Cirrhosis medical therapy: Difference between revisions
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===Pruritus=== | ===Pruritus=== | ||
* [[Pruritus]] is a common symptom in [[primary biliary cirrhosis]] and [[Hepatitis C]]. | * [[Pruritus]] is a common symptom in [[primary biliary cirrhosis]] and [[Hepatitis C]]. | ||
* Endogenous [[Opioid|opioids]] and increased serum bile acid levels are considered responsible for causing [[Itch|pruritus]]. | * Endogenous [[Opioid|opioids]] and increased serum [[bile acid]] levels are considered responsible for causing [[Itch|pruritus]]. | ||
* Preferred regimen for [[Itch|pruritus]] in chronic liver disease: | * Preferred regimen for [[Itch|pruritus]] in [[chronic liver disease]]: | ||
** [[Cholestyramine]] | ** [[Cholestyramine]] | ||
* Preferred regimen for mild [[Itch|itching]]: | * Preferred regimen for mild [[Itch|itching]]: | ||
** [[antihistamines]] | ** [[antihistamines]] | ||
** Ammonium lactate topical solution | ** [[Ammonium lactate]] [[topical]] solution | ||
* Preferred regimen for severe [[Itch|itching]]: | * Preferred regimen for severe [[Itch|itching]]: | ||
** Ultraviolet light therapy | ** [[Ultraviolet|Ultraviolet light therapy]] | ||
** [[plasmapheresis]] | ** [[plasmapheresis]] | ||
* Alternative regimens for [[Itch|pruritus]]: | * Alternative regimens for [[Itch|pruritus]]: | ||
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** [[ursodeoxycholic acid]] | ** [[ursodeoxycholic acid]] | ||
** [[rifampin]] | ** [[rifampin]] | ||
** [[naltrexone]] (opiate) | ** [[naltrexone]] ([[opiate]]) | ||
===Hypogonadism=== | ===Hypogonadism=== | ||
| Line 49: | Line 49: | ||
** At risk for [[osteoporosis]] | ** At risk for [[osteoporosis]] | ||
** On [[corticosteroids|corticosteroid]] therapy for autoimmune [[liver]] disease | ** On [[corticosteroids|corticosteroid]] therapy for autoimmune [[liver]] disease | ||
* Preferred regimen for [[osteoporosis]]: Alendronate sodium | * Preferred regimen for [[osteoporosis]]: [[Alendronate|Alendronate sodium]] | ||
===Pain management in Cirrhosis=== | ===Pain management in Cirrhosis=== | ||
* [[Cirrhosis|Cirrhotic]] patients can develop pain from [[ascites]] ([[back pain|back]] and [[abdominal pain]]) and pain from [[gynecomastia]] ([[mastalgia]]). | * [[Cirrhosis|Cirrhotic]] patients can develop pain from [[ascites]] ([[back pain|back]] and [[abdominal pain]]) and pain from [[gynecomastia]] ([[mastalgia]]). | ||
* [[Pain]] management in [[cirrhosis]] needs special consideration as many [[analgesic]] and [[Non-steroidal anti-inflammatory drug|anti-inflammatory drugs]] are metabolized by the [[liver]] and dosage regulations are required to prevent further [[liver]] damage and drug toxicity. | * [[Pain]] management in [[cirrhosis]] needs special consideration as many [[analgesic]] and [[Non-steroidal anti-inflammatory drug|anti-inflammatory drugs]] are metabolized by the [[liver]] and dosage regulations are required to prevent further [[liver]] damage and drug toxicity. | ||
* Drug dosages should be titrated as per the level of hepatic functioning in the patient. | * Drug dosages should be titrated as per the level of [[Liver|hepatic]] functioning in the [[patient]]. | ||
* Dosage changes are required in the | * Dosage changes are required in the following [[Patient|patients]]: | ||
** [[Portal hypertension]] | ** [[Portal hypertension]] | ||
** [[Renal failure]] | ** [[Renal failure]] | ||
** Alcoholic patient on multiple medications | ** Alcoholic patient on multiple medications | ||
* Non-selective [[Non-steroidal anti-inflammatory drug|NSAIDs]] should be avoided in patients with [[cirrhosis]] because of the following complications: | * Non-selective [[Non-steroidal anti-inflammatory drug|NSAIDs]] should be avoided in patients with [[cirrhosis]] because of the following complications: | ||
** Increased bleeding from [[varices]] | ** Increased [[bleeding]] from [[varices]] | ||
** Impaired [[renal function]] | ** Impaired [[renal function]] | ||
** Development of diuretic resistant [[ascites]] | ** Development of [[diuretic]] resistant [[ascites]] | ||
** Alternative regimen for [[pain]] in [[cirrhosis]]: [[celecoxib]] | ** Alternative regimen for [[pain]] in [[cirrhosis]]: [[celecoxib]] | ||
* [[Opioids]] should be used with caution in patients with [[cirrhosis]] because they are metabolized by the [[liver]] through oxidation and [[glucuronidation]]. | * [[Opioids]] should be used with caution in [[Patient|patients]] with [[cirrhosis]] because they are metabolized by the [[liver]] through oxidation and [[glucuronidation]]. | ||
* Patients with [[cirrhosis]] have reduced [[liver]] blood flow, protein binding and hepatic enzyme capacity, leading to drug accumulation and increased vulnerability to developing [[opiate]] toxicity. | * Patients with [[cirrhosis]] have reduced [[liver]] blood flow, [[protein]] binding and hepatic enzyme capacity, leading to drug accumulation and increased vulnerability to developing [[opiate]] toxicity. | ||
===Nutrition and exercise=== | ===Nutrition and exercise=== | ||
The following points need to be kept in mind regarding nutrition in cirrhosis patients:<ref name="pmid8328092">{{cite journal |vauthors=Kondrup J, Nielsen K, Hamberg O |title=[Nutritional therapy in patients with liver cirrhosis] |language=Danish |journal=Ugeskr. Laeg. |volume=155 |issue=29 |pages=2248–51 |year=1993 |pmid=8328092 |doi= |url=}}</ref><ref name="pmid1916467">{{cite journal |vauthors=Silk DB, O'Keefe SJ, Wicks C |title=Nutritional support in liver disease |journal=Gut |volume=Suppl |issue= |pages=S29–33 |year=1991 |pmid=1916467 |pmc=1405219 |doi= |url=}}</ref><ref name="pmid18627001">{{cite journal |vauthors=Plank LD, Gane EJ, Peng S, Muthu C, Mathur S, Gillanders L, McIlroy K, Donaghy AJ, McCall JL |title=Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial |journal=Hepatology |volume=48 |issue=2 |pages=557–66 |year=2008 |pmid=18627001 |doi=10.1002/hep.22367 |url=}}</ref><ref name="pmid16707194">{{cite journal |vauthors=Plauth M, Cabré E, Riggio O, Assis-Camilo M, Pirlich M, Kondrup J, Ferenci P, Holm E, Vom Dahl S, Müller MJ, Nolte W |title=ESPEN Guidelines on Enteral Nutrition: Liver disease |journal=Clin Nutr |volume=25 |issue=2 |pages=285–94 |year=2006 |pmid=16707194 |doi=10.1016/j.clnu.2006.01.018 |url=}}</ref> | The following points need to be kept in mind regarding nutrition in [[cirrhosis]] patients:<ref name="pmid8328092">{{cite journal |vauthors=Kondrup J, Nielsen K, Hamberg O |title=[Nutritional therapy in patients with liver cirrhosis] |language=Danish |journal=Ugeskr. Laeg. |volume=155 |issue=29 |pages=2248–51 |year=1993 |pmid=8328092 |doi= |url=}}</ref><ref name="pmid1916467">{{cite journal |vauthors=Silk DB, O'Keefe SJ, Wicks C |title=Nutritional support in liver disease |journal=Gut |volume=Suppl |issue= |pages=S29–33 |year=1991 |pmid=1916467 |pmc=1405219 |doi= |url=}}</ref><ref name="pmid18627001">{{cite journal |vauthors=Plank LD, Gane EJ, Peng S, Muthu C, Mathur S, Gillanders L, McIlroy K, Donaghy AJ, McCall JL |title=Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial |journal=Hepatology |volume=48 |issue=2 |pages=557–66 |year=2008 |pmid=18627001 |doi=10.1002/hep.22367 |url=}}</ref><ref name="pmid16707194">{{cite journal |vauthors=Plauth M, Cabré E, Riggio O, Assis-Camilo M, Pirlich M, Kondrup J, Ferenci P, Holm E, Vom Dahl S, Müller MJ, Nolte W |title=ESPEN Guidelines on Enteral Nutrition: Liver disease |journal=Clin Nutr |volume=25 |issue=2 |pages=285–94 |year=2006 |pmid=16707194 |doi=10.1016/j.clnu.2006.01.018 |url=}}</ref> | ||
* [[Anorexia]] is common in [[cirrhosis]] patients with [[ascites]] due to the direct compression of the [[Intestine|bowel]] by the ascitic fluid. | * [[Anorexia]] is common in [[cirrhosis]] patients with [[ascites]] due to the direct compression of the [[Intestine|bowel]] by the ascitic fluid. | ||
* Adequate [[Calorie|calories]] and [[Protein|proteins]] should be added to the [[Diet (nutrition)|diet]] of the [[patient]]. | * Adequate [[Calorie|calories]] and [[Protein|proteins]] should be added to the [[Diet (nutrition)|diet]] of the [[patient]]. | ||
* [[Patient|Patients]] should consume a balanced [[Diet (nutrition)|diet]] and one [[multivitamin]] daily. | * [[Patient|Patients]] should consume a balanced [[Diet (nutrition)|diet]] and one [[multivitamin]] daily. | ||
* [[Vitamin D]] and [[Vitamin K|K]] supplementation is recommended in [[Patient|patients]] with [[cholestasis]]. | * [[Vitamin D]] and [[Vitamin K|K]] supplementation is recommended in [[Patient|patients]] with [[cholestasis]]. | ||
* [[Patient|Patients]] frequently benefit from the addition of commonly available liquid and powdered nutritional supplements to the [[Diet (nutrition)|diet]]. | * [[Patient|Patients]] frequently benefit from the addition of commonly available liquid and powdered [[Dietary supplement|nutritional supplements]] to the [[Diet (nutrition)|diet]]. | ||
* [[Patient|Patients]] are encouraged to exercise regularly to prevent [[Muscle atrophy|muscle wasting]]. | * [[Patient|Patients]] are encouraged to [[Physical exercise|exercise]] regularly to prevent [[Muscle atrophy|muscle wasting]]. | ||
* An exercise program under the direct supervision of a physical therapist may be proposed for patients. | * An exercise program under the direct supervision of a physical therapist may be proposed for [[Patient|patients]]. | ||
==== Protein ==== | ==== Protein ==== | ||
* The [[Diet (nutrition)|diet]] of [[cirrhosis]] [[Patient|patients]] should be adequately titrated for [[protein]]. | * The [[Diet (nutrition)|diet]] of [[cirrhosis]] [[Patient|patients]] should be adequately titrated for [[protein]]. | ||
* Excessive [[protein]] in the [[Diet (nutrition)|diet]] places the patient at risk for [[hepatic encephalopathy]]. | * Excessive [[protein]] in the [[Diet (nutrition)|diet]] places the patient at risk for [[hepatic encephalopathy]]. | ||
