Chapter 52. Emergencies in Renal Failure and Dialysis Patients

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. Factitious anemia reflects changes in plasma volume related to dialysis. Abnormal hemostasis in ESRD is multifactorial in origin, resulting in an increased risk of gastrointestinal (GI) tract bleeding, subcapsular liver hematomas, subdural hematomas, and intraocular bleeding. Immunologic compromise, caused by impaired leukocyte chemotaxis and phagocytosis, leads to high mortality rates from infection. Dialysis does not appear to improve immune system function.

Anorexia, nausea, and vomiting are common symptoms of uremia, and are used as an indication to initiate dialysis, and assess its efficacy. Chronic constipation is common, due to decreased fluid intake, and the use of phosphate-binding gels.

Hypotension is the most frequent complication of HD. Excessive ultrafiltration from underestimation of the patient's ideal blood volume (dry weight) is the most common cause of intradialytic hypotension. Cardiac compensation for fluid loss may be compromised by diastolic dysfunction common in ESRD patients. Other causes of intradialytic hypotension include myocardial dysfunction from ischemia, hypoxia, arrhythmias, and pericardial tamponade; abnormalities of vascular tone secondary to sepsis, overproduction of nitric oxide, and antihypertensive medications; and volume loss from inadequate oral intake, vomiting, diarrhea, GI bleeding, or blood tubing or filter leaks. Treatment consists of Trendelenberg positioning, oral salt solution, or infusion of parenteral normal saline solution. If these interventions fail, excessive ultrafiltration is unlikely, and further evaluation will be required.

Dialysis disequilibrium, caused by cerebral edema following large solute clearances, is characterized by nausea, vomiting, and hypertension, which can progress to seizures, coma, and death. Treatment consists of terminating dialysis, and administering mannitol intravenously to increase serum osmolarity. This syndrome should be distinguished from other neurologic disorders, such as subdural hematoma, stroke, hypertensive crisis, hypoxia, and seizures.

Complications of vascular access account for more inpatient hospital days than any other complication of HD. Thrombosis or stenosis present with loss of the bruit and a thrill over the access. These need to be treated within 24 hours with angiographic clot removal, angioplasty, or direct injection of thrombolytic (eg, alteplase 2.2 milligrams) into the access. Vascular access infections often present with signs of systemic sepsis, including fever, hypotension, and an elevated white blood cell (WBC) count. Classic signs of pain, erythema, swelling, and discharge are often missing. Staphylococcus aureus is the most common infecting organism, followed by gram-negative bacteria. Patients usually require hospitalization, and treatment with vancomycin (15 milligrams/kilogram), and an aminoglycoside (eg, gentamycin 100 milligrams intravenously). Potential life-threatening hemorrhage from a vascular access may result from a ruptured aneurysm or anastomosis, or over-anticoagulation. Bleeding can often be controlled with 5 to 10 min of pressure at the puncture site. If this fails, the addition of an adsorbable gelatin sponge soaked in reconstituted thrombin, or a prothrombotic gauze (eg, HemCon or QuikClot), followed by 10 min of direct pressure may be effective. Life-threatening hemorrhage may require placement of a tourniquet proximal to the access, and vascular surgery consultation. If the etiology is excessive anticoagulation, the effects of heparin can be reversed with protamine 0.01 milligram/unit heparin dispensed during dialysis (10 to 20 milligrams protamine if the heparin dose is unknown). If a newly inserted vascular access continues to bleed, desmopressin acetate (0.3 microgram/kilogram intravenously) can be given as an adjunct to direct pressure.

Peritonitis is the most common complication of peritoneal dialysis (PD). Signs and symptoms are similar to those seen in other patients with peritonitis, and include fever, abdominal pain, and rebound tenderness. A cloudy effluent supports the diagnosis. Peritoneal fluid should be sent to the laboratory for cell count, Gramstain, culture, and sensitivity. With peritonitis, cell counts usually reveal > 100 leukocytes/mm3, with > 50% neutrophils. Gram stain is positive in only 10% to 40% of culture-proven peritonitis. Organisms isolated include Staphylococcus epidermidis, S aureus, Streptococcus species, and gram-negative bacteria. Empiric therapy begins with a few rapid exchanges of dialysate to decrease the number of inflammatory cells within the peritoneum. The addition of heparin (500 to 1000 units/L dialysate) decreases fibrin clot formation. Empiric antibiotics, covering gram-positive organisms (eg, cephalothin or vancomycin 500 milligrams/L dialysate) and gram-negative organisms (eg, gentamycin 100 milligrams/L dialysate), are added to the dialysate. Inpatient versus outpatient treatment of PD-related peritonitis should be based on clinical presentation.

Infections around the PD catheter are characterized by pain, erythema, swelling, and discharge. Causative organisms are S aureus and Pseudomonas aeruginosa. Outpatient treatment consists of a first-generation cephalosporin or ciprofloxacin.