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• W2022220300 abstract "The 3 major and potentially fatal complications of cirrhosis of the liver result from portal hypertension and include variceal bleeding, ascites, and encephalopathy. The cause of other complications, eg, thyroid dysfunction and hepatopulmonary syndrome, is uncertain. Several recent advances have occurred in the treatment of varices. However, treatment of ascites is still primarily confined to achieving a negative sodium balance, and therapy for encephalopathy centers on the use of lactulose. Although effective therapy may be available for most complications of cirrhosis, a major complication indicates a poor longterm prognosis. Liver transplantation is the only effective long-term treatment of complications due to cirrhosis. The 3 major and potentially fatal complications of cirrhosis of the liver result from portal hypertension and include variceal bleeding, ascites, and encephalopathy. The cause of other complications, eg, thyroid dysfunction and hepatopulmonary syndrome, is uncertain. Several recent advances have occurred in the treatment of varices. However, treatment of ascites is still primarily confined to achieving a negative sodium balance, and therapy for encephalopathy centers on the use of lactulose. Although effective therapy may be available for most complications of cirrhosis, a major complication indicates a poor longterm prognosis. Liver transplantation is the only effective long-term treatment of complications due to cirrhosis. Cirrhosis of the liver is the result of various disease processes and is characterized by diffuse fibrosis and conversion of the normal liver architecture into structurally abnormal nodules. Most complications (Table 1) arise as a consequence of either development of portal hypertension (defined as a hepatic venous pressure gradient >6 mm Hg) or a decrease in synthetic function of the liver. Although hepatocellular carcinoma has an association with cirrhosis in general, an increased risk seems to be associated with cirrhosis related to chronic viral hepatitis, hemochromatosis, α1-antitrypsin deficiency, and alcoholism. A major complication usually indicates advanced disease and underscores the need for consideration of liver transplantation.Table 1Complications of CirrhosisGastrointestinalAscites, bleeding varices (esophageal, gastric, cctopic). portal hypertensive gastropathyCentral nervous systemHepatic encephalopathyRenalHepatorenal syndromePulmonaryHepatic hydrothorax, hepatopulmonary syndrome, portopulmonary syndromeNutritionalProtein-energy malnutrition, fat-soluble vitamin deficiencyEndocrineThyroid dysfunction, gonadal dysfunction, glucose intoleranceCirculatoryHigh-output cardiac failureInfectiousSystemic infections, spontaneous bacterial peritonitis Open table in a new tab The average lifetime risk of variceal bleeding in patients with cirrhosis who have had no previous bleeding is 30%.1Roberts LR Katmath PS Pathophysiology and treatment of variceal hemorrhage.Mayo Clin Proc. 1996; 71: 973-983PubMed Google Scholar Independent predictors of initial bleeding from esophageal varices include Child class C cirrhosis, large varices, and red wale markings. Alcohol use is also a risk factor for both initial and subsequent variceal bleeding and should be discontinued. Nonselective β-blockers (propranolol, nadolol) have been shown to reduce the risk of initial variceal bleeding, with a trend toward decreased mortality, and should be considered in all patients with large varices and red markings. β-Blockers decrease portal pressure and portal collateral flow through a combination of decreased cardiac output and unopposed α-mediated splanchnic vasoconstriction, resulting in decreased splanchnic blood flow. Generally, propranolol is used as a long-acting preparation with an initial dose of 60 mg/d; the mean dose is 160 mg/d and is preferably administered in the evening. The dose should be titrated weekly to decrease the resting heart rate by 25% but not less than 55 beats/min and the systolic blood pressure to no lower than 90 mm Hg. Adverse effects of propranolol may be severe enough to warrant discontinuation of therapy in up to 27% of patients. Nadolol, another long-acting