* Low protein levels in the [[Diet (nutrition)|diet]] cause [[Muscle atrophy|muscle wasting]]. | * Low [[protein]] levels in the [[Diet (nutrition)|diet]] cause [[Muscle atrophy|muscle wasting]]. | ||
* As per the guidelines by the American Association for the Study of Liver Diseases and the American College of Gastroenterology, [[cirrhosis]] patients with [[protein]] [[malnutrition]] require multiple feedings per day with breakfast and a nightly snack.<ref name="pmid19904248">{{cite journal |vauthors=O'Shea RS, Dasarathy S, McCullough AJ |title=Alcoholic liver disease |journal=Am. J. Gastroenterol. |volume=105 |issue=1 |pages=14–32; quiz 33 |year=2010 |pmid=19904248 |doi=10.1038/ajg.2009.593 |url=}}</ref><ref name="pmid15246205">{{cite journal |vauthors=Córdoba J, López-Hellín J, Planas M, Sabín P, Sanpedro F, Castro F, Esteban R, Guardia J |title=Normal protein diet for episodic hepatic encephalopathy: results of a randomized study |journal=J. Hepatol. |volume=41 |issue=1 |pages=38–43 |year=2004 |pmid=15246205 |doi=10.1016/j.jhep.2004.03.023 |url=}}</ref><ref name="pmid18627001">{{cite journal |vauthors=Plank LD, Gane EJ, Peng S, Muthu C, Mathur S, Gillanders L, McIlroy K, Donaghy AJ, McCall JL |title=Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial |journal=Hepatology |volume=48 |issue=2 |pages=557–66 |year=2008 |pmid=18627001 |doi=10.1002/hep.22367 |url=}}</ref> | * As per the guidelines by the American Association for the Study of Liver Diseases and the American College of Gastroenterology, [[cirrhosis]] patients with [[protein]] [[malnutrition]] require multiple feedings per day with breakfast and a nightly snack.<ref name="pmid19904248">{{cite journal |vauthors=O'Shea RS, Dasarathy S, McCullough AJ |title=Alcoholic liver disease |journal=Am. J. Gastroenterol. |volume=105 |issue=1 |pages=14–32; quiz 33 |year=2010 |pmid=19904248 |doi=10.1038/ajg.2009.593 |url=}}</ref><ref name="pmid15246205">{{cite journal |vauthors=Córdoba J, López-Hellín J, Planas M, Sabín P, Sanpedro F, Castro F, Esteban R, Guardia J |title=Normal protein diet for episodic hepatic encephalopathy: results of a randomized study |journal=J. Hepatol. |volume=41 |issue=1 |pages=38–43 |year=2004 |pmid=15246205 |doi=10.1016/j.jhep.2004.03.023 |url=}}</ref><ref name="pmid18627001">{{cite journal |vauthors=Plank LD, Gane EJ, Peng S, Muthu C, Mathur S, Gillanders L, McIlroy K, Donaghy AJ, McCall JL |title=Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial |journal=Hepatology |volume=48 |issue=2 |pages=557–66 |year=2008 |pmid=18627001 |doi=10.1002/hep.22367 |url=}}</ref> | ||
* Branched-chain amino acids (BCAA) can function as pharmacologic nutrients for patients with decompensated [[cirrhosis]]. | * [[Branched-chain amino acids]] [[Branched chain amino acids|(BCAA)]] can function as pharmacologic [[Nutrient|nutrients]] for patients with decompensated [[cirrhosis]]. | ||
====Zinc==== | ====Zinc==== | ||
* [[Zinc]] deficiency is commonly observed in [[Patient|patients]] with [[cirrhosis]]. | * [[Zinc]] deficiency is commonly observed in [[Patient|patients]] with [[cirrhosis]]. | ||
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====Genotypes HCV 1 and 4==== | ====Genotypes HCV 1 and 4==== | ||
* Preferred regimen (1): Peginterferon plus [[ribavirin]] for 48 weeks. The dose for peginterferon alfa-2a is 180 µg subcutaneously per week together with [[ribavirin]] using doses of 1,000 mg for those <75 kg in weight and 1,200 mg for those >75 kg; the dose for peginterferon alfa-2b is 1.5 µg/kg subcutaneously per week together with [[ribavirin]] using doses of 800 mg for those weighing <65 kg; 1,000 mg for those weighing >65 kg to 85 kg, 1,200 mg for >85 kg to 105 kg, and 1,400 mg for >105 kg.<ref name="pmid24747798">{{cite journal |vauthors=Vierling JM, Zeuzem S, Poordad F, Bronowicki JP, Manns MP, Bacon BR, Esteban R, Flamm SL, Kwo PY, Pedicone LD, Deng W, Dutko FJ, DiNubile MJ, Koury KJ, Helmond FA, Wahl J, Bruno S |title=Safety and efficacy of boceprevir/peginterferon/ribavirin for HCV G1 compensated cirrhotics: meta-analysis of 5 trials |journal=J. Hepatol. |volume=61 |issue=2 |pages=200–9 |year=2014 |pmid=24747798 |doi=10.1016/j.jhep.2014.03.022 |url=}}</ref> | * Preferred regimen (1): Peginterferon plus [[ribavirin]] for 48 weeks. The dose for peginterferon alfa-2a is 180 µg subcutaneously per week together with [[ribavirin]] using doses of 1,000 mg for those <75 kg in weight and 1,200 mg for those >75 kg; the dose for [[Pegylated interferon alfa-2b|peginterferon alfa-2b]] is 1.5 µg/kg subcutaneously per week together with [[ribavirin]] using doses of 800 mg for those weighing <65 kg; 1,000 mg for those weighing >65 kg to 85 kg, 1,200 mg for >85 kg to 105 kg, and 1,400 mg for >105 kg.<ref name="pmid24747798">{{cite journal |vauthors=Vierling JM, Zeuzem S, Poordad F, Bronowicki JP, Manns MP, Bacon BR, Esteban R, Flamm SL, Kwo PY, Pedicone LD, Deng W, Dutko FJ, DiNubile MJ, Koury KJ, Helmond FA, Wahl J, Bruno S |title=Safety and efficacy of boceprevir/peginterferon/ribavirin for HCV G1 compensated cirrhotics: meta-analysis of 5 trials |journal=J. Hepatol. |volume=61 |issue=2 |pages=200–9 |year=2014 |pmid=24747798 |doi=10.1016/j.jhep.2014.03.022 |url=}}</ref> | ||
====Genotypes HCV 2 and 3==== | ====Genotypes HCV 2 and 3==== | ||
| Line 122: | Line 122: | ||
:[[Hepatitis_B/Medical_Therapy|Hepatitis B Medical Therapy]]<ref name="pmid1701755">{{cite journal |vauthors=Perrillo RP |title=Factors influencing response to interferon in chronic hepatitis B: implications for Asian and western populations |journal=Hepatology |volume=12 |issue=6 |pages=1433–5 |year=1990 |pmid=1701755 |doi= |url=}}</ref><ref name="pmid9011789">{{cite journal |vauthors=Hoofnagle JH, di Bisceglie AM |title=The treatment of chronic viral hepatitis |journal=N. Engl. J. Med. |volume=336 |issue=5 |pages=347–56 |year=1997 |pmid=9011789 |doi=10.1056/NEJM199701303360507 |url=}}</ref><ref name="pmid7477217">{{cite journal |vauthors=Dienstag JL, Perrillo RP, Schiff ER, Bartholomew M, Vicary C, Rubin M |title=A preliminary trial of lamivudine for chronic hepatitis B infection |journal=N. Engl. J. Med. |volume=333 |issue=25 |pages=1657–61 |year=1995 |pmid=7477217 |doi=10.1056/NEJM199512213332501 |url=}}</ref><ref name="pmid12512035">{{cite journal |vauthors=Dienstag JL, Goldin RD, Heathcote EJ, Hann HW, Woessner M, Stephenson SL, Gardner S, Gray DF, Schiff ER |title=Histological outcome during long-term lamivudine therapy |journal=Gastroenterology |volume=124 |issue=1 |pages=105–17 |year=2003 |pmid=12512035 |doi=10.1053/gast.2003.50013 |url=}}</ref><ref name="pmid15470215">{{cite journal |vauthors=Liaw YF, Sung JJ, Chow WC, Farrell G, Lee CZ, Yuen H, Tanwandee T, Tao QM, Shue K, Keene ON, Dixon JS, Gray DF, Sabbat J |title=Lamivudine for patients with chronic hepatitis B and advanced liver disease |journal=N. Engl. J. Med. |volume=351 |issue=15 |pages=1521–31 |year=2004 |pmid=15470215 |doi=10.1056/NEJMoa033364 |url=}}</ref><ref name="pmid14999707">{{cite journal |vauthors=Lok AS, McMahon BJ |title=Chronic hepatitis B: update of recommendations |journal=Hepatology |volume=39 |issue=3 |pages=857–61 |year=2004 |pmid=14999707 |doi=10.1002/hep.20110 |url=}}</ref><ref name="pmid15987916">{{cite journal |vauthors=Hadziyannis SJ, Tassopoulos NC, Heathcote EJ, Chang TT, Kitis G, Rizzetto M, Marcellin P, Lim SG, Goodman Z, Ma J, Arterburn S, Xiong S, Currie G, Brosgart CL |title=Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B |journal=N. Engl. J. Med. |volume=352 |issue=26 |pages=2673–81 |year=2005 |pmid=15987916 |doi=10.1056/NEJMoa042957 |url=}}</ref><ref name="pmid16230074">{{cite journal |vauthors=Chang TT, Gish RG, Hadziyannis SJ, Cianciara J, Rizzetto M, Schiff ER, Pastore G, Bacon BR, Poynard T, Joshi S, Klesczewski KS, Thiry A, Rose RE, Colonno RJ, Hindes RG |title=A dose-ranging study of the efficacy and tolerability of entecavir in Lamivudine-refractory chronic hepatitis B patients |journal=Gastroenterology |volume=129 |issue=4 |pages=1198–209 |year=2005 |pmid=16230074 |doi=10.1053/j.gastro.2005.06.055 |url=}}</ref><ref name="pmid14647053">{{cite journal |vauthors=Schiff ER, Lai CL, Hadziyannis S, Neuhaus P, Terrault N, Colombo M, Tillmann HL, Samuel D, Zeuzem S, Lilly L, Rendina M, Villeneuve JP, Lama N, James C, Wulfsohn MS, Namini H, Westland C, Xiong S, Choy GS, Van Doren S, Fry J, Brosgart CL |title=Adefovir dipivoxil therapy for lamivudine-resistant hepatitis B in pre- and post-liver transplantation patients |journal=Hepatology |volume=38 |issue=6 |pages=1419–27 |year=2003 |pmid=14647053 |doi=10.1016/j.hep.2003.09.040 |url=}}</ref><ref name="urlEASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection - Journal of Hepatology">{{cite web |url=http://www.journal-of-hepatology.eu/article/S0168-8278(12)00167-5/abstract |title=EASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection - Journal of Hepatology |format= |work= |accessdate=}}</ref><ref name="pmid15470215">{{cite journal |vauthors=Liaw YF, Sung JJ, Chow WC, Farrell G, Lee CZ, Yuen H, Tanwandee T, Tao QM, Shue K, Keene ON, Dixon JS, Gray DF, Sabbat J |title=Lamivudine for patients with chronic hepatitis B and advanced liver disease |journal=N. Engl. J. Med. |volume=351 |issue=15 |pages=1521–31 |year=2004 |pmid=15470215 |doi=10.1056/NEJMoa033364 |url=}}</ref> | :[[Hepatitis_B/Medical_Therapy|Hepatitis B Medical Therapy]]<ref name="pmid1701755">{{cite journal |vauthors=Perrillo RP |title=Factors influencing response to interferon in chronic hepatitis B: implications for Asian and western populations |journal=Hepatology |volume=12 |issue=6 |pages=1433–5 |year=1990 |pmid=1701755 |doi= |url=}}</ref><ref name="pmid9011789">{{cite journal |vauthors=Hoofnagle JH, di Bisceglie AM |title=The treatment of chronic viral hepatitis |journal=N. Engl. J. Med. |volume=336 |issue=5 |pages=347–56 |year=1997 |pmid=9011789 |doi=10.1056/NEJM199701303360507 |url=}}</ref><ref name="pmid7477217">{{cite journal |vauthors=Dienstag JL, Perrillo RP, Schiff ER, Bartholomew M, Vicary C, Rubin M |title=A preliminary trial of lamivudine for chronic hepatitis B infection |journal=N. Engl. J. Med. |volume=333 |issue=25 |pages=1657–61 |year=1995 |pmid=7477217 |doi=10.1056/NEJM199512213332501 |url=}}</ref><ref name="pmid12512035">{{cite journal |vauthors=Dienstag JL, Goldin RD, Heathcote EJ, Hann HW, Woessner M, Stephenson SL, Gardner S, Gray DF, Schiff ER |title=Histological outcome during long-term lamivudine therapy |journal=Gastroenterology |volume=124 |issue=1 |pages=105–17 |year=2003 |pmid=12512035 |doi=10.1053/gast.2003.50013 |url=}}</ref><ref name="pmid15470215">{{cite journal |vauthors=Liaw YF, Sung JJ, Chow WC, Farrell G, Lee CZ, Yuen H, Tanwandee T, Tao QM, Shue K, Keene ON, Dixon JS, Gray DF, Sabbat J |title=Lamivudine for patients with chronic hepatitis B and advanced liver disease |journal=N. Engl. J. Med. |volume=351 |issue=15 |pages=1521–31 |year=2004 |pmid=15470215 |doi=10.1056/NEJMoa033364 |url=}}</ref><ref name="pmid14999707">{{cite journal |vauthors=Lok AS, McMahon BJ |title=Chronic hepatitis B: update of recommendations |journal=Hepatology |volume=39 |issue=3 |pages=857–61 |year=2004 |pmid=14999707 |doi=10.1002/hep.20110 |url=}}</ref><ref name="pmid15987916">{{cite journal |vauthors=Hadziyannis SJ, Tassopoulos NC, Heathcote EJ, Chang TT, Kitis G, Rizzetto M, Marcellin P, Lim SG, Goodman Z, Ma J, Arterburn S, Xiong S, Currie G, Brosgart CL |title=Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B |journal=N. Engl. J. Med. |volume=352 |issue=26 |pages=2673–81 |year=2005 |pmid=15987916 |doi=10.1056/NEJMoa042957 |url=}}</ref><ref name="pmid16230074">{{cite journal |vauthors=Chang TT, Gish RG, Hadziyannis SJ, Cianciara J, Rizzetto M, Schiff ER, Pastore G, Bacon BR, Poynard T, Joshi S, Klesczewski KS, Thiry A, Rose RE, Colonno RJ, Hindes RG |title=A dose-ranging study of the efficacy and tolerability of entecavir in Lamivudine-refractory chronic hepatitis B patients |journal=Gastroenterology |volume=129 |issue=4 |pages=1198–209 |year=2005 |pmid=16230074 |doi=10.1053/j.gastro.2005.06.055 |url=}}</ref><ref name="pmid14647053">{{cite journal |vauthors=Schiff ER, Lai CL, Hadziyannis S, Neuhaus P, Terrault N, Colombo M, Tillmann HL, Samuel D, Zeuzem S, Lilly L, Rendina M, Villeneuve JP, Lama N, James C, Wulfsohn MS, Namini H, Westland C, Xiong S, Choy GS, Van Doren S, Fry J, Brosgart CL |title=Adefovir dipivoxil therapy for lamivudine-resistant hepatitis B in pre- and post-liver transplantation patients |journal=Hepatology |volume=38 |issue=6 |pages=1419–27 |year=2003 |pmid=14647053 |doi=10.1016/j.hep.2003.09.040 |url=}}</ref><ref name="urlEASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection - Journal of Hepatology">{{cite web |url=http://www.journal-of-hepatology.eu/article/S0168-8278(12)00167-5/abstract |title=EASL Clinical Practice Guidelines: Management of chronic hepatitis B virus infection - Journal of Hepatology |format= |work= |accessdate=}}</ref><ref name="pmid15470215">{{cite journal |vauthors=Liaw YF, Sung JJ, Chow WC, Farrell G, Lee CZ, Yuen H, Tanwandee T, Tao QM, Shue K, Keene ON, Dixon JS, Gray DF, Sabbat J |title=Lamivudine for patients with chronic hepatitis B and advanced liver disease |journal=N. Engl. J. Med. |volume=351 |issue=15 |pages=1521–31 |year=2004 |pmid=15470215 |doi=10.1056/NEJMoa033364 |url=}}</ref> | ||
* Patients with HBeAg-positive chronic hepatitis B<ref name="pmid16083710">{{cite journal |vauthors=Lai CL, Leung N, Teo EK, Tong M, Wong F, Hann HW, Han S, Poynard T, Myers M, Chao G, Lloyd D, Brown NA |title=A 1-year trial of telbivudine, lamivudine, and the combination in patients with hepatitis B e antigen-positive chronic hepatitis B |journal=Gastroenterology |volume=129 |issue=2 |pages=528–36 |year=2005 |pmid=16083710 |doi=10.1016/j.gastro.2005.05.053 |url=}}</ref> | * Patients with HBeAg-positive chronic [[hepatitis B]]<ref name="pmid16083710">{{cite journal |vauthors=Lai CL, Leung N, Teo EK, Tong M, Wong F, Hann HW, Han S, Poynard T, Myers M, Chao G, Lloyd D, Brown NA |title=A 1-year trial of telbivudine, lamivudine, and the combination in patients with hepatitis B e antigen-positive chronic hepatitis B |journal=Gastroenterology |volume=129 |issue=2 |pages=528–36 |year=2005 |pmid=16083710 |doi=10.1016/j.gastro.2005.05.053 |url=}}</ref> | ||
:'''a.''' [[ALT]] greater than 2 times normal or moderate/severe hepatitis on biopsy, and HBV DNA >20,000 IU/mL - treatment may be initiated with any of the 7 approved antiviral medications, but pegIFN-α, [[tenofovir]] or [[entecavir]] are preferred. | :'''a.''' [[ALT]] greater than 2 times normal or moderate/severe hepatitis on biopsy, and HBV DNA >20,000 IU/mL - treatment may be initiated with any of the 7 approved [[antiviral]] medications, but [[Interferon alfa-2b|pegIFN-α]], [[tenofovir]] or [[entecavir]] are preferred. | ||
:'''b.''' [[Alanine transaminase|ALT]] persistently normal or minimally elevated (<2 times normal) - should not be initiated on treatment. | :'''b.''' [[Alanine transaminase|ALT]] persistently normal or minimally elevated (<2 times normal) - should not be initiated on treatment. | ||
:'''c.''' Children with elevated [[Alanine transaminase|ALT]] greater than 2 times normal - treatment may be initiated with [[IFN-α]] or [[lamivudine]] if [[Alanine transaminase|ALT]] levels remain elevated at this level for longer than 6 months. | :'''c.''' Children with elevated [[Alanine transaminase|ALT]] greater than 2 times normal - treatment may be initiated with [[IFN-α]] or [[lamivudine]] if [[Alanine transaminase|ALT]] levels remain elevated at this level for longer than 6 months. | ||
* Patients with HBeAg-negative chronic [[hepatitis B]] (serum HBV DNA >20,000 IU/mL and elevated ALT >2 times normal) should be considered for treatment with pegIFN-α, [[tenofovir]] or [[entecavir]].<ref name="pmid19616339">{{cite journal |vauthors=Manolakopoulos S, Triantos C, Theodoropoulos J, Vlachogiannakos J, Kougioumtzan A, Papatheodoridis G, Tzourmakliotis D, Karamanolis D, Burroughs AK, Archimandritis A, Raptis S, Avgerinos A |title=Antiviral therapy reduces portal pressure in patients with cirrhosis due to HBeAg-negative chronic hepatitis B and significant portal hypertension |journal=J. Hepatol. |volume=51 |issue=3 |pages=468–74 |year=2009 |pmid=19616339 |doi=10.1016/j.jhep.2009.05.031 |url=}}</ref> | * Patients with HBeAg-negative chronic [[hepatitis B]] (serum HBV DNA >20,000 IU/mL and elevated ALT >2 times normal) should be considered for treatment with [[Interferon alfa-2b|pegIFN-α]], [[tenofovir]] or [[entecavir]].<ref name="pmid19616339">{{cite journal |vauthors=Manolakopoulos S, Triantos C, Theodoropoulos J, Vlachogiannakos J, Kougioumtzan A, Papatheodoridis G, Tzourmakliotis D, Karamanolis D, Burroughs AK, Archimandritis A, Raptis S, Avgerinos A |title=Antiviral therapy reduces portal pressure in patients with cirrhosis due to HBeAg-negative chronic hepatitis B and significant portal hypertension |journal=J. Hepatol. |volume=51 |issue=3 |pages=468–74 |year=2009 |pmid=19616339 |doi=10.1016/j.jhep.2009.05.031 |url=}}</ref> | ||
* Patients with compensated [[cirrhosis]] - best treated with [[tenofovir]] or [[entecavir]]. | * Patients with compensated [[cirrhosis]] - best treated with [[tenofovir]] or [[entecavir]]. | ||
* Patients with decompensated [[cirrhosis]] — [[Lamivudine]] or [[telbivudine]] may be used as initial treatment in combination with [[adefovir]] or [[tenofovir]] to reduce the risk of drug resistance.<ref name="pmid10613747">{{cite journal |vauthors=Villeneuve JP, Condreay LD, Willems B, Pomier-Layrargues G, Fenyves D, Bilodeau M, Leduc R, Peltekian K, Wong F, Margulies M, Heathcote EJ |title=Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B |journal=Hepatology |volume=31 |issue=1 |pages=207–10 |year=2000 |pmid=10613747 |doi=10.1002/hep.510310130 |url=}}</ref><ref name="pmid12198698">{{cite journal |vauthors=Fontana RJ, Hann HW, Perrillo RP, Vierling JM, Wright T, Rakela J, Anschuetz G, Davis R, Gardner SD, Brown NA |title=Determinants of early mortality in patients with decompensated chronic hepatitis B treated with antiviral therapy |journal=Gastroenterology |volume=123 |issue=3 |pages=719–27 |year=2002 |pmid=12198698 |doi= |url=}}</ref> | * Patients with decompensated [[cirrhosis]] — [[Lamivudine]] or [[telbivudine]] may be used as initial treatment in combination with [[adefovir]] or [[tenofovir]] to reduce the risk of drug resistance.<ref name="pmid10613747">{{cite journal |vauthors=Villeneuve JP, Condreay LD, Willems B, Pomier-Layrargues G, Fenyves D, Bilodeau M, Leduc R, Peltekian K, Wong F, Margulies M, Heathcote EJ |title=Lamivudine treatment for decompensated cirrhosis resulting from chronic hepatitis B |journal=Hepatology |volume=31 |issue=1 |pages=207–10 |year=2000 |pmid=10613747 |doi=10.1002/hep.510310130 |url=}}</ref><ref name="pmid12198698">{{cite journal |vauthors=Fontana RJ, Hann HW, Perrillo RP, Vierling JM, Wright T, Rakela J, Anschuetz G, Davis R, Gardner SD, Brown NA |title=Determinants of early mortality in patients with decompensated chronic hepatitis B treated with antiviral therapy |journal=Gastroenterology |volume=123 |issue=3 |pages=719–27 |year=2002 |pmid=12198698 |doi= |url=}}</ref> | ||
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* Immunosuppressive treatment based on serum aspartate aminotransferase ([[Aspartate transaminase|AST]]), serum alanine aminotransferase ([[Alanine transaminase|ALT]]), serum gamma-globulin levels, and histological features | * Immunosuppressive treatment based on serum aspartate aminotransferase ([[Aspartate transaminase|AST]]), serum alanine aminotransferase ([[Alanine transaminase|ALT]]), serum gamma-globulin levels, and histological features | ||
