Alkohoolne hepatiit

Alkohoolne hepatiit kujuneb meestel pikaaegsel 60-80 g alkoholi tarvitamisel päevas. Naistel piisab vähemast. Peamiselt on meestel, sest nendel on alkoholi kuritarvitamine suurem. Alkohoolne hepatiit võib esineda nii koos kui ka ilma alkohoolse maksatsirroosita.

Keskmine aste maksa alkoholtõvel. Sellest kergem on alkohoolne rasvmaks ja raskem alkohoolne tsirroos.

* Kokkuvõte
* Mälupalee

## Diagnoos

Tuleb tuvastada patsiendi alkoholitarve. Selle selgitamiseks kasuta küsimusi: Kas pole suutnud kontrollida alkot. Kas tunned süüdi, et liiga palju. Kas inimesed tihti ütlevad, et peaks vähendama. Kas kasutad hommikuti peatervendust. 2 = positiivne.

### Kaebused

Tavaliselt esinevad ebaspetsiifilised sümptomid nagu iiveldus/oskendamine, anoreksia, kaalulangus, nõrkus ja subfebriilne palavik. Tõsisematel juhtudel, kui sümptomeid indutseerivad maksafunsktiooni häriest tulenevad portaalhüpertensioon, võib esineda astsiit, GI veritsus, entsefalopaatia (segadus, letargia).

Kui patsient pöördub suure alkoholi tarbe järel häirunud vaimse seisundi või persisteeruva oksendamisega, peaks välistama ka subduraalset hematoomi, ägedat pankreatiiti või GI veritsust. Lisaks sellele hindama ärajäämanähtude (krambid, delirium tremens) ilmnemist.

### Objektiivne leid

Sõltub kaasuvatest haigustest objektiivne leid, portallhüpertensioon või tsirroos võivad anda ikteruse, spleonmegaalia, hüpogonadismi, palmaarse erüteemi.

Tavaliselt esineb palavik ja tahhükardia. Võib esineda ka kerge tahhüpnea primaarse respiratoorse alkaloosiga. Maks on palpatsioonil tundlik ja suurenenud (steatoos ja kahjustusest tulenev turse).

Portaalhüpertensioonist tulenevad sümptomid on ikteerilised skleerad, tume uriin, splenomegaalia, asterixis, perifeersed tursed ja astsiit.

Tsirroosistaadiumis haigel võib leida ämblikangioome, proksimaalsed lihasatroofiat, günekomastiat.

### Analüüsid

Laborianalüüsides esineb transaminaaside tõus (AST rohkem) kuni 10x, kaasneva paratsetamoolitoksilisusega isegi rohkem. Saab kasutada prognoosiks igast skoore. INR korreleerub tõsiduse astmega. Täpsustamiseks UH. GGT, AST:ALT suhe. Alkohoolse geneesi kahtlusi kinnitab mitokondriaalne AST.

#### Approach Considerations

Kui anamneesis on selge alkohoolne taust ja esineb tüüpiline kliiniline pilt, siis ei ole vaja lisauuringuid. Kergematel juhtudel on abi AST elevatsioonist. Uuringute andmeil on CRV täpne marker. Elektrolüütide kõrvalkalded võivad tekkida oksendamisest, portaalhüpertensioonist koos vähenenud ringleva vere mahuga, alkohoolsest ketoatsidoosist või respiratoorset alkaloosist. Alatoitumisest võivad tekkida hüpofosfateemia ja hüpomagneseemia.

Piltdiagnostika ei ole üldjuhul diagnoosiks vajalik, ent aitab välistada teisi põhjuseid. UH uuring on kõige levinum madala hinna, mitteinvasiivsuse ja laia kättesaadavuse tõttu. KT ja MRT võib kaaluda ainult maksavähi diagnoosi kahtlusel.

#### Complete Blood Count

Kliinilise vere analüüsis võib esineda nõrk-mõõdukas neutrofiilne leukotsütoos. Kuna alkhohol on otsene luuüdi supresseerija, siis võib ilmneda aneemiat MCV tõusuga. Trombotsütoos esineb põletikulise vastunena, samas trombotsütopeenia võib ilmneda läbi põrnast tuleneva trombotsüütide sekvestratsiooni.

