An error occurred while setting your user cookie. Please set your. browser to accept cookies to continue. This cookie stores just a. ID; no other information is captured. Accepting the NEJM cookie is. TV Programs News Programs Radio Shows. Commercials and Advertisements Journalism and Mass Communications (documentaries on TV & society) Popular Culture. The AXS Cookie Policy. This website, like most others, uses cookies in order to give you a great online experience. By continuing to use our website you accept to our. Manage your page to keep your users updated View some of our premium pages: google.com. Upgrade to a Premium Page. ![]() Management and Treatment of Patients with Cirrhosis and Portal Hypertension. The definitive version of this article is available in Am J Gastroenterol 2. PDF version)Abstract. Cirrhosis represents the end stage of any chronic liver disease. Hepatitis C and alcohol are currently the main causes of cirrhosis in the United States. Although initially cirrhosis is compensated, it eventually becomes decompensated, as defined by the presence of ascites, variceal hemorrhage, encephalopathy, and/or jaundice. These management recommendations are divided according to the status, compensated or decompensated, of the cirrhotic patient, with a separate section for the screening, diagnosis, and management of hepatocellular carcinoma (HCC), as this applies to patients with both compensated and decompensated cirrhosis. ![]() ![]() In the compensated patient, the main objective is to prevent variceal hemorrhage and any practice that could lead to decompensation. Hepatorenal syndrome is also a severe complication of cirrhosis but one that usually occurs in patients who are already in the hospital and, as it represents an extreme of the hemodynamic alterations that lead to ascites formation, it is placed under treatment of ascites. Recent advances in the pathophysiology of the complications of cirrhosis have allowed for a more rational management of cirrhosis and also for the stratification of patients into different risk groups that require different management. When few or no data exist from well- designed prospective trials, emphasis is given to results from large series and consensus conferences with involvement of recognized experts. A rational management of cirrhosis will result in improvements in quality of life, treatment adherence, and, ultimately, in outcomes. Introduction. Cirrhosis represents the end stage of any chronic liver disease. Hepatitis C and alcohol are currently the main causes of cirrhosis in the United States. Two major syndromes result from cirrhosis, namely portal hypertension and hepatic insufficiency. In addition, peripheral and splanchnic vasodilatation with the resulting hyperdynamic circulatory state is typical of cirrhosis and portal hypertension. The hyperdynamic circulatory state is characterized by low arterial pressure, high cardiac output, and decreased peripheral vascular resistance. Similarly, any sign of portal hypertension detected by physical examination (splenomegaly, caput medusae), laboratory investigation (even a subtle decrease in platelet count, such as a count < 1. Moreover, even subtle indicators of liver insufficiency (albumin levels < 3. Compensatory Enlargement of Human Atherosclerotic Coronary Arteries. Seymour Glagov, M.D., Elliot Weisenberg, B.A., Christopher K. Treatment of acute exacerbations of multiple sclerosis (MS) when the acute relapse is characterized by functionally disabling symptoms with documented evidence of. Overview of Acs e349 3. Initial Evaluation and Management e350 4. Early Hospital Care e359. Following is an alphabetical listing of prominent authors who regularly appear/appeared in the newsgroups mentioned above along with a brief description of their stories. INR, international normalized ratio, > 1. Decompensated cirrhosis is marked by the development of any of the following complications: jaundice, variceal hemorrhage, ascites, or encephalopathy (1). Jaundice results from hepatic insufficiency and, other than liver transplantation, there is no specic therapy for this complication. However, it is important to recognize and treat superimposed entities (e. The other complications of cirrhosis occur mainly as a consequence of portal hypertension and hyperdynamic circulation. Gastroesophageal varices result almost solely from portal hypertension, although hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. Hepatorenal syndrome (HRS) results from severe peripheral vasodilatation, which leads to renal vasoconstriction. Hepatic encephalopathy (HE) is a consequence of shunting of blood through portosystemic collaterals (as a result of portal hypertension), brain edema (cerebral vasodilatation), and hepatic insufficiency. ![]() Patients who belong to CTP class A are compensated and those in CTP classes B and C are decompensated. Nevertheless, the management of cirrhosis also involves the diagnosis and management of HCC. Therefore, the following treatment recommendations for cirrhosis are divided according to the status- -compensated or decompensated- -of the cirrhotic patient with a separate section for the screening, diagnosis, and management of HCC, as this applies to both patients with compensated and decompensated cirrhosis. When few or no data exist from well- designed prospective trials, emphasis is given to results from large series and consensus conferences with involvement of recognized experts. Clinical considerations may justify a course of action that differs from these recommendations. To link to this poem, put the URL below