NEW 2020: The Korean Association for the Study of the Liver (KASL) 2020 (The Korean Association for the Study of the Liver (KASL)
A. Esophageal Vein Guide: PREVENTION AND PREVENTION According to The Korean Association for the Study of the Liver (KASL) 2020
1. Gastroesophageal varices
• Gastroesophageal varices encountered # 52.2% of patients with cirrhosis were screened through endoscopy. The prevalence is higher in cirrhotic patients Child A compared with Child B/C (35–43% vs. 48–72%).
• Portal hypertension is the most common complication and the main cause of esophageal varices.
• Rate of gastroesophageal varices # 5–9% at 1 year and 14–17% at 2 years. Small esophageal varices often progress to large with an incidence of 12% at 1 year and 25% at 2 years.
• Independent risk factors for developing esophageal varices such as: alcoholic cirrhosis, decompensated cirrhosis and splenomegaly.
• Bleeding rate from varices in 1 year (no previous history) # 12% (5% small esophageal varices and 15% large esophageal varices). The main risk factors for bleeding are dilatation, red dots on dilated veins, and decompensated cirrhosis.
• Mortality #12–22% and 1-year recurrence rate without secondary prevention # 60%.
2. How to monitor gastroesophageal varices?
a. Endoscopic monitoring of gastroesophageal varices
• Endoscopic screening for esophageal varices and assessment of bleeding risk in patients with first diagnosis of cirrhosis
• A suggested term for patients with severe cirrhosis (F3) is compensated advanced chronic liver disease (cACLD), which distinguishes between severe fibrosis and cirrhosis. Liver elastography <10 kPa may rule out cACLD, 10-15 kPa suggests cACLD and >15kPa suggests high cACLD.
• Endoscopy in all cACLD patients is not necessary, Baveno VI criteria suggest avoiding follow-up endoscopy in cACLD patients with hepatic elastography < 20kPa and platelets >150,000 mm3 because of the very low risk of true varicose veins. management needs treatment.
b. Monitor esophageal varices
• Patients with compensated cirrhosis: endoscopic follow-up for 2-3 years
• Patients with decompensated cirrhosis: endoscopic follow-up for 1-2 years
• On endoscopy, esophageal varices are classified as F1 (small), F2, F3 (large) and red dot on varicose veins.
• Alcoholic and decompensated cirrhosis are the two highest risk factors for developing esophageal varices
c. Prevents the formation and progression of esophageal varices
• Treating the underlying disease can improve liver fibrosis as well as portal hypertension.
• In patients with cirrhosis caused by hepatitis B, approximately 74% of liver biopsies after 5 years of tenofovir disoproxil fumarate therapy showed regressing cirrhosis (1). In a meta-analysis (2) improvement of liver histology in hepatitis C patients treated with pegylated interferon±ribavirin (2). The incidence of esophageal varices was significantly lower in patients with hepatitis C with sustained virologic response (SVR) to pegylated interferon+ribavirin than in the SVR group.
• NSBBs (propranolol and nadolol) are not recommended to prevent esophageal varices formation.
• In patients with small esophageal varices, no red dots NSBBs (propranolol and nadolol) or carvedilol are considered to prevent progressive varices (B2)
d. Primary prevention of bleeding esophageal varices
• Cirrhotic patients with esophageal varices => annual bleeding rate due to varices # 5-15%.
• Active prevention is recommended in patients at high risk of bleeding such as: enlarged (F2-F3), decompensated cirrhosis, dilatation with red mark on dilated veins.
• Prevention in patients with small esophageal varices (F1): small esophageal varices with red markings or in patients with decompensated cirrhosis will be prevented with NSBBs (B1) (with differences in recommendations). Report B1 and B2 compared to stretch without red mark)
• Prevention in patients with large esophageal varices (F2, F3): NSBBs or ligation are recommended. Select patient tolerance, side effects, contraindications to NSBBs, and facility conditions.
• Carvedilol: better portal depressurization effect than propanolol. In studies comparing the efficacy of carvedilol, NSBBs and esophageal venous ligation (EVL) for primary prevention => efficacy is similar to NSBBs and EVL, or sometimes superior to EVL => use is recommended for primary prevention in patients with large esophageal varices (A1)
• Combination of NSBBs and EVL: Theoretically, we see a combination of 2 methods for synergistic effect of both radicalizing varicose veins and reducing portal pressure. However, studies have not shown consistent results for primary prevention compared with NSBBs and EVL monotherapy => recommended use and level of recommendation B2.
• ISMN alone or in combination with NSBBs is not recommended for primary prevention
B. MANAGEMENT OF HEART DISEASE
• HE is a neuropsychiatric syndrome caused by liver dysfunction. Clinical presentation with variable psychological and neurological abnormalities.
• Classification: HE is divided into latent hepatic encephalopathy (Covert hepatic encephalopathy) and clinical hepatic encephalopathy (Overt HE (OHE).
• Frequency of HE # 10-14% of patients with compensated cirrhosis and 16-21% of patients with decompensated cirrhosis.
• HE is classified according to the etiology, clinical stage, precipitating factors and neurologic severity.
