This post attempts to explain some of the basics surrounding the management of chronic liver disease and to provide a strategy for treating the most common complications of chronic liver disease.
Three key questions exist when working up a patient with liver disease.
- Is this an acute or chronic exacerbation of liver disease
- What is the underlying cause – i.e Infection (Hep B/C), Toxins (Alcohol, Paracetamol, INH), Vascular (Budd Chiari, Shock Liver), Autoimmune (Wilsons, ALD) or Obstetric
- Is there any evidence of complications
Chronic liver disease can be further divided in two categories: Compensated (stable) vs. Decompensated (unstable). Decompensated liver disease presents with symptoms related directly to the various functions of the liver – which are outlined in the diagram below.
Portal Hypertension (1) and Loss of liver function (2) can each explain the various symptoms uncovered during work-up of the patient with chronic liver disease.
1. Portal Hypertension (SAVE)
- S – Splenomegaly
- A – Ascites
- V – Varices (Rectal, Esophageal and Caput Medusae)
- E – Encephalopathy
2. Loss of Function
- Jaundice (Conjugated)
- Hypoalbuminemia – Peripheral Oedema, Ascites, Leuconychia
- Coagulopathy + Bleeding
- Peripheral Venous Dilation
Other risks associated with chronic liver disease included spontaneous bacterial peritonitis (>250 neutrophils in ascites fluid aspirate) & an increased risk of Hepatocellular Carcinoma
Management of Decompensated Chronic Liver Disease:
1. General Management
- Good nutrition + Early involvement of dietitian
- Abstinance from alcohol
- Colestyramine for pruritis
- Screening – Endoscopy for varices & U.S + AFP for Hepatocellular Ca.
- Discriminant function score (Answer: Do I give steroids in Alcohol Hepatitis)
- Child-Pugh Score (Answer: Estimates severity & prognosis in Cirrhosis)
2. Management of Ascites
Ascites in liver disease is due to mesenteric vasodilatation due to increased levels of endogenous nitrous oxide –> splanchnic and peripheral vasodilation –> decreased kidey perfusion –> activation of the renin-angiotensin-aldosterone system (RAAS) –> retention of Na+ & Water.
The diuretic treatment of ascites aims to target these specific neurohormonal factors.
- A) Salt Restriction – nB* not fluid restriction – Check urine sodium, if the patient has a urine sodium of > 80mEq the patient is likely taking too much salt in the diet. In practicality, salt restriction involves not adding any extra salt to the patients diet.
- B) Diuresis – Spironolactone + Loop Diuretic (100mg:40mg Ratio) – Spironolactone targets the overactive RAAS while the loop diuretic decreases Na+/Water resorbtion. Note that high doses of loop diuretics deplete the intravascular volume too quickly to allow for the ascitic fluid to move back to the vascular system. Moral = Go slow with Loop Diuretics in CLD!
- C) Paracentesis – There is no maximum volume to drain off as long as the patient is haemodynamically stable. If shifting dullness is present during examination this indicates that at least 2.5 Litres of fluid is present in the peritoneum. If too much volume is drained rapidly (esp. if patient with chronic ascites) renal failure may occur. For each litre of abdominal fluid drained – aim to give approximately 60 grams of Albumin. Send ascites fluid for microscopy + culture.
If these measures fail then the patient may need to be worked up for either
- TIPSS – transjugular intrahepatic portosystemic shunt
- Liver Transplant
3. Management of GI Bleed
- ABC MOVE – as covered in previous posts + Senior Help
- 2 wide bore cannulae in AC Fossa
- If acutely encephalopathic – involve anaesthetics – intubate
- Agressive fluid resuscitation with colloids + blood – avoid overtransfusion – Targets: Keep HgB >8, HCT > 20.
- Terlipressin (Variceal Vasoconstrictor) – 2mg stat dose followed by 1mg every 2 hours
- Endoscopy – Banding + Ligation. A Sengsten Blakemore tube can be inserted if the patient is responding poorly to terlipressin/octreotide/fluids
- Antibiotic Coverage – Ciprofloxacin or Cefotaxime x 5 days duration post Upper GI Bleed – Antibiotic coverage must be given to all liver disease patients following upper GI bleed as translocation of upper GI bacteria during bleeding can lead to SBP/Bacteraemia/Rebleeding due to Sepsis.
On dischage – patients should be maintained on Propranolol (Non-Cardioselective Beta Blocker) – Approx 20 – 40mg BD PO.
Propranolol has vasoconstritive effects particularly in the mesenteric arteries. Remember to r/o bronchial asthma + heart block on ECG before commencing B-Blocker. A target of 70% of the patients resting HR on admission should be used – this target will typically produce a portal pressure of less than 10mmHg.
(Last Updated – June 2016)