Biokeemia maksa analüüsides esineb mõõdukas AST tõus, kuid ALT püsib referentsväärtuses või on vähesel määral tõusnud (vastupidine teistele maksahaigustele). AST/ALT suhe üle 1 viitab alkohoolsele geneesile. Samas ei tohiks AST väärtused olla tugevalt tõusnud (>500 U/L), vastasel juhul peaks mõtlema alternatiivsele diagnoosile (viraalne, ravim-indutseeritud)

võib olla näidustatud B-hepatiidi ja C-hepatiidi test

#### Screening Blood Tests

Screening blood tests to exclude other conditions (appropriate in any patient with alcoholic hepatitis) may include the following:

* Hepatitis B surface antigen (HBsAg) detects hepatitis B
* Anti–hepatitis C virus by enzyme-linked immunosorbent assay (ELISA) detects hepatitis C
* Ferritin and transferrin saturation detect hemochromatosis
* Marked elevation of aminotransferase levels should raise concern for viral hepatitis or drug hepatotoxicity; in particular, people who are alcoholics may develop severe liver necrosis from standard therapeutic doses of acetaminophen
* Rapid deterioration of liver function (see Liver Tests) should raise the possibility of hepatocellular carcinoma (HCC), which can be tested for by determination of alpha-fetoprotein (AFP) levels as well as findings on an imaging study of the liver
* Jaundice with fever can be caused by gallstones producing cholangitis and is suggested by a disproportionate elevation of the alkaline phosphatase (ALP) level

#### Liver Tests

An AST/ALT ratio greater than 1 is almost universal in persons with alcoholic hepatitis. Even in severe disease, the elevations of aminotransferase levels are modest, and an AST level greater than 500 U/L should raise suspicion of an alternative diagnosis. An AST/ALT ratio greater than 1 may accompany cirrhosis of any cause and, therefore, is less diagnostically specific in the setting of cirrhosis.

Alkaline phosphatase (ALP) level elevations are typically mild in persons with alcoholic hepatitis. Levels greater than 500 U/L occur in a small percentage of patients, but abnormalities of this magnitude suggest a coexisting infiltrative or biliary obstructive process.

The gamma-glutamyl transpeptidase (GGTP) level is elevated markedly by alcohol use. Although a normal value helps to exclude alcohol as a cause of liver disease, an elevated level is of no value in distinguishing between simple alcoholism and alcoholic hepatitis.

##### Liver function tests

Common liver function tests include albumin level, bilirubin level, and prothrombin time (PT). Hypoalbuminemia occurs because of decreased hepatic synthetic function and coexisting protein-energy malnutrition (PEM). Hyperbilirubinemia is typically a mixture of unconjugated and conjugated bilirubin, with the latter predominating. Bilirubinuria is normally present in patients who are icteric. Coagulopathy predominantly affects the extrinsic pathway of coagulation (measured by PT). It is usually unresponsive to vitamin K.

The severity of hyperbilirubinemia and coagulopathy reflects the severity of alcoholic hepatitis and is of prognostic value.

##### Serum biomarkers

*Ash test*

The diagnostic value of serum biomarkers, such as the Ash test (ie, the 6 components of the FibroTest-ActiTest plus AST), was tested and validated in 275 patients with alcoholic hepatitis.[18]Both the sensitivity and the specificity of the Ash test in predicting alcoholic steatohepatitis were impressive (0.80 and 0.84, respectively).[18]

### Uuringud

Histoloogia on mõttekas võtta, see aitab ka diferentsida, ega tegu pole Wilsoni tõvega (seerumi tseruloplasmiin langenud), päriliku hemokromatoosiga (raud tõusnud), HCV (anti HCV).
Biopsial tavaliselt perilobulaarsed ja tsentrilobulaarsed PMN infiltraadid ja hepatotsüütide turse. Spetsiifilised on Mallory kehade esinemine koos PMN-ga ja megamitokondritega.

#### Ultrasonography

In general, real-time ultrasonography is the preferred imaging study in evaluating patients with suspected alcoholic hepatitis, because it is inexpensive, noninvasive, and widely available. This modality provides a good evaluation of the liver and other viscera, and it permits guided liver biopsy.

On ultrasonograms, the liver in patients with alcoholic hepatitis appears enlarged and diffusely hyperechoic. Features suggestive of coexistent portal hypertension and/or cirrhosis include the presence of varices, splenomegaly, and ascites.

Ultrasonography is also helpful in excluding gallstones, bile duct obstruction, and hepatic or biliary neoplasms. Jaundice with fever can be caused by gallstones producing cholangitis; ultrasonographic examination of the abdomen is usually sufficient to exclude this possibility. However, if stones are found or fever persists, cholangiography may be necessary.

Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma, which can be tested for by performing imaging studies (eg, ultrasonography, computed tomography [CT] scanning, magnetic resonance imaging [MRI]) of the liver.

#### Liver Biopsy

Liver biopsy is not always required in the evaluation of alcoholic hepatitis, but it may be useful in establishing the diagnosis, in determining the presence or absence of cirrhosis, and in excluding other causes of liver disease.

The 2010 American Association for the Study of Liver Diseases (AASLD) alcoholic liver disease (ALD) practice guideline recommends considering liver biopsy for patients whose diagnosis is reasonably uncertain and for patients likely to undergo medical treatment for severe alcoholic hepatitis. The risk of performing the biopsy should be weighed against the risk associated with the probable course of therapy, or the possible risk of an investigational treatment.[3]

##### Percutaneous liver biopsy

Percutaneous biopsy can be performed at the bedside by an experienced practitioner, usually a gastroenterologist or a hepatologist. Real-time ultrasonographic guidance may be desirable to optimize the biopsy site selection and to reduce the risk of complications.

Usually, a biopsy should be avoided in the presence of severe thrombocytopenia or coagulopathy because of the risk of serious (possibly fatal) hemorrhage.

##### Transjugular liver biopsy

If biopsy information is considered essential and the risk of percutaneous biopsy appears excessive, an alternative approach is to perform a biopsy angiographically via a catheter passed into the hepatic vein under fluoroscopic guidance. In principle, the risk of hemorrhage should be reduced, because the puncture site is contained within the venous system.

At the time of transjugular liver biopsy, the angiographer can determine the transhepatic venous pressure gradient. In alcoholic hepatitis and cirrhosis, the pressure measurement obtained with a catheter wedged retrograde in a branch of the hepatic vein accurately reflects the portal venous pressure.

#### Histologic Features

In alcoholic hepatitis, liver injury is characteristically most prominent in the centrilobular (perivenular) areas (zone 3 of Rappaport). Hepatocytes exhibit ballooning with necrosis. Focal accumulation of polymorphonuclear leukocytes, as shown in the image below, is noted in the areas of injury. Lymphocytes may also be present, especially in the portal tracts.

Ropy eosinophilic hyaline inclusions termed Mallory bodies may be observed in the perinuclear cytoplasm. With electron microscopy, Mallory bodies may be observed to be composed of fibril clumps that histochemically are identifiable as intermediate filaments. Mallory bodies are characteristic of alcoholic hepatitis, but are not always present, and occasionally, they can be observed in a variety of other disorders.

Macrovesicular steatosis, perivenular fibrosis, and frank cirrhosis commonly coexist with alcoholic hepatitis.

### Diferentsiaaldiagnoosid

Common considerations in alcoholic patients with jaundice include chronic pancreatitis with biliary strictures and pancreaticobiliary neoplasms.

A disorder histologically resembling alcoholic hepatitis can occur in patients who do not use alcohol. This syndrome, termed nonalcoholic steatohepatitis (NASH), is being recognized with increasing frequency. It occurs most frequently in the setting of obesity, hyperlipidemia, or type 2 diabetes mellitus. NASH is also observed in the setting of chronic parenteral hyperalimentation and in individuals who undergo jejunoileal bypass surgery for treatment of obesity. In most cases, NASH is indolent; however, in some individuals, it may progress insidiously to cirrhosis. NASH is currently believed to be responsible for a large fraction of cases of what was previously termed cryptogenic cirrhosis. In most patients with NASH, the ratio of aspartate aminotransferase (AST) to alanine aminotransferase (ALT) is less than 1, unless cirrhosis is present.

Changes in the mental status of patients with alcoholic hepatitis do not always imply the presence of hepatic encephalopathy. Other conditions (eg, subdural hematomas) should be excluded by obtaining a computed tomography (CT) scan of the brain.

