Cirrhosis medical therapy: Difference between revisions

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{{Cirrhosis}}
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{{CMG}} {{AE}} {{RT}}
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==Overview==
==Overview==
The change that cirrhosis causes to the liver is irreversible, therefore treatment is mostly centered on ameliorating the complications of cirrhosis. This entails treating [[pain]], [[osteoporosis]], [[hypogonadism]], [[constipation]], [[itching]], [[malnutrition]], as well as any identified underlying causes.
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 [[Symptom|symptoms]] such as [[pruritus|pruritus,]] [[hypogonadism]], [[osteoporosis]], and [[anorexia]] must be treated in [[Patient|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==
==Medical Therapy==
* Treatment of [[cirrhosis]] is mostly directed towards the treatment of complications such as:
* Treatment of [[cirrhosis]] is mostly directed towards the treatment of complications such as:<ref name="pmid11179247">{{cite journal |vauthors=Garcia-Tsao G |title=Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis |journal=Gastroenterology |volume=120 |issue=3 |pages=726–48 |year=2001 |pmid=11179247 |doi= |url=}}</ref><ref name="pmid22729954">{{cite journal |vauthors=Tsochatzis EA, Bosch J, Burroughs AK |title=New therapeutic paradigm for patients with cirrhosis |journal=Hepatology |volume=56 |issue=5 |pages=1983–92 |year=2012 |pmid=22729954 |doi=10.1002/hep.25915 |url=}}</ref>
** [[ascites]]  
** [[Ascites]]  
** [[hepatic encephalopathy]]
** [[Hepatic encephalopathy]]
** [[spontaneous bacterial peritonitis]]
** [[Spontaneous bacterial peritonitis]]
** [[esophageal varices]]  
** [[Esophageal varices]]  
** [[hepatorenal syndrome]]  
** [[Hepatorenal syndrome]]  
* Chronic constitutional symptoms enlisted below are also treated:
* Chronic constitutional [[Symptom|symptoms]] enlisted below are also treated:
** [[pruritus]]   
** [[Pruritus]]   
** [[hypogonadism]]  
** [[Hypogonadism]]  
** [[osteoporosis]]   
** [[Osteoporosis]]   
** [[anorexia]]  
** [[Anorexia]]  
* Alcohol abstinence:
* [[Alcohol]] abstinence:
** [[Alcohol]] should be avoided by all patients with cirrhosis. Improvement in liver function is noticed in patients with alcohol induced cirrhosis after abstinence from alcohol.
** [[Alcohol]] should be avoided by all patients with [[cirrhosis]]. Improvement in [[liver]] function is noticed in patients with [[alcohol]] induced [[cirrhosis]] after abstinence from [[alcohol]].<ref name="urlEffects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis - Gastroenterology">{{cite web |url=http://www.gastrojournal.org/article/S0016-5085(97)70142-2/fulltext |title=Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis - Gastroenterology |format= |work= |accessdate=}}</ref><ref name="pmid22633836">{{cite journal |vauthors= |title=EASL clinical practical guidelines: management of alcoholic liver disease |journal=J. Hepatol. |volume=57 |issue=2 |pages=399–420 |year=2012 |pmid=22633836 |doi=10.1016/j.jhep.2012.04.004 |url=}}</ref>


===Pruritus===
===Pruritus===
* [[Pruritus]] is a common symptom in chronic liver disease.   
* [[Pruritus]] is a common symptom in [[primary biliary cirrhosis]] and [[Hepatitis C]].   
* Endogenous opioids are considered responsible for causing pruritus.
* Endogenous [[Opioid|opioids]] and increased serum [[bile acid]] levels are considered responsible for causing [[Itch|pruritus]].
* Preferred regimen for pruritus in chronic liver disease:
* Preferred regimen for [[Itch|pruritus]] in [[chronic liver disease]]:
** [[Cholestyramine]]
** [[Cholestyramine]]
* Preferred regimen for mild itching:
* Preferred regimen for mild [[Itch|itching]]:
** [[antihistamines]]  
** [[H1 antihistamine|Antihistamines]]  
** Ammonium lactate topical solution.
** [[Ammonium lactate]] [[topical]] solution
* Preferred regimen for severe itching:  
* Preferred regimen for severe [[Itch|itching]]:  
** Ultraviolet light therapy
** [[Ultraviolet|Ultraviolet light therapy]]
** [[plasmapheresis]]  
** [[Plasmapheresis]]  
* Alternative regimens for pruritus:
* Alternative regimens for [[Itch|pruritus]]:
** [[diphenhydramine]]
** [[Diphenhydramine]]
** [[hydroxyzine]]
** [[Hydroxyzine]]
** [[ursodeoxycholic acid]]  
** [[Ursodeoxycholic acid]]  
** [[rifampin]]  
** [[Rifampin]]  
** [[naltrexone]] (opiate)
** [[Naltrexone]] ([[opiate]])


===Hypogonadism===
===Hypogonadism===
* Males with [[cirrhosis]] sometimes complain of loss of libido due to [[hypogonadism]].  
* Males with [[cirrhosis]] sometimes complain of loss of [[libido]] due to [[hypogonadism]].  
* Preferred regimen: Topical [[testosterone]] preparations
* Preferred regimen (1): Topical [[testosterone]] preparations
* Preferred regimen (2): [[Growth hormone]] therapy


