6.6 Liver Disease

Question 1

How would end stage hepatic disease present to anaesthetists?

Answer 1

1. Acute decompensation secondary to
   * Infection
   * Hypovolemia
   * Hypotension
   * Diuretics
   * Gastrointestinal haemorrhage
   * Excess dietary protein
   * Electrolyte imbalance
2. Infection
   * Flare-up of hepatitis (A, B, or C)
   * Prone to acquiring fungal infections, TB
3. Portal hypertension
   * Ascites—diaphragmatic splinting and respiratory distress
   * Spontaneous bacterial peritonitis
   * Varices—variceal bleeding
   * Splenomegaly—thrombocytopenia
4. Bleeding
   * Due to decreased production of clotting factors (II, VII, IX, X) and
   splenomegaly-related thrombocytopenia
   Haematemesis
5. Hepatic encephalopathy

Question 2

What is the pathophysiology of liver injury in alcoholic liver disease?

Answer 2

Conventionally divided into three histological types, although may co-exist:

1. • Steatosis
     ° Metabolism of ethanol causes the accumulation of lipid in liver cells.
2. • Alcoholic hepatitis
     ° Ethanol metabolism generates reactive oxygen species and
     neoantigens, which promote inflammation.
3. • Cirrhosis
     ° Prolonged hepatocellular damage generates myofibroblast-like cells
     that produce collagen, resulting in fibrosis.
     ° As hepatocytes are destroyed and liver architecture changes, hepatic
     function falls and increased resistance to portal blood flow produces
     portal hypertension.

Question 3

List the common clinical findings in patients with alcoholic liver disease.

Answer 3

1. • Signs of acute hepatitis
     ° Jaundice
     ° Tender hepatomegaly
     ° Fever (< 38.5ºC, often sawtooth)
2. • Signs of chronic liver disease
     ° Leuconychia/palmar erythema/dupuytren’s contracture/spider naevi
     ° Telangiectasia/bruising
     ° oedema (hypoalbuminaemia)
     ° Parotid swelling/hepatomegaly
     ° Gynaecomastia/testicular atrophy
     ° Encephalopathy
3. • Portal hypertension
     ° Ascites/splenomegaly/caput medusa
4. • Poor nutrition
     ° Muscle wasting/weight loss/cachexia/glossitis

Question 4

What is hepatorenal syndrome?

Answer 4

1. • Hepatorenal syndrome (HRS)
     is the reduced glomerular filtration rate (GFR) and
     consequent decline in renal function
     caused by advanced liver disease.
2. • Serum creatinine of > 133 μmol/litre
     in a patient with cirrhosis and ascites
     that persists after all possible pathologies
     have been excluded or treated.

• Due to generalised vasodilatation and altered hormone release
  (renin–angiotensin, ADH, and sympathetic systems)

subjecting the kidney to
hypotension, hypovolaemia, and local vasoconstriction.

Question 5

What are they types of HRS

Answer 5

1. HRS type 1:
   A rapid and severe progressive
   renal failure occurring in under 2 weeks.

As a result of some precipitating factors, (e.g. Alcoholic hepatitis,
gastrointestinal bleeding, NSAIDs, aminoglycosides, or infection).

2. HRS type 2:
   A slowly progressive moderate deterioration in function.
   Refractory ascites is the dominant clinical feature.

Question 6

What is hepatic encephalopathy?

Answer 6

Occurrence of confusion,
altered level of consciousness,
and coma due to liver failure

Grading:

I: Confused, altered mood

II: Inappropriate, drowsy

III: Stuporose, but rousable, very confused, agitated

IV: Coma, unresponsive to painful stimulus

Question 7

How would you assess the prognosis of liver disease and how is this assessment tool useful?

Answer 7

• The Model for End-Stage Liver Disease (MELD) score uses
  bilirubin, INR, and creatinine.
• The Child-Pugh score
  [Pugh’s modification (1972) of Child’s criteria (1964)]

is used to determine the prognosis,

as well as the required strength of treatment
and the necessity of liver transplantation.

Question 8

Child Pugh Score

Answer 8

1-3 score

Encephalopathy grade
None Minimal (1&2) Advanced (3&4)

Ascites
None Easily controlled Poor control

Serum bilirubin mg/dL
< 2 2–3 > 3

Serum albumin g/dL
> 3.5 2.8–3.5 < 2.8

Prothrombin time (seconds > control)
1–4 4–6 > 6

Question 9

What are the anaesthetic implications for anaesthetising patients with end-stage liver failure (for nonhepatic surgery)?

Pre operative

Answer 9

Preoperative

1. • Comprehensive assessment of suitability
     and work-up for procedure—
     multidisciplinary approach
2. • Preoperative optimisation of fluid and nutritional status,
     as well as any electrolyte disturbance or coagulopathy
3. • Consider preoperative abdominal paracentesis
4. • Delayed gastric emptying—antacid prophylaxis
     +/− rapid sequence induction

Question 10

What are the anaesthetic implications for
anaesthetising patients with end-stage liver failure

(for nonhepatic surgery)?

Intraoperative

Answer 10

Intraoperative
* Drugs
° Altered drug handling
° Increased sensitivity to sedative agents
° Reduced metabolism of many drugs including opioids
° Increased volume of distribution and altered protein binding
° Short-acting drugs preferred (desflurane, remifentanil)

• Technique
  ° Extreme caution with epidural anaesthesia and other regional
  procedures due to associated coagulopathy
• Monitoring
  ° Invasive monitoring for major surgery
  (oesophageal doppler contraindicated in the presence of varices)
• Others
  ° Glycaemic control
  ° Thermoregulation
  ° Antibiotic prophylaxis and strict adherence to aseptic technique

Question 11

What are the anaesthetic implications for anaesthetising patients with end-stage liver failure (for nonhepatic surgery)?

Post op

Answer 11

Postoperative
Care on high-dependency unit or ITU