into your page: <a href="http:// of Myself by Walt Whitman</a> Plain for ![]() The median survival of patients with compensated cirrhosis is ~9 years (3), but it is as long as 1. The treatment of the underlying liver disease is beyond the scope of these recommendations. The main recommendations specific to patients with newly diagnosed cirrhosis are screening for varices and HCC (see below: Screening, diagnosis, and management of HCC). The objective of EGD is to detect the presence/size of varices for determining whether the patient should receive therapy for prevention of first variceal hemorrhage (primary prophylaxis). Their presence correlates with the severity of liver disease; although only 4. CTP class A patients have varices, they are present in 8. CTP class C patients (7). Patients with gastroesophageal varices develop variceal hemorrhage at the rate of 1. The mortality rate with each episode of variceal hemorrhage is approximately 1. Therefore, one of the main preventive measures for the patient with compensated cirrhosis is the prevention of first variceal hemorrhage (primary prophylaxis). Recommendations stated below follow recent treatment recommendations endorsed by the AASLD (American Association for the Study of Liver Diseases) and the ACG (American College of Gastroenterology) (5; 6). Three factors identify patients at a high risk of bleeding from varices: large variceal size, red wale marks on the varices (defined as longitudinal dilated venules resembling whip marks on the variceal surface), and advanced liver disease (CTP class B or C) (8). Patients with large varices or patients with high risk small varices (those with red signs or those occurring in a CTP class C patient) are at the highest risk of bleeding. Other patients with small varices (non- high risk) are at a low risk of bleeding, but are at risk for variceal growth. Two therapies are currently accepted in the prevention of the first episode of variceal hemorrhage, namely nonselective beta- blockers (NSBBs) and endoscopic variceal ligation (EVL) (Supplementary Table 2). Therefore, selective beta- 1- blockers (e. Results from RCTs show that, in patients with varices, NSBBs significantly reduce the incidence of first variceal hemorrhage, from 2. The effect is more evident in patients with medium/large- sized varices (3. ![]() NSBB- treated patients). Mortality is lower in the beta- blocker group compared with that in the control group, and this difference has been shown to be statistically significant (1. The incidence of first variceal hemorrhage in patients with small varices, although low, is reduced with beta- blockers (from 7 to 2% over a period of 2 years); however, these numbers are too small to show statistical significance. In patients with small varices that are not at a high risk of hemorrhage, NSBBs have been effective in delaying variceal growth, and thereby preventing variceal hemorrhage (1. EVL has been compared with NSBB in several randomized trials in patients with large varices with or without red wale markings. Two meta- analyses show that EVL is associated with a small but significantly lower incidence of first variceal hemorrhage without differences in mortality (1. However, a more recent meta- analysis showed that the estimated effect of EVL in some trials may be biased and was associated with the duration of follow- up (the shorter the follow- up, the more positive the estimated effect of EVL (1. EVL is cost- effective when cost per quality- adjusted life year is considered (1. NSBB by both patients and physicians (1. However, NSBBs have other advantages, such as prevention of bleeding from other portal hypertension sources (portal hypertensive gastropathy and gastric varices) and a possible reduction in the incidence of spontaneous bacterial peritonitis (SBP) (1. Given the lack of correlation between decreases in heart rate and decreases in portal pressure (1. ![]() ![]() NSBB is adjusted to the maximal tolerated doses to heart rates of 5. Propranolol is administered twice a day (BID) and is usually started at a dose of 2. BID. Nadolol is administered QD (once a day) and is started at a dose of 2. QD. The NSBB on the Department of Veterans Affairs (VA) National Formulary is propranolol (1. On the basis of data showing recurrent bleeding on discontinuation of beta- blockers (2. NSBBs be continued indefinitely. Importantly, once NSBBs are initiated and the dose is appropriately adjusted there is no need for repeat EGD. Approximately 1. 5% of patients have contraindications to the use of NSBB, such as asthma, insulin- dependent diabetes (with episodes of hypoglycemia), and peripheral vascular disease. The most common side effects related to NSBB in cirrhosis are lightheadedness, fatigue, and shortness of breath. Some of these side effects disappear with time or after a reduction in the dose of NSBB. ![]() ![]() In clinical trials, side effects have led to treatment discontinuation in ~1. The rate of side effects in trials in which nadolol was used (~1. The most common complications are transient dysphagia and chest discomfort. Shallow ulcers at the site of each ligation are the rule, and the use of proton pump inhibitors after ligation seems to reduce their size (2. However, there have been reports of bleeding from ligation- induced esophageal ulcers that has resulted in death (2. These therapies are summarized in (Supplementary Table 2). Nitrates (such as isosorbide mononitrate, ISMN) are ineffective in preventing first variceal hemorrhage in patients with large varices (2.
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