===Osteoporosis===
===Osteoporosis===
* [[Cirrhosis]]is is one of the major causes of [[osteoporosis]].<ref name="pmid17153457">{{cite journal |author=Giouleme OI, Vyzantiadis TA, Nikolaidis NL, ''et al.'' |title=Pathogenesis of osteoporosis in liver cirrhosis |journal=Hepatogastroenterology |volume=53 |issue=72 |pages=938–43 |year=2006 |pmid=17153457 |doi= |url=}}</ref>
* [[Cirrhosis]]is is one of the major causes of [[osteoporosis]].<ref name="pmid17153457">{{cite journal |author=Giouleme OI, Vyzantiadis TA, Nikolaidis NL, ''et al.'' |title=Pathogenesis of osteoporosis in liver cirrhosis |journal=Hepatogastroenterology |volume=53 |issue=72 |pages=938–43 |year=2006 |pmid=17153457 |doi= |url=}}</ref>
* Preferred regimen: [[Calcium]] and [[vitamin D]] supplementation for all the following patients:  
* [[Calcium]] and [[vitamin D]] supplementation for all the following [[Patient|patients]]:
** 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|Alendronate sodium]]


===Pain management in Cirrhosis===
===Pain management in 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 secondary to [[ascites]] ([[back pain|back]] and [[abdominal pain]]) and [[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.  
* [[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 follwing patients:  
* 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 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===
===Nutrition and exercise===
* [[Anorexia]] is common in cirrhosis patients with [[ascites]] due to the direct compression of the bowel by the ascitic fluid.  
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>
* Adequate calories and proteins should be added to the diet of the patient.
* [[Anorexia]] is common in [[cirrhosis]] patients with [[ascites]] due to the direct compression of the [[Intestine|bowel]] by the ascitic fluid.  
* Patients should consume a balanced diet and one multivitamin daily.
* Adequate [[Calorie|calories]] and [[Protein|proteins]] should be added to the [[Diet (nutrition)|diet]] of the [[patient]].
* [[Vitamin D]] and [[Vitamin K|K]] supplementation is recommended in patients with [[cholestasis]].  
* [[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]].
* [[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 [[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 [[Patient|patients]].  


==== Protein ====
==== Protein ====
* The diet of cirrhosis 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 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 cause muscle wasting.  
* Low [[protein]] levels in the [[Diet (nutrition)|diet]] cause [[Muscle atrophy|muscle wasting]].  
* Branched-chain amino acids (BCAA) can function as pharmacologic nutrients for patients with decompensated cirrhosis.
* 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]] [[Branched chain amino acids|(BCAA)]] can function as pharmacologic [[Nutrient|nutrients]] for patients with decompensated [[cirrhosis]].
====Zinc====
====Zinc====
* Zinc deficiency is commonly observed in patients with [[cirrhosis]].   
* [[Zinc]] deficiency is commonly observed in [[Patient|patients]] with [[cirrhosis]].   
* Zinc supplementation can also help resolve [[muscle cramps]].
* [[Zinc]] supplementation can also help resolve [[muscle cramps]].
* Low dose Zn supplementation could prevent deterioration of the clinical status of cirrhosis and prevent excess Cu accumulation in non-alcoholic cirrhotic patients.  
* Low dose [[zinc]] supplementation could prevent deterioration of the clinical status of [[cirrhosis]] and prevent excess [[copper]] accumulation in non-alcoholic [[Cirrhosis|cirrhotic]] patients.  
* Zn supplementation produces metabolic effects and trends towards improvements in liver function, [[hepatic encephalopathy]], and nutritional status.<ref name="pmid22827782">{{cite journal |author=Somi MH, Rezaeifar P, Ostad Rahimi A, Moshrefi B |title=Effects of Low Dose Zinc Supplementation on Biochemical Markers in Non-alcoholic Cirrhosis: A Randomized Clinical Trial |journal=Arch Iran Med |volume=15 |issue=8 |pages=472–6 |year=2012 |month=August |pmid=22827782 |doi=012158/AIM.006 |url=}}</ref>
* [[Zinc]] supplementation produces metabolic effects and trends towards improvements in [[liver]] function, [[hepatic encephalopathy]], and nutritional status.<ref name="pmid22827782">{{cite journal |author=Somi MH, Rezaeifar P, Ostad Rahimi A, Moshrefi B |title=Effects of Low Dose Zinc Supplementation on Biochemical Markers in Non-alcoholic Cirrhosis: A Randomized Clinical Trial |journal=Arch Iran Med |volume=15 |issue=8 |pages=472–6 |year=2012 |pmid=22827782 |url=}}</ref>
* Supplementation with 220 mg Zinc twice a day orally may improve [[dysgeusia]] and also helps in stimulating the patient's appetite.  
* 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:
** [[Hepatitis A]]
** [[Streptococcus pneumoniae|Pneumococci]]
** [[Influenza]]


==Treatment of Underlying Causes==
==Treatment of Underlying Causes==
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:[[Alcoholic_liver_disease_medical_therapy|Alcoholic Liver Disease Medical Therapy]]
:[[Alcoholic_liver_disease_medical_therapy|Alcoholic Liver Disease Medical Therapy]]


