Consequences of liver cirrhosis, and management approaches · Portopulmonary hypertension is rare,...

$: Consequences of liver cirrhosis, and management approaches · Portopulmonary hypertension is rare, yet its prevalence increases to 1620% of patients with - refractory ascites. It$
International Journal of Scientific & Engineering Research Volume 9, Issue 5, May-2018 1128 ISSN 2229-5518

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Consequences of liver cirrhosis, and management approaches

Sami Ayyadah Ghareeb Alshammari, Atheer Musaed Aljuhani, Abdullah Ahmed Alkhalaf, Abdulaziz Moqbel Faleh Alshammary, Mutab Suliman saif AlShammari, Ahmed Hamed Maleh alshammari, Khalid Sukhail G

Alshammari, Ahmed Farhan Alhaysuni, Hamoud Khalid Alshaya

Abstract:

This review will focus on the consequences and treatment strategies currently recommended in

the management of patients with cirrhosis. We searched the electronic medical databases

PubMed, Embase, to identified relevant articles, trials, and studies that were published until

January, 2018 in English language and only concerning human subject. We searched relevant

studies discussing the Consequences of liver cirrhosis, and management strategies. Cirrhosis

has multisystem impacts and consequences. Numerous pulmonary changes could take place as an

outcome of cirrhosis. Patients with cirrhosis frequently have neurologic indications and

symptoms. One of the most common and most commonly recognized of these is hepatic

encephalopathy. Patients with cirrhosis usually have abnormalities in systemic and pulmonary

circulation defined by increased cardiac output, associated with lowered systemic vascular

resistance and blood pressure. Extrahepatic manifestations need to be taken into factor to

consider when treating a cirrhotic patient to enhance clinical results. Although some extrahepatic

sequelae of cirrhosis may be reversible after liver transplantation, some may not, or presented the

clinical seriousness, some could endanger the feasibility of the transplant process. The utmost

treatment for cirrhosis and end phase liver disease is liver transplantation.

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Introduction:

Liver cirrhosis (LC) is a critical stage of chronic liver illness with bad results. Substantial

information have shown that poor liver function and the occurrence of hepatocellular carcinoma

(HCC) are accountable for the shortened survival of LC patients [1], [2], [3].

Cirrhotic patients are prone to develop dangerous complications that call for emergency care and

ICU admission. They can present specific decompensations associated with cirrhosis such as

variceal bleeding and hepatorenal syndrome (HRS) or other critical occasions likewise observed

in the general population such as extreme sepsis or septic shock. Clinical management of all these

entities requires a certain method in cirrhosis. Cirrhotic patients have a hyperdynamic circulation

with high cardiac output and reduced systemic vascular resistance in the lack of infection

[4].Blood circulation disorder enhances the susceptibility of critically-ill cirrhotic patients to

establish numerous organ failure and undermines vascular reactivity to vasopressor medicines

[5]. HRS, a severe functional renal failure happening in patients with advanced cirrhosis and

ascites, is also secondary to this blood circulation disorder that leads to an extreme renal

vasoconstriction [4].Moreover, hypotensive cirrhotic patients require a carefully well balanced

replacement of volemia, considering that over transfusion enhances portal hypertension and the

danger of variceal bleeding and under transfusion causes tissue hypoperfusion which increases

the threat of numerous organ failure [6]. Cirrhotic patients are also at a high risk for development

of other bleeding complications and are extra prone to nosocomial infections [7].This extreme

complexity of critically-ill cirrhotic patients requires a particular medical approach that needs to

be known by general intensivists considering that it has a negative influence on patient prognosis.

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This review will focus on the consequences and treatment strategies currently recommended in

the management of patients with cirrhosis.

Methodology:

We searched the electronic medical databases PubMed, Embase, to identified relevant articles,

trials, and studies that were published until January, 2018 in English language and only

concerning human subject. We searched relevant studies discussing the Consequences of liver

cirrhosis, and management strategies. furthermore, references list of identified studies to revel

more concerned studies to our studied topic.

