mEq/L. What is the most appropriate next step in management?
A. Start renal replacement therapy (RRT) and manage hyperkalaemia with calcium gluconate, insulin-dextrose, and sodium bicarbonate
B. Continue aggressive fluid resuscitation with normal saline and reassess in 24 hours
C. Perform urgent renal ultrasound to rule out obstructive uropathy
D. Initiate loop diuretics (furosemide 240 mg IV) to promote urine output
Explanation
Clinical Diagnosis: ATN in Sepsis-Induced AKI
Key Point
This patient has established acute tubular necrosis (ATN) with sepsis-induced acute kidney injury (AKI). The muddy brown casts, elevated FENa (>2%), and oliguria despite fluid resuscitation confirm intrinsic renal failure, not prerenal azotaemia.
Diagnostic Criteria for ATN
Table
Feature
ATN
Prerenal
Postrenal
FENa
>2%
<1%
Variable
Urine casts
Muddy brown, granular
Hyaline
None
Response to fluids
Poor
Rapid improvement
Depends on obstruction
Urine osmolality
<400 mOsm/kg
>500 mOsm/kg
Variable
Management Algorithm for ATN with Hyperkalaemia and Oliguria
Life-threatening hyperkalaemia (K+ >6.5 mEq/L with ECG changes)
4.
Severe metabolic acidosis (pH <7.15)
5.
Pulmonary oedema (fluid overload unresponsive to diuretics)
This patient meets criteria 1, 2, and 3.
Immediate Management of Hyperkalaemia
Clinical Pearl
Hyperkalaemia in ATN is an emergency because the kidneys cannot excrete potassium. Immediate interventions shift K+ intracellularly and stabilize the myocardium:
1.
Calcium gluconate 10% (10 mL IV over 2–5 min) — stabilizes cardiac membrane; does NOT lower K+ but prevents dysrhythmia
2.
Insulin 10 units IV + dextrose 25 g IV — shifts K+ into cells; onset 10–20 min; duration 4–6 hours
3.
Sodium bicarbonate 50 mEq IV — alkalinizes serum, shifts K+ intracellularly; less effective in acidosis
4.
RRT — definitive removal of potassium and correction of acidosis
Warning
Loop diuretics are contraindicated in oliguric ATN because:
The tubules are damaged and cannot respond to diuretics
Diuretics may worsen dehydration and further reduce glomerular filtration rate
Furosemide will not increase urine output in established ATN
Why Fluid Resuscitation Alone Is Insufficient
Key Point
The patient has already received aggressive fluid resuscitation for 18 hours with no improvement in urine output or creatinine. Continuing fluids without RRT will cause:
Pulmonary oedema
Hypertension
Worsening hyperkalaemia (K+ cannot be excreted)
Metabolic acidosis
Fluid responsiveness has been exhausted; RRT is now the definitive therapy.
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