Care of the Patient with End-Stage Renal Disease

Chapter 26


Care of the Patient with End-Stage Renal Disease image




End-stage renal disease (ESRD) or stage 5 chronic kidney disease (CKD) and its treatment influence virtually every aspect of critical care in affected patients. ESRD designates advanced renal failure in which hemodialysis (HD), peritoneal dialysis (PD), or a renal allograft is required to ameliorate symptoms and prolong life. Stage 5 CKD designates estimated glomerular filtration rate (eGFR) below 15 mL/min/1.73 sq-m. However, dialysis does not completely correct the complex derangements of uremia, whereas both dialysis and immunosuppressive treatment for renal transplantation introduce additional risks of their own.



Common Problems in Patients with End-Stage Renal Disease in the Intensive Care Unit


Some aspects of ESRD contribute to the genesis of critical illnesses, whereas others complicate their management (Box 26.1).



BOX 26.1   Common Problems in Patients with End-Stage Renal Disease in the ICU










Cardiovascular Complications


Fluid overload resulting from patient noncompliance with regular dialysis or from iatrogenic fluid administration should be distinguished from primary heart failure by echocardiography. Left ventricular hypertrophy is extremely common in dialysis patients, resulting primarily from chronic hypertension. It progresses to diastolic dysfunction (reduced left ventricular compliance) and ultimately to dilated cardiomyopathy with systolic dysfunction and hypotension.


Systolic dysfunction is rarely exacerbated by placement of an arteriovenous (AV) fistula (usually an upper arm fistula between the brachial artery and vein). Bradycardia during transient occlusion of an AV fistula is a specific but not sensitive marker of high-output heart failure (Branham sign) (but is not recommended due to associated risk of clotting off the fistula). Hypotension complicates HD treatments in hemodynamically unstable intensive care unit (ICU) patients as well as in patients undergoing routine outpatient dialysis. Hypotension occurs in part because the normal homeostatic response to fluid removal—namely, vasoconstriction—is impaired during HD. Hypotension, in turn, may result in vascular access thrombosis, usually in association with underlying stenosis of the venous anastomosis (Box 26.2).



BOX 26.2   Treatment of Vascular Access Thrombosis


Perform emergency dialysis if necessary through a temporary venous catheter


Clot is removed by surgical thrombectomy or by mechanical (wire) thrombolysis, usually by interventional radiologists; avoid thrombolytics if there is a bleeding risk


Thrombosed central venous catheters are treated by thrombolytic instillation or by catheter replacement


After thrombectomy or thrombolysis, fistulography should be performed to detect an underlying vascular access stenosis


Pulmonary edema may result from fluid overload, an episode of accelerated hypertension, or myocardial infarction, all of which are often superimposed on prior left ventricular dysfunction. Patients sometimes present with pulmonary edema caused by occult fluid overload. In these circumstances, the patient’s body weight is maintained by fluid accumulation, and the loss of lean body mass is not recognized during outpatient care. Coronary artery disease, a common cause of death in patients with ESRD, is due to diverse “nontraditional” metabolic abnormalities associated with uremia, including specific lipid abnormalities, vascular calcification, inflammatory mediators and advanced glycosylation end products, and endothelial dysfunction.


Pericarditis may precede the initiation of maintenance dialysis or it may occur in chronic dialysis patients. The incidence of uremic pericarditis has significantly decreased as standard practice has shifted toward earlier initiation and more intensive dialysis. Patients with poor adherence to prescribed treatment, or those with access malfunction, remain at risk. In addition, patients with ESRD secondary to autoimmune diseases like lupus or rheumatoid arthritis may develop a flare with serositis and effusions. Finally, antihypertensive medications including hydralazine or minoxidil may cause a lupus-like syndrome or hemorrhagic pericarditis, respectively.


Arrhythmias are the most common cause of cardiac death in the dialysis population and most likely when nearing the end of a 72-hour dialysis-free “weekend” obligated by the thrice weekly outpatient hemodialysis schedule. Arrhythmias are also exacerbated by dialysis against inappropriately low dialysate potassium concentrations.