Discussion:

• COMPLICATIONS OF CIRRHOSIS

Significant advancements have been made in recent times to both avoid and manage the typical

problems of cirrhosis such as variceal blood loss, ascites, spontaneous microbial peritonitis and

encephalopathy [8-14],( Table 1). It is very important to note that bacterial infections are regular,

specifically in decompensated cirrhotics, exacerbating hepatic dysfunction, encephalopathy and

portal hypertension and highlighting the demand for vigilance and rigorous antibiotic therapy in

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cirrhosis. Enhanced bacterial translocation from the intestinal tract, a jeopardized immune

function and an extreme proinflammatory cytokine launch have been implicated in the

pathogenesis of the cirrhosis-associated systemic inflammatory disorder [15].An instance is the

failure to control esophageal variceal bleeding with associated bacterial infection [16].

Table 1.Complications of cirrhosis, their prevention and treatment

Complications Prevention Treatment Variceal bleeding [8-10]

Non selective beta blockers Variceal band ligation

Acute: Resuscitation Vasocontrictors Sclerotherapy Band Ligation TIPSS Surgical Shunts Chronic: Variceal obliteration TIPS Surgical Shunts

Ascites [8],[12] Low Na diet Low Na diet Diuretics Large volume paracentesis TIPSS (LeVeen / Denver shunts)

Renal failure [13] Avoid hypovolemia Discontinue diuretics Rehydration Albumin infusion Hepatorenal syndrome: Add Terlipressin or Midodrine (Noradrenaline) and Somatostatin (Octreotide)

Encephalopathy [14]

Avoid precipitants Treat precipitating factors: Infection Bleeding Electrolyte imbalance Sedatives High protein intake Lactulose Neomycin, Metronidazole, Rifaximin

Spontaneous bacterial peritonitis [8]

Treat ascites Early diagnosic paracentesis: Neutrophils >250/cc → antibiotics iv Secondary prophlaxis with a po antibiotic such as Levofloxacin

TIPSS: Transjugular intrahepatic porto-systemic shunt; vasoconstrictors: vasopressin, octreotide/somatostatin, terlipressin; non-selective beta blockers: nadolol, propranolol

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An essential understanding for the clinician is that as soon as problems have created, suited

patients should be referred to a Liver Center that specializes in both the care of patients with end

phase liver condition and liver transplantation. Special focus has additionally to be paid to the

blood circulation and cardiac abnormalities in cirrhosis that could avert transplant eligibility. The

hepatopulmonary syndrome which takes place in 15-20% of cirrhotics results from overflow of

NO and overexpression of the endothelin B receptor with consequent pulmonary arteriolar

vasodilation and hypoxemia [17], [18].It is mostly relatively easy to fix after transplantation.

Portopulmonary hypertension is rare, yet its prevalence increases to 16-20% of patients with

refractory ascites. It is most likely brought on by an extra of pulmonary arteriolar

vasoconstrictors and profibrogenic aspects like TGFβ1 [19].The problem is considered

irreversible and a pulmonary artery pressure > 40 mmHg prevents liver transplantation

[20].Cirrhotic cardiomyopathy is defined by a blunted stress reaction of the heart, combined with

hypertrophy [21].Serious kinds raise postoperative mortality and preclude transplantation.

Hepatocellar Carcinoma

HCC is just one of the commonest solid body organ tumors around the world and cirrhosis is the

significant risk factor for progression to HCC [22-24].Other threat variables are listed in Table 2.

The pathogenic appears to be the advancement of regenerative nodules with little cell dysplasia

then invasive HCC. The mortality rate of HCC connected with cirrhosis is rising in most

developed regions, whereas mortality from non-HCC difficulties of cirrhosis is decreasing

[25].Cirrhosis due to HCV is connected with the greatest HCC occurrence in Japan compared

with the West, complied with by hereditary hemochromatosis (5-year cumulative occurrence 17-

30%). In cirrhosis due to HBV, the significant cause for HCC-related deaths in the world, the 5-

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year advancing incidence of HCC is 15% in high endemic locations and 10% in the West. 5-year

HCC incidence is reduced in alcoholic cirrhotics, or in patients with biliary cirrhosis (8% and 4%,

respectively). HCC is increasing in the USA, where its incidence had enhanced from 1.8 per

100,000 to 2.5 each 100,000 over one decade, mainly attributable to HCV infection [26].