** [[Prednisone]] or prednisolone with azathioprine (adults) | ** [[Prednisone]] or [[prednisolone]] with [[azathioprine]] (adults) | ||
** [[Prednisone]] with [[azathioprine]] or [[6-mercaptopurine]] (children) | ** [[Prednisone]] with [[azathioprine]] or [[6-mercaptopurine]] (children) | ||
** [[Prednisone]] or [[prednisolone]] alone. | ** [[Prednisone]] or [[prednisolone]] alone. | ||
| Line 149: | Line 149: | ||
:[[Primary_sclerosing_cholangitis_medical_therapy|Primary Sclerosing Cholangitis Medical Therapy]] | :[[Primary_sclerosing_cholangitis_medical_therapy|Primary Sclerosing Cholangitis Medical Therapy]] | ||
* Standard treatment includes [[ursodiol]] which has been shown to lower elevated liver enzyme numbers in people with PSC. | * Standard treatment includes [[ursodiol]] which has been shown to lower elevated liver enzyme numbers in people with [[Primary sclerosing cholangitis|PSC]]. | ||
* Symptomatic treatment includes: | * Symptomatic treatment includes: | ||
** Anti-histaminics - for [[Itch|itching]] | ** Anti-histaminics - for [[Itch|itching]] | ||
** [[Cholestyramine]] - bile acid sequestrant | ** [[Cholestyramine]] - [[bile acid sequestrant]] | ||
** Antibiotics - for infections | ** [[Antibiotic|Antibiotics]] - for [[Infection|infections]] | ||
** [[Vitamin]] supplemantation - Vitamin A, D and K. | ** [[Vitamin]] supplemantation - [[Vitamin A]], [[Vitamin D|D]] and [[Vitamin K|K]]. | ||
===Wilson's Disease=== | ===Wilson's Disease=== | ||
| Line 160: | Line 160: | ||
* Avoid intake of foods and water with high concentrations of [[copper]]. | * Avoid intake of foods and water with high concentrations of [[copper]]. | ||
* Initial treatment for symptomatic patients includes a [[Chelation|chelating]] agent ([[D-penicillamine]], [[trientine]] or zinc). | * Initial treatment for symptomatic [[Patient|patients]] includes a [[Chelation|chelating]] agent ([[D-penicillamine]], [[trientine]] or zinc). | ||
* Patients with acute [[Hepatic failure|liver failure]] due to [[Wilson's disease]], or unresponsive to [[chelation]] treatment - should be referred to [[liver transplantation]]. | * Patients with acute [[Hepatic failure|liver failure]] due to [[Wilson's disease]], or unresponsive to [[chelation]] treatment - should be referred to [[liver transplantation]]. | ||
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* Salt restriction to less than 2000 mg per day. | * Salt restriction to less than 2000 mg per day. | ||
* Fluid restriction unless the serum sodium is less than 120 - 125 mmol/L. | * Fluid restriction unless the serum sodium is less than 120 - 125 mmol/L. | ||
* Diuretics are the first line drugs for the treatment of [[ascites]]. | * [[Diuretic|Diuretics]] are the first line drugs for the treatment of [[ascites]]. | ||
* Therapeutic [[paracentesis]] in tense [[ascites]]. Serial therapeutic paracentesis is a treatment option for refractory ascites. | * Therapeutic [[paracentesis]] in tense [[ascites]]. Serial therapeutic [[paracentesis]] is a treatment option for refractory ascites. | ||
*Intravenous [[albumin]] infusion may also be considered in refractory cases. <ref name="pmid11772973">{{cite journal |vauthors=Moreau R, Asselah T, Condat B, de Kerguenec C, Pessione F, Bernard B, Poynard T, Binn M, Grangé JD, Valla D, Lebrec D |title=Comparison of the effect of terlipressin and albumin on arterial blood volume in patients with cirrhosis and tense ascites treated by paracentesis: a randomised pilot study |journal=Gut |volume=50 |issue=1 |pages=90–4 |year=2002 |pmid=11772973 |pmc=1773081 |doi= |url=}}</ref> | *Intravenous [[albumin]] infusion may also be considered in refractory cases. <ref name="pmid11772973">{{cite journal |vauthors=Moreau R, Asselah T, Condat B, de Kerguenec C, Pessione F, Bernard B, Poynard T, Binn M, Grangé JD, Valla D, Lebrec D |title=Comparison of the effect of terlipressin and albumin on arterial blood volume in patients with cirrhosis and tense ascites treated by paracentesis: a randomised pilot study |journal=Gut |volume=50 |issue=1 |pages=90–4 |year=2002 |pmid=11772973 |pmc=1773081 |doi= |url=}}</ref> | ||
*[[Transjugular intrahepatic portosystemic shunt|TIPS]] may be used in refractory cases of ascites.<ref name="pmid17678653">{{cite journal |vauthors=Salerno F, Cammà C, Enea M, Rössle M, Wong F |title=Transjugular intrahepatic portosystemic shunt for refractory ascites: a meta-analysis of individual patient data |journal=Gastroenterology |volume=133 |issue=3 |pages=825–34 |year=2007 |pmid=17678653 |doi=10.1053/j.gastro.2007.06.020 |url=}}</ref> | *[[Transjugular intrahepatic portosystemic shunt|TIPS]] may be used in refractory cases of [[ascites]].<ref name="pmid17678653">{{cite journal |vauthors=Salerno F, Cammà C, Enea M, Rössle M, Wong F |title=Transjugular intrahepatic portosystemic shunt for refractory ascites: a meta-analysis of individual patient data |journal=Gastroenterology |volume=133 |issue=3 |pages=825–34 |year=2007 |pmid=17678653 |doi=10.1053/j.gastro.2007.06.020 |url=}}</ref> | ||
===Esophageal Variceal Bleeding=== | ===Esophageal Variceal Bleeding=== | ||
:[[Esophageal varices#Treatment|Esophageal Varices Treatment]]<ref name="pmid15646423">{{cite journal |vauthors=de Franchis R, Dell'Era A, Iannuzzi F |title=Diagnosis and treatment of portal hypertension |journal=Dig Liver Dis |volume=36 |issue=12 |pages=787–98 |year=2004 |pmid=15646423 |doi=10.1016/j.dld.2004.08.001 |url=}}</ref><ref name="pmid20200386">{{cite journal |vauthors=Garcia-Tsao G, Bosch J |title=Management of varices and variceal hemorrhage in cirrhosis |journal=N. Engl. J. Med. |volume=362 |issue=9 |pages=823–32 |year=2010 |pmid=20200386 |doi=10.1056/NEJMra0901512 |url=}}</ref> | :[[Esophageal varices#Treatment|Esophageal Varices Treatment]]<ref name="pmid15646423">{{cite journal |vauthors=de Franchis R, Dell'Era A, Iannuzzi F |title=Diagnosis and treatment of portal hypertension |journal=Dig Liver Dis |volume=36 |issue=12 |pages=787–98 |year=2004 |pmid=15646423 |doi=10.1016/j.dld.2004.08.001 |url=}}</ref><ref name="pmid20200386">{{cite journal |vauthors=Garcia-Tsao G, Bosch J |title=Management of varices and variceal hemorrhage in cirrhosis |journal=N. Engl. J. Med. |volume=362 |issue=9 |pages=823–32 |year=2010 |pmid=20200386 |doi=10.1056/NEJMra0901512 |url=}}</ref> | ||
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**Non-selective [[beta blockers]] should be used to prevent the first [[Esophageal varices|variceal bleeding]]<ref name="pmid12668985">{{cite journal |vauthors=Abraldes JG, Tarantino I, Turnes J, Garcia-Pagan JC, Rodés J, Bosch J |title=Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis |journal=Hepatology |volume=37 |issue=4 |pages=902–8 |year=2003 |pmid=12668985 |doi=10.1053/jhep.2003.50133 |url=}}</ref><ref name="pmid19344721">{{cite journal |vauthors=Villanueva C, Aracil C, Colomo A, Hernández-Gea V, López-Balaguer JM, Alvarez-Urturi C, Torras X, Balanzó J, Guarner C |title=Acute hemodynamic response to beta-blockers and prediction of long-term outcome in primary prophylaxis of variceal bleeding |journal=Gastroenterology |volume=137 |issue=1 |pages=119–28 |year=2009 |pmid=19344721 |doi=10.1053/j.gastro.2009.03.048 |url=}}</ref><ref name="pmid24076364">{{cite journal |vauthors=Ge PS, Runyon BA |title=The changing role of beta-blocker therapy in patients with cirrhosis |journal=J. Hepatol. |volume=60 |issue=3 |pages=643–53 |year=2014 |pmid=24076364 |doi=10.1016/j.jhep.2013.09.016 |url=}}</ref><ref name="pmid7029276">{{cite journal |vauthors=Lebrec D, Poynard T, Hillon P, Benhamou JP |title=Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study |journal=N. Engl. J. Med. |volume=305 |issue=23 |pages=1371–4 |year=1981 |pmid=7029276 |doi=10.1056/NEJM198112033052302 |url=}}</ref><ref name="pmid3306385">{{cite journal |vauthors=Pascal JP, Cales P |title=Propranolol in the prevention of first upper gastrointestinal tract hemorrhage in patients with cirrhosis of the liver and esophageal varices |journal=N. Engl. J. Med. |volume=317 |issue=14 |pages=856–61 |year=1987 |pmid=3306385 |doi=10.1056/NEJM198710013171403 |url=}}</ref><ref name="pmid16306522">{{cite journal |vauthors=Groszmann RJ, Garcia-Tsao G, Bosch J, Grace ND, Burroughs AK, Planas R, Escorsell A, Garcia-Pagan JC, Patch D, Matloff DS, Gao H, Makuch R |title=Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis |journal=N. Engl. J. Med. |volume=353 |issue=21 |pages=2254–61 |year=2005 |pmid=16306522 |doi=10.1056/NEJMoa044456 |url=}}</ref> | **Non-selective [[beta blockers]] should be used to prevent the first [[Esophageal varices|variceal bleeding]]<ref name="pmid12668985">{{cite journal |vauthors=Abraldes JG, Tarantino I, Turnes J, Garcia-Pagan JC, Rodés J, Bosch J |title=Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis |journal=Hepatology |volume=37 |issue=4 |pages=902–8 |year=2003 |pmid=12668985 |doi=10.1053/jhep.2003.50133 |url=}}</ref><ref name="pmid19344721">{{cite journal |vauthors=Villanueva C, Aracil C, Colomo A, Hernández-Gea V, López-Balaguer JM, Alvarez-Urturi C, Torras X, Balanzó J, Guarner C |title=Acute hemodynamic response to beta-blockers and prediction of long-term outcome in primary prophylaxis of variceal bleeding |journal=Gastroenterology |volume=137 |issue=1 |pages=119–28 |year=2009 |pmid=19344721 |doi=10.1053/j.gastro.2009.03.048 |url=}}</ref><ref name="pmid24076364">{{cite journal |vauthors=Ge PS, Runyon BA |title=The changing role of beta-blocker therapy in patients with cirrhosis |journal=J. Hepatol. |volume=60 |issue=3 |pages=643–53 |year=2014 |pmid=24076364 |doi=10.1016/j.jhep.2013.09.016 |url=}}</ref><ref name="pmid7029276">{{cite journal |vauthors=Lebrec D, Poynard T, Hillon P, Benhamou JP |title=Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study |journal=N. Engl. J. Med. |volume=305 |issue=23 |pages=1371–4 |year=1981 |pmid=7029276 |doi=10.1056/NEJM198112033052302 |url=}}</ref><ref name="pmid3306385">{{cite journal |vauthors=Pascal JP, Cales P |title=Propranolol in the prevention of first upper gastrointestinal tract hemorrhage in patients with cirrhosis of the liver and esophageal varices |journal=N. Engl. J. Med. |volume=317 |issue=14 |pages=856–61 |year=1987 |pmid=3306385 |doi=10.1056/NEJM198710013171403 |url=}}</ref><ref name="pmid16306522">{{cite journal |vauthors=Groszmann RJ, Garcia-Tsao G, Bosch J, Grace ND, Burroughs AK, Planas R, Escorsell A, Garcia-Pagan JC, Patch D, Matloff DS, Gao H, Makuch R |title=Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis |journal=N. Engl. J. Med. |volume=353 |issue=21 |pages=2254–61 |year=2005 |pmid=16306522 |doi=10.1056/NEJMoa044456 |url=}}</ref> | ||
