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Protracted waiting times for patients awaiting orthotopic liver transplantation (OLT) place them at risk for developing potentially lethal complications of liver disease. In this chapter, we address the evaluation and management of these complications, including ascites, encephalopathy, pruritus, esophageal varices, and malnutrition.


Ascites remains one of the most difficult management problems in the OLT candidate (Fig. 3.1.). Paracentesis should be performed on initial presentation to confirm portal hypertension as the cause of ascites. As an initial treatment, salt restriction is efficacious in less than 20% of patients, thus necessitating diuretic use. Fluid restriction is recommended only if the serum sodium is less than 120 mEq/L. Rapid correction of hyponatremia should be avoided as it has been implicated in the pathogenesis of central pontine myelinolysis post-OLT.

Spironolactone is frequently used alone or in conjunction with furosemide. Dosages can be titrated up as necessary to achieve adequate natriuresis. Addition of hydrochlorothiazide may induce satisfactory diuresis in patients who continue to have significant ascites despite large doses of spironolactone and furosemide. Electrolytes, blood urea nitrogen, and serum creatinine should be monitored on

Criteri Congruenza Dei Triangoli

diuretic therapy. Diuretics should be discontinued if serum sodium falls below 120 mEq/L, or if the creatinine rises above 2 mg/dL. Hyponatremia in these circumstances reflects an excess of free water and should not be managed with hypertonic saline infusion. Alternative diuretic choices to spironolactone include amiloride or triamterene. In patients who are sulfa-allergic, ethacrynic acid may be used instead of furosemide.

3.2.1. Refractory Ascites

Refractory ascites (< 10% of cases) is defined as the inability to effectively diurese patients despite salt restriction and intensive diuretic treatment (spironolactone 400 mg/day and furosemide 160 mg/day). The limiting factor is usually the development of electrolyte abnormalities or renal insufficiency. It is important to exclude other causes of renal dysfunction, such as nonsteroidal anti-inflammatory drugs (NSAIDs). A 24-hour urine collection may be useful to confirm salt restriction and efficacy of diuretic therapy. Continued weight gain in a patient excreting greater than 78 mEq/L of urinary sodium in a 24-hour period suggests dietary noncompliance.

Repeat paracentesis may be performed every 2 or 3 weeks, though it is time-consuming, cumbersome, and may lead to excessive protein loss. The need for more frequent paracentesis suggests medical and/or dietary noncompliance. A transjugular intrahepatic portosystemic shunt (TIPS) may result in a significant decrease in ascites. However, TIPS may lead to compromised hepatic perfusion, with an increased risk of ischemic hepatocellular failure and intractable encephalopathy. Thus, TIPS is relatively contraindicated in Child-Pugh-Turcotte (CPT) Class C cirrhotic patients due to increased morbidity and mortality. Absolute and relative contraindications are listed in Table 3.1. Following TIPS regular surveillance for shunt stenosis with Doppler ultrasound is recommended. Most shunt occlusions can be revised radiographically.

Peritoneovenous shunting (LeVeen and Denver shunts) function by drawing ascitic fluid through a subcutaneous tube into the intrathoracic vascular space. Limitations include a high rate of shunt occlusion, disseminated intravascular coagulation, and increased perioperative mortality.

3.2.2. Spontaneous Bacterial Peritonitis (SBP): Treatment

SBP usually presents in cirrhotic patients as an unexplained clinical deterioration, as the classical signs of peritonitis, including fever, chills, and abdominal pain, may be absent. The mortality due to SBP remains high, reflecting the severity of the underlying liver disease. Paracentesis is diagnosed by finding an absolute neutrophil count (ANC) of greater than 250/mm3 in the ascitic fluid. Culture bottles should be promptly inoculated at the bedside to increase the yield. Empiric therapy should be directed at Gram-negative aerobic organisms and consist of a third-generation cephalosporin, such as cefotaxime, administered for 5 days. Antibiotic therapy should be tailored depending on the susceptibility profile of the infecting organism. Follow-up paracentesis is necessary if the patient does not appear to be responding to antibiotic therapy and to document a decrease

TABLE 3.1. Contraindications to Transjugular Intrahepatic Portosystemic Shunt

Re I alive


Systemic sepsis

Intractable encephalopathy nut precipitated by gastttiintestinal bleeding

Hepatic neoplasms

Right-sided cardiac failure

Portal vein thrombosis

Severe hepatocellular failure

Polycystic liver disease

in neutrophil count. Secondary peritonitis (i.e., due to a perforated viscus) should be suspected if the ascitic fluid Gram stain shows a polymicrobial flora, neutrophil count > 10,000/mm3, brownish color, glucose < 50 mg/dL, lactic dehydrogenase (LDH) > 225 IU/L, or protein > 1 mg/dL.

3.2.3. Spontaneous Bacterial Peritonitis: Prophylaxis

Patients with a total ascitic protein of less than 1 g/dL, previous SBP, or recent upper gastrointestinal bleeding are at increased risk of developing spontaneous bacterial peritonitis and should receive prophylactic antibiotics (Table 3.2). Prophylactic antibiotic therapy is effective in reducing the incidence of SBP and is also cost-effective. Although there has been concern about the selection of resistant organisms with prophylactic antibiotic use, the clinical impact is unclear.

3.2.4. Hepatorenal Syndrome (HRS)

HRS occurs in approximately 10% of hospitalized cirrhotic patients. Diagnostic criteria for HRS are shown in Table 3.3. Currently, two distinct forms of hepatorenal syndrome are recognized. Type I HRS is defined as a rapid deterioration in renal function, with virtually all patients expiring within 10 weeks of onset. In contrast, type II HRS is insidious, with a life expectancy of several months. The major clinical consequence of HRS type II is the development of refractory ascites. Before a diagnosis of HRS can be established, other specific causes of renal dysfunction must be excluded, such as obstruction, volume depletion, glomerulonephritis, acute tubular necrosis, and drug-induced nephrotoxicity. A urinary catheter, renal ultrasound, and fluid challenge are useful in this setting. The recent use of nephrotoxic drugs (NSAIDs, aminoglycosides) is ruled out by history.

The treatment of HRS has been disappointing. Renal vasodilators (dopamine, prostaglandin, prostaglandin analogues), systemic vasocontrictors (norepineph-

TABLE 3.2. Prophylactic Antibiotics against Spontaneous Bacterial Peritonitis


Dosage (oral)


750 mg weekly


400 mg daily


5 times per week

tdoLihle strength)

TABLE 3.3. Diagnostic Criteria for Hepatorenal Syndrome

Principal Supporting

Chronic or acute liver disease with advanced Urine volume < 500 mL/day hepatocellular Failure and portal hypertension Urine sodium < 10 mEq/L

Scrum creatinine (>1.5 mg/dL or 24-hour creatinine Unremarkable urine sediment clearance < 40 mL/min) Fractional excretion of sodium **' \% Absence of shock, ongoing bactcrial in feet ion, use of nephrotoxic drugs No sustained improvement with diuretic withdrawal and expansion of plasma volume with 1.5 L isotonic saline No obstructive uropathy or parenchymal renal disease rine, octapressin), and antagonists of renal vasoconstriction (angiotensin II receptor antagonists, intrarenal phentolamine) have all been generally unsuccessful. Preliminary data suggest that the combination of volume expansion and systemic vasoconstrictors may help reverse HRS. In addition, a modified extracorporeal dialysis system may also improve HRS. TIPS may be useful, but its precise role remains to be defined for this indication.

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