* Mild to moderate alcoholic hepatitis:
* Mild to moderate [[alcoholic hepatitis]]:
** Abstinence from alcohol.
** Abstinence from [[alcohol]]
** Aggressive enteral nutrition therapy.
** Preferred regimen (1): Aggressive enteral nutrition therapy
* Severe Alcoholic hepatitis:
* Severe [[Alcoholic hepatitis]]:
** 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 (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).
** [[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
** 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===
===Hepatitis C===
:[[Hepatitis_C/Medical_Therapy|Hepatitis C Medical Therapy]]
:[[Hepatitis_C/Medical_Therapy|Hepatitis C Medical Therapy]]<ref name="pmid8898645">{{cite journal |vauthors=Lai MY, Kao JH, Yang PM, Wang JT, Chen PJ, Chan KW, Chu JS, Chen DS |title=Long-term efficacy of ribavirin plus interferon alfa in the treatment of chronic hepatitis C |journal=Gastroenterology |volume=111 |issue=5 |pages=1307–12 |year=1996 |pmid=8898645 |doi= |url=}}</ref><ref name="pmid15777574">{{cite journal |vauthors=Everson GT |title=Management of cirrhosis due to chronic hepatitis C |journal=J. Hepatol. |volume=42 Suppl |issue=1 |pages=S65–74 |year=2005 |pmid=15777574 |doi=10.1016/j.jhep.2005.01.009 |url=}}</ref><ref name="pmid11984517">{{cite journal |vauthors=Poynard T, McHutchison J, Manns M, Trepo C, Lindsay K, Goodman Z, Ling MH, Albrecht J |title=Impact of pegylated interferon alfa-2b and ribavirin on liver fibrosis in patients with chronic hepatitis C |journal=Gastroenterology |volume=122 |issue=5 |pages=1303–13 |year=2002 |pmid=11984517 |doi= |url=}}</ref><ref name="pmid12883493">{{cite journal |vauthors=Poynard T, McHutchison J, Manns M, Myers RP, Albrecht J |title=Biochemical surrogate markers of liver fibrosis and activity in a randomized trial of peginterferon alfa-2b and ribavirin |journal=Hepatology |volume=38 |issue=2 |pages=481–92 |year=2003 |pmid=12883493 |doi=10.1053/jhep.2003.50319 |url=}}</ref><ref name="pmid19403902">{{cite journal |vauthors=McHutchison JG, Everson GT, Gordon SC, Jacobson IM, Sulkowski M, Kauffman R, McNair L, Alam J, Muir AJ |title=Telaprevir with peginterferon and ribavirin for chronic HCV genotype 1 infection |journal=N. Engl. J. Med. |volume=360 |issue=18 |pages=1827–38 |year=2009 |pmid=19403902 |doi=10.1056/NEJMoa0806104 |url=}}</ref><ref name="pmid21449783">{{cite journal |vauthors=Poordad F, McCone J, Bacon BR, Bruno S, Manns MP, Sulkowski MS, Jacobson IM, Reddy KR, Goodman ZD, Boparai N, DiNubile MJ, Sniukiene V, Brass CA, Albrecht JK, Bronowicki JP |title=Boceprevir for untreated chronic HCV genotype 1 infection |journal=N. Engl. J. Med. |volume=364 |issue=13 |pages=1195–206 |year=2011 |pmid=21449783 |pmc=3766849 |doi=10.1056/NEJMoa1010494 |url=}}</ref>


* Abstinence from alcohol as alcohol aggravates HCV associated [[fibrosis]], cirrhosis and makes [[liver cancer]] more likely.
* Abstinence from [[alcohol]] as [[alcohol]] aggravates [[Hepatitis C|HCV]] associated [[fibrosis]], cirrhosis and makes [[liver cancer]] more likely.


====Genotypes HCV 1 and 4====
====Genotypes HCV 1 and 4====
* Treatment with [[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.
* 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====
* Treatment with [[peginterferon]] plus ribavirin should be administered for 24 weeks, using a [[ribavirin]] dose of 800 mg.
* Preferred regimen (1): [[Pegylated interferon alfa-2a|peginterferon]] plus [[ribavirin]] should be administered for 24 weeks, using a [[ribavirin]] dose of 800 mg.<ref name="urlMedscape Log In">{{cite web |url=https://www.medscape.com/viewarticle/833771 |title=Medscape Log In |format= |work= |accessdate=}}</ref>
 
* Alternative regimen (1): Triple therapy- [[Pegylated interferon alfa-2a|peginterferon]] plus [[ribavirin]] along with an additional dose of 100mg of [[amantadine]] q12h.
For "nonresponders" - people who do not respond to previous treatments addition of 100mg of [[amantadine]] twice a day has been suggested by a few studies and this is sometimes referred to as "triple therapy".


===Hepatitis B===
===Hepatitis B===
:[[Hepatitis_B/Medical_Therapy|Hepatitis B Medical Therapy]]
:[[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
* 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.''' 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 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.
:'''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]].
* 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.
* 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>


===Autoimmune Hepatitis===
===Autoimmune Hepatitis===
:[[Autoimmune_hepatitis#Treatment|Autoimmune Hepatitis Medical Therapy]]
:[[Autoimmune_hepatitis#Treatment|Autoimmune Hepatitis Medical Therapy]]


* Immunosuppressive treatment based on serum aspartate aminotransferase (AST), serum alanine aminotransferase (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.
* Alternative drug therapies for suboptimal response - ([[cyclosporine]], [[tacrolimus]], or [[mycophenolate mofetil]])
* Alternative drug therapies for suboptimal response - ([[cyclosporine]], [[tacrolimus]], or [[mycophenolate mofetil]])


Line 133: Line 143:


* There is no known cure, but medication may slow the progression so that a normal lifespan and quality of life may be attainable.
* 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.
** [[Ursodiol|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]].
** [[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]].


Line 139: 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 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===
:[[Wilson's_disease_medical_therapy|Wilson's Disease Medical Therapy]]
:[[Wilson's_disease_medical_therapy|Wilson's Disease Medical Therapy]]


* 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 chelating agent ([[D-penicillamine]] or [[trientine]]).
* Initial treatment for symptomatic [[Patient|patients]] includes a [[Chelation|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.
* Patients with acute [[Hepatic failure|liver failure]] due to [[Wilson's disease]], or unresponsive to [[chelation]] treatment - should be referred to [[liver transplantation]].


