Peritoneal Dialysis (PD) is a form of treatment for kidney failure that uses the lining of the abdomen, the peritoneal membrane, as a natural filter. A sterile fluid called dialysate is introduced into the abdominal cavity, where it draws waste products and excess water from the blood across the membrane. The removal of this excess fluid is known as ultrafiltration (UF), a process driven primarily by sugar (dextrose) in the dialysate creating an osmotic pressure gradient. When the body fails to remove enough fluid, a condition known as low ultrafiltration, it can lead to fluid overload and is a serious complication that often requires a change in treatment. This failure can stem from complex changes within the peritoneal membrane, errors in the dialysis regimen, or physical blockages.
Alterations in Peritoneal Membrane Function
The most intricate causes of low ultrafiltration are rooted in changes to the peritoneal membrane itself, which is a dynamic surface. Over time, particularly with long-term exposure to glucose-based dialysate, the membrane’s efficiency in removing fluid can decline. This decline often results from the membrane becoming overly permeable, leading to a condition known as high solute transport status.
In patients with this status, the glucose in the dialysate, which acts as the osmotic agent, is absorbed too rapidly into the bloodstream. This quick absorption causes the osmotic pressure gradient to dissipate prematurely, significantly reducing net ultrafiltration as the driving force for fluid removal disappears early in the exchange cycle.
Another significant physiological change is the thickening and scarring of the membrane, a process referred to as peritoneal fibrosis, which can progress to severe conditions like encapsulating peritoneal sclerosis. Chronic inflammation, often triggered by repeated infections (peritonitis) or the long-term presence of high glucose concentrations, stimulates this scarring. This fibrosis reduces the effective surface area available for transport and can impair the function of specialized water channels called aquaporins, which are responsible for the removal of solute-free water.
The body naturally reabsorbs some dialysate fluid through the lymphatic system. If this peritoneal fluid loss rate increases significantly, it directly counteracts ultrafiltration. Fluid pulled into the peritoneal cavity is reabsorbed before it can be drained out, leading to a net loss of fluid removal.
Issues Related to Dialysis Prescription and Technique
Beyond the membrane’s health, inadequate ultrafiltration can be caused by preventable errors in the dialysis prescription or in how the treatment is performed. The timing of the exchange, known as the dwell time, is a careful balance that can undermine fluid removal if incorrect. If the dialysate is drained too early, the osmotic gradient may not have reached its peak fluid removal capacity.
However, if the dialysate remains in the abdomen for too long, the glucose concentration will have significantly decreased due to absorption, and the osmotic pull will have dissipated. At this point, the gradient may reverse, causing the body to reabsorb fluid from the dialysate, resulting in little to no net ultrafiltration.
The effectiveness of the osmotic pull is directly related to the concentration of glucose in the dialysate. Standard solutions come in various concentrations (e.g., 1.5%, 2.5%, 4.25% dextrose). Using a lower concentration than required creates a weaker osmotic gradient, limiting the amount of water transferred into the dialysate and leading to insufficient fluid removal.
The volume of dialysate introduced into the abdomen, known as the fill volume, also plays a role in ultrafiltration capacity. When the prescribed fill volume is too low, the overall surface area of the peritoneal membrane exposed to the dialysate is reduced. This limits the total potential for both fluid and waste removal, directly contributing to low ultrafiltration.
Physical and Mechanical Obstructions
Physical problems with the catheter or the anatomical structure of the abdominal cavity can mimic ultrafiltration failure by preventing fluid from being properly drained, despite successful fluid removal across the membrane. A common issue is the malfunction or obstruction of the peritoneal catheter, which is the conduit for fluid inflow and outflow. Obstruction can be caused by intraluminal fibrin clots, which are small strands of protein that block the catheter lumen.
The catheter tip can also migrate out of its optimal position in the pelvis or become wrapped in the omentum, a fatty layer of tissue in the abdomen, causing it to kink or restrict flow. These issues result in incomplete drainage of the dialysate, which is then measured as a low ultrafiltration volume, even if the fluid transfer across the membrane was successful.
Another physical issue is a dialysate leak, where fluid escapes the peritoneal cavity into surrounding tissues or spaces. Leaks can occur externally around the catheter exit site, or internally into the abdominal wall, genital area (causing swelling), or even into the chest cavity (pleural leak or hydrothorax). When dialysate leaks, the total volume drained is significantly lower than expected, leading to a false appearance of ultrafiltration failure.
Internal scarring, or adhesions, can cause fluid sequestration or loculation. These adhesions create pockets that trap the dialysate, preventing it from mixing freely or reaching the catheter’s drainage holes. The catheter cannot retrieve the entire instilled volume, and the trapped fluid remains in the body, manifesting as a failure to achieve target fluid removal.