Figure 60.1. Continuous Ambulatory Peritoneal Dialysis (CAPD). In CAPD, dialysate is instilled into the peritoneal cavity through the peritoneal dialysis catheter.

VASCULAR ACCESS

Vascular access remains the Achilles heel of hemodialysis. Dialysis access complications are a major source of morbidity for ESRD patients and account for more than $1 billion per year in health care expenditures.

    The three primary types of hemodialysis access devices are the arteriovenous (AV) fistula, the AV graft, and the dialysis catheter. The native AV fistula (Figure 60.2A) is the best and the preferred long-term dialysis access. It offers several advantages over the other hemodialysis access types: (1) it has the longest life; (2) because it has no synthetic material, it rarely becomes infected; and (3) it requires fewer interventions to maintain patency. The AV fistula is created by anastomosis of an artery to a vein, usually in the nondominant arm, resulting in arterialization and dilation of the vein. The most commonly created fistulae are the radiocephalic (Brescio-Cimino) fistula at the wrist and the brachiocephalic fistula at the elbow. The vascular access surgeon may use preoperative venous mapping with ultrasound to determine the best site for fistula creation.

    An AV fistula may require 2–3 months to mature; that is, to be of sufficient caliber such that it can be cannulated with two 16-gauge needles and support a blood flow through the dialysis circuit of 300–450 mL/min. Therefore, the patient with stage 4–5 CKD should be referred to the vascular access surgeon at least 6 months before the predicted need for initiation of dialysis. KDOQI guidelines suggest that patients be referred for vascular access when the serum creatinine is >4 mg/dL or the glomerular filtration rate is <25 mL/min. The failure to refer the CKD patient for vascular access in a timely manner puts that patient at risk of starting dialysis with a catheter, which in and of itself carries a greater mortality risk than starting dialysis with an AV fistula. Patients with CKD should also be educated regarding the importance of preserving veins for vascular access. Venipuncture should be avoided in the nondominant arm in order to better preserve those veins for vascular access.

    When the vasculature is not suitable for creation of an AV fistula based on physical examination or preoperative ultrasound venous mapping, the surgeon and nephrologist may decide that the best option is placement of an AV graft (Figure 60.2B). The AV graft is created by interposing a synthetic tube, usually made from polytetrafluoroethane (PTFE), between the artery and the vein. The most commonly placed AV grafts are the straight graft between the radial artery and the basilic vein and the loop graft between the brachial artery and the basilic vein. AV grafts have the advantage of being suitable for dialysis within 2–3 weeks of creation. However, grafts thrombose more frequently than fistulae and require more interventions to remain patent, and even with interventions to maintain patency most grafts last only about 2 years. Many trials have attempted to prove that use of antiplatelet agents or systemic anticoagulation decreases graft thrombosis, but so far the only agent that has a proven benefit without increasing bleeding complications is dipyridamole. In patients that have no upper arm blood vessels suitable for access placement, an experienced vascular surgeon may be able to create a femoral AV graft, but these are associated with high rates of infection and thrombosis and are considered a vascular access of last resort.

    Dialysis catheters are generally reserved for patients who have no other vascular access options or for patients who require a catheter as a “bridge” until a fistula is mature. Dual-lumen cuffed catheters are placed in the internal jugular vein and tunneled through subcutaneous tissues, usually under ultrasound guidance. The subclavian vein should be avoided because of the risk of subclavian vein thrombosis, which can render the whole upper extremity unsuitable for future vascular access creation. Nontunneled, noncuffed catheters are often used in cases of acute kidney injury in which a short course of dialysis (1–2 weeks at most) is anticipated. These catheters may be placed at the bedside with ultrasound guidance in the internal jugular or femoral vein. If the patient needs a longer course of dialysis, the nontunneled, noncuffed catheter should be exchanged for a more permanent tunneled, cuffed catheter.

COMPLICATIONS RELATED TO DIALYSIS ACCESS

Infectious complications are the second most common cause of mortality for patients with ESRD. ESRD patients may have impaired cellular and humoral immunity. Furthermore, hemodialysis and peritoneal dialysis catheters carry infection risks because they are foreign bodies.

    Hemodialysis catheter infections occur at a rate of 2 to 5.5 per 1000 patient days. Catheter-related bacteremia should be suspected in any patient who has fever and/or shaking chills. Empirical antibiotic therapy to cover both gram-positive and gram-negative organisms should begin after blood cultures have been obtained. The gold standard treatment for hemodialysis catheter–related infections is to remove the catheter and to place a new tunneled catheter after the patient has been afebrile for 48 hours and surveillance blood cultures are documented as negative. This approach, however, may require that the patient remain in the hospital for several days and that the patient have a temporary (nontunneled, noncuffed) catheter placed for dialysis.