nonselective β-blocker, may be tried as an alternative to propranolol. Nadolol is less lipophilic and does not cross the blood-brain barrier, and its use has been shown to result in discontinuation of therapy in only 4% of patients. The usual daily dose ranges from 20 to 240 mg/d. Measurement of the hepatic venous pressure gradient at baseline and after 1 month of stable therapy is useful in ascertaining response and in guiding further management. Hemodynamic studies have shown that the benefit of β-blockers is noted only in patients in whom the hepatic venous pressure gradient is reduced to less than 12 mm Hg or 20% below the baseline. Risk reduction with β-blockade averages less than 50%, and maximum benefit is seen in patients with Child class A and B cirrhosis. More than 30% of patients have no decrease in portal pressure despite adequate β-blockade.2Garcia-Tsao G Grace ND Grozmann RJ et al.Short-term effects of propranolol on portal venous pressure.Hepatology. 1986; 6: 101-106Crossref PubMed Scopus (260) Google Scholar 2 The addition of long-acting nitrates to nonselective β-blockers has been shown to enhance their hemodynamic effect and reduce the risk of bleeding from esophageal varices and therefore should be considered in patients who do not respond to β-blockers. Endoscopic variceal sclerotherapy has been used in the primary prophylaxis of variceal bleeding; however, the results are poorer compared with pharmacotherapy Thus, endoscopic sclerotherapy is currently not recommended. More recently, however, endoscopic variceal band ligation EVL was shown to be safe and more effective than propranolol for the primary prevention of variceal bleeding.3Sarin SK Lamba GS Kumar M Misra A Murthy NS Comparison of endoscopic ligation and propranolol for Ihe primary prevention of varieeal bleeding.N Engl J Med. 1999; 340: 988-993Crossref PubMed Scopus (326) Google Scholar Further confirmation of these results is needed before this approach can be adopted as routine clinical practice. Patients suspected of having bleeding varices should be managed in an intensive care setting. Adequate venous access should be established, preferably with 2 large-bore peripheral cannulas. Replenishment of blood volume and correction of coagulopathy must be done with packed erythrocytes (to increase hemoglobin concentration to 10 g/dL) and fresh frozen plasma. Care must be taken not to overexpand the plasma volume, which may increase portal pressure and result in exacerbation of variceal bleeding and worsening ascites. In unstable patients, the airway must be protected by endotracheal intubation. Antibiotics such as norfloxacin should be administered at a dose of 400 mg twice a day, especially in patients with ascites, to prevent spontaneous bacterial peritonitis (SBP) and gram-negative systemic infections. Emergency endoscopy of the upper gastrointestinal tract must be performed in all patients suspected of having a variceal hemorrhage. Once the site of bleeding has been confirmed, various treatment modalities are available, and the physician must select the most appropriate modality for each patient. Pharmacological therapy may be initiated while the patient is awaiting endoscopy. The various agents that have been used include vasopressin either alone or in combination with nitroglycerin, terlipressin somatostatin, and octreotide. Vasopressin alone, although effective in controlling bleeding, is associated with major complications (arrhythmias, myocardial infarction, bowel necrosis, cerebrovascular accidents, and local tissue necrosis) and is no longer recommended. The combination of vasopressin with nitroglycerin has been shown to be more effective than vasopressin alone in the control of acute variceal bleeding and in reducing the rate of cardiac complications.1Roberts LR Katmath PS Pathophysiology and treatment of variceal hemorrhage.Mayo Clin Proc. 1996; 71: 973-983PubMed Google Scholar Terlipressin, an analogue of vasopressin has a longer half-life than vasopressin and can be given as a bolus infusion every 4 hours. It has efficacy similar to vasopressin in controlling acute variceal bleeding and is associated with fewer adverse effects. Terlipressin has not received Food and Drug Administration approval and is not