==Treatment of Complications==
==Treatment of Complications==
===Ascites===
===Ascites===
:[[Ascites medical therapy|Ascites Treatment]]
:[[Ascites medical therapy|Ascites Treatment]]<ref name="pmid25954497">{{cite journal |vauthors=Pedersen JS, Bendtsen F, Møller S |title=Management of cirrhotic ascites |journal=Ther Adv Chronic Dis |volume=6 |issue=3 |pages=124–37 |year=2015 |pmid=25954497 |pmc=4416972 |doi=10.1177/2040622315580069 |url=}}</ref><ref name="pmid15084697">{{cite journal |vauthors=Ginès P, Cárdenas A, Arroyo V, Rodés J |title=Management of cirrhosis and ascites |journal=N. Engl. J. Med. |volume=350 |issue=16 |pages=1646–54 |year=2004 |pmid=15084697 |doi=10.1056/NEJMra035021 |url=}}</ref><ref name="pmid19475696">{{cite journal |vauthors=Runyon BA |title=Management of adult patients with ascites due to cirrhosis: an update |journal=Hepatology |volume=49 |issue=6 |pages=2087–107 |year=2009 |pmid=19475696 |doi=10.1002/hep.22853 |url=}}</ref><ref name="pmid22334252">{{cite journal |vauthors=Hernández-Gea V, Aracil C, Colomo A, Garupera I, Poca M, Torras X, Miñana J, Guarner C, Villanueva C |title=Development of ascites in compensated cirrhosis with severe portal hypertension treated with β-blockers |journal=Am. J. Gastroenterol. |volume=107 |issue=3 |pages=418–27 |year=2012 |pmid=22334252 |doi=10.1038/ajg.2011.456 |url=}}</ref><ref name="pmid19570764">{{cite journal |vauthors=Angeli P, Fasolato S, Mazza E, Okolicsanyi L, Maresio G, Velo E, Galioto A, Salinas F, D'Aquino M, Sticca A, Gatta A |title=Combined versus sequential diuretic treatment of ascites in non-azotaemic patients with cirrhosis: results of an open randomised clinical trial |journal=Gut |volume=59 |issue=1 |pages=98–104 |year=2010 |pmid=19570764 |doi=10.1136/gut.2008.176495 |url=}}</ref><ref name="pmid20633946">{{cite journal |vauthors= |title=EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis |journal=J. Hepatol. |volume=53 |issue=3 |pages=397–417 |year=2010 |pmid=20633946 |doi=10.1016/j.jhep.2010.05.004 |url=}}</ref><ref name="pmid3360270">{{cite journal |vauthors=Ginès P, Titó L, Arroyo V, Planas R, Panés J, Viver J, Torres M, Humbert P, Rimola A, Llach J |title=Randomized comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis |journal=Gastroenterology |volume=94 |issue=6 |pages=1493–502 |year=1988 |pmid=3360270 |doi= |url=}}</ref><ref name="pmid23463403">{{cite journal |vauthors=Runyon BA |title=Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012 |journal=Hepatology |volume=57 |issue=4 |pages=1651–3 |year=2013 |pmid=23463403 |doi=10.1002/hep.26359 |url=}}</ref><ref name="pmid23523582">{{cite journal |vauthors=Morando F, Maresio G, Piano S, Fasolato S, Cavallin M, Romano A, Rosi S, Gola E, Frigo AC, Stanco M, Destro C, Rupolo G, Mantoan D, Gatta A, Angeli P |title=How to improve care in outpatients with cirrhosis and ascites: a new model of care coordination by consultant hepatologists |journal=J. Hepatol. |volume=59 |issue=2 |pages=257–64 |year=2013 |pmid=23523582 |doi=10.1016/j.jhep.2013.03.010 |url=}}</ref>


* Abstinence from alcohol.
* Abstinence from [[alcohol]].
* 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>
*[[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]]
:[[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>