• Factors promoting HE such as: gastrointestinal bleeding, uremia, sedatives, diuretics, protein overload, infection, constipation, dehydration, electrolyte disturbances…
2. Diagnosis of HE:
• To diagnose clinical hepatic encephalopathy (OHE) other neuropsychiatric causes must be ruled out, and diagnosis of HE is based on clinical symptoms (A1)
• HE is classified as either OHE which can be diagnosed on the basis of clinical symptoms or CHE (latent hepatic encephalopathy) requiring cognitive function testing (B1)
• In patients suggestive of hepatic encephalopathy, imaging studies such as cranial MRI or neurological function testing will be performed to rule out other causes of cognitive impairment (B2)
• If the patient suggests hepatic encephalopathy with normal NH3 concentration => find other causes of cognitive dysfunction (B1)
3. Management of clinical hepatic encephalopathy (OHE):
– Identify and manage predisposing factors: Predisposing factors are detected in #80-90% of cirrhotic patients. In many cases, HE is improved when the promoter is removed => timely detection and correction of predisposing factors such as bleeding, infection, fluid loss, constipation, etc. is an important requirement in patients. patient HE
Non-absorbable disaccharides Lactulose (20–30 g)x 3–4 times/day. Aim to have soft stools 2-3 times/day
– Neomycin and metronidazole are not recommended because of many side effects such as: decreased intestinal absorption, nephrotoxicity, ototoxicity and peripheral neuropathy
4. Prevention of hepatic encephalopathy
• Approximately 50-70% of hepatic encephalopathy recur within 1 year, so secondary prevention should be initiated after the primary episode.
• Nonabsorbable disaccharides (lactulose, lactuto) is the first choice, the dose of 30-60ml/time ensures 2-3 bowel movements/day.
• In case the patient is intolerant to lactulose/lactitol => rifaximin is an option (400 mg x 3 times/day or 550 mg x 2 times/day).
• Combination of Non-absorbable disaccharide and rifaximin may reduce OHE recurrence compared with monotherapy (2) (3)=> recommended for secondary prevention (B1)
• According to a case-control study (1) rifaximin prevention for 2 years on average significantly reduced the recurrence rate of OHE compared with controls ((31.5% vs. 47%, P=0.034). Bass et al in one study prospective study (2) prevention of rifaxinmin for 6 months significantly reduced relapse rate compared with placebo (hazard ratio [HR], 0.42; 95% CI, 0.28–0.64). Long-term use of rifaximin increases the risk of Clostridium difficile infection, however recent studies have not shown that (4) (5)
• Long-term use of recommended BCAA-Branched Chain Amino Acids (B2) to improve symptoms as well as risk of OHE recurrence (6) (7)
• In patients with intractable ascites, intravenous albumin (40g/week) can prevent OHE as well as improve mortality (9) (recommendation B2)
• Diet provides energy from 35-40kcal/kg/day, protein 1.2-1.5g/day. Prolonged protein reduction can cause liver dysfunction, muscle weakness, and protein metabolism. Divide into many small sessions during the day, 4-6 times/day, including the night before going to bed.
Diagram of treatment and prevention of hepatic encephalopathy:
1. Vlachogiannakos J, Viazis N, Vasianopoulou P, Vafiadis I, Karamanolis DG, Ladas SD. Long-term administration of rifaximin improves the prognosis of patients with decompensated alcoholic alcoholic. J Gastroenterol Hepatol 2013;28:450-455
2. Bass NM, Mullen KD, Sanyal A, Poordad F, Neff G, Leevy CB, et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med 2010;362:1071-1081.
3. Acharya C, Bajaj JS. Current management of hepatic encephalopathy. Am J Gastroenterol 2018;113:1600-1612.
4. Mullen KD, Sanyal AJ, Bass NM, Poordad FF, Sheikh MY, Frederick RT, et al. Rifaximin is safe and well tolerated for long-term maintenance of remission from overt hepatic encephalopathy. Clin Gastroenterol Hepatol 2014;12:1390-1397.e2.
5. Neff GW, Jones M, Jonas M, Ravinuthala R, Novick D, Kaiser TE, et al. Lack of Clostridium difficile infection in patients treated with rifaximin for hepatic encephalopathy: a retrospective analysis. J Clin Gastroenterol 2013;47:188-192
6. Gluud LL, Dam G, Les I, Marchesini G, Borre M, Aagaard NK, et al. Branched-chain amino acids for people with hepatic encephalopathy. Cochrane Database Syst Rev 2017;5:CD001939
7. Park JG, Tak WY, Park SY, Kweon YO, Jang SY, Lee YR, et al. Effects of branched-chain amino acids (BCAAs) on the progression of advanced liver disease: a Korean quality, multicenter, retrospective, observational, cohort study. Medicine (Baltimore) 2017;96:e6580
8. Varakanahalli S, Sharma BC, Srivastava S, Sachdeva S, Dahale AS. Secondary prevention of hepatic encephalopathy in cirrhosis of liver: a double-blind randomized controlled trial of L-ornithine L-aspartate versus placebo. Eur J Gastroenterol Hepatol 2018;30:951-958.
9. Caraceni P, Riggio O, Angeli P, Alessandria C, Neri S, Foschi FG, et al. Long-term albumin administration in decompensated cirrhosis (ANSWER): an open-label randomised trial. Lancet 2018;391:2417-2429.
Author: BS. Huynh Trung
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