Alkohoolne tsirroos

Alkohoolne tsirroos kujuneb 20% kuritarvitajatest.

HCV + alkohol = lisandub viiekordne risk HCCks.

NB! Paratsetamool ja alkohoolik ei käi kokku. Alla 2g päevas, soovitatavalt mitte üldse.

Kõige raskem aste maksa alkoholtõvel. Sellest kergemad on alkohoolne hepatiit ja alkohoolne rasvmaks.

* Kokkuvõte
* Mälupalee

## Diagnoos

### Kaebused

Sümptomid sõltuvad sellest, kuivõrd suudab maks kompenseerida. Võivad olla suhteliselt vähesed (anoreksia, väsimus, tursed) aga üldiselt tugevamad ja sõltuvad ka nt HCC ja portallhüpertensiooni olemasolust.

### Objektiivne leid

Nii võivad sümptomiteks olla astsiit, splenomegaalia, vaariksi veritsused. Nahal kroonilise maksahaiguse stigmad (ämblikangioomid, palmaarne erüteem), alajäseme tursed, günekomastia ja hüpogonadistm, perifeerne neuropaatia, dementsus.

### Analüüsid

Laboratoorselt prognostilised on bilirubiin, albumiin ja INR. Neid on ka vaja Child Pugh skooris.

### Tüsistused

Most complications of alcoholic hepatitis are identical to those of cirrhosis.

*Variceal hemorrhage*

Acute variceal bleeding constitutes one of the most devastating emergencies, not only in gastroenterology but also in medicine at large. Resuscitation of the patient and protection of the airway are the 2 most important steps in the treatment of acute variceal bleeding. Cessation of the acute bleeding is usually achieved in more than 90% of patients with the combination of interventional endoscopy (sclerotherapy or banding ligation) and the intravenous infusion of pharmaceutical agents that lower the pressure within the portal system (somatostatin or one of its long-acting analogues [eg, octreotide]). Alternatively and for patients who continue to bleed in spite of interventional endoscopy and drug therapy, more invasive options, such as balloon tamponade, a transjugular intrahepatic portosystemic shunt, and an emergency portal-caval shunt, may be used.

*Hepatic encephalopathy*

The development of encephalopathy in patients with alcoholic hepatitis is invariably associated with a grave prognosis. Treatment consists of close monitoring of the patient and the administration of lactulose or nonabsorbable antibiotics. Low energy or low protein intake is not indicated, except transiently in severe cases. The use of benzodiazepine receptor antagonists (ie, flumazenil [Romazicon]) is still experimental. Rarely, rapidly progressive worsening of encephalopathy leading to deep coma may be associated with cerebral edema, as observed in fulminant hepatic failure. In selected instances, aggressive treatment with intracranial pressure monitoring and liver-assist devices may be considered.

*Coagulopathy and thrombocytopenia*

Profound hypoprothrombinemia may ensue during the course of severe alcoholic hepatitis, especially in patients with variceal bleeding. Administer fresh frozen plasma (FFP) to temporarily restore the depleted hepatic prothrombin stores. The value of parenteral administration of vitamin K is dubious, because the hepatocytes are incapable of synthesizing new prothrombin. Platelet transfusions are not usually necessary to correct thrombocytopenia, unless the patient is actively bleeding or requires an invasive procedure.

*Ascites*

Acute onset of ascites may develop in patients with alcoholic hepatitis, even in the absence of overtly decompensated liver disease and portal hypertension. The ascites is typically transudative, with a very low albumin concentration (

*Spontaneous bacterial peritonitis*

Spontaneous bacterial peritonitis may develop in patients with alcoholic hepatitis and ascites, especially in those with concomitant gastrointestinal bleeding. Following a confirmatory diagnostic paracentesis, broad-spectrum antibiotic therapy with a second- or third-generation cephalosporin is the treatment of choice.

*Iron overload*

Several histopathologic studies have shown that as many as 50% of patients with alcoholic liver disease have increased hepatic iron content compared with healthy controls. This excess deposition of iron may play a significant role in the progression of the alcoholic liver damage. Portosystemic shunts, especially the side-to-side variety, enormously increase the deposition of iron in the liver. Occasionally, this excessive iron deposition leads to a clinical and pathologic entity that is analogous to primary hemochromatosis. Attempts to treat alcoholic liver disease with phlebotomy to reduce iron overload have been hampered by the development of anemia, and no clear benefit has been observed.

## Ravi

Jätta ära alkohol.

Kompenseeritud tsirroosi elulemus 80%, mittekompenseeritud 50%. Edasijoodikutel 30%.

### Muu ravi

Definitiivne ravi transplantatsioon - elulemus sageli parem kui teiste haiguste puhul, sest vähem äratõukereaktsioone.