available for clinical use in the United States. Somatostatin has been shown to be superior to vasopressin and comparable to terlipressin balloon tamponade, and endoscopic variceal sclerotherapy in the control of acute variceal hemorrhage.1Roberts LR Katmath PS Pathophysiology and treatment of variceal hemorrhage.Mayo Clin Proc. 1996; 71: 973-983PubMed Google Scholar It is well tolerated and has few adverse effects. An initial intravenous bolus of 250 μg followed by a continuous intravenous infusion of 250 to 500 μg/h is the usual dosing schedule. Octreotide, a synthetic analogue of somatostatin, is widely used in the United States to control acute variceal hemorrhage and has been shown to be effective in controlling bleeding and in decreasing bleeding-related mortality. It is administered intravenously as a continuous infusion of 50 μg/h for 5 days. Endoscopic injection sclerotherapy controls active hemorrhage from esophageal varices in about 90% of patients.4Westaby D Hayes PC Gimson AE Polson RJ Williams R Controlled clinical trial of injection sclerotherapy for active variceal bleeding.Hepatology. 1989; 9: 274-277Crossref PubMed Scopus (189) Google Scholar More recently, EVL was shown to be comparable to endoscopic sclerotherapy in the control of bleeding. Compared with sclerotherapy EVL also significantly reduces rebleeding rates, mortality, procedure-related complications, and the number of sessions needed to eradicate varices. Therefore, EVL is currently the initial procedure of choice for patients with acute esophageal variceal bleeding. A second session may be done within 24 hours if bleeding is inadequately controlled. Complications of EVL include superficial ulceration and dysphagia, transient chest discomfort, and, rarely, esophageal strictures. Balloon tamponade is useful as a temporary measure to control acute variceal bleeding and to stabilize the patient while more definitive procedures are being planned. In the 10% of patients in whom bleeding cannot be controlled with 2 endoscopic therapeutic sessions within 24 hours, either surgery or a transjugular intrahepatic portosystemic shunt (TIPS) should be planned. Shunt surgery should be considered in patients with Child class A cirrhosis. A TIPS should be used in patients with Child class B or C cirrhosis as salvage therapy and preferably as a bridge to orthotopic liver transplantation. Rebleeding occurs in about two thirds of patients and is most likely to occur within 6 weeks of the initial episode. The preferred therapeutic method of choice is EVL at weekly or twice weekly intervals until the esophageal varices are obliterated. Once the varices are obliterated, endoscopy is performed at 3 months and then every 6 to 12 months thereafter. Recurrent varices are treated by ligation. The combination of sclerotherapy with EVL (ligation followed by 1 or 2 sessions of low-dose sclerotherapy when varices have disappeared or when small residual varices remain) may decrease the recurrence of varices and rebleeding rates compared with EVL alone. The addition of nonselective β-blockers to endoscopic therapy may enhance benefit. A TIPS is associated with a high incidence of hepatic encephalopathy and TIPS dysfunction and is not recommended as first-line therapy to prevent rebleeding from esophageal varices. However, in patients with uncontrolled bleeding, TIPS is useful as salvage therapy or as a bridge to liver transplantation. Surgical portocaval shunting should be considered in the patient with Child class A cirrhosis with recurrent bleeding. The prevalence of gastric varices in cirrhosis ranges from 6% to 20% and accounts for about 10% of all upper gastrointestinal bleeding in patients with portal hypertension. Most of the current regimens to treat gastric varices are derived from anecdotal evidence or are extrapolated from trials of esophageal varices. Methods proposed to treat bleeding gastric varices include endoscopic sclerotherapy with conventional sclerosants, thrombin or butyl-cyanoacrylate, TIPS, and surgery. However, controlled trials are lacking, and once fundal gastric varices bleed, TIPS or surgery is advisable. In published studies, the prevalence of portal hypertensive gastropathy (PHG) varies between 7% and 98%. In the cirrhotic patient, the reported prevalence of acute bleeding from PHG is 4% to 38% of all acute bleeding. Rebleeding seems to be common, with a prevalence of 62% and 75%.5Grace ND Groszmann RJ Garcia-Tsao G et al.Portal hypertension and variceal bleeding: an AASLD single topic symposium.Hepatology. 