Chronic Liver Disease Flashcards
CHRONIC LIVER DISEASE
• Viral (HBV, HCV), Toxic (Alcoholic, Drug induced),
Metabolic (NAFLD, Haemachromatosis, Wilson’s),
Autoimmune (AIH, PBC, PSC) and Right Heart
Failure can cause Chronic Liver Disease
• Patients may be asymptomatic or complain of non-
specific symptoms e.g. Fatigue; Specific symptoms
include RHP (Liver Distention), Abdominal
Distention (Ascites), Ankle Swelling
• Haematemesis and Melaena from GI Haemorrhage
(secondary to Varices and Portal HTN), Pruritus due
to Cholestasis (Bilirubin), Gynaecomastia, Loss of
Libido and Amenorrhoea due to Endocrine
dysfunction, Confusion and Drowsiness due to
Neuropsychiatric complications (Portosystemic Encephalopathy)
• Chest and Upper Body show spider naevi along distribution of SVC; >5 is diagnostic
• Palmar Erythema (Hyperdynamic circulation), Clubbing and Dupuytren’s Contracture (Due to
collagenous changes); Xanthoma (Cholesterol deposits) in Palmar crease or above eyes in PBC
• Initial Hepatomegaly followed by small liver in well-established Cirrhosis; Splenomegaly due
to Portal Hypertension
Ascites and Liver Disease
• Fluid within the Peritoneal Cavity; Common complication of Cirrhosis
• Renal Sodium and Water Retention as a result of Peripheral Arterial Vasodilation (NO, ANP,
Prostaglandins) and consequent reduction in effective blood volume due to activation of
RAAS and Sympathetic nervous system
• Portal Hypertension leads to local hydrostatic pressure; Hepatic and Splanchnic production of
Lymph and Transudation of fluid into Peritoneal Cavity
• Low Serum Albumin as a consequence of poor liver synthetic function
• Precipitating factors include high Sodium diet, Development of Hepatocellular Carcinoma or
Splanchnic Vein Thrombosis; Mild generalised Abdominal Pain and Discomfort are common
but if severe should raise suspicion of Spontaneous Bacterial Peritonitis
o Haematogenous spread of Bacteria (E coli, Klebsiella, Enterococcus) to Peritoneum;
Neutropaenia sufficient to start treatment; Third generation Cephalosporin for
treatment, recurrence is common so prevention antibiotics given
• Presence of fluid confirmed by Shifting dullness; Peripheral Oedema, Right sided Pleural
Effusion due to passage of Ascitic fluid through congenital diaphragmatic defects
Management of Ascites
• Diagnostic Aspiration of 10-20mL; Neutrophil
count (>250/mm3
) indicates Bacterial
Peritonitis, Gram stain and culture (Bacteria and
Acid-fast Bacilli), Protein (Serum-Ascites
gradient of >11g/L suggests Portal
Hypertension, otherwise Peritonitis/Neoplasia),
Cytology (for Malignancy) and Amylase
(Pancreatitic Ascites)
• Reduction in sodium intake; Daily weights, 2-
daily U/Es and Creatinine; Urine output daily
• Diet sodium restriction, Avoiding sodium
containing and retaining drugs
• Spironolactone (100mg OD) or Eplerenone
(25mg OD, does not cause Gynaecomastia);
Aim to lose 700ml in 24 hours or 1L if Peripheral Odema is present; Loop Diuretic (e.g.
Furosemide) added if response is poor; Discontinue if rise in Creatinine occurs
• Paracentesis – Symptomatic relief of tense ascites; Complications include Hypovolaemia and
Renal Dysfunction (Ascites reaccumulates at expense of circulating volume); More likely if >5L
removal and worse liver function; Can be overcome with Albumin infusion if Renal Function is
normal and no Hyponatraemia present
• Transjugular Intrahepatic Portosystemic Shunt (TIPS) for Resistant Ascites if there is no
Spontaneous Portosystemic Encephalopathy (PSE)
Portosystemic Encephalopathy (Hepatic)
• Occurs secondary to Chronic Cirrhosis; Due to spontaneous shunting in Portal Hypertension,
or in patients with surgical shunts or TIPS; Encephalopathy potentially reversible
• Portal blood bypasses liver via Collateral circulation, Toxic metabolites (Principally Ammonia)
pass directly to Brain to cause encephalopathy
o Ammonia induced alteration of Neurotransmitter balance, especially at Astrocyte-
Neurone interface, leads to pathophysiology
• PSE can be precipitated by High dietary protein, GI Haemorrhage, Constipation, Infection,
Fluid and Electrolyte disturbance, Drugs (especially CNS depressants), TIPS and other shunts,
Surgery, Progressive Liver Damage and Hepatocellular Carcinoma
• Acute Encephalopathy can also occur as part of Fulminant Hepatic Failure
• Increasing Drowsiness and Comatose; Chronic disorder with Personality, Mood and Intellect,
Reversal of sleep rhythm; Patient is irritable, confused, disoriented, slurred speech
• Nausea, Vomiting, Weakness; Hyperreflexia and Increased Tone; Convulsions are rare; Fetor
Hepaticus (Sweet smelling breath), Flapping tremor (Asterixis), Constructional Apraxia
(Unable to write or draw), Decreased Mental function
• Associated with poor prognosis; Should be referred for Liver Transplantation
Management of Portosystemic Encephalopathy
• Clinical diagnosis; LFTs reflect underlying Liver disease and not PSE
• EEG shows decreased normal α-waves; Visual evoked responses detect subclinical disease
• Arterial Blood ammonia is useful for monitoring but not readily available
• Purgation and Enema to empty bowel of nitrogenous substances as well as limit ammonia
absorption e.g. Lactulose, Lactilol
• Nutrition with adequate calories; Do not restrict protein for more than 48 hours
• Rifaximin (Low oral bioavailability) and Metronidazole
• IV fluids; Diuretics should be stopped or reduced