Table 2.Risk factors for hepatocellular carcinoma

Cirrhosis Decompensated cirrhosis Viral Hepatitis B and C NASH Type 2 diabetes Aflatoxin exposure Co-infection with multiple viruses; HBV, HCV and HIV (risk 2-6 fold) Increasing Age Male Sex Positive family history of HCC Associated secondary alcohol abuse (risk 2-4 fold) or NASH as a co-factor

Screening for HCC is among the most important tasks in complying with patients with cirrhosis.

Present AASLD and EASL standards recommend a minimum of one yearly screening for HCC in

patients with cirrhosis using imaging with ultrasound, triphasic CT scan or gadolinium enhanced

MRI [22-24].Serum alfa-fetoprotein, which was an essential element of prior screening

algorithms, is no longer advised because of its bad sensitivity and specificity. As soon as HCC is

detected, several treatment modalities are offered that depend upon tumor size, tumor number and

local expertise. In the non-cirrhotic patient, surgical resection is a choice and could be alleviative.

However, most patients with cirrhosis will not tolerate liver resection or have tiny satellite

lesions, and the most effective option for cure is with liver transplantation. The Milan

requirements have suggested that the death and recurrence rate of HCC is acceptable if liver

transplant is performed for either a solitary tumor <5cm in diameter or no greater than 3 tumors

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with the largest being <3cm in diameter. Alternative treatments for HCC patients who do not

meet the criteria for surgical resection or transplant are radiofrequency ablation,

chemoembolization, alcohol ablation and cyberknife radiotherapy [22-24].Choice of these

modalities relies on regional expertise, and randomized tests suggesting that they enhance long

term survival are scarce.

• MANAGEMENT

The importance of identifying etiology in management

The identification of the reason underlying liver cirrhosis is essential in beginning preventive

measures and designing specific intervention.Table 3 reveals one of the most ideal tests for

etiologic medical diagnosis of cirrhosis. Anti-mitochondrial antibodies are certain for primary

biliary cirrhosis, HBV-DNA or HCV-RNA positivity for liver disease B or C, low serum

ceruloplasmin levels for Wilson's condition, and high serum ferritin and transferrin saturation

index for genetic hemochromatosis. Of note, liver cirrhosis could arise from existing side-by-side

etiologic aspects (i.e. alcohol and viral infection, weight problems and virus, etc.).

Table 3.Diagnostic tests, suggested etiology, and current treatment for the most frequent forms of liver cirrhosis in adult patients

Abnormal test(s) Etiology Treatment γGT (high), MCV (high) Alcohol Abstinence HBsAg, HBV-DNA, HBc-IgM, HDV-RNA (positivity)

HBV + Delta virus infection

Interferon α-2b, nucleoside (Lamivudine, Telbivudine, Entecavir) and nucleotide (Adefovir, Tenofovir) analogues

HCV-RNA (positivity) HCV infection Interferon plus ribavirin

γGT (high), alkaline phosphatase (high), AMA (positivity)

Primary biliary cirrhosis Ursodeoxycholate

ANA, ASMA, LKM (positivity) Autoimmune hepatitis Prednisone, azathioprine Ferritin (high), transferring saturation index (> 45%), liver iron content (high), HFE gene mutation for hereditary

Hemochromatosis Phlebotomy, deferoxamine

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hemochromatosis (C282Y, H63D) Ceruloplasmin (low), serum (low) and 24 h urine copper excretion (high)

Wilson’s disease D-penicillamine, zinc

HDL-cholesterol (low), glucose (high), triglycerides (high)

NAFLD/NASH Low caloric diet, exercise, drugs lowering insulin-resistance

AMA: Anti-mitochondrial antibody; ANA: Antinuclear antibody; ASMA: Anti-smooth-muscle antibody; γGT: γ- glutamyltransferase; HBV-DNA: Hepatitis B virus DNA; HCV-RNA: Hepatitis C virus RNA; HBsAg: Hepatitis B surface antigen; HDL: High density lipoprotein; HDV-RNA: Hepatitis delta virus RNA; LKM: Liver kidney microsomes; MCV: Mean corpuscular volume; NASH: Nonalcoholic steatohepatitis; NAFLD: Nonalcoholic fatty liver disease.