1998; 28: 868-880Crossref PubMed Scopus (331) Google Scholar Propranolol is the treatment of choice for both acute and chronic bleeding from PHG.6Perez-Ayuso RM Pique JM Bosch J et al.Propranolol in prevention of recurrent bleeding from severe portal hypertensive gastropathy in cirrhosis.lancet. 1991; 337: 1431-1434Abstract PubMed Scopus (224) Google Scholar If drug therapy fails, a portosystemic shunt (surgery or TIPS) aimed at decreasing the elevated portal pressure should be considered. Ascites is the most common of the major complications of cirrhosis, and approximately 50% of patients with compensated cirrhosis will develop ascites during 10 years of observation.7Runyon BA Management of adult patients with ascites caused by cirrhosis.Hepatology. 1998; 27: 264-272Crossref PubMed Scopus (207) Google Scholar Ascites results from renal retention of salt and water with localization of this excess fluid into the peritoneal cavity due to portal hypertension. Treatment of ascites is therefore aimed at creating a negative sodium and water balance and, if this strategy is inadequate, at decreasing portal pressure by portosystemic shunting. Bed rest is advisable for patients with a large amount of ascites because an upright posture is associated with activation of the renin-angiotensin–aldosterone system and the sympathetic nervous system, with consequent reduction of the glomerular filtration rate and of sodium excretion. Dietary sodium is restricted to 90 mEq/d or even 45 mEq/d if necessary. Fluids are restricted to 1500 mL/d; however, in the presence of dilutional hyponatremia (serum sodium level < 120 mEq/L), fluids are limited to less than 1000 mL/d. The choice of diuretic therapy depends on the urinary sodium levels.8Roberts LR Kamath PS Ascites and hepatorenal syndrome: pathophysiology and management.Mayo Clin Proc. 1996; 71: 874-881Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar Patients with an initial urinary sodium level greater than 30 mEq/L can be managed with spironolactone alone; a combination of furosemide and spironolactone in a ratio of 40 mg and 100 mg is used if the urinary sodium level is 10 30 mEq/L. If the urinary sodium level is less than 10 mEq/L, large-volume paracentesis is needed in addition to diuretic therapy. Body weight and urinary sodium levels should be used to monitor therapeutic response. Target weight loss should be 1 kg/d in patients with peripheral edema and 0.5 kg/d in those without peripheral edema. Common complications of diuretic therapy include electrolyte imbalances hyponatremia and hypokalemia-hyperkalemia), hepatic encephalopathy, renal impairment, gynecomastia, and muscle cramps. Therapeutic paracentesis (large-volume or total abdominal paracentesis is indicated in patients with tense ascites. Therapeutic paracentesis with albumin infusion has been shown to have significantly lower complications hyponatremia renal impairment, and hepatic encephalopathy) compared with diuretic therapy. The preferred site of the paracentesis is the left lower quadrant, away from the rectus sheath to avoid injury to the inferior epigastric vessels.8Roberts LR Kamath PS Ascites and hepatorenal syndrome: pathophysiology and management.Mayo Clin Proc. 1996; 71: 874-881Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar In addition, the sigmoid colon on the left side is more mobile and has a thicker wall than the cecum on the right side; thus, the risk of perforation is minimized if the paracentesis needle inadvertently encounters the bowel wall. Concurrent plasma volume expansion with albumin (8 g/L of ascitic fluid removed) has been shown to be effective in preventing circulatory dysfunction after paracentesis and is currently recommended, as intravascular reequilibration occurs in 6 to 8 hours after ascitic fluid removal. Repeated therapeutic paracentesis may be necessary in a small number of patients whose condition is refractory to other forms of therapy. Refractory ascites