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Patients with end-stage renal disease (ESRD) may sustain multiple complications of their disease process and treatment. Emergent dialysis is most commonly required for hyperkalemia, severe metabolic acidosis, and pulmonary edema resistant to alternative therapy. (See the appropriate chapters for discussion of the management of hypertension, heart failure, bleeding disorders, and electrolyte disorders.)

Creatine protein kinase (and the MB fraction), troponin I, and troponin T are not significantly elevated in ESRD patients undergoing regular dialysis, and have been shown to be specific markers of myocardial ischemia in these patients. Hypertension occurs in 80% to 90% of patients starting dialysis. Management includes control of blood volume, followed by use of adrenergic-blocking drugs, angiotensin-converting enzyme inhibitors, or vasodilating agents. Congestive heart failure (CHF) may be caused by hypertension, coronary ischemia, and valvular disease, as well as uremic cardiomyopathy, fluid overload, and arteriovenous (AV) fistulas (high output failure). Treatment is similar to that in non-ESRD patients. Nitrates are helpful, and possibly furosemide (60 to 100 milligrams) may help, even in oliguric patients, as furosemide causes pulmonary vessel vasodilatation. Preload can be further reduced by inducing diarrhea with sorbitol and with phlebotomy (minimum 150 mL). Blood should be collected in a transfusion bag so that it may be transfused back to the patient during subsequent dialysis. Hemodialysis (HD) is the definitive treatment. Pericarditis in ESRD patients is usually due to worsening uremia. Electrocardiographic (ECG) changes typical of acute pericarditis are not seen. Pericardial friction rubs are louder than in most other forms of pericarditis, often palpable, and frequently persist after the metabolic abnormalities have been corrected. Uremic pericarditis is treated with intensive dialysis. Cardiac tamponade is the most serious complication of uremic pericarditis. It presents with changes in mental status, hypotension, or dyspnea. An enlarged heart on chest x-ray may suggest the diagnosis, which can be confirmed with echocardiography. Hemodynamically significant pericardial effusions require pericardiocentesis under fluoroscopic or ultrasonographic guidance.

Uremic encephalopathy presents with cognitive defects, memory loss, slurred speech, and asterixis. The progressive neurologic symptoms of uremia are the most common indications for initiating HD. It should remain a diagnosis of exclusion until structural, vascular, infectious, toxic, and metabolic causes of neurologic dysfunction have been ruled out. Peripheral neuropathy, manifested by paresthesias, diminished deep tendon reflexes, impaired vibration sense, muscle wasting, and weakness, occurs in 60% to 100% of patients with ESRD. Autonomic dysfunction, characterized by postural dizziness, gastric fullness, bowel dysfunction, reduced sweating, reduced heart rate variability, and baroreceptor control impairment, is common in ESRD patients, but is not responsible for intradialytic hypotension. Stroke is seen in 6% of HD patients, with 52% of cases caused by intracranial hemorrhage (subdural hematoma in particular). Stroke may be caused by cerebrovascular disease, head trauma, bleeding dyscrasias, anticoagulation, excessive ultrafiltration, or hypertension. It should be considered in any ESRD patient presenting with a change in mental status.

Anemia is caused by decreased erythropoietin, blood loss from dialysis, frequent phlebotomy, and decreased red cell survival. ...

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