Kidney replacement therapy and dialysis in children: Case

This girl has severe acute kidney injury complicating the low cardiac output state that follows cardiopulmonary bypass and cardiac surgery, and she meets several of the AEIOU indications for urgent kidney replacement therapy. She has refractory hyperkalaemia with electrocardiogram changes, severe metabolic acidosis, and fluid overload with pulmonary oedema, and she is haemodynamically unstable on noradrenaline, which together dictate the modality of choice. [1]

Clinical findings

The picture is that of post-cardiac surgery acute kidney injury, a classic trigger in paediatric intensive care because cardiopulmonary bypass, the inflammatory response, and perioperative low cardiac output injure the renal tubules. Her oliguria of under 0.5 mL per kg per hour for 8 hours, her doubling creatinine, and her metabolic and electrolyte derangement place her in the failure stage of the modified RIFLE criteria. The hyperkalaemia to 7.0 mmol per litre with QRS widening is immediately life-threatening and reflects failure of renal potassium excretion. Her fluid overload of 11 percent with crackles and rising ventilator pressures signals that the excess fluid is now compromising her lungs, and her ongoing need for noradrenaline marks her as haemodynamically unstable. [1]

The three clinical questions at the bedside are whether she needs dialysis now, which modality is feasible, and what access is available. The answer to the first is clearly yes, because her disturbances are refractory and progressive with end-organ effects. The answer to the second follows her haemodynamic state, and the answer to the third is a central line, favouring the right internal jugular vein and avoiding the subclavian to preserve the veins she may one day need for a fistula. [1]

Management and outcome

Management began with immediate treatment of the hyperkalaemia as a bridge to definitive removal. Ten percent calcium gluconate at 0.5 mL per kg was given slowly intravenously to stabilise the myocardium and narrow the QRS, followed by insulin with dextrose and nebulised salbutamol to shift potassium into cells, and sodium bicarbonate for her severe acidosis. These measures were recognised as bridges only, buying time while the dialysis circuit was prepared, because none of them remove potassium. [1]

Continuous renal replacement therapy was chosen because she was haemodynamically unstable on noradrenaline and could not tolerate the rapid fluid and solute shifts of intermittent haemodialysis. A right internal jugular central line was placed, and a continuous venovenous haemodiafiltration circuit was started at an effluent dose of 30 mL per kg per hour, with regional citrate anticoagulation chosen over heparin because of her perioperative bleeding risk. The ionised calcium and the total to ionised calcium ratio were monitored closely to detect citrate accumulation. Fluid removal was set to bring her gently toward her dry weight over the next 36 hours, guided by her blood pressure, lactate, and ventilator pressures rather than a fixed rate. [1]

Over the following days her potassium and acidosis normalised, her ventilator pressures fell as the fluid was removed, and her noradrenaline was weaned. Her urine output gradually returned as her cardiac output recovered, the continuous therapy was weaned and then stopped on day 5, and her creatinine returned to near baseline over the following week. She did not develop dialysis disequilibrium because, although her urea was moderately raised, it was not extreme and the clearance was gentle and continuous. The lesson is that continuous therapy matched to her haemodynamic state allowed safe fluid and solute removal while her heart and kidneys recovered. [3]

The counterfactual: peritoneal dialysis in an infant

If this had been a 6-month-old infant with end-stage kidney disease from dysplastic kidneys rather than a reversible post-surgical injury, the modality would have been chronic peritoneal dialysis, not continuous renal replacement therapy. Peritoneal dialysis uses the peritoneal membrane as a native filter, needs no vascular access or needles, tolerates low blood pressure, and fits a small body where building a fistula or managing a blood circuit is difficult, which is why it is the first-line modality for infants. The prescription would use dwell volumes of 600 to 1100 mL per square metre, beginning low, with an overnight automated cycler and aggressive nutritional support, often via a gastrostomy, to drive growth. This counterfactual illustrates that the right modality depends on whether the failure is acute or chronic, the child's age and size, and the haemodynamic state, and that the goal of chronic dialysis is always to bridge the child to transplantation. [2]