Peritonitis and Catheter-Related Infections
Peritonitis remains a leading complication of PD. It contributes to technique failure, hospitalization, and patient mortality. Peritonitis is thought to occur most often by touch contamination, but may also occur in the setting of a catheter exit site or tunnel infection, by transmural migration of bacteria through the intestinal wall, or rarely by the hematogenous or transvaginal route. Patients with peritonitis usually present with cloudy peritoneal fluid and abdominal pain. When a patient presents with these complaints the abdomen should be drained and the effluent sent for cell count with differential, Gram stain, and culture. At least two of the following three conditions should be present to make the diagnosis of peritonitis: symptoms and signs of peritoneal inflammation, an effluent white blood cell count of more than 100/mm3 with at least 50% polymorphonuclear neutrophil cells, and a positive culture from the dialysate. Using appropriate culture techniques an organism can be isolated from the peritoneal fluid in over 80% of cases. Infections due to gram-positive cocci (Staphylococcus epidermidis and Staphylococcus aureus) tend to be most common (60–70% episodes) compared to infections with gram-negative bacteria (15–25%) or fungi (2–3%). Infection with mycobacteria can also occur but is rare. Peritonitis with multiple organisms or anaerobes should raise the concern of intrabdominal pathology and lead to abdominal computed tomography (CT) scan and surgical evaluation.
Patients who present with signs and symptoms of peritonitis should always be treated empirically with antibiotics. Various antibiotics can be used to treat peritonitis, but empiric therapy must cover both gram-positive and gram-negative organisms. Guidelines outlining empiric antibiotic regimens are published and have changed over the years in response to concern over the development of vancomycin-resistant organisms and appreciation of the importance of preservation of residual renal function. Gram-positive organisms may be covered by vancomycin or a cephalosporin, and gram-negative organisms by a third-generation cephalosporin or aminoglycoside. Numerous combinations are possible, but the choice of antibiotics should take into account the patient's infection history and the center's history of resistant organisms. Antibiotics are usually administered by the intraperitoneal route and can be given by intermittent (once daily) or continuous (in each exchange) dosing (Table 51–2). Most patients will show considerable clinical improvement within 48 hours of starting antibiotic therapy. Final antibiotic therapy should be guided by culture results and sensitivities. Treatment should be continued for a total of 2 weeks, while more severe infections due to S aureus, pseudomonas, or multiple gram-negative organisms should be treated for 3 weeks. If there is no clinical improvement after 48 hours, cell counts and cultures should be repeated. Refractory peritonitis is defined as failure to respond to appropriate antibiotics within 5 days and should be managed by catheter removal. Other indications for catheter removal are fungal peritonitis, relapsing peritonitis, peritonitis in the setting of severe exit site or tunnel infection, and infection due to multiple enteric organisms in the setting of a surgical abdomen. During peritonitis the permeability of the peritoneal membrane increases due to inflammation, and patients often will need a more concentrated dialysis solution in order to maintain fluid removal. Protein losses will also increase during peritonitis. Peritonitis is also often associated with increased fibrin clot production that can occlude the dialysis catheter. Heparin can be added to each bag of dialysis solution (500–1000 units/L) to decrease fibrin clot production.
Table 51–2. Intraperitoneal Antibiotic Dosing for Treatment of Peritonitis.1 ||Download (.pdf)
Table 51–2. Intraperitoneal Antibiotic Dosing for Treatment of Peritonitis.1
Intermittent (per Exchange, Once Daily)
Continuous (mg/L, All Exchanges)
LD 500, MD 125
LD 500, MD 125
15–30 mg/kg every 5–7 days
LD 1000, MD 25
LD 8, MD 4
LD 25, MD 12
LD 1000, MD 250
Catheter-related infections can occur at the exit site or in the subcutaneous tunnel. An exit-site infection is defined by the presence of purulent drainage at the catheter–epidermal interface that may or may not be accompanied by erythema, tenderness, or crust formation. A tunnel infection may present as erythema, edema, or tenderness of the subcutaneous tunnel, but may be clinically occult. Exit-site and tunnel infections may be caused by a variety of microorganisms, with S aureus and Pseudomonas aeruginosa being responsible for the majority. A gram stain and culture of exit-site drainage should be performed. Empiric therapy may be initiated immediately and should always cover S aureus. Oral antibiotic therapy is as effective as intraperitoneal therapy. In some cases, intensified local care or a local antibiotic cream may be sufficient. A patient with an exit-site infection that progresses to peritonitis or who presents with an exit site infection in conjunction with peritonitis will usually require catheter removal. Patients should be taught to perform routine exitsite care in order to prevent catheter infections. Daily cleansing with antibacterial soap and water is recommended by most centers. The daily application of mupirocin or gentamicin cream to the exit site has been shown to be effective in reducing catheter infections and related peritonitis.