#### Differential Diagnoses

* Chronic Pancreatitis
* Hepatitis B
* Hepatitis C

### Tüsistused

Sagedasemad: Portaalhüpertensioon, söögitoru vaariksite verejooks, astsiit, entsefalopaatia, hepatorenaalne sündroom ja spontaanne bakteriaalne peritoniit. Maks suurenenud

#### Medscape

The long-term prognosis of individuals with alcoholic hepatitis depends heavily on whether patients have established cirrhosis and whether they continue to drink. With abstinence, patients with this disease exhibit progressive improvement in liver function over months to years, and the histologic features of active alcoholic hepatitis resolve. If alcohol abuse continues, alcoholic hepatitis invariably persists and progresses to cirrhosis over months to years. In one study, the estimated 5-year survival after hospitalization for severe alcoholic hepatitis was 31.8%. Abstinence was the only independent predictor of long-term survival.[9]

Mild alcoholic hepatitis is a benign disorder with negligible short-term mortality. However, when alcoholic hepatitis is of sufficient severity to cause hepatic encephalopathy, jaundice, or coagulopathy, mortality can be substantial.

The overall 30-day mortality rate in patients hospitalized with alcoholic hepatitis is approximately 15%; however, in patients with severe liver disease, the rate approaches or exceeds 50%. In those lacking encephalopathy, jaundice, or coagulopathy, the 30-day mortality rate is less than 5%. Overall, the 1-year mortality rate after hospitalization for alcoholic hepatitis is approximately 40%.

In one study, the overall mortality among patients with severe alcoholic hepatitis was 66%. Age, white blood cell (WBC) count, prothrombin time (PT), and female sex were all independent risk factors for the dismal outcome.[10]

*Model for end-stage liver disease (MELD) score*

Several retrospective studies have shown that the MELD score is useful in predicting the 30- and 90-day mortality in patients with alcoholic hepatitis (see the MELD Score calculator). Moreover, the MELD score seems to contain some practical and statistical advantages over Maddrey's DF in predicting mortality among these patients. In a cohort of 73 patients with alcoholic hepatitis at the Mayo Clinic, the MELD score was the only independent predictor of mortality.[12]Likewise, in another much larger retrospective study of 202 patients with alcoholic hepatitis, the MELD score was found superior to not only Maddrey's DF but also to the classic Child-Turcotte-Pugh (CTP) score.[13]

*Glasgow alcoholic hepatitis score (GAHS)*

The GAHS is one of the most recently described predictors of outcome in patients with alcoholic hepatitis. This scoring system uses 5 different variables, including age, bilirubin level, blood urea nitrogen (BUN) level, PT, and WBC count. The overall accuracy of GAHS, which was validated in 195 patients with alcoholic hepatitis, was 81%, when predicting 28-day outcome.[14]In contrast, the modified DF had an overall accuracy of only 50%.[14]

## Ravi

Alkoholi tarbimine lõpetada. Sel juhul paljudel paraneb seisund 6 kuu jooksul, kuid tesitel ei aita üldse. 5 aasta elulemus 60%. Kes jätkavad on 5 aasta elulemus 30%

Dieet korda, võimalik et vältida valke, eriti kui entsefalopaatia. Ei tohi olla alatoitunud

### Farmakoloogiline

Ravi on peamiselt toetav!

Tuleb ravida vajadusel tüsistusi.

Kortikosteroidid tõsisema haiguspildi(entsefalopaatia, GI veritsuse) korral abiks

Pentoksifülliin TNF-a Kuppferi rakude oma - aitab.

### Muu ravi

Transplantatsoon on võimalik, kuid vastuoluline. Igal juhul peab 6 kuud tilkagi mitte jooma.

### Medscape

#### Approach Considerations

In most patients with alcoholic hepatitis, the illness is mild. The short-term prognosis is good, and no specific treatment is required. Hospitalization is not always necessary. Alcohol use must be stopped, and care should be taken to ensure good nutrition; providing supplemental vitamins and minerals, including folate and thiamine, is reasonable. Patients who are coagulopathic should receive vitamin K parenterally. Anticipate symptoms of alcohol withdrawal, and manage them appropriately.

In contrast, patients with severe acute alcoholic hepatitis are at a high risk of early death, at a rate of 50% or greater within 30 days. In multiple studies, the strongest factor predictive of short-term mortality was hepatic encephalopathy. In some studies, a combination of hyperbilirubinemia and coagulopathy has also been found to independently predict a high short-term mortality rate. Individuals with these findings or with other complications, such as azotemia or gastrointestinal bleeding, should be hospitalized. Usually, observing the patient in an intensive care unit (ICU) until liver function is stable and the patient is clinically improving is prudent.