is defined as ascites that cannot be mobilized or early recurrence that cannot be prevented because of either a lack of response to salt restriction and diuretics (diuretic-resistant ascites) or the development of diuretic-induced complications (diuretic-intractable ascites). This condition is seen in about 10% to 20% of patients with ascites and available therapies include repeated large-volume paracentesis peritoneovenous shunts, and TIPS. However, peritoneovenous shunting is rarely used because of its attendant complications (shunt occlusion, infection and sepsis, vena caval thrombosis, and peritoneal fibrosis) and the introduction of alternative therapies such as paracentesis.7Runyon BA Management of adult patients with ascites caused by cirrhosis.Hepatology. 1998; 27: 264-272Crossref PubMed Scopus (207) Google Scholar Although shown to be effective in patients with refractory ascites in conjunction with improved renal function, TIPS may result in deterioration of liver function and increased mortality compared with repeated paracentesis and albumin replacement and thus is recommended only in a study setting.9Lebrec D Giuily N Hudengue A et al.French Group of Clinicians and a Group of Biologists. Transjugular intrahepatic portosystemic shunts: comparison with paracentesis in patients with cirrhosis and refractory ascites; a randomized trial.J Hepatol. 1996; 25: 135-144Abstract Full Text PDF PubMed Scopus (385) Google Scholar The prognosis of patients with refractory ascites is extremely poor (1-year survival <50%), and liver transplantation should be considered. The hepatorenal syndrome (HRS), a state of functional renal failure in patients with end-stage liver disease, is characterized by an increased creatinine level, relatively hyperosmolar urine, and a urinary sodium excretion of less than 10 mEq/L. The probability of occurrence of HRS in patients with cirrhosis is 18% at 1 year and 39% at 5 years. The prognosis for HRS is extremely poor, and the only proven treatment is liver transplantation.8Roberts LR Kamath PS Ascites and hepatorenal syndrome: pathophysiology and management.Mayo Clin Proc. 1996; 71: 874-881Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar It is important to correct hypovolemia and to avoid use of all nephrotoxic agents (aminoglycoside antibiotics, nonsteroidal anti-inflammatory drugs, diuretics, and contrast agents) in cirrhotic patients with renal impairment. An algorithmic approach to patients with cirrhosis, ascites and impaired renal function is presented in Figure 1.8Roberts LR Kamath PS Ascites and hepatorenal syndrome: pathophysiology and management.Mayo Clin Proc. 1996; 71: 874-881Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar Arteriolar vasoconstrictors and TIPS have been used more recently without definite benefit. In hospitalized patients, the prevalence of SBP ranges between 10% and 30%. The clinical manifestations may be subtle, and a high degree of suspicion is necessary for the diagnosis. Diagnostic paracentesis should be performed routinely in all patients with ascites in patients who develop signs of peritonitis, and in those whose clinical condition deteriorates. A neutrophil count greater than 250/mm3 (0.25 × 109/L) in the absence of an intra-abdominal source of infection in the ascitic fluid is suggestive of SBP and should prompt administration of antibiotics.7Runyon BA Management of adult patients with ascites caused by cirrhosis.Hepatology. 1998; 27: 264-272Crossref PubMed Scopus (207) Google Scholar More than 92% of all cases of SBP are monomicrobial, with Escherichia coli being the most common isolate, followed by Klebsiella species and other gram-negative bacteria. Gram-positive organisms are the etiologic agents in almost 25% of cases, with streptococcal species being the most common. Anaerobic infection is rare; it probably represents no more than 5% of all cases and, as with poly-microbial bacteria or fungi, clinicians should consider a diagnosis of secondary bacterial peritonitis. Cefotaxime at a dose of 2 g every 8 hours, administered intravenously for 5 to 7 days, is the treatment of choice.8Roberts LR Kamath PS Ascites and hepatorenal syndrome: pathophysiology and management.Mayo Clin Proc. 1996; 71: 