The increased intrabdominal pressure that occurs during PD can be associated with a variety of mechanical complications. Hernias are quite common and can be inguinal, incisional (pericatheter or other), umbilical, or ventral. Risk factors for hernia formation include large dwell volumes, recent abdominal surgery, and polycystic kidney disease. Hernias usually present as painless swelling but can be associated with intestinal strangulation. The performance of a CT scan with the instillation of intraperitoneal contrast can aid in the diagnosis of a hernia. Treatment usually involves surgical repair with temporary cessation of PD and conversion to hemodialysis. In some situations PD can be resumed postoperatively with low volume exchanges and with the patient supine [as in nocturnal intermittent peritoneal dialysis (NIPD)] in order to maintain low intraabdominal pressure and facilitate healing. Leaks may also occur at the catheter site or through other defects into the abdominal wall. The diagnosis of abdominal wall leaks may sometimes be difficult. Patients may present with decreased ultrafiltration and weight gain due to fluid accumulation in the tissues. Patients with leaks may also present with scrotal or labial edema, which may be difficult to distinguish from fluid migration through a patent processus vaginalis. Abdominal CT with intraperitoneal contrast will assist in making the proper diagnosis in this situation. Leaks can sometimes heal with conversion to NIPD or hemodialysis, but they often will require surgical repair. Hydrothorax formation due to the passage of dialysate through defects in the hemidiaphragm is a rare complication of PD. Thoracentesis will yield a transudative fluid with a very high glucose concentration. Diagnosis can also be made by radionuclide scanning after technetium-labeled albumin is added to the peritoneal fluid and allowed to dwell for several hours. Definitive treatment will usually involve surgical repair of the diaphragmatic defect.
Encapsulating Peritoneal Sclerosis
Encapsulating peritoneal sclerosis (EPS) is a rare but serious condition characterized by extensive intraperitoneal fibrosis and encasement of bowel loops. This entity should not be confused with the more benign and subclinical peritoneal fibrosis that can occur in most patients on PD. EPS is typically associated with a progressive loss of ultrafiltration and poor solute transport. Patients may present with bloody effluent, malnutrition, abdominal pain, nausea, and bowel obstruction. The diagnosis is usually based on clinical suspicion and can be confirmed on CT by the presence of peritoneal thickening and calcification along with encapsulation and cocooning of bowel loops. It can also be confirmed by peritoneal biopsy. The cause of EPS is unknown but may be related to prior episodes of severe peritonitis, a reaction to foreign substances such as plasticizers or disinfectants, and an extended duration of peritoneal dialysis. No uniformly successful therapy for EPS exists at this time and mortality remains quite high (>50%). Described treatment strategies have included cessation of PD, bowel rest, and total parenteral nutrition. Surgery may be beneficial but can be technically difficult. Immunosuppression with corticosteroids and azathioprine has been reported in several small series to be beneficial.