*Patients with no varices and bleeding:
*Patients with no [[varices]] and [[bleeding]]:<ref name="pmid163065222">{{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>
**EGD should be performed at regular intervals.
**[[Esophagogastroduodenoscopy|EGD]] should be performed at regular intervals.<ref name="pmid25034836">{{cite journal |vauthors=Hwang JH, Shergill AK, Acosta RD, Chandrasekhara V, Chathadi KV, Decker GA, Early DS, Evans JA, Fanelli RD, Fisher DA, Foley KQ, Fonkalsrud L, Jue T, Khashab MA, Lightdale JR, Muthusamy VR, Pasha SF, Saltzman JR, Sharaf R, Cash BD |title=The role of endoscopy in the management of variceal hemorrhage |journal=Gastrointest. Endosc. |volume=80 |issue=2 |pages=221–7 |year=2014 |pmid=25034836 |doi=10.1016/j.gie.2013.07.023 |url=}}</ref>
*Patients with small varices that have not bled:
*[[Patient|Patients]] with small [[varices]] that have not bled:<ref name="pmid10655253">{{cite journal |vauthors=Merkel C, Marin R, Sacerdoti D, Donada C, Cavallarin G, Torboli P, Amodio P, Sebastianelli G, Bolognesi M, Felder M, Mazzaro C, Gatta A |title=Long-term results of a clinical trial of nadolol with or without isosorbide mononitrate for primary prophylaxis of variceal bleeding in cirrhosis |journal=Hepatology |volume=31 |issue=2 |pages=324–9 |year=2000 |pmid=10655253 |doi=10.1002/hep.510310210 |url=}}</ref><ref name="pmid18042114">{{cite journal |vauthors=Gluud LL, Klingenberg S, Nikolova D, Gluud C |title=Banding ligation versus beta-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials |journal=Am. J. Gastroenterol. |volume=102 |issue=12 |pages=2842–8; quiz 2841, 2849 |year=2007 |pmid=18042114 |doi=10.1111/j.1572-0241.2007.01564.x |url=}}</ref><ref name="pmid1674104">{{cite journal |vauthors=Poynard T, Calès P, Pasta L, Ideo G, Pascal JP, Pagliaro L, Lebrec D |title=Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clinical trials. Franco-Italian Multicenter Study Group |journal=N. Engl. J. Med. |volume=324 |issue=22 |pages=1532–8 |year=1991 |pmid=1674104 |doi=10.1056/NEJM199105303242202 |url=}}</ref><ref name="pmid20513005">{{cite journal |vauthors=Bosch J |title=Carvedilol for portal hypertension in patients with cirrhosis |journal=Hepatology |volume=51 |issue=6 |pages=2214–8 |year=2010 |pmid=20513005 |doi=10.1002/hep.23689 |url=}}</ref><ref name="pmid19610055">{{cite journal |vauthors=Tripathi D, Ferguson JW, Kochar N, Leithead JA, Therapondos G, McAvoy NC, Stanley AJ, Forrest EH, Hislop WS, Mills PR, Hayes PC |title=Randomized controlled trial of carvedilol versus variceal band ligation for the prevention of the first variceal bleed |journal=Hepatology |volume=50 |issue=3 |pages=825–33 |year=2009 |pmid=19610055 |doi=10.1002/hep.23045 |url=}}</ref><ref name="urlPrimary prevention of variceal haemorrhage: A pharmacological approach - Journal of Hepatology">{{cite web |url=http://www.journal-of-hepatology.eu/article/S0168-8278(10)00119-4/fulltext |title=Primary prevention of variceal haemorrhage: A pharmacological approach - Journal of Hepatology |format= |work= |accessdate=}}</ref><ref name="pmid15300580">{{cite journal |vauthors=Merkel C, Marin R, Angeli P, Zanella P, Felder M, Bernardinello E, Cavallarin G, Bolognesi M, Donada C, Bellini B, Torboli P, Gatta A |title=A placebo-controlled clinical trial of nadolol in the prophylaxis of growth of small esophageal varices in cirrhosis |journal=Gastroenterology |volume=127 |issue=2 |pages=476–84 |year=2004 |pmid=15300580 |doi= |url=}}</ref><ref name="pmid8985266">{{cite journal |vauthors=Bernard B, Lebrec D, Mathurin P, Opolon P, Poynard T |title=Beta-adrenergic antagonists in the prevention of gastrointestinal rebleeding in patients with cirrhosis: a meta-analysis |journal=Hepatology |volume=25 |issue=1 |pages=63–70 |year=1997 |pmid=8985266 |doi=10.1053/jhep.1997.v25.pm0008985266 |url=}}</ref>
**Non-selective [[beta blockers]] should be used to prevent the first variceal bleeding
**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 EGD every 2 years
**Those not receiving [[beta blockers]], should be followed up with [[Esophagogastroduodenoscopy|EGD]] every 2 years
**If the liver decompensates, 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 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: <ref name="pmid180421142">{{cite journal |vauthors=Gluud LL, Klingenberg S, Nikolova D, Gluud C |title=Banding ligation versus beta-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials |journal=Am. J. Gastroenterol. |volume=102 |issue=12 |pages=2842–8; quiz 2841, 2849 |year=2007 |pmid=18042114 |doi=10.1111/j.1572-0241.2007.01564.x |url=}}</ref><ref name="pmid182932742">{{cite journal |vauthors=Bosch J, Abraldes JG, Berzigotti A, Garcia-Pagan JC |title=Portal hypertension and gastrointestinal bleeding |journal=Semin. Liver Dis. |volume=28 |issue=1 |pages=3–25 |year=2008 |pmid=18293274 |doi=10.1055/s-2008-1040318 |url=}}</ref>
**Esophageal 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
**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 endoscopic [[Esophageal varices|variceal]] ligation reserved for those who are unable to tolerate the [[:Category:Drugs|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 variceal hemorrhage:
*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
**[[Blood transfusions]] to keep [[hemoglobin]] above 8gms/dl
**[[Blood transfusions]] to keep [[hemoglobin]] above 8gms/dl
**Antibiotics prophylaxis
**[[Antibiotic|Antibiotics]] prophylaxis
***Oral [[norfloxacin]]- 400mg BD
***Oral [[norfloxacin]]- 400mg BD
***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
**[[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>
**Esophageal variceal ligation
**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
**[[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]])
**[[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 variceal bleed:
*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 esophageal variceal ligation (EVL) and non-selective [[beta blockers]]
**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
**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.
**Refractory cases should be referred for [[Liver transplantation|transplantation]].
 
{{#ev:youtube|9Vrmq8XKuXo|500}}
===Hepatic Encephalopathy===
===Hepatic Encephalopathy===
The treatment of [[hepatic encephalopathy]] in [[cirrhosis]] is as follows: <ref name="pmid1346515">{{cite journal |vauthors=Butterworth RF |title=Pathogenesis and treatment of portal-systemic encephalopathy: an update |journal=Dig. Dis. Sci. |volume=37 |issue=3 |pages=321–7 |year=1992 |pmid=1346515 |doi= |url=}}</ref>
:[[Hepatic_encephalopathy#Treatment|Hepatic Encephalopathy Treatment]]
:[[Hepatic_encephalopathy#Treatment|Hepatic Encephalopathy Treatment]]


*[[Lactulose]]: orally or rectally to effect a bowel purge
*[[Lactulose]]: orally or rectally to effect a [[Intestine|bowel]] purge
*Those who progress to Grade III or IV encephalopathy should undergo [[endotracheal intubation]]
*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
*[[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
*[[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]]
*[[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>
**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


