Acute kidney injury: SAQ

This boy presents septic shock with acute kidney injury. The creatinine has risen to 2.3 times the baseline of 48 micromoles per litre, placing him in KDIGO stage 2, and the oliguria for 12 hours confirms the staging. The potassium of 6.8 mmol per litre with peaked T waves is immediately life-threatening, the metabolic acidosis with a pH of 7.22 reflects the accumulating acid and the failing clearance, and the shock from the presumed sepsis is the precipitating cause. The immediate priority is to treat the hyperkalaemia and to resuscitate the shock in parallel with the diagnostic workup. ^[1]

Question 1 (10 marks)

Outline the immediate management of this child, including the staged treatment of his hyperkalaemia and the resuscitation of his shock. ^[2]

The first priority is the hyperkalaemia with ECG changes, which is an immediate threat of cardiac arrest. I would give intravenous calcium gluconate at 0.5 mL per kg of the 10 percent solution over 5 to 10 minutes with cardiac monitoring to stabilise the myocardial cell membrane. Calcium does not lower the potassium, so I would immediately follow it with agents that shift potassium into the cells: intravenous insulin with glucose plus nebulised salbutamol, which are recommended in combination for a synergistic effect; sodium bicarbonate's role remains uncertain and I would reserve it for severe comorbidity with metabolic acidosis. I would recheck the potassium after each intervention because the effect is transient, and I would arrange for renal replacement therapy if the hyperkalaemia is refractory. ^[2]

In parallel I would resuscitate the shock. I would establish intravenous access and give an isotonic crystalloid bolus of 10 to 20 mL per kg, with reassessment after each bolus, because restoring the perfusion may reverse a pre-renal component of his injury. The PRoMPT BOLUS trial showed no difference between balanced crystalloids and 0.9 percent saline in children with septic shock, so either is acceptable. I would send blood cultures, commence broad-spectrum antibiotics within the first hour, and identify and control the source of the sepsis. I would be cautious with further fluid boluses once he is no longer shocked, because fluid overload has an independent and synergistic effect with AKI on mortality in critically ill children. ^[2]

I would stop all nephrotoxic drugs and adjust every drug dose to the current estimated GFR. I would monitor him in a high-dependency or intensive care setting with hourly urine output, continuous cardiac monitoring, and serial creatinine, electrolytes, and blood gases. I would involve the paediatric nephrologist and the intensivist early, and I would establish the indications for renal replacement therapy, which include refractory hyperkalaemia, severe metabolic acidosis, fluid overload causing pulmonary oedema, and uraemic complications. ^[2]