Patients with severe alcoholic hepatitis may benefit over the short term from specific therapies directed toward reducing liver injury, enhancing hepatic regeneration, and suppressing inflammation. Glucocorticosteroids are widely used for this purpose, although their benefits have not been proven unequivocally. Various other treatments remain experimental. For the long term, goals include improvement of liver function, prevention of progression to cirrhosis, and reduction of mortality. Only prolonged alcohol abstinence is of demonstrated benefit in all these areas.

Among future therapeutic directions, gene therapy is perhaps the most appealing modality. Various genes involved in hepatic fibrogenesis, inflammatory response, and oxidative stress are overexpressed in alcoholic hepatitis. Moreover, some candidate genes correlate well with the histologic findings and disease severity, thus suggesting that they may be potential targets for such therapy.[21]

#### Surgical considerations

Patients with acute alcoholic hepatitis are at a high risk of developing hepatic failure following general anesthesia and major surgery. Because postoperative mortality rates are high, surgery should be avoided in the setting of acute alcoholic hepatitis unless it is absolutely necessary. If patients remain abstinent, alcoholic hepatitis usually resolves over time, permitting surgery to be undertaken with a substantially reduced risk.

#### Transfer

Patients with alcoholic hepatitis of mild to moderate severity can be treated in a primary care setting. In general, for patients with severe alcoholic hepatitis or cirrhosis, observation by a gastroenterologist or a hepatologist is desirable, particularly if the illness is of sufficient severity or complexity to require intensive care.

If patients become comatose or have complications that may require surgical intervention, the treating physician should consider emergent transfer to a tertiary care center with experience in the treatment of liver failure. In selected cases, the use of novel liver-assist devices (artificial livers) may provide transient improvement in the manifestations of liver failure.

#### Cessation of Alcohol Intake

Cessation of alcohol use is the mainstay of treatment of alcoholic hepatitis. The 2010 American Association for the Study of Liver Diseases (AASLD) alcoholic liver disease (ALD) guideline states that complete abstinence should be enjoined on all alcoholic hepatitis patients.[3]

In general, alcoholic hepatitis resolves or improves greatly following 6-12 months of alcohol abstinence, and continued improvement may be observed for several years. Mild alcoholic hepatitis often resolves completely, but, following severe alcoholic hepatitis, residual cirrhosis can usually be demonstrated. If alcohol abuse persists, alcoholic hepatitis invariably persists and progresses to cirrhosis, and the prognosis is dramatically worse.

Some experts have questioned whether complete abstinence is necessary or whether reduced amounts of alcohol would be sufficient for recovery in most patients. Given the addictive nature of alcohol in most patients who use it heavily, counseling complete abstinence is prudent. Patients should be referred to a program of rehabilitation and support, and they should be strongly encouraged to attend. Also, patients should be fully informed regarding the serious potential health consequences of continued ethanol use.

#### Diet and Nutritional Support

For patients with milder alcoholic hepatitis, a general diet containing 100 g/d of protein is appropriate. Provide supplemental multivitamins and minerals, including folate and thiamine. Salt restriction may be required in patients with ascites.

Additional treatment includes nutritional support. The 2010 American Association for the Study of Liver Diseases (AASLD) alcoholic liver disease (ALD) guideline recommends testing all patients with alcoholic hepatitis for protein-energy malnutrition (PEM) and for vitamin and mineral deficiencies.[3]

Protein-energy malnutrition is almost universal in patients hospitalized for alcoholic hepatitis. In a large Veterans Administration Cooperative Study of Alcoholic Hepatitis, the severity of protein-energy malnutrition correlated with the severity of alcoholic hepatitis and the predicted mortality rate.[22]In patients with alcoholic hepatitis and severe protein-energy malnutrition, the mortality rate was 50%, compared with a mortality rate of less than 10% in patients with mild protein-energy malnutrition.[22]

##### Oral intake vs parenteral/enteral hyperalimentation

Some studies have suggested that improved energy and protein intake may improve the survival rate in patients with severe alcoholic hepatitis. However, complications associated with parenteral hyperalimentation (eg, sepsis, hemothorax) or enteral hyperalimentation (eg, aspiration pneumonia) may outweigh the benefits of these approaches. Thus, if patients are able to take food orally, this is the route of choice, and formal nutritional support can be reserved for those instances in which patients are unable to ingest enough by mouth to meet their needs. Energy (caloric) intake should be carefully measured to ensure adequate consumption. The use of nutritional supplements and appetite stimulants may be appropriate.