Liver Transplantation

Liver transplantation is thought about as a viable treatment option for patients with acute liver

failing and end-stage liver disease. In liver cirrhosis, transplantation is typically taken into

consideration when a patient has suffered from either a difficulty of portal hypertension or an

indication of endangered hepatic synthetic function [27]. However, provided the high costs,

mortality rate, and the paucity of donor organs, transplantation is presently justified just when it

comes to long-term prognosis, and psychological, intellectual, economic and family members

assistance. Appropriately, patients might be considered as current, future or unacceptable

candidates. Selection consists of a search for contraindications and PCPs are actively involved in

this procedure (i.e. alcohol and medicine usage) [28].Presently, patients are normally put on a

waiting listing once Child-Pugh class B or a MELD score of over 13 is reached [29].Start of

issues may prepare for referral, yet significantly decompensated or crippled patients are typically

discarded. Existing indications and relative and absolute contraindications to liver transplantation

are reported in Table 4.

Table 4.Current indications and contraindications to orthotopic liver transplantation in adult patients with liver cirrhosis.

Indications Contraindications Advanced chronic liver failure Relative Child-Pugh score > 7 HIV seropositivity

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Qualifying MELD score Methadone dependence Stage 3 hepatocellular carcinoma Acute liver failure Absolute Drug, toxins or virus induced fulminant hepatitis Extrahepatic malignant disease AIDS Cholangiocarcinoma Severe, uncontrolled systemic infection Multiorgan failure Advanced cardiopulmonary disease Active substance abuse General No alternative available treatment No absolute contraindications Willingness to comply with follow-up care and family assistance

AIDS: Acquired immunodeficiency syndrome; HIV: Human immunodeficiency virus; MELD: Model for end stage liver disease.

Monitoring alcohol and drug abuse

Alcoholic abuse causes 25% of liver cirrhosis and adds to one more 25% -50% of cases. PCPs

play a crucial duty in the application of long-lasting detoxification programs, therapy, assistance,

and surveillance. This step is critical, since recuperated abusers are taken into consideration for

antiviral treatment or transplantation just after 6 months of continual abstaining.

Ascites

Ascites is the most common difficulty and reason for a hospital stay of cirrhotic patients,

however it is also the difficulty which could be better treated in the house. Portal hypertension,

reduced albumin synthesis, decreased plasma oncotic pressure, and sodium retention are all

identifying aspects. Paracentesis generally eliminates a transudative liquid (i.e. albumin < 1 g/dL;

serum/ascites albumin gradient > 1.1). Patients exhibiting stomach discomfort, tense ascites and

fever could have a spontaneous bacterial peritonitis (SBP), a condition characterized by an ascitic

granulocyte matter going beyond 250/mm3. SBP could speed up cirrhosis in the direction of renal

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and liver failure. Treatment consists of high doses of albumin to prevent renal failing and

intravenous cefotaxime at dosages of 2 g twice a day. Long term prophylaxis of SBP recurrence

with norfloxacin is indicated in endured patients. Ascites is considered refractory if it continues

regardless of using diuretic medications at the maximum tolerable dosage. Although some

research studies indicate the utility of bed rest as a remedy, no controlled trials have been done in

support to this method. Therefore, preliminary therapy is dietary salt restriction [30], [31].

Treatment starts with spironolactone at dosages ranging from 100 to 400 mg/d. Furosemide might

be included (40 to 160 mg/d) when spironolactone does not successfully enhance fluid retention.

Weight needs to be monitored daily and electrolytes must be regularly checked. Albumin

infusion is required to prevent post-paracentesis blood circulation disorder [32] complying with

large quantity paracentesis [33].Such therapies can be handled by PCPs or in an incorporated care

system with expert professionals. Preventive measures consist of the evasion of NSAIDs, since

they advertise sodium retention. In the case of recurrent or refractory ascites, before taking into

consideration the patient for a transjugular intrahepatic portosystemic shunt (TIPS), large

quantity paracentesis is possible in the house. Paracentesis is secure and rarely speeds up

hepatorenal disorder. Patients with SBP or refractory ascites have an advanced condition with a

poorer prognosis, therefore require hospitalization. Patients and their family members have to be

educated the relevance of a day-to-day body weight check, and to refer FD when it increases by

2-4 kg over a short duration of monitoring.