===Hepatorenal Syndrome===
===Hepatorenal Syndrome===
:[[Hepatorenal syndrome#Treatment|Hepatorenal Syndrome Treatment]]
:[[Hepatorenal syndrome#Treatment|Hepatorenal Syndrome Treatment]]<ref name="pmid1435935">{{cite journal |vauthors=Epstein M |title=The hepatorenal syndrome--newer perspectives |journal=N. Engl. J. Med. |volume=327 |issue=25 |pages=1810–1 |year=1992 |pmid=1435935 |doi=10.1056/NEJM199212173272509 |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="pmid14654322">{{cite journal |vauthors=Ginès P, Guevara M, Arroyo V, Rodés J |title=Hepatorenal syndrome |journal=Lancet |volume=362 |issue=9398 |pages=1819–27 |year=2003 |pmid=14654322 |doi=10.1016/S0140-6736(03)14903-3 |url=}}</ref><ref name="pmid10347109">{{cite journal |vauthors=Angeli P, Volpin R, Gerunda G, Craighero R, Roner P, Merenda R, Amodio P, Sticca A, Caregaro L, Maffei-Faccioli A, Gatta A |title=Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide |journal=Hepatology |volume=29 |issue=6 |pages=1690–7 |year=1999 |pmid=10347109 |doi=10.1002/hep.510290629 |url=}}</ref>


*[[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 242: Line 254:


===Spontaneous Bacterial Peritonitis===
===Spontaneous Bacterial Peritonitis===
:[[Spontaneous bacterial peritonitis medical therapy|Spontaneous Bacterial Peritonitis Medical Therapy]]
:[[Spontaneous bacterial peritonitis medical therapy|Spontaneous Bacterial Peritonitis Medical Therapy]]<ref name="pmid8428722">{{cite journal |vauthors=Toledo C, Salmerón JM, Rimola A, Navasa M, Arroyo V, Llach J, Ginès A, Ginès P, Rodés J |title=Spontaneous bacterial peritonitis in cirrhosis: predictive factors of infection resolution and survival in patients treated with cefotaxime |journal=Hepatology |volume=17 |issue=2 |pages=251–7 |year=1993 |pmid=8428722 |doi= |url=}}</ref><ref name="pmid7843703">{{cite journal |vauthors=Solà R, Andreu M, Coll S, Vila MC, Oliver MI, Arroyo V |title=Spontaneous bacterial peritonitis in cirrhotic patients treated using paracentesis or diuretics: results of a randomized study |journal=Hepatology |volume=21 |issue=2 |pages=340–4 |year=1995 |pmid=7843703 |doi= |url=}}</ref><ref name="pmid2019378">{{cite journal |vauthors=Runyon BA, McHutchison JG, Antillon MR, Akriviadis EA, Montano AA |title=Short-course versus long-course antibiotic treatment of spontaneous bacterial peritonitis. A randomized controlled study of 100 patients |journal=Gastroenterology |volume=100 |issue=6 |pages=1737–42 |year=1991 |pmid=2019378 |doi= |url=}}</ref><ref name="pmid9049193">{{cite journal |vauthors=Novella M, Solà R, Soriano G, Andreu M, Gana J, Ortiz J, Coll S, Sàbat M, Vila MC, Guarner C, Vilardell F |title=Continuous versus inpatient prophylaxis of the first episode of spontaneous bacterial peritonitis with norfloxacin |journal=Hepatology |volume=25 |issue=3 |pages=532–6 |year=1997 |pmid=9049193 |doi=10.1002/hep.510250306 |url=}}</ref><ref name="pmid19277033">{{cite journal |vauthors=Saab S, Hernandez JC, Chi AC, Tong MJ |title=Oral antibiotic prophylaxis reduces spontaneous bacterial peritonitis occurrence and improves short-term survival in cirrhosis: a meta-analysis |journal=Am. J. Gastroenterol. |volume=104 |issue=4 |pages=993–1001; quiz 1002 |year=2009 |pmid=19277033 |doi=10.1038/ajg.2009.3 |url=}}</ref><ref name="pmid17030175">{{cite journal |vauthors=Fernández J, Ruiz del Arbol L, Gómez C, Durandez R, Serradilla R, Guarner C, Planas R, Arroyo V, Navasa M |title=Norfloxacin vs ceftriaxone in the prophylaxis of infections in patients with advanced cirrhosis and hemorrhage |journal=Gastroenterology |volume=131 |issue=4 |pages=1049–56; quiz 1285 |year=2006 |pmid=17030175 |doi=10.1053/j.gastro.2006.07.010 |url=}}</ref>


*[[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===
{{MedCondContrAbs
{{MedCondContrAbs


|MedCond = Cirrhosis|Acetazolamide|Methazolamide|Ranolazine|Ticagrelor|Triamterene}}
|MedCond = Cirrhosis|Acetazolamide|Methazolamide|Ranolazine|Ticagrelor|Triamterene}}<ref name="pmid23638982">{{cite journal |vauthors=Lewis JH, Stine JG |title=Review article: prescribing medications in patients with cirrhosis - a practical guide |journal=Aliment. Pharmacol. Ther. |volume=37 |issue=12 |pages=1132–56 |year=2013 |pmid=23638982 |doi=10.1111/apt.12324 |url=}}</ref>


==References==
==References==

Latest revision as of 16:43, 2 September 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sudarshana Datta, MD [2]

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

Pruritus

Hypogonadism

Osteoporosis

Pain management in cirrhosis

Nutrition and exercise

The following points need to be kept in mind regarding nutrition in cirrhosis patients:[6][7][8][9]

Protein

Zinc

Vaccination

Treatment of Underlying Causes

Alcoholic Liver Disease

Alcoholic Liver Disease Medical Therapy
  • 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

Hepatitis C Medical Therapy[13][14][15][16][17][18]

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

Hepatitis B

Hepatitis B Medical Therapy[21][22][23][24][25][26][27][28][29][30][25]
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.

