Alcoholic Liver Disease: Clinical Presentation, Diagnosis, and Treatment

00:01 The clinical presentation is going to be related to what stage we're in if it's fatty liver disease that's going to be somewhat different than if we're at steatohepatitis, than if we're at cirrhosis.

00:11 With alcoholic steatosis or just fatty liver.

00:13 It's largely asymptomatic.

00:15 There may be vague abdominal discomfort, the liver is actually somewhat expanded by the accumulation of fat and by stretching glistens capsule around the liver, you may have that vague sense of, I don't feel so good.

00:28 And we may actually formally be able to distinguish that there is hepatomegaly on exam, we'll be able to feel the liver edge below the right costal margin.

00:39 With more severe disease, now alcoholic hepatitis.

00:42 It's inflammation, so there'll be a low grade fever.

00:45 There'll be a lot of other systemic manifestations including anorexia and nausea.

00:50 There will be that right upper quadrant discomfort, the patient may be jaundice because we are impacting the ability of the hepatocytes to function, So we may not be metabolizing bilirubin appropriately.

01:02 There'll be the same hepatomegaly that we saw with fatty liver disease.

01:05 And depending on the extent of inflammation, we may be starting to see the beginning of portal hypertension with associated ascites and addition, we may be able to see some effects on the CNS with hepatic encephalopathy.

01:21 And then frank alcoholic cirrhosis that's in stage disease, and I would actually refer you to the entire talk in the Lecturio files that's all about cirrhosis.

01:33 But we'll see as indicated here, fatigue, malaise, weight loss, severe jaundice.

01:38 Pruritus from deposition of bile salts, so the patient becomes quite itchy.

01:42 With alcoholic cirrhosis, we'll see hepatic encephalopathy including signs like asterixis, where you have the patient close their eyes and try to stop traffic and their palms do that they have a flap.

01:54 They may be tired, confused, even be in a frank coma.

01:59 Ascites occurs due to portal hypertension and decreased albumin and we may have GI bleeding because of esophageal varices associated with the portal hypertension.

02:11 Skin changes will include things related to elevated estrogen such as telangiectasias.

02:18 We may also have other portosystemic shunts so that you have a Caput Medusae.

02:24 Palmar erythema is associated with elevated estrogens.

02:27 Clubbed nails may be a secondary and rare manifestation and then patients will get into patrons contracture usually have the ring finger where they have abnormal fibrosis and holds that finger in that position.

02:40 Dupuytren's contractures are associated with other entities and can be completely idiopathic, but our seem at a certain frequency and alcoholic cirrhosis.

02:49 And then other hyper estrogenic effects.

02:52 Gynecomastia, hypogonadism, reduced libido, erectile dysfunction, infertility, and amenorrhea.

03:01 Finally, there may be alopecia and or the effects of diminished vitamin.

03:06 So if the individual is drinking more than they're actually eating and not getting adequate nutrition, they may have B12, or folate deficiencies, they have iron deficiencies and then we'll see a glossitis, a smooth and inflamed tongue.

03:21 Or you may have an anemia associated with vitamin deficiency.

03:26 In making the diagnosis, clearly it's related to history.

03:30 How much alcohol? How frequently do you do it? What's the duration of that? Keep in mind that with alcohol disorders, anything else that potentially causes injury to the liver is going to exacerbate the alcohol related injury.

03:46 So we want to assess and see whether there are other causes such as hemochromatosis, abnormal copper, metabolism, Wilson's disease, Alpha-1 antitrypsin, viral hepatitis, or other medications that may synergize with alcohol.

04:00 In terms of laboratory studies, classically, the AST is more elevated than the ALT in terms of identifying enzyme elevation with abnormal liver function.

04:13 And the gamma glutamyl transferase is also a very sensitive indicator of alcohol intake.

04:21 Typically, classically, the AST to ALT ratio is greater than 2.

04:25 And that's something you can tuck away in the back of your head because that's frequently asked on rounds.

04:32 Any AST or any ALT that is greater than 500 says, as something else is going on here.

04:37 We usually don't see elevations, more than 500 and pure alcoholic disease.

04:44 And the alkaline phosphatase is certainly going to be elevated when there's a lot of inflammation.