Hepatorenal syndrome (HRS) is a life-threatening difficulty in patients with refractory ascites.

Medical diagnosis includes the following standards: innovative chronic liver failure with portal

hypertension; serum creatinine exceeding 1.5 mg/dL or a 24-h creatinine clearance of less

compared to 40 mL/min; absence of shock, continuous bacterial infection, or current treatment

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with nephrotoxic drugs; no sustained improvement in kidney function adhering to diuretic

withdrawal and the expansion of plasma volume with 1.5 L saline; much less compared to 500

mg/dL proteinuria and no ultrasonographic evidence of obstructive uropathy or parenchymal

kidney condition [34]. While awaiting transplantation, patients with HRS, eligible for

transplantation, could improve with medications, namely albumin, terlipressin, and vasoactive

drugs or TIPS [35].

Portal hypertension

Active variceal hemorrhage represent about one-third of all fatalities associated with cirrhosis.

Steps connected to the prevention and treatment of variceal hemorrhage consists of: prediction of

patients at risk, prophylaxis versus an initial bleed, treatment of an active bleed, and avoidance of

rebleeding. Diagnosing and treating portal hypertension is a way to stop esophageal variceal

bleeding, and PCPs may play an active function in this respect. Varices look must be checked by

upper endoscopy every 2-3 years, with a follow-up after 2 years for low-risk bleeding or yearly

for high-risk bleeding. Non-selective β-blockers are effective in minimizing the threat of blood

loss by reducing the relaxing heart rate by 25%.Endoscopic band ligation is indicated for patients

at risk of risky blood loss and for those who have already bled [36].TIPS is an alternative choice

for patients with formerly failed treatments [37].A current research study has shown that early

use TIPS is connected with significant decreases in treatment failing and death [38].

Hepatic encephalopathy

Hepatic encephalopathy is a chronically debilitating complication of hepatic cirrhosis and

incorporates a wide spectrum of potentially reversible neuropsychiatric abnormalities seen in

patients with liver dysfunction. This problem is considered as the start of brain disorder as a

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result of metabolic abnormalities, which happens consequently of liver failure. Hepatic

encephalopathy is mostly triggered by a lowered clearance of gut-deriving neurotoxins, and is a

possibly reversible condition ranging from refined personality modifications to coma, with

flapping tremor as a regular initial finding. PCPs should look for acid-base and electrolyte

disruptions, irregularity, infections, gastrointestinal bleeding, and inappropriate use of sedative

medicines. Treatment contains determining and correcting the speeding up aspects, colon

cleansing and acidification with lactulose. Dietary protein limitation is no more advocated

because it might facilitate malnutrition and the look of complications. Rifaximin, a minimally

taken in oral antibiotic, has an antimicrobial impact against enteric microorganisms and has

gotten authorization from the United States Food and Drug Administration for reducing the risk

of obvious hepatic encephalopathy reoccurrence. In a randomized, double-blind, placebo-

controlled trial, six-month rifaximin therapy at a dosage of 550 mg two times daily was compared

to a placebo in patients with chronic liver disease that were in remission from recurrent hepatic

encephalopathy. Rifaximin maintained remission more efficiently compared to the placebo as

well as significantly decreased the threat of hospitalization for hepatic encephalopathy

[39].Venous infusion of branched-chain amino acids or flumazenil may work when it comes to

comas. Patients might be taken care of in your home; admission to healthcare facility is booked

for those that are non-responsive after 12 h therapy.

Conclusion:

Cirrhosis has multisystem impacts and consequences. Numerous pulmonary changes could take

place as an outcome of cirrhosis. Patients with cirrhosis frequently have neurologic indications

and symptoms. One of the most common and most commonly recognized of these is hepatic

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encephalopathy. Patients with cirrhosis usually have abnormalities in systemic and pulmonary

circulation defined by increased cardiac output, associated with lowered systemic vascular

resistance and blood pressure. Extrahepatic manifestations need to be taken into factor to

consider when treating a cirrhotic patient to enhance clinical results. Although some extrahepatic

sequelae of cirrhosis may be reversible after liver transplantation, some may not, or presented the

clinical seriousness, some could endanger the feasibility of the transplant process. The utmost

treatment for cirrhosis and end phase liver disease is liver transplantation. The significant

problems that remain in the care of the patient post liver transplantation are recurrent disease in

the transplant, particularly HCV, and longterm consequences of immunosuppressive

representatives such as hypertension, hyperlipidemia and kidney illness.