The 2010 AASLD ALD guideline states that patients with advanced disease should receive aggressive enteral nutritional therapy.[3]Patients with mild to moderate alcoholic hepatitis (Maddrey discriminant function [MDF] score <32, no liver encephalopathy) that improves during the first week of hospitalization (ie, lower serum bilirubin level or decreased MDF) and who are treated with nutritional therapy and abstinence will probably neither need nor benefit from other interventions, but these individuals should be monitored closely.[3]

##### Protein restriction vs normal protein intake

Except in patients with severe encephalopathy, protein restriction is unnecessary and should be avoided because a protein-deficient diet impairs liver regeneration and worsens liver function. Even in the presence of hepatic encephalopathy, patients are usually able to ingest a minimum of 60-100 g/d of dietary protein if other measures to control encephalopathy have been aggressively pursued. In rare instances, restricting dietary proteins may be necessary. In these cases, alternatives include provision of high-quality protein via the parenteral route or provision of oral amino acid supplements that are selectively enriched with branched-chain amino acids.

#### Pharmacotherapy

Use of medications in alcoholic hepatitis has been considered controversial. Many treatments discussed in the Medication section are still investigational.[23]However, according to the 2010 American Association for the Study of Liver Diseases (AASLD) alcoholic liver disease (ALD) guideline[3]: (1) Naltrexone or acamprosate may be used, in addition to counseling, to assist patients who have achieved abstinence to avoid relapsing; and (2) in patients with severe disease (Maddrey discriminant function [MDF] score ≥32), unless steroids are contraindicated, prednisolone should be considered. Pentoxifylline may be considered, especially if prednisolone cannot be used.

Prednisolone and pentoxifylline are recommended for the treatment of severe alcoholic hepatitis,[1]but uncertainty about their benefit persists.

Results of the Steroids or Pentoxifylline for Alcoholic Hepatitis (STOPAH) trial involving 1,103 subjects showed that treatment with the steroid prednisolone reduced 28-day mortality in patients with severe alcoholic hepatitis, whereas treatment with the oral phosphodiesterase inhibitor pentoxifylline did not.[24, 25] However, the benefit of prednisolone did not extend beyond 28 days. There was no difference in the mortality rates between the two treatments at 1 year. Mortality at 28 days was 13.5% with prednisolone and pentoxifylline combined, 14.3% with prednisolone and placebo, 19.4% with pentoxifylline and placebo, and 16.7% with double placebo. For all patients treated with prednisolone, the mortality rate was 13.9%; for those treated only with pentoxifylline or placebo, the rate was 18.0%. Mortality rates were similar in patients who received pentoxifylline treatment (16.4%) and those who did not (15.5%).[24, 25]

Significant predictors of 28-day mortality included prednisone use, prothrombin time ratio, bilirubin level, age, white blood cell count, urea level, creatinine level, and hepatic encephalopathy.[24, 25]Neither treatment was significantly associated with a survival benefit beyond 28 days. Infections were significantly more frequent in the prednisolone group than in the no-prednisolone group. Patients who did not reduce or increased their alcohol use had a 3-fold increased risk of death compared with those who abstained.[24, 25]

Tort claims regarding steroid-induced aseptic necrosis of the hip are very common. Physicians treating patients with alcoholic hepatitis for longer than the recommended period should discuss the issue with the patient and the patient's family, and obtain consent. Patients with mild forms of alcoholic hepatitis should not be treated with steroids.

#### Liver Transplantation

Orthotopic liver transplantation is widely used in patients with end-stage liver disease.[26, 1]Most patients with active alcoholic hepatitis are excluded from transplantation because of ongoing alcohol abuse. In most liver transplantation programs in the United States, patients must abstain from alcohol for at least 6 months before they can be considered for transplantation, and a thorough psychosocial evaluation must demonstrate that patients have a low likelihood of reverting to alcohol abuse.

Patients with alcoholic hepatitis may be informed that their liver injury can be expected to subside, and liver function will improve following at least 6 months of abstinence. If they still develop cirrhosis and its complications, they can be considered for transplantation if they remain committed to sustained abstinence. The prospect of liver transplantation can be a powerful motivational tool for encouraging abstinence.

##### Challenges to liver transplantation policies

Current policies pertaining to liver transplantation in patients with end-stage alcoholic liver disease (ie, cirrhosis), especially those with severe alcoholic hepatitis, have been challenged.[27, 28]

First, the societal aspects of the issue (ie, the public perception and reservation regarding the use of donated livers for self-inflicted disease) should not be any different than those of intravenous (IV) drug addicts with the hepatitis C virus or even the fast-food generation of obese persons with nonalcoholic steatohepatitis (NASH).