**Those not receiving [[beta blockers]], should be followed up with [[Esophagogastroduodenoscopy|EGD]] every 2 years | **Those not receiving [[beta blockers]], should be followed up with [[Esophagogastroduodenoscopy|EGD]] every 2 years | ||
**If the liver decompensates, [[Esophagogastroduodenoscopy|EGD]] should be performed at that time and then annually | **If the [[liver]] decompensates, [[Esophagogastroduodenoscopy|EGD]] should be performed at that time and then annually | ||
**Those who recieve [[beta blockers]] may not require a regular follow up with [[Esophagogastroduodenoscopy|EGD]] | **Those who recieve [[beta blockers]] may not require a regular follow up with [[Esophagogastroduodenoscopy|EGD]] | ||
*Patients with medium/large varices that have not bled: | *Patients with medium/large [[varices]] that have not bled: | ||
** | **[[EVL|Endoscopic variceal ligation]] or non-selective [[beta blockers]] may be used to prevent first [[Esophageal varices|variceal]] bleeding, as these patients are at a higher risk for bleeding with [[beta blockers]] being the first choice of treatment and esophageal [[Esophageal varices|variceal]] ligation reserved for those who are unable to tolerate the drugs | ||
**[[Nitrates]], [[sclerotherapy]] and shunts alone are not used as primary prophylaxis to prevent bleeding | **[[Nitrates]], [[sclerotherapy]] and shunts alone are not used as primary prophylaxis to prevent [[bleeding]] | ||
*Patients with [[cirrhosis]] and an acute episode of [[Esophageal varices|variceal]] [[Bleeding|hemorrhage]]:<ref name="pmid7623904">{{cite journal |vauthors=Besson I, Ingrand P, Person B, Boutroux D, Heresbach D, Bernard P, Hochain P, Larricq J, Gourlaouen A, Ribard D |title=Sclerotherapy with or without octreotide for acute variceal bleeding |journal=N. Engl. J. Med. |volume=333 |issue=9 |pages=555–60 |year=1995 |pmid=7623904 |doi=10.1056/NEJM199508313330904 |url=}}</ref><ref name="urlEndoscopic management of acute esophageal variceal bleeding - Techniques in Gastrointestinal Endoscopy">{{cite web |url=http://www.giejournal.org/article/S1096-2883(17)30029-3/pdf |title=Endoscopic management of acute esophageal variceal bleeding - Techniques in Gastrointestinal Endoscopy |format= |work= |accessdate=}}</ref> | *Patients with [[cirrhosis]] and an acute episode of [[Esophageal varices|variceal]] [[Bleeding|hemorrhage]]:<ref name="pmid7623904">{{cite journal |vauthors=Besson I, Ingrand P, Person B, Boutroux D, Heresbach D, Bernard P, Hochain P, Larricq J, Gourlaouen A, Ribard D |title=Sclerotherapy with or without octreotide for acute variceal bleeding |journal=N. Engl. J. Med. |volume=333 |issue=9 |pages=555–60 |year=1995 |pmid=7623904 |doi=10.1056/NEJM199508313330904 |url=}}</ref><ref name="urlEndoscopic management of acute esophageal variceal bleeding - Techniques in Gastrointestinal Endoscopy">{{cite web |url=http://www.giejournal.org/article/S1096-2883(17)30029-3/pdf |title=Endoscopic management of acute esophageal variceal bleeding - Techniques in Gastrointestinal Endoscopy |format= |work= |accessdate=}}</ref> | ||
**[[Fluid]] replacement | **[[Fluid]] replacement | ||
| Line 194: | Line 194: | ||
***Intravenous [[ciprofloxacin]] | ***Intravenous [[ciprofloxacin]] | ||
***Intravenous [[ceftriaxone]] (1 gm/day) in centers with high prevalence of [[quinolone]] resistance | ***Intravenous [[ceftriaxone]] (1 gm/day) in centers with high prevalence of [[quinolone]] resistance | ||
**[[Somatostatin]] or its analogues [[octreotide]] and [[vapreotide]]; [[terlipressin]] should be initiated as soon as variceal bleeding is suspected and continued for 3 to 5 days after diagnosis is performed <ref name="pmid8103145">{{cite journal |vauthors=Sung JJ, Chung SC, Lai CW, Chan FK, Leung JW, Yung MY, Kassianides C, Li AK |title=Octreotide infusion or emergency sclerotherapy for variceal haemorrhage |journal=Lancet |volume=342 |issue=8872 |pages=637–41 |year=1993 |pmid=8103145 |doi= |url=}}</ref> | **[[Somatostatin]] or its analogues [[octreotide]] and [[vapreotide]]; [[terlipressin]] should be initiated as soon as [[Esophageal varices|variceal bleeding]] is suspected and continued for 3 to 5 days after diagnosis is performed <ref name="pmid8103145">{{cite journal |vauthors=Sung JJ, Chung SC, Lai CW, Chan FK, Leung JW, Yung MY, Kassianides C, Li AK |title=Octreotide infusion or emergency sclerotherapy for variceal haemorrhage |journal=Lancet |volume=342 |issue=8872 |pages=637–41 |year=1993 |pmid=8103145 |doi= |url=}}</ref> | ||
** | **[[EVL|Endoscopic variceal ligation]] <ref name="pmid8101900">{{cite journal |vauthors=Gimson AE, Ramage JK, Panos MZ, Hayllar K, Harrison PM, Williams R, Westaby D |title=Randomised trial of variceal banding ligation versus injection sclerotherapy for bleeding oesophageal varices |journal=Lancet |volume=342 |issue=8868 |pages=391–4 |year=1993 |pmid=8101900 |doi= |url=}}</ref><ref name="pmid11870374">{{cite journal |vauthors=Bañares R, Albillos A, Rincón D, Alonso S, González M, Ruiz-del-Arbol L, Salcedo M, Molinero LM |title=Endoscopic treatment versus endoscopic plus pharmacologic treatment for acute variceal bleeding: a meta-analysis |journal=Hepatology |volume=35 |issue=3 |pages=609–15 |year=2002 |pmid=11870374 |doi=10.1053/jhep.2002.31354 |url=}}</ref> | ||
**Sclerotherapy <ref name="pmid17060770">{{cite journal |vauthors=Krige JE, Kotze UK, Bornman PC, Shaw JM, Klipin M |title=Variceal recurrence, rebleeding, and survival after endoscopic injection sclerotherapy in 287 alcoholic cirrhotic patients with bleeding esophageal varices |journal=Ann. Surg. |volume=244 |issue=5 |pages=764–70 |year=2006 |pmid=17060770 |pmc=1856595 |doi=10.1097/01.sla.0000231704.45005.4e |url=}}</ref><ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid1579136">{{cite journal |vauthors=Stiegmann GV, Goff JS, Michaletz-Onody PA, Korula J, Lieberman D, Saeed ZA, Reveille RM, Sun JH, Lowenstein SR |title=Endoscopic sclerotherapy as compared with endoscopic ligation for bleeding esophageal varices |journal=N. Engl. J. Med. |volume=326 |issue=23 |pages=1527–32 |year=1992 |pmid=1579136 |doi=10.1056/NEJM199206043262304 |url=}}</ref> | **[[Sclerotherapy]] <ref name="pmid17060770">{{cite journal |vauthors=Krige JE, Kotze UK, Bornman PC, Shaw JM, Klipin M |title=Variceal recurrence, rebleeding, and survival after endoscopic injection sclerotherapy in 287 alcoholic cirrhotic patients with bleeding esophageal varices |journal=Ann. Surg. |volume=244 |issue=5 |pages=764–70 |year=2006 |pmid=17060770 |pmc=1856595 |doi=10.1097/01.sla.0000231704.45005.4e |url=}}</ref><ref name="pmid9683971">{{cite journal |vauthors=Williams EJ, Iredale JP |title=Liver cirrhosis |journal=Postgrad Med J |volume=74 |issue=870 |pages=193–202 |year=1998 |pmid=9683971 |pmc=2360862 |doi= |url=}}</ref><ref name="pmid1579136">{{cite journal |vauthors=Stiegmann GV, Goff JS, Michaletz-Onody PA, Korula J, Lieberman D, Saeed ZA, Reveille RM, Sun JH, Lowenstein SR |title=Endoscopic sclerotherapy as compared with endoscopic ligation for bleeding esophageal varices |journal=N. Engl. J. Med. |volume=326 |issue=23 |pages=1527–32 |year=1992 |pmid=1579136 |doi=10.1056/NEJM199206043262304 |url=}}</ref> | ||
**[[Transjugular intrahepatic portosystemic shunt]] ([[TIPS]])<ref name="pmid20573925">{{cite journal |vauthors=García-Pagán JC, Caca K, Bureau C, Laleman W, Appenrodt B, Luca A, Abraldes JG, Nevens F, Vinel JP, Mössner J, Bosch J |title=Early use of TIPS in patients with cirrhosis and variceal bleeding |journal=N. Engl. J. Med. |volume=362 |issue=25 |pages=2370–9 |year=2010 |pmid=20573925 |doi=10.1056/NEJMoa0910102 |url=}}</ref><ref name="pmid12761727">{{cite journal |vauthors=Boyer TD |title=Transjugular intrahepatic portosystemic shunt: current status |journal=Gastroenterology |volume=124 |issue=6 |pages=1700–10 |year=2003 |pmid=12761727 |doi= |url=}}</ref><ref name="pmid10320885">{{cite journal |vauthors=Patel NH, Chalasani N, Jindal RM |title=Current status of transjugular intrahepatic portosystemic shunts |journal=Postgrad Med J |volume=74 |issue=878 |pages=716–20 |year=1998 |pmid=10320885 |pmc=2431632 |doi= |url=}}</ref><ref name="pmid24115809">{{cite journal |vauthors=Loffroy R, Estivalet L, Cherblanc V, Favelier S, Pottecher P, Hamza S, Minello A, Hillon P, Thouant P, Lefevre PH, Krausé D, Cercueil JP |title=Transjugular intrahepatic portosystemic shunt for the management of acute variceal hemorrhage |journal=World J. Gastroenterol. |volume=19 |issue=37 |pages=6131–43 |year=2013 |pmid=24115809 |pmc=3787342 |doi=10.3748/wjg.v19.i37.6131 |url=}}</ref><ref name="pmid7918921">{{cite journal |vauthors=McCormick PA, Dick R, Burroughs AK |title=Review article: the transjugular intrahepatic portosystemic shunt (TIPS) in the treatment of portal hypertension |journal=Aliment. Pharmacol. Ther. |volume=8 |issue=3 |pages=273–82 |year=1994 |pmid=7918921 |doi= |url=}}</ref> | **[[Transjugular intrahepatic portosystemic shunt]] ([[TIPS]])<ref name="pmid20573925">{{cite journal |vauthors=García-Pagán JC, Caca K, Bureau