Chronic Liver Disease:

Complication and Treatment

Syifa Mustika

A Patient Case…

54 year old gentleman presents to internist with increasing swelling of his abdomen and feet over the last 2 months. He has been increasing tired over this time and feels nauseous and is off his food. His wife has commented that his eyes have turned yellow over the last few days. He works in as a truck driver and smokes 10 cigarettes a day. He admits to drinking 2 cans of beer every weekend since young. His wife also says he sometimes drinks a bottle of whisky.

On examination he is jaundiced but has no hepatic flap and is orientated in time, place and person. His abdomen is distended but soft and non-tender. There is no palpable organomegaly but there is shifting dullness.

What are your main differential diagnoses for this gentleman?

Differential Diagnosis

• (Decompensated) Alcoholic liver disease

• Viral liver disease

• Hepatocellular Carcinoma

• Pancreatic Cancer

• Cryptogenic Liver Cirrhosis

• Autoimmune liver disease

What further history would be needed?

What signs would you look for on examination?

Signs of CLD

How would you investigate this

patient? Bedside

• Observations, BM, fluid balance, weight

Blood tests

• LFTs (pre/post) (including albumin), INR

• CBC, RFT, CRP

• Liver screen: viral hepatitis serology, autoantibodies, alpha-1 antitrypsin

Imaging

• US abdomen + portal vein doppler

• CXR, CT, MRI, MRCP

Special tests

• Ascitic tap, Endoscopic examination (oesophageal varices), liver biopsy

What is your management plan?

Conservative

• Alcohol abstinence, optimise nutrition, low salt diet, fluid restriction

Medical

• Vitamin B supplementation

• Diuretics

• Beta-blocker

• Paracentesis (give albumin)

• NG feeding

• Antibiotics (? SBP)

• Lactulose (in hepatic encephalopathy)

Surgical

• TIPS

• Liver transplantation

What is possible complications and the

prognosis of this patient?

• Portal hypertension: esophageal varices, ascites

• SBP

• Hepatic encephalopathy (constipation, GI bleed, infection, renal failure)

• Hepatocellular carcinoma

• Coagulopathy

• Hepato-renal syndrome

• Liver failure

Prognostic :

Calculates Child Pugh Score: bilirubin, INR, albumin, ascites, hepatic encephalopathy

Outline

Epidemiology

Definition, Etiologies and Classification

Clinical Presentation

Diagnostic Approach

Progostic Measurement

Management

Complications: Variceal Hemorrhage, HE, HRS

Epidemiology

Cirrhosis is the 12th leading cause of death in the

United States.

It accounted for 29,165 deaths in 2007, with a mortality

rate of 9.7 per 100,000 persons.

Cirrhosis is a major risk factor for the development of

hepatocellular carcinoma; the incidence of this

malignancy tripled from 1975 to 2005.

Definitions and Etiologies

The word cirrhosis is derived from the Greek word

kirrhos, meaning orange or tawny, and osis, meaning

condition.

World Health Organization definition of cirrhosis is a

diffuse process characterized by fibrosis and the

conversion of normal liver architecture into structurally

abnormal nodules that lack normal lobular

organization.

Classification

Morphologic classification is less useful because of considerable overlap.

Micronodular cirrhosis, with uniform nodules less than 3 mm in diameter:

causes include alcohol, hemochromatosis, biliary obstruction, hepatic

venous outflow obstruction, jejunoileal bypass, and Indian childhood

cirrhosis.

Macronodular cirrhosis, with nodular variation greater than 3 mm in

diameter: causes include chronic hepatitic C, chronic hepatitis B, alpha-1

antitrypsin deficiency, and primary biliary cirrhosis,

Mixed cirrhosis, a combination of micronodular and macronodular cirrhosis:

micronodular cirrhosis frequently evolves into macronodular cirrhosis

Clinical Presentation

Diagnostic Approach

Prognostic Measurement

Management

Management focuses on the treatment of complications

Surveillence for hepatocellular carcinoma with serial USG and

serum alpha fetoprotein measurements at frequent intervals

(e.g., every 6 months) Vaccination of cirrhotic patients against

hepatitis A and B is recommended if patients lack serologic

evidence of immunity.

Cirrhotic patients should be advised to avoid alcohol and

other hepatotoxins.

In end-stage cirrhosis, liver transplantation can be a lifesaving procedure if the patient is an appropriate candidate

Complication

Ascites

Variceal Hemmorhage

Hepatic Encephalopathy

Hepatorenal Syndrome

Spontaneus Bacterial Peritonitis

Malnutrition

Hepatocellular Carcinoma

Variceal Hemorrhage

• ABC

- Protect airway

- High flow O2

- Haemodynamically stable?

- Bloods (Hb, Urea, Crossmatch 4-6 units), ABG

- Fluid resuscitation – anything, blood is best

• Correct clotting abnormalities (vitamin K, FFP)

• Emergency endoscopy: banding, adrenaline injections

• Somatostatin or Octreotide

• IV omeprazole, antibiotics

Rockall Risk Score:

Age, Co-morbidities, Shock, Diagnosis, evidence of bleeding (OGD)

• Reversible decrease in neurological function

secondary to liver disease

• Acute: seen with acute liver failure

• Acute on chronic: established cirrhosis

• Diagnosis :

Clinical (most important)

The drawing tests

EEG

CT/MRI may show cerebral atrophy

Hepatic Encephalopathy

Hepatic Encephalopathy

West Haven Criteria for Hepatic Encephalopathy

• Grade 1: shorted attention span, reversal of sleep-wake cycle, impaired

performance of addiction or substraction (anxiety, irritability)

• Grade 2: lethargy, subtle personality change, disorientation minimal of

time and place. Asterixis.

• Grade 3: stupor but responsive, severe confusion and disorientation,

abnormal behaviour, incomprehensible speech, confusion and gross

disorientation.

• Grade 4: coma (unresponsive to verbal and stimuli)

• Identify and treat precipitation factor

• Treat underlying liver disease

• Low to normal protein diet

• Antibiotics (Neomycin, metronidazole)

• Lactulose

• BCAA

• LOLA

• Liver Transplantation

Hepatic Encephalopathy - Treatment

Hepatorenal Syndrome

• Progressive renal failure

• Type 1 : rapidly progressive, high mortality

• Type 2: slower progression

• R/O volume depletion secondary to diuretics

• IV vasoconstrictors

• Liver transplantation

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