Second, the current fixed interval of ethanol abstinence, often at the behest of third-party payers, as a prerequisite for transplantation remains controversial as a predictor of future alcoholic relapse (ie, recidivism).[29, 30]

Finally, other investigators have proposed the conduct of pilot studies, on only a small cohort of patients, to determine whether liver transplantation improves the survival of patients with severe alcoholic hepatitis.[31]

##### 2010 AASLD ALD recommendation

The recommendation of the 2010 American Association for the Study of Liver Diseases (AASLD) alcoholic liver disease (ALD) guideline report is that patients with end-stage alcoholic liver disease be evaluated for liver transplantation in the same way as other possible candidates, after medical and psychosocial factors have been carefully evaluated.[3]A formal assessment of the probability of long-term abstinence should be included in the evaluation.[3]

#### Consultations

Largely, mild and moderate alcoholic hepatitis can be managed on a hospital medical floor, requiring only a brief hospital stay. In fact, patients with the mildest forms of the disease may never seek medical attention, or they can be treated safely in outpatient settings. By contrast, severe acute alcoholic hepatitis requires intensive medical care and often a multidisciplinary approach.

##### Nutrition services and gastroenterology/hepatology

Adequate nutritional support is of paramount importance for the survival and recovery of patients with alcoholic hepatitis. The complexity of the disease and the wide variation in nutritional regimens and modalities mandate consultation with a nutritionist. Customarily, the gastroenterology service of the hospital should be able to handle this issue and should be instrumental in treatment.

In patients with alcoholic hepatitis who have developed cirrhosis, especially those with coexistent chronic viral hepatitis B or C, consider periodic surveillance for hepatocellular carcinoma. A common algorithm includes the determination of serum alpha-fetoprotein (AFP) levels at 6-month intervals along with annual diagnostic ultrasonography. The finding of a liver nodule or an elevated AFP level should lead to referral to a liver specialist and additional diagnostic studies.

In general, for patients with severe alcoholic hepatitis or cirrhosis, observation by a gastroenterologist or a hepatologist is desirable, particularly if the illness is of sufficient severity or complexity to require intensive care.

##### Nephrology

The onset of acute renal failure may indicate the development of hepatorenal syndrome or, alternatively, an episode of acute tubular necrosis resulting either from the use of nephrotoxic drugs or from acute intravascular volume changes. In these instances, obtaining consultation with a nephrologist is advisable.

##### Neurology

If a patient with alcoholic hepatitis exhibits mental status changes, focal neurologic findings, or seizures, consider consultation with a neurologist.

##### Infectious disease

The fever and leukocytosis that accompany alcoholic hepatitis often raise concerns regarding possible sepsis or other infectious processes. Routine evaluation with urinalysis, chest radiography, and cultures of blood and urine is appropriate, and findings from these tests are usually negative. If concerns persist, consultation with an infectious disease specialist is appropriate.

#### Long-Term Monitoring

In the absence of complications, patients generally can be discharged from acute medical inpatient care facilities once alcohol withdrawal symptoms have cleared; liver function has begun to improve; and the complications of liver failure, such as encephalopathy, have resolved with appropriate treatment.

In patients who have a potential for rehabilitation, transferring them to an inpatient substance abuse treatment program rather than discharging them from the hospital may be appropriate.

Patients recently discharged from the hospital following an acute bout of alcoholic hepatitis should generally be observed within 2 weeks of their discharge. Subsequent periodic follow-up visits, at intervals ranging from weeks to several months, are appropriate to monitor patients' responses to treatment, including obtaining electrolyte levels and liver test results, and to encourage sobriety.

In patients with alcoholic hepatitis who have developed cirrhosis, especially those with coexistent chronic viral hepatitis B or C, consider periodic surveillance for hepatocellular carcinoma. A common algorithm includes determination of the serum alpha-fetoprotein (AFP) level at 6-month intervals along with annual diagnostic ultrasonography. The finding of a liver nodule or an elevated AFP level should lead to referral to a liver specialist and additional diagnostic studies.

Immunizing patients with alcoholic liver disease against common infectious pathogens, including hepatitis A virus, hepatitis B virus, pneumococci, and influenza A virus, is prudent.