04:50 Other findings with alcoholic hepatitis, we'll see abnormal bilirubin metabolism and or release, we will see diminished albumin synthesis, we will see diminished coagulation factor synthesis and we will may or may not see evidence of anemia either macrocytic from B12 or folate or microcytic due to iron and iron and blood loss occurs also with alcoholic gastritis.

05:18 With alcoholic cirrhosis now, at the end stage, you may actually not see an elevation in AST or ALT.

05:24 At that point, the hepatocytes are no longer susceptible to any further damage.

05:29 They're in stage.

05:31 So it's usually a modest elevation.

05:34 Bilirubin will certainly be elevated because we are not metabolizing or releasing bilirubin appropriately, the gamma glutamyl transpeptidase still ends up being a relatively sensitive marker.

05:44 And alkaline phosphatase will be quite elevated because the fibrosis in the cirrhotic state is markedly impacting the ability of the biliary tree to do its appropriate actions.

05:58 And as a manifestation of that alkaline phosphatase is markedly elevated.

06:02 Other laboratory studies with cirrhosis, elevated ammonia, markedly diminished protein synthesis.

06:09 The PT is down.

06:11 Platelets are down for a combination of reasons.

06:14 One is you have hypersplenism due to portal hypertension, and that sucks up platelets, but also the liver makes thrombopoietin and thrombopoietin is going to be necessary for getting the bone marrow to synthesize and make new platelets.

06:27 You may have anemia and hyponatremia.

06:31 The hyponatremia is because of the effects of chronic alcohol and cirrhotic disease altering the normal renal cycle that is responsible for maintaining water and sodium within limits.

06:48 Imaging to make a diagnosis, ultrasound is quite good.

06:51 It shows an irregular trunk and liver.

06:54 CT scan can also be employed.

06:56 And then the gold standard overall is to do a liver biopsy.

07:00 How do you manage this? Well, you know, basically stopped drinking.

07:05 Okay, that's easier said than done.

07:07 Also want to make sure the patients are in a healthy diet.

07:09 So they're getting adequate nutrition and an adequate vitamin intake.

07:13 In alcoholic hepatitis, it's the same story, stop drinking.

07:17 Make sure that there is adequate hydration and normal electrolyte correction, supplement the nutrition, and make sure that there's not something else concurrent that is exacerbating the injury.

07:30 Additional treatments for alcoholic hepatitis include: glucocorticoids to limit inflammation.

07:35 And pentoxifylline is another drug that is used for patients who can't have steroids.

07:41 And what this does is start to do is limit the production of various pro-inflammatory mediators such as tumor necrosis factor.

07:49 So with cirrhosis at the end stage, it's going to be largely supportive.

07:55 You will do similar things that you've done for a patient as alcoholic hepatitis, you just don't want the disease to get any worse.

08:03 So you want to minimize any damage.

08:05 So you want to quit drinking, you may have to salt and water restrict because of the aberrations in the normal renal function.

08:12 You give diuretics and or a therapeutic paracentesis to remove the excess fluid from the ascites.

08:19 For the hepatic encephalopathy, you restrict protein intake.

08:22 So you need to have a low protein burden.

08:26 The more protein you have, the greater the severity of the encephalopathy.

08:31 And similarly, you can reduce the microbiota, which is a major source of protein as well in the GI tract by giving oral lactulose oral neomycin.

08:41 And finally, for patients who have quit drinking, then you can offer the possibility of a liver transplant, but with a limited resource and if a patient is not able to abstain forever from alcohol, then they are not a candidate for that for that procedure.

09:00 So what's the outlook for these patients? If the patient has alcoholic hepatitis, they tend to progress at a rate of about 10 to 20% per year to cirrhosis.

09:10 In most cases, that's because they continue to drink, abstinence reduces that risk substantially.

09:17 The median survival for compensated cirrhosis without significant complications such as bleeding without hepatic encephalopathy, without hepatorenal syndrome, with the renal aberrations is about 12 years.

09:32 The median survival when there is really severe disease is much less on the order of months.

09:37 And the model for assessing, whether a patient has really severe liver disease or moderate or mild is this model for end stage liver disease, otherwise called the MELD score.

09:50 We're not going into the details.

09:52 But when you become a hepatologist or a liver transplanter, you will use the MELD score to determine where on the transplant list your patient will be.

10:04 With that, we have finally come to the end of alcoholic liver disease.

10:10 Go have a drink.