    As an alternative approach to treating dialysis catheter–related bacteremia, some centers have successfully used the strategy of catheter exchange over a guidewire when there is no sign of a tunnel infection and the patient shows rapid clinical improvement with antibiotic therapy. Another treatment approach is to “lock” the infected catheter with an antibiotic solution in order to eliminate the layer of biofilm that adheres to the catheter surface.

    Regardless of which treatment approach is used, the patient with catheter-related bacteremia warrants close monitoring for development of signs of a metastatic infection such as endocarditis, septic arthritis, osteomyelitis, discitis, or epidural abscess. These metastatic infections often are not clinically apparent for weeks to months following the episode of bacteremia. Staphylococcus aureus is the most virulent organism with respect to metastatic infections, and attempts at catheter salvage in cases of S. aureus bacteremia may lead to unacceptably high rates of metastatic infections.

    Noninfectious complications of vascular access are frequent and include vascular access stenosis, thrombosis, limb ischemia, aneurysm, and congestive heart failure. Stenosis, which is narrowing of blood vessels, may occur at any location in the access circuit but most commonly occurs at the site of the arteriovenous anastomosis leading to decreased inflow of blood, or in the central veins causing blood to recirculate in the access. Both conditions can significantly decrease dialysis adequacy. Because stenosis also increases the risk of access thrombosis, which itself leads to fistula and graft failure, KDOQI recommends routine surveillance of fistulae at the discretion of the clinician. Doppler ultrasound is an excellent noninvasive method of assessing access stenosis, but its use is limited to the arm; central stenosis is better assessed with conventional venography. Stenotic lesions can be treated with angioplasty and stenting using interventional radiology techniques, while thrombosis is treated with thrombectomy. In cases of access thrombosis, it is important to diagnose and treat concurrent stenosis in order to decrease the risk of repeated thromboses. Limb ischemia can occur from both AV fistulae and grafts, as tissues distal to the access may not receive adequate perfusion. Severe ischemia, characterized by pain at rest, nonhealing ulcers, or evidence of nerve injury, requires urgent surgical revascularization of affected tissues. Aneurysms of access result from repeated needle sticks, and rupture of an aneurysm can lead to catastrophic exsanguination. Congestive heart failure may occur if blood flow in an access is >1000 mL/min and may be treated by banding to decrease the size of the access.

    The major infectious complication related to peritoneal dialysis access is peritonitis. Peritonitis is one of the major causes of failure of the modality and transfer to hemodialysis. Peritonitis may be asymptomatic, with the patient noticing only that the dialysate effluent is cloudy. When symptoms develop they typically include abdominal pain, fever, nausea, and vomiting. The workup for peritonitis should include laboratory examination of the effluent for cell count, Gram stain, and culture. A cell count >100/µL with more than 50% PMNs is suggestive of peritonitis. Empirical antibiotics should be administered to cover both gram-positive and gram-negative organisms. Antibiotics may be administered intravenously or by the intraperitoneal route by adding them to the dialysis solution. If the cultures are positive for more than one organism, abdominal imaging and surgical consultation should be obtained because polymicrobial peritonitis is often associated with an intra-abdominal catastrophe such as a perforated viscus. Peritonitis with mycobacterium or fungus almost always mandates removal of the catheter because these organisms are very difficult to eradicate with antimicrobial therapy alone.

    Nasal carriage of S. aureus is a major risk factor for exit-site infections, tunnel infections, and peritonitis with this organism. The application of an antibiotic cream to the exit site has been shown to reduce peritoneal dialysis infections. Mupirocin applied to the exit site daily reduces rates of S. aureus infections; however, it does not help with gram-negative infections, particularly Pseudomonas. More recent data indicate that gentamicin cream applied to the exit site prevents peritoneal dialysis catheter–related infections from both gram-positive and gram-negative organisms.

    There are several noninfectious causes of peritoneal dialysis catheter malfunction. It is not uncommon for patients to experience problems with drainage of fluid after a dwell. This is most often due to constipation, which should be aggressively treated with laxatives that do not contain magnesium or phosphorous. Catheter migration may also occur, where the catheter tip that is normally coiled and resting in the floor of the pelvis moves to another intra-abdominal location. Abdominal x-ray will help to diagnose both of these problems. Occasionally strands of fibrin, which can be a result of peritonitis, will be visible in peritoneal dialysis effluent, but this may also occur spontaneously. Heparin may be added to dialysate bags at 500 or 1000 units/L to prevent fibrin plugging, but if this is ineffective, thrombolytics like tissue plasminogen activator (tPA) may be used to unclog the catheter.