C, Laleman W, Appenrodt B, Luca A, Abraldes JG, Nevens F, Vinel JP, Mössner J, Bosch J |title=Early use of TIPS in patients with cirrhosis and variceal bleeding |journal=N. Engl. J. Med. |volume=362 |issue=25 |pages=2370–9 |year=2010 |pmid=20573925 |doi=10.1056/NEJMoa0910102 |url=}}</ref><ref name="pmid12761727">{{cite journal |vauthors=Boyer TD |title=Transjugular intrahepatic portosystemic shunt: current status |journal=Gastroenterology |volume=124 |issue=6 |pages=1700–10 |year=2003 |pmid=12761727 |doi= |url=}}</ref><ref name="pmid10320885">{{cite journal |vauthors=Patel NH, Chalasani N, Jindal RM |title=Current status of transjugular intrahepatic portosystemic shunts |journal=Postgrad Med J |volume=74 |issue=878 |pages=716–20 |year=1998 |pmid=10320885 |pmc=2431632 |doi= |url=}}</ref><ref name="pmid24115809">{{cite journal |vauthors=Loffroy R, Estivalet L, Cherblanc V, Favelier S, Pottecher P, Hamza S, Minello A, Hillon P, Thouant P, Lefevre PH, Krausé D, Cercueil JP |title=Transjugular intrahepatic portosystemic shunt for the management of acute variceal hemorrhage |journal=World J. Gastroenterol. |volume=19 |issue=37 |pages=6131–43 |year=2013 |pmid=24115809 |pmc=3787342 |doi=10.3748/wjg.v19.i37.6131 |url=}}</ref><ref name="pmid7918921">{{cite journal |vauthors=McCormick PA, Dick R, Burroughs AK |title=Review article: the transjugular intrahepatic portosystemic shunt (TIPS) in the treatment of portal hypertension |journal=Aliment. Pharmacol. Ther. |volume=8 |issue=3 |pages=273–82 |year=1994 |pmid=7918921 |doi= |url=}}</ref> | ||
**[[Balloon tamponade]]: temporary measure to stop bleeding for 24 hours until one of the above procedures is initiated | **[[Balloon tamponade]]: temporary measure to stop [[bleeding]] for 24 hours until one of the above procedures is initiated | ||
*Patients who have [[cirrhosis]] and have recovered from a [[Esophageal varices|variceal]] [[Bleeding|bleed]]:<ref name="pmid2029994">{{cite journal |vauthors=Conn HO, Grace ND, Bosch J, Groszmann RJ, Rodés J, Wright SC, Matloff DS, Garcia-Tsao G, Fisher RL, Navasa M |title=Propranolol in the prevention of the first hemorrhage from esophagogastric varices: A multicenter, randomized clinical trial. The Boston-New Haven-Barcelona Portal Hypertension Study Group |journal=Hepatology |volume=13 |issue=5 |pages=902–12 |year=1991 |pmid=2029994 |doi= |url=}}</ref><ref name="pmid12648985">{{cite journal |vauthors=Bosch J, García-Pagán JC |title=Prevention of variceal rebleeding |journal=Lancet |volume=361 |issue=9361 |pages=952–4 |year=2003 |pmid=12648985 |doi=10.1016/S0140-6736(03)12778-X |url=}}</ref><ref name="pmid18626050">{{cite journal |vauthors=Gonzalez R, Zamora J, Gomez-Camarero J, Molinero LM, Bañares R, Albillos A |title=Meta-analysis: Combination endoscopic and drug therapy to prevent variceal rebleeding in cirrhosis |journal=Ann. Intern. Med. |volume=149 |issue=2 |pages=109–22 |year=2008 |pmid=18626050 |doi= |url=}}</ref> | *Patients who have [[cirrhosis]] and have recovered from a [[Esophageal varices|variceal]] [[Bleeding|bleed]]:<ref name="pmid2029994">{{cite journal |vauthors=Conn HO, Grace ND, Bosch J, Groszmann RJ, Rodés J, Wright SC, Matloff DS, Garcia-Tsao G, Fisher RL, Navasa M |title=Propranolol in the prevention of the first hemorrhage from esophagogastric varices: A multicenter, randomized clinical trial. The Boston-New Haven-Barcelona Portal Hypertension Study Group |journal=Hepatology |volume=13 |issue=5 |pages=902–12 |year=1991 |pmid=2029994 |doi= |url=}}</ref><ref name="pmid12648985">{{cite journal |vauthors=Bosch J, García-Pagán JC |title=Prevention of variceal rebleeding |journal=Lancet |volume=361 |issue=9361 |pages=952–4 |year=2003 |pmid=12648985 |doi=10.1016/S0140-6736(03)12778-X |url=}}</ref><ref name="pmid18626050">{{cite journal |vauthors=Gonzalez R, Zamora J, Gomez-Camarero J, Molinero LM, Bañares R, Albillos A |title=Meta-analysis: Combination endoscopic and drug therapy to prevent variceal rebleeding in cirrhosis |journal=Ann. Intern. Med. |volume=149 |issue=2 |pages=109–22 |year=2008 |pmid=18626050 |doi= |url=}}</ref> | ||
**Combination of | **Combination of [[EVL|endoscopic variceal ligation (EVL)]] and non-selective [[beta blockers]] | ||
**[[EVL]] should be repeated every 1-2 weeks until obliteration with first surveillance EVL performed 1-3 months and then every 6-12 months to check for recurrence | **[[EVL]] should be repeated every 1-2 weeks until obliteration with first surveillance [[EVL]] performed 1-3 months and then every 6-12 months to check for recurrence | ||
**Refractory cases should be referred for [[Liver transplantation|transplantation]]. | **Refractory cases should be referred for [[Liver transplantation|transplantation]]. | ||
| Line 213: | Line 213: | ||
*[[Intracranial pressure]] is monitored and frequent [[neurological examination]] is done in those with high grade encephalopathy | *[[Intracranial pressure]] is monitored and frequent [[neurological examination]] is done in those with high grade encephalopathy | ||
**[[Mannitol]] bolus (0.5-1.0 gm/kg body weight) is recommended as first-line therapy | **[[Mannitol]] bolus (0.5-1.0 gm/kg body weight) is recommended as first-line therapy | ||
**In patients at highest risk for cerebral edema (serum [[ammonia]] >150 µM, grade 3/4 [[hepatic encephalopathy]], [[acute renal failure]], requiring vasopressors to maintain [[mean arterial pressure]] [MAP]), the prophylactic induction of [[hypernatremia]] with [[hypertonic saline]] to a [[sodium]] level of 145-155 mEq/L is recommended | **In patients at highest risk for [[cerebral edema]] (serum [[ammonia]] >150 µM, grade 3/4 [[hepatic encephalopathy]], [[acute renal failure]], requiring vasopressors to maintain [[mean arterial pressure]] [MAP]), the prophylactic induction of [[hypernatremia]] with [[hypertonic saline]] to a [[sodium]] level of 145-155 mEq/L is recommended | ||
**Short acting [[barbiturates]] and induction of [[hypothermia]] in refractory cases as a bridge to [[liver transplantation]]. | **Short acting [[barbiturates]] and induction of [[hypothermia]] in refractory cases as a bridge to [[liver transplantation]]. | ||
Prevention of [[hepatic encephalopathy]]: | Prevention of [[hepatic encephalopathy]]: | ||
*Reduced [[protein]] intake | *Reduced [[protein]] intake | ||
**May lead to [[protein]] [[malnutrition]] and negative nitrogen balance | **May lead to [[protein]] [[malnutrition]] and negative [[nitrogen]] balance | ||
*Correction of [[hypokalemia]] | *Correction of [[hypokalemia]] | ||
*[[Lactulose]] | *[[Lactulose]] | ||
**Decreases absorption of [[ammonia]] from the gastrointestinal tract | **Decreases absorption of [[ammonia]] from the gastrointestinal tract | ||
**Works as a [[laxative]], increasing the transit time and reducing absorption of [[ammonia]] | **Works as a [[laxative]], increasing the transit time and reducing absorption of [[ammonia]] | ||
**[[Lactulose]] can be given rectally for patients who cannot take oral medications.<ref name="pmid4682313">{{cite journal |author=Kersh ES, Rifkin H |title=Lactulose enemas |journal=Ann. Intern. Med. |volume=78 |issue=1 |pages=81-4 |year=1973 |pmid=4682313 |doi=}}</ref><ref name="pmid240347">{{cite journal |author=Ratnaike RN, Hicks EP, Hislop IG |title=The rectal administration of lactulose |journal=Australian and New Zealand journal of medicine |volume=5 |issue=2 |pages=137-40 |year=1975 |pmid=240347 |doi=}}</ref><ref name="pmid3301614">{{cite journal |author=Uribe M, Campollo O, Vargas F, ''et al'' |title=Acidifying enemas (lactitol and lactose) vs. nonacidifying enemas (tap water) to treat acute portal-systemic encephalopathy: a double-blind, randomized clinical trial |journal=Hepatology |volume=7 |issue=4 |pages=639-43 |year=1987 |pmid=3301614 |doi=}}</ref> One regimen is 300 mL (200 gm) of [[lactulose]] syrup (10 gm/15 ml) in 1 L of water which is retained for 1 hour, with the patient in the [[Trendelenburg position]].<ref name="pmid11467622">{{cite journal |author=Blei AT, Córdoba J |title=Hepatic Encephalopathy |journal=Am. J. Gastroenterol. |volume=96 |issue=7 |pages=1968-76 |year=2001 |pmid=11467622 |doi=10.1111/j.1572-0241.2001.03964.x}}</ref> | **[[Lactulose]] can be given [[Rectal|rectally]] for patients who cannot take oral medications.<ref name="pmid4682313">{{cite journal |author=Kersh ES, Rifkin H |title=Lactulose enemas |journal=Ann. Intern. Med. |volume=78 |issue=1 |pages=81-4 |year=1973 |pmid=4682313 |doi=}}</ref><ref name="pmid240347">{{cite journal |author=Ratnaike RN, Hicks EP, Hislop IG |title=The rectal administration of lactulose |journal=Australian and New Zealand journal of medicine |volume=5 |issue=2 |pages=137-40 |year=1975 |pmid=240347 |doi=}}</ref><ref name="pmid3301614">{{cite journal |author=Uribe M, Campollo O, Vargas F, ''et al'' |title=Acidifying enemas (lactitol and lactose) vs. nonacidifying enemas (tap water) to treat acute portal-systemic encephalopathy: a double-blind, randomized clinical trial |journal=Hepatology |volume=7 |issue=4 |pages=639-43 |year=1987 |pmid=3301614 |doi=}}</ref> One regimen is 300 mL (200 gm) of [[lactulose]] syrup (10 gm/15 ml) in 1 L of water which is retained for 1 hour, with the patient in the [[Trendelenburg position]].<ref name="pmid11467622">{{cite journal |author=Blei AT, Córdoba J |title=Hepatic Encephalopathy |journal=Am. J. Gastroenterol. |volume=96 |issue=7 |pages=1968-76 |year=2001 |pmid=11467622 |doi=10.1111/j.1572-0241.2001.03964.x}}</ref> | ||
*Antibiotics | *Antibiotics | ||