Reference: 1. Wilt TJ, Shamliyan T, Shaukat A, Taylor BC, MacDonald R, Yuan JM, Johnson JR,

Tacklind J, Rutks I, Kane RL. Management of chronic hepatitis B. Evid Rep Technol Assess (Full Rep) 2008;(174):1–671.

2. Alazawi W, Cunningham M, Dearden J, Foster GR. Systematic review: outcome of compensated cirrhosis due to chronic hepatitis C infection. Aliment Pharmacol Ther. 2010;32:344–355.

3. Schwartz JM, Reinus JF. Prevalence and natural history of alcoholic liver disease. Clin Liver Dis. 2012;16:659–666.

4. Arroyo V, Fern´andez J, Gin ´es P. Pathogenesis and treatment of hepatorenal syndrome. Semin Liver Dis 2008;28:81–95.

5. Albillos A, Rossi I, Cacho G, Mart´ınez MV, Millan I, Abreu L, et al. Enhanced endothelium-dependent vasodilation in patients with cirrhosis. Am J Physiol 1995;268:459–464.

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6. Casta ˜neda B, Morales J, Lionetti R, Moitinho E, Andreu V, P ´erez-Del-Pulgar S, et al. Effects of blood volume restitution following a portal hypertensiverelated bleeding in anesthetized cirrhotic rats. Hepatology 2001;33:821– 825.

7. Tandon P, Garcia-Tsao G. Bacterial infections, sepsis, and multiorgan failure in cirrhosis. Semin Liver Dis 2008;28:26–42.

8. Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology. 2001;120:726–48.

9. Bosch J, Garcia-Pagan JC. Prevention of variceal rebleeding. Lancet. 2003;361:952–4. 10. de Franchis R, Dell’Era A, Iannuzzi F. Diagnosis and treatment of portal

hypertension. Dig Liver Dis. 2004;36:787–98. 11. Boyer TD. Transjugular intrahepatic portosystemic shunt: current

status. Gastroenterology. 2003;124:1700–10. 12. Gines P, Cardenas A, Arroyo V, Rodes J. Management of cirrhosis and ascites. N Engl J

Med. 2004;350:1646–54. 13. Gines P, Guevara M, Arroyo V, Rodes J. Hepatorenal syndrome. Lancet. 2003;362:1819–

27. 14. Butterworth RF. Complications of cirrhosis III. Hepatic encephalopathy. J

Hepatol. 2000;32(1 Suppl):171–80. 15. Riordan SM, Williams R. The intestinal flora and bacterial infection in cirrhosis. J

Hepatol. 2006;45:744–57. 16. Papatheodoridis GV, Patch D, Webster GJ, Brooker J, Barnes E, Burroughs AK. Infection

and hemostasis in decompensated cirrhosis: a prospective study using thrombelastography. Hepatology. 1999;29:1085–90.

17. Arguedas MR, Abrams GA, Krowka MJ, Fallon MB. Prospective evaluation of outcomes and predictors of mortality in patients with hepatopulmonary syndrome undergoing liver transplantation. Hepatology. 2003;37:192–7.

18. Fallon MB. Mechanisms of pulmonary vascular complications of liver disease: hepatopulmonary syndrome. J Clin Gastroenterol. 2005;39(4 Suppl 2):S138–42.

19. Blendis L, Wong F. Portopulmonary hypertension: an increasingly important complication of cirrhosis. Gastroenterology. 2003;125:622–4.

20. Colle IO, Moreau R, Godinho E, et al. Diagnosis of portopulmonary hypertension in candidates for liver transplantation: a prospective study. Hepatology. 2003;37:401–9.

21. Gaskari SA, Honar H, Lee SS. Therapy insight: Cirrhotic cardiomyopathy. Nat Clin Pract Gastroenterol Hepatol. 2006;3:329–37.