874-881Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar Oral ofloxacin (400 mg every 12 hours) has been shown to be as effective as cefotaxime in the treatment of uncomplicated SBP. However, in critically ill patients or in those with impaired oral absorption, the intravenous route is preferred. Antibiotic therapy should be further modified based on the results of ascitic fluid culture and antibiotic sensitivities of the isolated organisms. Although 75% to 90% of patients with SBP respond to third-generation cephalosporins, the mortality rate of hospitalized patients remains high (between 20% and 40%).7Runyon BA Management of adult patients with ascites caused by cirrhosis.Hepatology. 1998; 27: 264-272Crossref PubMed Scopus (207) Google Scholar Renal impairment has been shown to be the single most adverse prognostic factor in predicting survival. After an episode of SBP, long-term survival is only about 30% at the end of 2 years, and therefore patients should be considered for liver transplantation. Since the recurrence rate of SBP is about 60% at the end of 1 year, secondary prophylaxis with oral norfloxacin (400 mg/d) is indicated in all patients after an episode of SBP. Secondary peritonitis from gut perforation should also be considered in any patient with neutrocytic ascites. Patients do not develop a classic surgical abdomen, even with free perforation of the colon into ascitic fluid. Gut perforation should be suspected and pursued aggressively if the initial ascitic fluid is neutrocytic and fulfills 2 of the following 3 criteria: total protein greater than 1 g/dL, glucose less than 50 mg/dL, and lactate dehydrogenase higher than the upper limit of normal for serum. In addition, a leukocyte count greater than 10.0 × 109/L and the presence of multiple organisms in the ascitic fluid should raise the suspicion of secondary bacterial peritonitis. Cefotaxime plus metronidazole seems to be excellent empirical therapy for suspected secondary peritonitis. Abdominal radiography, computed tomography, or water soluble contrast studies of the upper and lower gastrointestinal tract must be performed to exclude bowel perforation or intra-abdominal abscesses. Emergency surgery with antibiotic coverage is the treatment of choice for secondary peritonitis. Variants of SBP include culture-negative neutrocytic ascites when the ascitic fluid neutrophil count is greater than 250/mm3 but the fluid is sterile, and monomicrobial nonneutrocytic bacterascites, which is diagnosed when ascitic fluid cultures are positive but the neutrophil count is less than 250/mm3, both in the absence of a secondary cause of peritonitis. Patients with culture-negative neutrocytic ascites and symptomatic patients with monomicrobial nonneutrocytic bacterascites should be treated as if they had SBP.10Gilbert JA Kamalh PS Spontaneous bacterial peritonitis: an update.Mayo Clin Proc. 1995; 70: 365-370Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar The issue of primary prophylaxis is controversial, and the potential problems of emergence of antibiotic resistance and changes in bacterial flora remain unresolved. In patients admitted to the hospital after an episode of upper gastrointestinal hemorrhage, prophylaxis with oral, poorly absorbed antibiotics (norfloxacin or ciprofloxacin) for 7 days has been shown to decrease the incidence of infections and improve survival, and thus these antibiotics should be administered to all such patients. Hepatic encephalopathy is a term applied to a wide range of neuropsychiatric manifestations in patients with severe liver dysfunction. It encompasses features ranging from subtle changes in behavior detected only on psychometric testing to deep coma. Hepatic encephalopathy in the setting of chronic liver disease is often precipitated by various factors (Table 2) or develops as a result of spontaneous portosystemic shunting.11Riordan SM Williams R Treatment of hepatic enccphalopathy.N Engl J Med. 1997; 337: 473-479Crossref PubMed Scopus (338) Google Scholar Ammonia is thought to have an important role in the pathogenesis of hepatic encephalopathy, and most treatment measures of proven value are based on this hypothesis. However, several other mechanisms, such as production of false neurotransmitters and