Fluid balance management is one of the primary functions of renal replacement therapy. PD is an excellent modality for fluid removal due to the continuous, more physiologic nature of this modality. However, there remains an unacceptably high incidence of hypertension and cardiovascular disease in the PD population. Patients are trained to adjust their ultrafiltration by choosing the correct concentration of dextrose in their dialysis solution regimen depending on their dietary intake and volume status. Ultrafiltration failure can be defined as the failure of PD fluid removal to match the volume balance needs of the patient. Patients presenting with the clinical syndrome of volume overload need to be carefully evaluated prior to being labeled with ultrafiltration failure. It is important to consider the numerous factors that can alter fluid balance. Reversible causes such as dietary indiscretion, loss of residual renal function, noncompliance with dialysis, mechanical problems such as leaks or catheter malfunction, and inappropriate dialysis prescription need to be initially ruled out. Inappropriate tailoring of a PD prescription to a patient's transport type (eg, using long dwell times with low glucose concentrations in a high transporter) should not be attributed to technique failure. After these reversible causes of impaired fluid removal have been ruled out, the next diagnostic step is to evaluate the ultrafiltration and transport functions of the peritoneal membrane in parallel (Figure 51–4). This can be accomplished by performing a modification of the standard PET using a 4.25% dextrose solution. A net ultrafiltration volume of less than 400 mL with a 4-hour dwell is considered abnormal. A net ultrafiltration volume greater than 400 mL rules out alterations in peritoneal membrane function and the patient should be reevaluated clinically focusing on dietary indiscretion, noncompliance, inappropriate prescription, or loss of residual renal function.
Evaluation of volume overload in peritoneal dialysis patients.
If the net ultrafiltration volume is less than 400 mL, then small solute transport characteristics should be measured. Patients with a low drain volume and high transport characteristics represent the largest group of patients with ultrafiltration failure. Patients falling into this profile include those with inherently high transport (approximately 10% of patients starting PD) and recent peritonitis and those who have developed high transport during long-term PD. In general it is easy to maintain solute clearance goals in these patients despite a tendency toward clinical volume overload. The combination of low ultrafiltration volume and low transport tends to be rare. This usually represents disruption of the peritoneal membrane or inadequate distribution of the peritoneal fluid such as seen with severe adhesions or encapsulating peritoneal sclerosis. These patients will have inadequate solute clearance and fluid overload and will be difficult to maintain on PD if they have no residual renal function. Patients with low ultrafiltration volume and low average or high average transport may have mechanical problems, high peritoneal/lymphatic absorption rates, or aquaporin deficiency.
General therapeutic strategies to prevent fluid overload include routine monitoring of desired weight, residual renal function, daily ultrafiltration volumes, and PET results. Dietary counseling concerning salt and fluid intake should be ongoing. Protection of residual renal function should be a priority and high-dose loop diuretics may be used in patients with residual renal function to enhance fluid removal.
Hyperglycemia must be controlled in diabetic patients to allow maintenance of an osmotic gradient and adequate ultrafiltration. Preservation of peritoneal membrane function by prevention of peritonitis, the timely removal of peritoneal catheters when necessary, and the use of more biocompatible dialysis solutions should also be a priority. Specific therapeutic interventions in patients with poor ultrafiltration and high transport include converting to APD if the patient is undergoing CAPD. With continuous cycling peritoneal dialysis (CCPD) the long daytime dwell may still result in fluid absorption in very high transporters, in which case a manual exchange can be performed in the middle of the day. Another option is to use the polyglucose solution icodextrin in the long dwell cycle. Icodextrin is poorly absorbed and has been shown to be superior to glucose-based solutions in maintaining net ultrafiltration during long dwells. Patients with poor ultrafiltration and low solute transport will be difficult to maintain on PD if they have no residual renal function and transfer to hemodialysis is usually necessary. Therapeutic options for patients with poor ultrafiltration and low or high average transport include the use of icodextrin in long dwells and shorter dwell times for glucose-based exchanges. There are no pharmacologic agents currently available to decrease lymphatic absorption.
PD can be associated with a number of metabolic abnormalities. Glucose absorption will vary depending on a patient's transport characteristics, but can amount to 100–150 g/day. This, in addition to the hyperinsulinemia that ensues, can lead to weight gain and possibly also increased atherosclerosis. Glucose absorption is likely responsible for the lipid abnormalities that are commonly seen in PD patients. PD patients typically have high total and low-density lipoprotein (LDL) cholesterol, high triglycerides, and low high-density lipoprotein (HDL) cholesterol. This glucose loading may also result in hyperglycemia requiring the initiation or intensification of diabetes therapy. Protein malnutrition is common in PD patients and is partially due to protein loss across the peritoneum, which can be substantial (>10 g/day) in patients with high peritoneal transport or with peritonitis. PD patients may also have a suppressed appetite due to absorption of glucose during dialysis and a feeling of abdominal fullness. A protein intake of at least 1.2 g/kg is recommended for PD patients.