Autoimmune Hepatitis

Autoimmune Hepatitis Medical Therapy

Primary Biliary Cirrhosis

Primary Biliary Cirrhosis Medical Therapy

Primary Sclerosing Cholangitis

Primary Sclerosing Cholangitis Medical Therapy

Wilson's Disease

Wilson's Disease Medical Therapy

Treatment of Complications

Ascites

Ascites Treatment[35][36][37][38][39][40][41][42][43]
  • 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

Esophageal Varices Treatment[46][47]

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Hepatic Encephalopathy

The treatment of hepatic encephalopathy in cirrhosis is as follows: [82]

Hepatic Encephalopathy Treatment

Prevention of hepatic encephalopathy:

Hepatorenal Syndrome

Hepatorenal Syndrome Treatment[92][72][93][94]

Other treatment modalities:

Spontaneous Bacterial Peritonitis

Spontaneous Bacterial Peritonitis Medical Therapy[96][97][98][99][100][101]

Contraindicated medications

Cirrhosis is considered an absolute contraindication to the use of the following medications:

References

  1. ↑ Garcia-Tsao G (2001). "Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis". Gastroenterology. 120 (3): 726–48. PMID 11179247.
  2. ↑ Tsochatzis EA, Bosch J, Burroughs AK (2012). "New therapeutic paradigm for patients with cirrhosis". Hepatology. 56 (5): 1983–92. doi:10.1002/hep.25915. PMID 22729954.
  3. ↑ "Effects of ethanol consumption on hepatic hemodynamics in patients with alcoholic cirrhosis - Gastroenterology".
  4. ↑ "EASL clinical practical guidelines: management of alcoholic liver disease". J. Hepatol. 57 (2): 399–420. 2012. doi:10.1016/j.jhep.2012.04.004. PMID 22633836.
  5. ↑ Giouleme OI, Vyzantiadis TA, Nikolaidis NL; et al. (2006). "Pathogenesis of osteoporosis in liver cirrhosis". Hepatogastroenterology. 53 (72): 938–43. PMID 17153457.
  6. ↑ Kondrup J, Nielsen K, Hamberg O (1993). "[Nutritional therapy in patients with liver cirrhosis]". Ugeskr. Laeg. (in Danish). 155 (29): 2248–51. PMID 8328092.
  7. ↑ Silk DB, O'Keefe SJ, Wicks C (1991). "Nutritional support in liver disease". Gut. Suppl: S29–33. PMC 1405219. PMID 1916467.
  8. ↑ 8.0 8.1 Plank LD, Gane EJ, Peng S, Muthu C, Mathur S, Gillanders L, McIlroy K, Donaghy AJ, McCall JL (2008). "Nocturnal nutritional supplementation improves total body protein status of patients with liver cirrhosis: a randomized 12-month trial". Hepatology. 48 (2): 557–66. doi:10.1002/hep.22367. PMID 18627001.
  9. ↑ Plauth M, Cabré E, Riggio O, Assis-Camilo M, Pirlich M, Kondrup J, Ferenci P, Holm E, Vom Dahl S, Müller MJ, Nolte W (2006). "ESPEN Guidelines on Enteral Nutrition: Liver disease". Clin Nutr. 25 (2): 285–94. doi:10.1016/j.clnu.2006.01.018. PMID 16707194.
  10. ↑ O'Shea RS, Dasarathy S, McCullough AJ (2010). "Alcoholic liver disease". Am. J. Gastroenterol. 105 (1): 14–32, quiz 33. doi:10.1038/ajg.2009.593. PMID 19904248.
  11. ↑ Córdoba J, López-Hellín J, Planas M, Sabín P, Sanpedro F, Castro F, Esteban R, Guardia J (2004). "Normal protein diet for episodic hepatic encephalopathy: results of a randomized study". J. Hepatol. 41 (1): 38–43. doi:10.1016/j.jhep.2004.03.023. PMID 15246205.
  12. ↑ Somi MH, Rezaeifar P, Ostad Rahimi A, Moshrefi B (2012). "Effects of Low Dose Zinc Supplementation on Biochemical Markers in Non-alcoholic Cirrhosis: A Randomized Clinical Trial". Arch Iran Med. 15 (8): 472–6. PMID 22827782.
  13. ↑ Lai MY, Kao JH, Yang PM, Wang JT, Chen PJ, Chan KW, Chu JS, Chen DS (1996). "Long-term efficacy of ribavirin plus interferon alfa in the treatment of chronic hepatitis C". Gastroenterology. 111 (5): 1307–12. PMID 8898645.
  14. ↑ Everson GT (2005). "Management of cirrhosis due to chronic hepatitis C". J. Hepatol. 42 Suppl (1): S65–74. doi:10.1016/j.jhep.2005.01.009. PMID 15777574.
  15. ↑ Poynard T, McHutchison J, Manns M, Trepo C, Lindsay K, Goodman Z, Ling MH, Albrecht J (2002). "Impact of pegylated interferon alfa-2b and ribavirin on liver fibrosis in patients with chronic hepatitis C". Gastroenterology. 122 (5): 1303–13. PMID 11984517.
  16. ↑ Poynard T, McHutchison J, Manns M, Myers RP, Albrecht J (2003). "Biochemical surrogate markers of liver fibrosis and activity in a randomized trial of peginterferon alfa-2b and ribavirin". Hepatology. 38 (2): 481–92. doi:10.1053/jhep.2003.50319. PMID 12883493.
  17. ↑ McHutchison JG, Everson GT, Gordon SC, Jacobson IM, Sulkowski M, Kauffman R, McNair L, Alam J, Muir AJ (2009). "Telaprevir with peginterferon and ribavirin for chronic HCV genotype 1 infection". N. Engl. J. Med. 360 (18): 1827–38. doi:10.1056/NEJMoa0806104. PMID 19403902.
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  20. ↑ "Medscape Log In".
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  25. ↑ 25.0 25.1 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 (2004). "Lamivudine for patients with chronic hepatitis B and advanced liver disease". N. Engl. J. Med. 351 (15): 1521–31. doi:10.1056/NEJMoa033364. PMID 15470215.