activation of central γ-aminobutyric acid–benzodiazepine receptors by ligands of endogenous origin, altered cerebral metabolism, disturbed activity of sodium-potassium–adenosine triphosphatase, zinc deficiency, and deposition of manganese, have been thought to contribute to the development of hepatic encephalopathy.Table 2Factors Precipitating Hepatic Encephalopathy in Patients With Chronic Liver DiseasePossible mechanismPrecipitantIncreased ammonia productionExcess dietary protein,*Common precipitants. constipation (anorexia, fluid restriction),*Common precipitants. gastrointestinal hemorrhage,*Common precipitants. infection (including bacterial peritonitis),*Common precipitants. blood transfusionIncreased diffusion of ammonia across blood-brain barrierAzotemia,*Common precipitants. hypokalemia,*Common precipitants. systemic alkalosis*Common precipitants.Activation of central γ-aminobutyric acid-benzodiazepinc receptors, compounding of central nervous system depressant effectUse of other psychoactivc drugsReduced metabolism of toxins because of hepatic hypoxiaDehydration (fluid restriction, diuretic effect, excessive paracentcsis, diarrhea due to osmotic laxatives), arterial hypotension (gastrointestinal hemorrhage, peripheral vascular dilatation), arterial hypoxemia, anemia, use of benzodiazepinesReduced hepatic metabolism of toxins because of diversion of portal bloodPortosystemic shunts (spontaneous, surgical, transjugular intrahepatic portosystemic shunt)*Common precipitants.Reduced hepatic metabolism of toxins because of decreased functional reserveProgressive hepatic parenchymal damage*Common precipitants.Multiple factorsDevelopment of hepatocellular carcinoma*Common precipitants.* Common precipitants. Open table in a new tab There are no specific manifestations of hepatic encephalopathy, and therefore it is important to exclude other causes of an altered sensorium (Table 3). Levels of arterial ammonia correlate poorly with the grade of hepatic encephalopathy and cannot be totally relied on in arriving at the diagnosis. Subclinical encephalopathy may be detected by simple bedside tests such as the number connection and trail-making tests. Once other causes of encephalopathy are excluded, precipitating factors must be identified and corrected.Table 3Differential Diagnosis of Hepatic EncephalopathyDisorderDiagnostic testMetabolic encephalopathiesBlood chemical analysis Hypoglycemia,*This diagnosis is especially pertinent to patients with liver disease electrolyte imbalance,*This diagnosis is especially pertinent to patients with liver disease hypoxia,*This diagnosis is especially pertinent to patients with liver disease carbon dioxide narcosis, azotemia,*This diagnosis is especially pertinent to patients with liver disease ketoacidosisToxic encephalopathies Alcohol*This diagnosis is especially pertinent to patients with liver diseaseMeasurement of blood alcohol level, erythrocyie transketolase activity, therapeutic response to thiamine (acute intoxication, withdrawal syndrome, Wernicke-Korsakoff syndrome) Psychoactive drugs, salicylates, heavy metalsToxicologic screeningIntracranial lesionsComputed tomography, lumbar puncture, arteriography, clectroencephalography, virological testing Subarachnoid, subdural, or intracerebral hemorrhage,*This diagnosis is especially pertinent to patients with liver disease cerebral infarction, cerebral tumor, cerebral abscess, meningitis, encephalitis, epilepsy or encephalopathy after seizureNeuropsychialric disordersTests for organic brain syndromes* This diagnosis is especially pertinent to patients with liver disease Open table in a new tab Conventional treatment of hepatic encephalopathy relies primarily on reducing the production and absorption of ammonia. Nonabsorbable disaccharides such as lactulose (β-galactosido fructose) or lactitol (β-galactoside sorbitol) help to remove both dietary and endogenous ammoniagenic substrates from the intestinal lumen and have been shown to improve hepatic encephalopathy.12Conn HO Leevy CM Vlahcevic ZR et al.Comparison of lactulose and neomycin in the treatment of chronic portal-systemic encephalopathy: a double blind controlled trial.Gastroenterology. 1977;" @default.
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