Pulmonary Complications


Uremic lung refers to putative increased pulmonary capillary leakiness in patients with ESRD. Clinical confirmation of this entity is lacking, and it may be due entirely to volume overload. Pleural effusion may be due to fluid overload, uremic serositis, tuberculosis (from an increased incidence of reactivation of tuberculosis in ESRD patients), or diaphragmatic leak associated with PD. Dyspnea during dialysis can be due to dialysis-induced hypoxemia, which is generally modest (i.e., a reduction of Pao2 of 10 to 15 mm Hg) but can be problematic in patients with chronic lung disease. Dyspnea can also be due to an anaphylactoid reaction to the dialyzer. Peritoneal dialysis fluid can elevate the diaphragm, especially when the patient is supine, and compromise ventilation in patients with pulmonary disease. Sleep apnea syndrome occurs in 40% of patients with ESRD. These patients have an increased sensitivity to drugs that worsen their sleep-disordered breathing and cause respiratory depression. Sirolimus, an immunosuppressant, may cause hemorrhagic pneumonitis, which may manifest as diffuse alveolar hemorrhage.



Hematologic Complications


The anemia of ESRD is mainly due to deficiency of kidney-produced erythropoietin. Full response to recombinant erythropoietin requires 4 to 8 weeks, and therefore cannot correct anemia in the acutely ill patient. In addition, inflammation, infection, and even minor surgery blunt the normal marrow response to erythropoietin to a remarkable degree. Uremic bleeding is due to a functional defect in von Willebrand factor, inhibition of adenosine diphosphate (ADP)-induced platelet aggregation, and anemia. Measurement of bleeding time can quantify bleeding risk, but its predictive power is limited for any individual patient. Although inadequate dialysis can prolong the bleeding time, intensive dialysis may not fully correct it. Anemia also increases bleeding time because of a rheologic mechanism: at a hematocrit of less than 30%, platelets stream in the center of blood vessels away from the vessel wall.



Infectious Complications


Dialysis patients receiving chronic dialysis have decreased host defenses. Impaired granulocyte functions include chemotaxis, phagocytosis, and intracellular killing. Impaired lymphocyte functions include defective antibody production and inadequate response to vaccines. These defects result from both the uremic state and exposure to bioincompatible dialysis membranes. Bioincompatibility connotes complement activation and cytokine release stimulated by exposure to the dialysis membrane. These changes in granulocyte and lymphocyte function in dialysis patients manifest as increased susceptibility to common bacterial pathogens rather than to opportunistic pathogens (e.g., Pneumocystis jiroveci). Infectious risk in renal transplant recipients varies with time after transplant, influencing both intensity of immunosuppression and use of prophylactic strategies. In the earliest postoperative period, donor-derived and nosocomial infections are of greatest concern, whereas in the late posttransplant period, community-acquired infections predominate.


Infected vascular access sites, especially central venous catheters, are the leading cause of bacteremia in dialysis patients. Offending organisms are usually staphylococci and streptococci but may include gram-negative rods. PD patients suffer from catheter-associated peritonitis, characterized by bouts of abdominal pain, an elevated peritoneal fluid white blood cell count (> 100 cells/μL), cloudy effluent, and positive peritoneal fluid cultures with the same spectrum of pathogens as affect hemodialysis catheters. Tunneling of the dialysis catheter, meticulous catheter care, and local antibiotic at the exit site reduce infectious risk. Urinary tract infections are also common in dialysis patients and may occur even if urine output is minimal.



Neurologic Complications


Uremic encephalopathy causes somnolence, confusion, seizures, and coma. Physical signs include hyperreflexia, asterixis, and myoclonus. Patients on maintenance HD may have unrecognized uremic encephalopathy resulting from access malfunction or noncompliance. Severe elevation of blood urea nitrogen (BUN), which may be due to bleeding, catabolism, or total parenteral nutrition (TPN), has no effect on neurologic function and is not by itself an indicator of uremic encephalopathy. Alterations in mental status may respond to intensive dialysis. Subdural hematomas may be spontaneous rather than traumatic. Both uremic platelet dysfunction and exposure to heparin during HD may contribute. Because active metabolites of morphine or meperidine accumulate in renal failure (the latter causes seizures), their use should be avoided. Hydromorphone and fentanyl are preferred analgesics in ESRD. Renal transplant recipients are at increased risk of infectious neurologic complications including meningitis and encephalitis, as well as medication-induced posterior leukoencephalopathy.

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Jul 7, 2016 | Posted by in CRITICAL CARE | Comments Off on Care of the Patient with End-Stage Renal Disease

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