ANEMIA MANAGEMENT

The anemia of chronic kidney disease usually becomes apparent before patients require renal replacement therapy. Although deficiency of the sialoglycoprotein erythropoietin (EPO) is an important cause of the anemia of CKD, numerous other factors play a role (box 60.1) including iron deficiency, chronic inflammation, occult blood loss, and secondary hyperparathyroidism. The mainstays of treatment of anemia in dialysis patients are administration of recombinant erythropoiesis-stimulating agents (ESAs) and intravenous iron. ESAs are typically administered intravenously or subcutaneously to hemodialysis patients and subcutaneously to peritoneal dialysis patients. Intravenous iron is given in the hemodialysis unit to maintain the transferrin saturation (serum iron/total iron binding capacity × 100%) at >30%. The administration of intravenous iron improves the bone marrow response to ESAs and reduces the total amount of ESAs required to maintain the hemoglobin at its target. Lower doses of ESAs confer substantial cost savings to the healthcare system because ESA costs are a major expenditure for the ESRD program. Intravenous iron is available in several different preparations in the United States: iron sucrose (Venofer), iron gluconate (Ferrlecit), ferumoxytol (Feraheme), and iron dextran. Iron dextran is used less commonly because it is associated with a substantial rate of anaphylactic reactions.

Box 60.1 CAUSES OF EPO RESISTANCE

    The recommended targets for hemoglobin in both CKD patients and dialysis patients have come under increased scrutiny since the publication of several studies showing that higher hemoglobins are associated with increased risk of cardiovascular events and strokes in both predialysis and dialysis patients. KDIGO, the Kidney Disease Improving Global Outcomes, published guidelines in 2012 that recommended that ESA therapy should be used to avoid hemoglobin levels lower than 9 g/dL and maintain hemoglobin levels not exceeding 11.5 g/dL. The US FDA recommends that the hemoglobin should not exceed 11 g/dL in CKD patients being treated with ESAs. Notably, KDIGO recommends caution and if possible withholding of ESAs in patients with a history of stroke or malignancy. Regular monitoring of the hemoglobin is recommended for any patient who is receiving an ESA in order to avoid the potentially dangerous overcorrection of anemia.

BONE DISEASE AND MINERAL METABOLISM MANAGEMENT

Disordered mineral metabolism may begin in CKD patients as early as stage 2. Prompt evaluation and treatment of mineral disorders is important to prevent more severe complications by the time the patient requires renal replacement therapy. The kidney’s ability to excrete phosphorous decreases as GFR falls because there are fewer nephrons and their function is impaired. Furthermore, levels of vitamin 1,25-(OH)₂D₃ (calcitriol) decline because there are fewer renal tubular cells producing 1-alpha-hydroxylase, the enzyme responsible for its activation. The rise in serum phosphate levels and the fall in serum calcium both feed back on the parathyroid gland to increase production of parathyroid hormone (PTH). High levels of PTH lead to a condition of high bone turnover and resorption with eventual sclerosis, called osteitis fibrosa but can also lead to the accumulation of unmineralized bone, known as osteomalacia. Uncontrolled hyperparathyroidism may lead to other systemic complications. Throughout the body, abnormal mineral metabolism fueled by high levels of PTH leads to calcification of the intima of arteries and arterioles, another pathologic change that leads to cardiovascular disease in patients with ESRD. This pathophysiology is responsible for calcific uremic arteriolopathy (CUA), previously known as calciphylaxis, an unusual yet devastating and painful disease in which arteriolar calcification leads to tissue ischemia in the skin and subcutaneous tissues.

    Dietary phosphate restriction is an important early step in preventing secondary hyperparathyroidism. In animal studies, a rise in PTH can be prevented by stringent dietary phosphate restriction. In CKD stages 4 and 5, and particularly in dialysis patients for whom malnutrition may already be an issue, phosphate binders may be given with meals to control serum phosphate levels (table 60.1). Aluminum hydroxide is the most potent binder of dietary phosphorus but should not be used chronically because of the risk of aluminum toxicity. It may be used in short courses of 2–3 days for severe hyperphosphatemia. Calcium acetate (Phoslo) and calcium carbonate are commonly used phosphate binders but carry the risk of causing hypercalcemia, especially when given with a vitamin D analogue. Sevelamer hydrochloride (Renagel), sevelamer carbonate (Renvela), and lanthanum carbonate (Fosrenol) are non–calcium-based binders that should be used preferentially when serum calcium levels are higher than serum calcium levels are greater than 9.5 mg/dL. Sevelamer also has the advantage of lowering LDL cholesterol.

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