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  27. ↑ 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 (2005). "Long-term therapy with adefovir dipivoxil for HBeAg-negative chronic hepatitis B". N. Engl. J. Med. 352 (26): 2673–81. doi:10.1056/NEJMoa042957. PMID 15987916.
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  49. ↑ Hwang JH, Shergill AK, Acosta RD, Chandrasekhara V, Chathadi KV, Decker GA, Early DS, Evans JA, Fanelli RD, Fisher DA, Foley KQ, Fonkalsrud L, Jue T, Khashab MA, Lightdale JR, Muthusamy VR, Pasha SF, Saltzman JR, Sharaf R, Cash BD (2014). "The role of endoscopy in the management of variceal hemorrhage". Gastrointest. Endosc. 80 (2): 221–7. doi:10.1016/j.gie.2013.07.023. PMID 25034836.
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  51. ↑ Gluud LL, Klingenberg S, Nikolova D, Gluud C (2007). "Banding ligation versus beta-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials". Am. J. Gastroenterol. 102 (12): 2842–8, quiz 2841, 2849. doi:10.1111/j.1572-0241.2007.01564.x. PMID 18042114.
  52. ↑ Poynard T, Calès P, Pasta L, Ideo G, Pascal JP, Pagliaro L, Lebrec D (1991). "Beta-adrenergic-antagonist drugs in the prevention of gastrointestinal bleeding in patients with cirrhosis and esophageal varices. An analysis of data and prognostic factors in 589 patients from four randomized clinical trials. Franco-Italian Multicenter Study Group". N. Engl. J. Med. 324 (22): 1532–8. doi:10.1056/NEJM199105303242202. PMID 1674104.
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  56. ↑ Merkel C, Marin R, Angeli P, Zanella P, Felder M, Bernardinello E, Cavallarin G, Bolognesi M, Donada C, Bellini B, Torboli P, Gatta A (2004). "A placebo-controlled clinical trial of nadolol in the prophylaxis of growth of small esophageal varices in cirrhosis". Gastroenterology. 127 (2): 476–84. PMID 15300580.
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  59. ↑ Villanueva C, Aracil C, Colomo A, Hernández-Gea V, López-Balaguer JM, Alvarez-Urturi C, Torras X, Balanzó J, Guarner C (2009). "Acute hemodynamic response to beta-blockers and prediction of long-term outcome in primary prophylaxis of variceal bleeding". Gastroenterology. 137 (1): 119–28. doi:10.1053/j.gastro.2009.03.048. PMID 19344721.
  60. ↑ Ge PS, Runyon BA (2014). "The changing role of beta-blocker therapy in patients with cirrhosis". J. Hepatol. 60 (3): 643–53. doi:10.1016/j.jhep.2013.09.016. PMID 24076364.
  61. ↑ Lebrec D, Poynard T, Hillon P, Benhamou JP (1981). "Propranolol for prevention of recurrent gastrointestinal bleeding in patients with cirrhosis: a controlled study". N. Engl. J. Med. 305 (23): 1371–4. doi:10.1056/NEJM198112033052302. PMID 7029276.
  62. ↑ Pascal JP, Cales P (1987). "Propranolol in the prevention of first upper gastrointestinal tract hemorrhage in patients with cirrhosis of the liver and esophageal varices". N. Engl. J. Med. 317 (14): 856–61. doi:10.1056/NEJM198710013171403. PMID 3306385.
  63. ↑ 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 (2005). "Beta-blockers to prevent gastroesophageal varices in patients with cirrhosis". N. Engl. J. Med. 353 (21): 2254–61. doi:10.1056/NEJMoa044456. PMID 16306522.
  64. ↑ Gluud LL, Klingenberg S, Nikolova D, Gluud C (2007). "Banding ligation versus beta-blockers as primary prophylaxis in esophageal varices: systematic review of randomized trials". Am. J. Gastroenterol. 102 (12): 2842–8, quiz 2841, 2849. doi:10.1111/j.1572-0241.2007.01564.x. PMID 18042114.
  65. ↑ Bosch J, Abraldes JG, Berzigotti A, Garcia-Pagan JC (2008). "Portal hypertension and gastrointestinal bleeding". Semin. Liver Dis. 28 (1): 3–25. doi:10.1055/s-2008-1040318. PMID 18293274.
  66. ↑ 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.
  67. ↑ "Endoscopic management of acute esophageal variceal bleeding - Techniques in Gastrointestinal Endoscopy".
  68. ↑ Sung JJ, Chung SC, Lai CW, Chan FK, Leung JW, Yung MY, Kassianides C, Li AK (1993). "Octreotide infusion or emergency sclerotherapy for variceal haemorrhage". Lancet. 342 (8872): 637–41. PMID 8103145.
  69. ↑ Gimson AE, Ramage JK, Panos MZ, Hayllar K, Harrison PM, Williams R, Westaby D (1993). "Randomised trial of variceal banding ligation versus injection sclerotherapy for bleeding oesophageal varices". Lancet. 342 (8868): 391–4. PMID 8101900.
  70. ↑ Bañares R, Albillos A, Rincón D, Alonso S, González M, Ruiz-del-Arbol L, Salcedo M, Molinero LM (2002). "Endoscopic treatment versus endoscopic plus pharmacologic treatment for acute variceal bleeding: a meta-analysis". Hepatology. 35 (3): 609–15. doi:10.1053/jhep.2002.31354. PMID 11870374.
  71. ↑ Krige JE, Kotze UK, Bornman PC, Shaw JM, Klipin M (2006). "Variceal recurrence, rebleeding, and survival after endoscopic injection sclerotherapy in 287 alcoholic cirrhotic patients with bleeding esophageal varices". Ann. Surg. 244 (5): 764–70. doi:10.1097/01.sla.0000231704.45005.4e. PMC 1856595. PMID 17060770.
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