Peritoneal Dialysis and Home Kidney Replacement Therapy — Advanced

Pseudomonas exit-site infections are optimally treated with anti-pseudomonal systemic therapy. Oral ciprofloxacin is an effective agent for Pseudomonas exit-site infections and is recommended when there is no systemic sepsis or tunnel infection; topical aminoglycoside (gentamicin) applied to the exit site can augment local control and reduce recurrence. Immediate catheter removal is not mandatory for isolated exit-site infection without tunnel or peritonitis unless infection is refractory. Flucloxacillin and mupirocin target Staphylococcus species and are ineffective against Pseudomonas. Intraperitoneal vancomycin is primarily for Gram‑positive peritonitis rather than exit-site Pseudomonas. Intravenous piperacillin–tazobactam would provide anti‑pseudomonal coverage but is overly invasive for a non-systemic exit-site infection and systemic antibiotics with oral ciprofloxacin are appropriate first-line; IV therapy is reserved for systemic or deep infection.

Empiric therapy for PD-associated peritonitis should cover both Gram-positive and Gram-negative organisms. Intraperitoneal administration achieves high local antibiotic concentrations and is preferred. A first-generation cephalosporin such as cefazolin provides Gram‑positive coverage (including many staphylococci), and an anti‑pseudomonal cephalosporin such as ceftazidime (or cefepime) provides Gram‑negative coverage; this combination is a widely accepted empiric regimen. Oral amoxicillin–clavulanate alone does not provide sufficient Gram‑negative/pseudomonal coverage and oral route is suboptimal in PD peritonitis. Intravenous vancomycin alone lacks Gram‑negative coverage and intraperitoneal administration is preferred where feasible. Flucloxacillin plus metronidazole misses Gram‑negative aerobes and anaerobes are rarely the primary cause. Oral doxycycline and topical measures are inappropriate for peritonitis.

In anuric patients, peritoneal clearance must provide the entire solute removal. The most direct way to raise weekly Kt/V is to increase total dialysate volume per week — by increasing number of exchanges, using larger fill volumes if tolerated, or switching to automated PD (APD) to increase total exchanges/clearance. Erythropoiesis-stimulating agents affect anaemia, not dialysis solute clearance. Routinely using very high glucose concentrations for all exchanges risks metabolic and peritoneal membrane damage and does not optimally increase small‑molecule clearance relative to increasing total volume. Converting to haemodialysis may be necessary if PD cannot meet targets despite optimisation, but the next step should be to intensify PD first. Restoring residual renal function is not possible in an anuric patient and stopping diuretics would not increase Kt/V.

High peritoneal transporters absorb glucose rapidly, which limits osmotic UF during long dwells; icodextrin provides sustained colloid osmotic effect and is specifically effective for the long dwell (typically daytime) in high transporters to improve UF. Repeated use of high glucose (4.25%) can increase risks of metabolic complications and may still be ineffective for long dwell in high transporters. Decreasing dwell volumes or shortening dwells might help solute clearance strategies but will not improve long-dwell UF; short dwells favour sodium sieving and may paradoxically worsen net fluid removal for the long dwell. Oral loop diuretics help patients with residual renal function but do not address peritoneal UF failure. Immediate transfer to haemodialysis is a later option if medical/prescription measures fail; the first-line prescription change for long-dwell UF failure is icodextrin.

Encapsulating peritoneal sclerosis is a serious, potentially life‑threatening complication of long-term PD. Management includes stopping PD, nutritional support, anti-inflammatory/immunomodulatory therapy (corticosteroids often used acutely) and tamoxifen has been used to stabilise disease; surgical adhesiolysis or enterolysis may be required for obstructive complications. Increasing PD exchanges or hypertonic glucose will not treat the fibrotic process and may worsen outcomes. Long-term antibiotics are not effective unless infection is documented. Switching to automated PD does not address EPS; stopping PD is generally necessary. While prognosis can be poor, active treatment (steroids, tamoxifen, and surgery when indicated) improves outcomes in many cases.

In patients with refractory volume overload, combining a long daytime icodextrin dwell with nocturnal APD using shorter, more frequent cycles can increase total ultrafiltration and improve sodium removal because icodextrin provides sustained long-dwell UF and short nocturnal cycles enhance convection and net sodium removal. Replacing all exchanges with icodextrin is impractical and not recommended due to cost and formulation limits. Reducing nightly volume may decrease overall clearance and UF. Using only low-glucose solutions will reduce osmotic UF. Reliance on hypertonic glucose alone without icodextrin increases glucose exposure and may be less effective for long-dwell UF; icodextrin is the preferred long-dwell solution for fluid-overloaded patients.

Faeculent effluent soon after catheter insertion strongly suggests bowel perforation. Immediate priorities are to stop PD (to avoid ongoing contamination), make the patient nil by mouth, start broad-spectrum intravenous antibiotics, obtain urgent surgical review and imaging, and usually remove the catheter. Continuing PD, flushing the catheter, or attempting to replace it locally risks worsening contamination and sepsis. Increasing exchanges would distribute contamination. Definitive surgical management is often required.

Peritoneal dialysis performed at home requires the ability to perform aseptic technique and manage exchanges, or reliable caregiver support. Significant cognitive impairment without a capable caregiver is a major contraindication to unsupervised home PD because of infection risk and treatment errors. Advanced age alone is not a contraindication if the patient is cognitively intact and has suitable environment/support. Diabetes, prior uncomplicated intra-abdominal surgery remote in time, and BMI in the overweight range are not absolute contra-indications; specific surgical adhesions or extensive previous abdominal surgery may pose problems but a remote uncomplicated appendicectomy usually does not.

PD is valuable in many AKI situations (especially paediatric/neonatal cases, low-resource settings, patients with bleeding risk) because it avoids vascular access and systemic anticoagulation. However, PD provides lower instantaneous solute and fluid clearance than haemodialysis/CRRT and is therefore least appropriate for patients needing very rapid, high-efficiency removal of potassium and fluid (life‑threatening hyperkalemia and pulmonary oedema) where haemodialysis or CRRT is preferred. The other scenarios listed are situations where PD can be appropriate or even advantageous.

To use PD for acute hyperkalaemia, potassium-free dialysate (commercial PD fluids typically contain no potassium) and a strategy of short dwells with frequent exchanges increases transperitoneal clearance of potassium because potassium diffuses down its gradient into the dialysate. A long icodextrin dwell is not optimal for rapid potassium removal because its slower solute clearance and long dwell time limit immediate K removal. Standard CAPD intervals are too long for acute emergency removal. Insulin–glucose should be given intravenously (not injected into the peritoneal cavity) as immediate temporising therapy. Haemodialysis is the fastest modality and preferable if available urgently, but PD can be used with potassium‑free solutions and frequent exchanges if HD access is delayed.