**Killing bacteria in the gut reduces the bacterial conversion of [[protein]] to [[ammonia]] | **Killing bacteria in the [[Gastrointestinal tract|gut]] reduces the bacterial conversion of [[protein]] to [[ammonia]] | ||
**[[Neomycin]] | **[[Neomycin]] | ||
**[[Metronidazole]] | **[[Metronidazole]] | ||
*[[Rifaximin]]<ref name="pmid20335583">{{cite journal |vauthors=Bass NM, Mullen KD, Sanyal A, Poordad F, Neff G, Leevy CB, Sigal S, Sheikh MY, Beavers K, Frederick T, Teperman L, Hillebrand D, Huang S, Merchant K, Shaw A, Bortey E, Forbes WP |title=Rifaximin treatment in hepatic encephalopathy |journal=N. Engl. J. Med. |volume=362 |issue=12 |pages=1071–81 |year=2010 |pmid=20335583 |doi=10.1056/NEJMoa0907893 |url=}}</ref><ref name="pmid20849805">{{cite journal |vauthors=Bajaj JS, Heuman DM, Wade JB, Gibson DP, Saeian K, Wegelin JA, Hafeezullah M, Bell DE, Sterling RK, Stravitz RT, Fuchs M, Luketic V, Sanyal AJ |title=Rifaximin improves driving simulator performance in a randomized trial of patients with minimal hepatic encephalopathy |journal=Gastroenterology |volume=140 |issue=2 |pages=478–487.e1 |year=2011 |pmid=20849805 |pmc=3020996 |doi=10.1053/j.gastro.2010.08.061 |url=}}</ref> | *[[Rifaximin]]<ref name="pmid20335583">{{cite journal |vauthors=Bass NM, Mullen KD, Sanyal A, Poordad F, Neff G, Leevy CB, Sigal S, Sheikh MY, Beavers K, Frederick T, Teperman L, Hillebrand D, Huang S, Merchant K, Shaw A, Bortey E, Forbes WP |title=Rifaximin treatment in hepatic encephalopathy |journal=N. Engl. J. Med. |volume=362 |issue=12 |pages=1071–81 |year=2010 |pmid=20335583 |doi=10.1056/NEJMoa0907893 |url=}}</ref><ref name="pmid20849805">{{cite journal |vauthors=Bajaj JS, Heuman DM, Wade JB, Gibson DP, Saeian K, Wegelin JA, Hafeezullah M, Bell DE, Sterling RK, Stravitz RT, Fuchs M, Luketic V, Sanyal AJ |title=Rifaximin improves driving simulator performance in a randomized trial of patients with minimal hepatic encephalopathy |journal=Gastroenterology |volume=140 |issue=2 |pages=478–487.e1 |year=2011 |pmid=20849805 |pmc=3020996 |doi=10.1053/j.gastro.2010.08.061 |url=}}</ref> | ||
**Dose of 400 mg taken orally 3 times a day was as effective as lactulose or lactilol at improving hepatic encephalopathy symptoms.<ref name="pmid8325041">{{cite journal |author=Bucci L, Palmieri GC |title=Double-blind, double-dummy comparison between treatment with rifaximin and lactulose in patients with medium to severe degree hepatic encephalopathy |journal=Current medical research and opinion |volume=13 |issue=2 |pages=109-18 |year=1993 |pmid=8325041 |doi=}}</ref> Similarly, rifaximin was as effective as neomycin and paromomycin.<ref name="pmid1751811">{{cite journal |author=Pedretti G, Calzetti C, Missale G, Fiaccadori F |title=Rifaximin versus neomycin on hyperammoniemia in chronic portal systemic encephalopathy of cirrhotics. A double-blind, randomized trial |journal=The Italian journal of gastroenterology |volume=23 |issue=4 |pages=175-8 |year=1991 |pmid=1751811 |doi=}}</ref><ref name="pmid22391344">{{cite journal |vauthors=Kalambokis GN, Mouzaki A, Rodi M, Pappas K, Fotopoulos A, Xourgia X, Tsianos EV |title=Rifaximin improves systemic hemodynamics and renal function in patients with alcohol-related cirrhosis and ascites |journal=Clin. Gastroenterol. Hepatol. |volume=10 |issue=7 |pages=815–8 |year=2012 |pmid=22391344 |doi=10.1016/j.cgh.2012.02.025 |url=}}</ref> | **Dose of 400 mg taken orally 3 times a day was as effective as lactulose or lactilol at improving hepatic encephalopathy symptoms.<ref name="pmid8325041">{{cite journal |author=Bucci L, Palmieri GC |title=Double-blind, double-dummy comparison between treatment with rifaximin and lactulose in patients with medium to severe degree hepatic encephalopathy |journal=Current medical research and opinion |volume=13 |issue=2 |pages=109-18 |year=1993 |pmid=8325041 |doi=}}</ref> Similarly, [[rifaximin]] was as effective as [[neomycin]] and [[Paromomycin sulfate|paromomycin]].<ref name="pmid1751811">{{cite journal |author=Pedretti G, Calzetti C, Missale G, Fiaccadori F |title=Rifaximin versus neomycin on hyperammoniemia in chronic portal systemic encephalopathy of cirrhotics. A double-blind, randomized trial |journal=The Italian journal of gastroenterology |volume=23 |issue=4 |pages=175-8 |year=1991 |pmid=1751811 |doi=}}</ref><ref name="pmid22391344">{{cite journal |vauthors=Kalambokis GN, Mouzaki A, Rodi M, Pappas K, Fotopoulos A, Xourgia X, Tsianos EV |title=Rifaximin improves systemic hemodynamics and renal function in patients with alcohol-related cirrhosis and ascites |journal=Clin. Gastroenterol. Hepatol. |volume=10 |issue=7 |pages=815–8 |year=2012 |pmid=22391344 |doi=10.1016/j.cgh.2012.02.025 |url=}}</ref> | ||
*[[Benzodiazepines]] receptor agonists | *[[Benzodiazepines]] receptor agonists | ||
**[[Flumazenil]]- 2 milligrams over 10 minutes | **[[Flumazenil]]- 2 milligrams over 10 minutes | ||
| Line 237: | Line 237: | ||
*[[Albumin]] infusion | *[[Albumin]] infusion | ||
**1 gm [[albumin]] per kg of body weight intravenously on day one followed by followed by 20-40 grams daily | **1 gm [[albumin]] per kg of body weight [[Intravenous therapy|intravenously]] on day one followed by followed by 20-40 grams daily | ||
*[[Octreotide]] | *[[Octreotide]] | ||
*[[Midodrine]] | *[[Midodrine]] | ||
*[[Vasopressin]] analogs | *[[Vasopressin]] analogs | ||
**Ornipressin- limited use by ischemic complications | **Ornipressin- limited use by [[Ischemia|ischemic]] complications | ||
**[[Terlipressin]] | **[[Terlipressin]] | ||
*[[Transjugular intrahepatic portosystemic shunt]] | *[[Transjugular intrahepatic portosystemic shunt]] | ||
| Line 257: | Line 257: | ||
*[[Abdominal paracentesis]] | *[[Abdominal paracentesis]] | ||
*Intravenous antibiotics- | *Intravenous [[Antibiotic|antibiotics]]- | ||
**[[Cefotaxime]] 2 g every 8 hours | **[[Cefotaxime]] 2 g every 8 hours | ||
**Oral [[ofloxacin]] (400 mg twice per day) as a substitute for [[cefotaxime]] | **Oral [[ofloxacin]] (400 mg twice per day) as a substitute for [[cefotaxime]] | ||
*Patients with ascitic fluid [[PMN]] counts greater than or equal to 250 cells/mm3 (0.25 X 109/L) and clinical suspicion of [[SBP]] who also have a [[serum creatinine]] greater than 1 mg/dL, [[blood urea nitrogen]] greater than 30 mg/dL, or total [[bilirubin]] greater than 4 mg/dL should receive 1.5 g [[albumin]] per kg body weight within 6 hours of detection and 1.0 g/kg on day 3. | *[[Patient|Patients]] with ascitic fluid [[PMN]] counts greater than or equal to 250 cells/mm3 (0.25 X 109/L) and clinical suspicion of [[SBP]] who also have a [[serum creatinine]] greater than 1 mg/dL, [[blood urea nitrogen]] greater than 30 mg/dL, or total [[bilirubin]] greater than 4 mg/dL should receive 1.5 g [[albumin]] per kg body weight within 6 hours of detection and 1.0 g/kg on day 3. | ||
===Contraindicated medications=== | ===Contraindicated medications=== | ||
Revision as of 21:55, 4 December 2017
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Cirrhosis Microchapters |
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Treatment |
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Cirrhosis medical therapy On the Web |
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American Roentgen Ray Society Images of Cirrhosis medical therapy |
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Risk calculators and risk factors for Cirrhosis medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2] Sudarshana Datta, MD [3]
Overview
The change that cirrhosis causes to the liver is irreversible, therefore treatment is mostly centered on ameliorating the complications of cirrhosis such as ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, esophageal varices and hepatorenal syndrome. Chronic constitutional symptoms such as pruritus, hypogonadism, osteoporosis and anorexia must be treated in patients. Maintenance of adequate nutrition (especially protein intake) is extremely important in cirrhosis patients. The underlying cause of cirrhosis needs to be managed and the treatment varies depending upon the cause of cirrhosis.
Medical Therapy
- Treatment of cirrhosis is mostly directed towards the treatment of complications such as:[1][2]
- Chronic constitutional symptoms enlisted below are also treated:
- Alcohol abstinence:
Pruritus
- Pruritus is a common symptom in primary biliary cirrhosis and Hepatitis C.
- Endogenous opioids and increased serum bile acid levels are considered responsible for causing pruritus.
- Preferred regimen for pruritus in chronic liver disease:
- Preferred regimen for mild itching:
- antihistamines
- Ammonium lactate topical solution
- Preferred regimen for severe itching:
- Alternative regimens for pruritus:
Hypogonadism
- Males with cirrhosis sometimes complain of loss of libido due to hypogonadism.
- Preferred regimen (1): Topical testosterone preparations
- Preferred regimen (2): Growth hormone therapy
Osteoporosis
- Cirrhosisis is one of the major causes of osteoporosis.[5]
- Calcium and vitamin D supplementation for all the following patients:
- At risk for osteoporosis
- On corticosteroid therapy for autoimmune liver disease
- Preferred regimen for osteoporosis: Alendronate sodium
Pain management in Cirrhosis
- Cirrhotic patients can develop pain from ascites (back and abdominal pain) and pain from gynecomastia (mastalgia).
- Pain management in cirrhosis needs special consideration as many analgesic and anti-inflammatory drugs are metabolized by the liver and dosage regulations are required to prevent further liver damage and drug toxicity.
- Drug dosages should be titrated as per the level of hepatic functioning in the patient.
- Dosage changes are required in the following patients:
- Portal hypertension
- Renal failure
- Alcoholic patient on multiple medications
- Non-selective NSAIDs should be avoided in patients with cirrhosis because of the following complications:
- Opioids should be used with caution in patients with cirrhosis because they are metabolized by the liver through oxidation and glucuronidation.
- Patients with cirrhosis have reduced liver blood flow, protein binding and hepatic enzyme capacity, leading to drug accumulation and increased vulnerability to developing opiate toxicity.
