Kidney replacement therapy and dialysis in children: SAQ

This boy has severe acute kidney injury complicating septic shock, and he meets several of the AEIOU criteria for urgent kidney replacement therapy: refractory hyperkalaemia with electrocardiogram changes, severe metabolic acidosis, and fluid overload with pulmonary oedema. Critically, he is haemodynamically unstable on two vasopressors, which dictates the modality of choice. [1]

Question 1 (10 marks)

Outline the kidney replacement therapy you would choose for this child, your immediate medical management while it is being prepared, and the principles of its prescription. [1]

This boy is in septic shock on high-dose dual vasopressors, so he cannot tolerate the rapid fluid and solute shifts of intermittent haemodialysis, which would precipitate circulatory collapse. The correct modality is continuous renal replacement therapy, the slow continuous blood circuit run at the bedside that removes fluid and solute gently over hours to days and tolerates low blood pressure. He needs a central venous access line, favouring the right internal jugular vein, and I would avoid a subclavian line because it stenoses the veins needed for a future fistula. [1]

While the circuit is being prepared I would treat the hyperkalaemia immediately as a bridge to definitive removal. Ten percent calcium gluconate at 0.5 mL per kg slow intravenously (maximum 20 mL) stabilises the myocardium and reduces the risk of arrhythmia from the peaked T waves. Insulin with dextrose, nebulised or intravenous salbutamol, and sodium bicarbonate for the acidosis shift potassium into cells. I would also review his vasopressors and ventilation to optimise renal perfusion, recognising that these measures are bridges, not solutions, and that definitive clearance by dialysis must follow. [3]

The prescription of continuous renal replacement therapy targets an effluent dose of 25 to 35 mL per kg per hour, balancing adequate clearance against the need to minimise filter clotting and protect his circulating volume. Anticoagulation is usually with heparin, but if he has a bleeding risk or coagulopathy from his sepsis I would use regional citrate anticoagulation, monitoring the ionised calcium and the total to ionised calcium ratio to avoid citrate accumulation, which is a particular risk in liver dysfunction. Fluid removal would be set to bring him gently back toward his dry weight over the next 24 to 48 hours, guided by his haemodynamics and oxygenation rather than a fixed target. [1]

Question 2 (10 marks)

Six months later you are asked to advise on kidney replacement therapy for an 8-month-old infant with end-stage kidney disease from bilateral dysplastic kidneys. Discuss the modality of choice, the principles of the prescription, and the complications the family must understand. [2]

The modality of choice for an infant with end-stage kidney disease is chronic peritoneal dialysis. Peritoneal dialysis is preferred in infants and small children because it uses the peritoneal membrane as a native filter, needs no vascular access or needles, requires no systemic anticoagulation, tolerates low blood pressure, and fits a small body where building a reliable arteriovenous fistula or managing the blood circuit of haemodialysis is technically difficult. The International Society for Peritoneal Dialysis guidelines endorse peritoneal dialysis as first-line for paediatric end-stage kidney disease, particularly in infants. [2]

The prescription is built around dwell volume, dwell time, glucose concentration, and the number of cycles. Dwell volumes are typically 600 to 1100 mL per square metre of body surface area, beginning low and titrating to comfort and the risk of dialysate leak, with an overnight automated cycler giving the family daytime freedom. Glucose-based dialysate provides the osmotic gradient for ultrafiltration, and icodextrin is used for the long overnight dwell to sustain fluid removal and spare glucose exposure. The peritoneal equilibration test personalises the prescription, because high transporters absorb glucose quickly and need shorter dwells while low transporters need longer dwells to reach adequacy, measured as a weekly Kt over V for urea. [2]

The family must understand the central role of nutrition and growth, because infants on dialysis need aggressive calorie support, often via a gastrostomy, to grow and develop, and failure to thrive is a major driver of poor outcome. The most important complication is peritoneal dialysis-related peritonitis, the leading cause of technique failure and catheter loss: it presents with cloudy effluent, abdominal pain, and fever, is diagnosed by an effluent white cell count above 100 per microlitre after a dwell, and is treated with empirical intraperitoneal antibiotics covering gram-positive and gram-negative organisms, then narrowed to culture. Infants carry the highest mortality of any dialysis group, driven by infection and cardiovascular disease, so the family must also understand that dialysis is a bridge to transplantation, which offers the best survival and quality of life and should be planned from the outset. [2]