22. Bruix J, Sherman M, Llovet JM, et al. Clinical management of hepatocellular carcinoma. Conclusions of the Barcelona-2000 EASL conference. European Association for the Study of the Liver. J Hepatol. 2001;35:421–30.

23. Llovet JM, Burroughs A, Bruix J. Hepatocellular carcinoma. Lancet. 2003;362:1907–17. 24. Sherman M, Klein A. AASLD single-topic research conference on hepatocellular

carcinoma: Conference proceedings. Hepatology. 2004;40:1465–73.

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25. Fattovich G, Stroffolini T, Zagni I, Donato F. Hepatocellular carcinoma in cirrhosis: Incidence and risk factors. Gastroenterology. 2004;127(5 Suppl 1):S35–50.

26. El-Serag HB. Hepatocellular carcinoma and hepatitis C in the United States. Hepatology. 2002;36:S74–83.

27. Steinman TI, Becker BN, Frost AE, Olthoff KM, Smart FW, Suki WN, Wilkinson AH; Clinical Practice Committee, American Society of Transplantation. Guidelines for the referral and management of patients eligible for solid organ transplantation. Transplantation. 2001;71:1189–1204.

28. Heidelbaugh JJ, Sherbondy M. Cirrhosis and chronic liver failure: part II. Complications and treatment. Am Fam Physician. 2006;74:767–776.

29. Wiesner R, Edwards E, Freeman R, Harper A, Kim R, Kamath P, Kremers W, Lake J, Howard T, Merion RM, Wolfe RA, Krom R; United Network for Organ Sharing Liver Disease Severity Score Committee. Model for end-stage liver disease (MELD) and allocation of donor livers. Gastroenterology. 2003;124:91–96.

30. Kashani A, Landaverde C, Medici V, Rossaro L. Fluid retention in cirrhosis: pathophysiology and management. QJM. 2008;101:71–85.

31. Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology. 2004;39:841–856.

32. Ginès A, Fernández-Esparrach G, Monescillo A, Vila C, Domènech E, Abecasis R, Angeli P, Ruiz-Del-Arbol L, Planas R, Solà R, et al. Randomized trial comparing albumin, dextran 70, and polygeline in cirrhotic patients with ascites treated by paracentesis. Gastroenterology. 1996;111:1002–1010.

33. Gentilini P, Bernardi M, Bolondi L, Craxi A, Gasbarrinie G, Ideo G, Laffi G, La Villa G, Salerno F, Ventura E, et al. The rational use of albumin in patients with cirrhosis and ascites. A Delphi study for the attainment of a consensus on prescribing standards. Dig Liver Dis. 2004;36:539–546.

34. Arroyo V, Ginès P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, Reynolds TB, Ring-Larsen H, Schölmerich J. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. Hepatology. 1996;23:164–176.

35. Runyon BA. AASLD Practice Guidelines Committee. Management of adult patients with ascites due to cirrhosis: an update. Hepatology. 2009;49:2087–2107.

36. Sarin SK, Lamba GS, Kumar M, Misra A, Murthy NS. Comparison of endoscopic ligation and propranolol for the primary prevention of variceal bleeding. N Engl J Med. 1999;340:988–993.

37. Grace ND. Diagnosis and treatment of gastrointestinal bleeding secondary to portal hypertension. American College of Gastroenterology Practice Parameters Committee. Am J Gastroenterol. 1997;92:1081–1091. 40. García-Pagán JC, Caca K, Bureau C, Laleman W, Appenrodt B, Luca A, Abraldes JG, Nevens F, Vinel JP, Mössner J, Bosch J; Early TIPS (Transjugular Intrahepatic Portosystemic Shunt) Cooperative Study Group. Early

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use of TIPS in patients with cirrhosis and variceal bleeding. N Engl J Med. 2010;362:2370–2379.

38. Bass NM, Mullen KD, Sanyal A, Poordad F, Neff G, Leevy CB, Sigal S, Sheikh MY, Beavers K, Frederick T, et al. Rifaximin treatment in hepatic encephalopathy. N Engl J Med. 2010;362:1071–1081.

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