Nutrition and exercise
The following points need to be kept in mind regarding nutrition in cirrhosis patients:[6][7][8][9]
- Anorexia is common in cirrhosis patients with ascites due to the direct compression of the bowel by the ascitic fluid.
- Adequate calories and proteins should be added to the diet of the patient.
- Patients should consume a balanced diet and one multivitamin daily.
- Vitamin D and K supplementation is recommended in patients with cholestasis.
- Patients frequently benefit from the addition of commonly available liquid and powdered nutritional supplements to the diet.
- Patients are encouraged to exercise regularly to prevent muscle wasting.
- An exercise program under the direct supervision of a physical therapist may be proposed for patients.
Protein
- The diet of cirrhosis patients should be adequately titrated for protein.
- Excessive protein in the diet places the patient at risk for hepatic encephalopathy.
- Low protein levels in the diet cause muscle wasting.
- As per the guidelines by the American Association for the Study of Liver Diseases and the American College of Gastroenterology, cirrhosis patients with protein malnutrition require multiple feedings per day with breakfast and a nightly snack.[10][11][8]
- Branched-chain amino acids (BCAA) can function as pharmacologic nutrients for patients with decompensated cirrhosis.
Zinc
- Zinc deficiency is commonly observed in patients with cirrhosis.
- Zinc supplementation can also help resolve muscle cramps.
- Low dose zinc supplementation could prevent deterioration of the clinical status of cirrhosis and prevent excess copper accumulation in non-alcoholic cirrhotic patients.
- Zinc supplementation produces metabolic effects and trends towards improvements in liver function, hepatic encephalopathy, and nutritional status.[12]
- Preferred regimen: 220 mg Zinc po q12h may improve dysgeusia and also helps in stimulating the patient's appetite.
Vaccination
- Patients with cirrhosis must be vaccinated against the following:
Treatment of Underlying Causes
Alcoholic Liver Disease
- Mild to moderate alcoholic hepatitis:
- Abstinence from alcohol
- Preferred regimen (1): Aggressive enteral nutrition therapy
- Severe Alcoholic hepatitis:
- Preferred regimen (1): Four week course of prednisolone (40 mg/day for 28 days), typically followed by discontinuation or a 2-week taper (if no contraindications for steroid use).
- Preferred regimen (2):Pentoxifylline therapy (400 mg orally 3 times daily for 4 weeks) is an alternative in severe disease, especially if there are contraindications to steroid therapy
Hepatitis C
- Abstinence from alcohol as alcohol aggravates HCV associated fibrosis, cirrhosis and makes liver cancer more likely.
Genotypes HCV 1 and 4
- Preferred regimen (1): Peginterferon plus ribavirin for 48 weeks. The dose for peginterferon alfa-2a is 180 µg subcutaneously per week together with ribavirin using doses of 1,000 mg for those <75 kg in weight and 1,200 mg for those >75 kg; the dose for peginterferon alfa-2b is 1.5 µg/kg subcutaneously per week together with ribavirin using doses of 800 mg for those weighing <65 kg; 1,000 mg for those weighing >65 kg to 85 kg, 1,200 mg for >85 kg to 105 kg, and 1,400 mg for >105 kg.[19]
Genotypes HCV 2 and 3
- Preferred regimen (1): peginterferon plus ribavirin should be administered for 24 weeks, using a ribavirin dose of 800 mg.[20]
- Alternative regimen (1): Triple therapy- peginterferon plus ribavirin along with an additional dose of 100mg of amantadine q12h.
Hepatitis B
- Patients with HBeAg-positive chronic hepatitis B[31]
- a. ALT greater than 2 times normal or moderate/severe hepatitis on biopsy, and HBV DNA >20,000 IU/mL - treatment may be initiated with any of the 7 approved antiviral medications, but pegIFN-α, tenofovir or entecavir are preferred.
- b. ALT persistently normal or minimally elevated (<2 times normal) - should not be initiated on treatment.
- c. Children with elevated ALT greater than 2 times normal - treatment may be initiated with IFN-α or lamivudine if ALT levels remain elevated at this level for longer than 6 months.
- Patients with HBeAg-negative chronic hepatitis B (serum HBV DNA >20,000 IU/mL and elevated ALT >2 times normal) should be considered for treatment with pegIFN-α, tenofovir or entecavir.[32]
- Patients with compensated cirrhosis - best treated with tenofovir or entecavir.
- Patients with decompensated cirrhosis — Lamivudine or telbivudine may be used as initial treatment in combination with adefovir or tenofovir to reduce the risk of drug resistance.[33][34]
Autoimmune Hepatitis
- Immunosuppressive treatment based on serum aspartate aminotransferase (AST), serum alanine aminotransferase (ALT), serum gamma-globulin levels, and histological features
- Prednisone or prednisolone with azathioprine (adults)
- Prednisone with azathioprine or 6-mercaptopurine (children)
- Prednisone or prednisolone alone.
- Alternative drug therapies for suboptimal response - (cyclosporine, tacrolimus, or mycophenolate mofetil)
Primary Biliary Cirrhosis
- There is no known cure, but medication may slow the progression so that a normal lifespan and quality of life may be attainable.
- Ursodeoxycholic acid (Ursodiol) is the most frequently used treatment.
- Cholestyramine (a bile acid sequestrant) may be prescribed to absorb bile acids in the gut and be eliminated, and in turn give relief from itching. Alternative agents include naltrexone and rifampicin.
Primary Sclerosing Cholangitis
- Standard treatment includes ursodiol which has been shown to lower elevated liver enzyme numbers in people with PSC.
- Symptomatic treatment includes:
- Anti-histaminics - for itching
- Cholestyramine - bile acid sequestrant
- Antibiotics - for infections
- Vitamin supplemantation - Vitamin A, D and K.
Wilson's Disease
- Avoid intake of foods and water with high concentrations of copper.
- Initial treatment for symptomatic patients includes a chelating agent (D-penicillamine, trientine or zinc).
- Patients with acute liver failure due to Wilson's disease, or unresponsive to chelation treatment - should be referred to liver transplantation.
Treatment of Complications
Ascites
- Abstinence from alcohol.
- Salt restriction to less than 2000 mg per day.
- Fluid restriction unless the serum sodium is less than 120 - 125 mmol/L.
- Diuretics are the first line drugs for the treatment of ascites.
- Therapeutic paracentesis in tense ascites. Serial therapeutic paracentesis is a treatment option for refractory ascites.
- Intravenous albumin infusion may also be considered in refractory cases. [44]
- TIPS may be used in refractory cases of ascites.[45]
Esophageal Variceal Bleeding
- Patients with no varices and bleeding:
- Patients with small varices that have not bled:[49][50][51][52][53][54]
- Non-selective beta blockers should be used to prevent the first variceal bleeding[55][56][57][58][59][60]
- Those not receiving beta blockers, should be followed up with EGD every 2 years
- If the liver decompensates, EGD should be performed at that time and then annually
- Those who recieve beta blockers may not require a regular follow up with EGD
- Patients with medium/large varices that have not bled:
- Endoscopic variceal ligation or non-selective beta blockers may be used to prevent first variceal bleeding, as these patients are at a higher risk for bleeding with beta blockers being the first choice of treatment and esophageal variceal ligation reserved for those who are unable to tolerate the drugs
- Nitrates, sclerotherapy and shunts alone are not used as primary prophylaxis to prevent bleeding
- Patients with cirrhosis and an acute episode of variceal hemorrhage:[61][62]
- Fluid replacement
- Blood transfusions to keep hemoglobin above 8gms/dl
- Antibiotics prophylaxis
- Oral norfloxacin- 400mg BD
- Intravenous ciprofloxacin
- Intravenous ceftriaxone (1 gm/day) in centers with high prevalence of quinolone resistance
- Somatostatin or its analogues octreotide and vapreotide; terlipressin should be initiated as soon as variceal bleeding is suspected and continued for 3 to 5 days after diagnosis is performed [63]
- Endoscopic variceal ligation [64][65]
- Sclerotherapy [66][67][68]
- Transjugular intrahepatic portosystemic shunt (TIPS)[69][70][71][72][73]
- Balloon tamponade: temporary measure to stop bleeding for 24 hours until one of the above procedures is initiated
- Patients who have cirrhosis and have recovered from a variceal bleed:[74][75][76]
- Combination of endoscopic variceal ligation (EVL) and non-selective beta blockers
- EVL should be repeated every 1-2 weeks until obliteration with first surveillance EVL performed 1-3 months and then every 6-12 months to check for recurrence
- Refractory cases should be referred for transplantation.
Hepatic Encephalopathy
The treatment of hepatic encephalopathy in cirrhosis is as follows: [77]
- Lactulose: orally or rectally to effect a bowel purge
- Those who progress to Grade III or IV encephalopathy should undergo endotracheal intubation
- Seizures can be controlled with phenytoin and benzodiazepines with short half lives
- Intracranial pressure is monitored and frequent neurological examination is done in those with high grade encephalopathy
- Mannitol bolus (0.5-1.0 gm/kg body weight) is recommended as first-line therapy
- In patients at highest risk for cerebral edema (serum ammonia >150 µM, grade 3/4 hepatic encephalopathy, acute renal failure, requiring vasopressors to maintain mean arterial pressure [MAP]), the prophylactic induction of hypernatremia with hypertonic saline to a sodium level of 145-155 mEq/L is recommended
- Short acting barbiturates and induction of hypothermia in refractory cases as a bridge to liver transplantation.
Prevention of hepatic encephalopathy:
- Reduced protein intake
- May lead to protein malnutrition and negative nitrogen balance
- Correction of hypokalemia
- Lactulose
- Decreases absorption of ammonia from the gastrointestinal tract
- Works as a laxative, increasing the transit time and reducing absorption of ammonia
- Lactulose can be given rectally for patients who cannot take oral medications.[78][79][80] One regimen is 300 mL (200 gm) of lactulose syrup (10 gm/15 ml) in 1 L of water which is retained for 1 hour, with the patient in the Trendelenburg position.[81]
- Antibiotics
- Killing bacteria in the gut reduces the bacterial conversion of protein to ammonia
- Neomycin
- Metronidazole
- Rifaximin[82][83]
- Benzodiazepines receptor agonists
- Flumazenil- 2 milligrams over 10 minutes
Hepatorenal Syndrome
- Albumin infusion
- 1 gm albumin per kg of body weight intravenously on day one followed by followed by 20-40 grams daily
- Octreotide
- Midodrine
- Vasopressin analogs
- Ornipressin- limited use by ischemic complications
- Terlipressin
- Transjugular intrahepatic portosystemic shunt
- Liver dialysis
Other treatment modalities:
Spontaneous Bacterial Peritonitis
- Abdominal paracentesis
- Intravenous antibiotics-
- Cefotaxime 2 g every 8 hours
- Oral ofloxacin (400 mg twice per day) as a substitute for cefotaxime
- Patients with ascitic fluid PMN counts greater than or equal to 250 cells/mm3 (0.25 X 109/L) and clinical suspicion of SBP who also have a serum creatinine greater than 1 mg/dL, blood urea nitrogen greater than 30 mg/dL, or total bilirubin greater than 4 mg/dL should receive 1.5 g albumin per kg body weight within 6 hours of detection and 1.0 g/kg on day 3.
Contraindicated medications
Cirrhosis is considered an absolute contraindication to the use of the following medications:
References
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- ↑ Besson I, Ingrand P, Person B, Boutroux D, Heresbach D, Bernard P, Hochain P, Larricq J, Gourlaouen A, Ribard D (1995). "Sclerotherapy with or without octreotide for acute variceal bleeding". N. Engl. J. Med. 333 (9): 555–60. doi:10.1056/NEJM199508313330904. PMID 7623904.
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