Chronic Liver Disease

BY PROF/ GOUDA ELLABBAN

Burden

Markedly decreased life expectancy 12th leading cause of death in US 25,000 deaths annually 373,00 hospital discharges High morbidity and mortality due to

complications

Cirrhosis

Alcoholic liver disease

Chronic hepatitis B

Chronic hepatitis C

Primary biliary cirrhosis

Primary sclerosing cholangitis

Autoimmune hepatitis

Hereditary hemochromatosis

Wilson’s disease

Alpha1-antitrypsin deficiency

Hepatic Fibrosis

Hepatic fibrosis

Fibrosis is a wound healing response in which damaged regions are encapsulated by an extracellular matrix or scar

Develops in almost all patients with chronic liver injury

                                                                                                                                    

   

Cirrhosis

Late stage of progressive hepatic fibrosis Characterized distortion of hepatic

architecture and formation of regenerative nodules

Generally irreversible in advanced stages

Case

55 yo man with h/o heavy ETOH use presents with abdominal swelling and pain

What other questions would you ask the patient???

What are you looking for on your exam???

Case

Exam Temp 99.5, BP 98/66, scleral icterus Chest- crackles in bases, scattered

“spiders” Abd- distended, dilated abd wall veins,

diffusely tender Ext- 2+ edema B

Case

AST 150, ALT 73, alk phos 153, GGT 320, bili 4.3/3.1, TP 8.3, alb 2.2, PT INR 1.9

WBC 2.2, H/H 11/33. Plt 78K Na 130

LFT’s

LFT’s is a misleading term Do not reflect how well the liver is

functioning Abnormal values can be caused by non-

hepatic diseases

LFT’s

Enzyme tests- AST ALT, Alk P and GGT Synthetic function- Albumin and PT Hepatic transport ability- Bilirubin

Patterns

Disproportionate elevation of transaminases seen with hepatocellular processes

Diproportionate elevation of Alk P in cholestatic process

Serum Bili can be elevated in both processes so not helpful in differentiating

Patterns Low albumin suggests a chronic prcess Normal albumin suggest acute process Elevated PT is either Vit K deficiency

(due to juandice and malabs of Vit K) or significant hepatocellular dysfunction

Failure of parenteral Vit K to correct PT indicates the latter

Bilirubin

Catabolic product of heme metabolism Elevated from:

Overproduction Impaired uptake, conjugation or exceretion Backwards leakage from damaged

hepatocytes or bile ducts

Case

AST 150, ALT 73, alk phos 153, GGT 320, bili 4.3/3.1, TP 8.3, alb 2.2, PT INR 1.9

WBC 2.2, H/H 11/33. Plt 78K Na 130

What would you do first in the evaluation of this patient??

Paracentesis

What information do you get from peritoneal fluid analysis???

What studies do you want to perform on the ascites fluid???

Ascitic fluid

Cloudy fluid Albumin 0.5 TP 0.7 Cell count- 425 WBC, 90% PMN’s Gram stain- many PMN’s, no bacteria

How do you interpret the results from your tap??

Serum-to ascites albumin gradient (SAAG)

SAAG= (serum albumin)-(ascitic fluid albumin) What is our patient’s SAAG???

SAAG > 1.1 indicates portal HTN SAAG < 1.1 indicates pt does not have

portal HTN

                        

                                                                                                   

                                                                                                                           

Diagnosis of SBP

Definition- ascitic fluid infection w/o intraabdominal source of infection

Positive ascitic fluid culture and/or PMN>250 Calculate this patient’s ascitic PMN count

Consider secondary peritonitis if: TP >1.0 Glucose <50 LDH > upper limit for serum

How will you treat SBP??

                                                       

                                                                       

                                                                                                                             

Antibiotic choice

Need to cover gut flora as well as Strep and Staph

3rd generation cephalosporin such as cefotaxime 2g IV q8hrs

Treat for 5 days and reassess patient If has had good response, d/c antibiotics If still has fever or abd pain, re-tap

PMN <250, stop antibiotics PMN > pre-treatment level, look for surgical cause PMN >250 but < pre-treatment level, give 48 hrs antibiotocs

and repeat tap

SBP Prophylaxis

Indicated for patients with h/o SBP or variceal bleed

Proven to decrease mortality, to prevent bacterial infections, and to be cost effective

SBP Prophylaxis Regimens

If h/o SBP, Norfloxacin 400 mg qd or Bactrim DS qd

If recent variceal bleed, Norfloxacin 400 mg BID or Bactrim DS BID for 7 days

Why do patients with cirrhosis develop ascites??

Ascites formation in cirrhosis

1st step is development of portal HTN (>12 mm Hg)

Portal HTN leads to splanchnic vasodilation Collateral vein formation Local production of vasodilators (NO)

Vasodilation leads to systemic effects

How will you treat the ascites??

Treatment of ascites

Goal is to minimize edema and ascites w/o intravacular volume depletion

No evidence that treatment of ascites improves survival, but pt’s feel better

Treat underlying disorder- ETOH and autoimmune hepatitis

Avoid NSAID’s Limit Na to 2g/day

Treatment of ascites

Start with combo of spironolactone and furosemide (100 mg and 40mg) or spironolactone alone

Max rec’d doses: spironolactone 400mg/d and furosemide 160 mg/d

Rec’d wt loss is 300-500g/d w/o edema and 800-1000g/d w/edema

Treatment of large volume ascites

Treatment of choice is large volume paracentesis

Faster, more effective and fewer adverse effects vs. diuresis

Diuretics should be given as maintenance therapy to prevent recurrence

Complications of cirrhosis

Variceal hemorrhage Ascites Spontaneous bacterial peritonitis Hepatorenal syndrome Hepatic encephalopahty Hepatopulmonary syndrome Hepatocellular carcinoma