liver cirrhosis

Question 1

what are complications of liver cirrhosis?

Answer 1

Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma

Question 2

why does cirrhosis lead to muscle wasting?

Answer 2

the liver damage leads to inability to store and process glucose so the body resorts to using other ways of getting energy- so breaks down muscles

Question 3

how can the complications of liver cirrhosis secondary to portal hypertension be remembered?

Answer 3

Ascites 
Bleeding 
Caput Medusa 
Decreased liver function 
Enlarged spleen

Question 4

what are hepatic causes of portal hypertension?

Answer 4

• cirrosis
• schistosomaisis
• sarcoidosis

Question 5

how can portal; hypertension be confirmed?

Answer 5

hepatic venous pressure gradient can be measured
- catheter is inserted into the IVC and the portal vein and the pressure difference is calculated

ct scan can be used to look for ascites, cirrhosis, splenomegaly and IVC dilatation

Question 6

what is a TIPS procedure?

Answer 6

an IR procedure where a tube is inserted between the portal vein and the hepatic vein, so the blood can flow directly between the two and skip the resistance caused by cirrhosis of the liver

Question 7

explain the pathophysiology of how and where you get varices in liver cirrhosis

Answer 7

• portal vein comes from the superior mesenteric vein and the splenic vein and delivers blood to the liver.
• Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back-pressure into the portal system. This is called “portal hypertension”. This back-pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous. These swollen, tortuous vessels are called varices. They occur at the:

Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)

• these can be at risk of bleeding

Question 8

how can stable varies be treated?

Answer 8

• Propranolol reduces portal hypertension by acting as a non-selective beta blocker
• Elastic band ligation of varices
• Injection of sclerosant (less effective than band ligation)
• TIPs procedure- transjugular intrahepatic portosystemic shunt

Question 9

how are bleeding oesophageal varicose managed?

Answer 9

1. resus
   - tellipressin-> causes vasoconstriction and slows bleeding
   - correct coagulopathies with vitamin K or fresh frozen plasma
   - give broad spectrum antibiotics
   - consider intubation and ITU is become life threateningly unwell
2. treat
   - urgent endoscopy and inject sclerosant
   - sengstaken blakemore tube

Question 10

what type of ascites is caused by cirrhosis?

Answer 10

• transudative - less protein content

Question 11

what is the management of ascites?

Answer 11

• Low sodium diet
• Anti-aldosterone diuretics (spironolactone)
• Paracentesis (ascitic tap or ascitic drain)
• Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
• Consider TIPS procedure in refractory ascites
• Consider transplantation in refractory ascites

Question 12

what is the effect of liver cirrhosis on the RAS system?

Answer 12

back up of blood in the portal system will cause leakage into the peritoneal cavity and fluid loss to the peritoneal space will reduce the amount of blood entering the kidneys

a reduction of blood pressure going to the kidneys will reduce and stimulate the production of renin. renin will stimulate aldosterone, which will lead to reabsorption of sodium and water from the distal convoluted tubule.

this can exacerbate ascites

Question 13

what is the prevalence of bacterial peritonitis?

Answer 13

• occurs in 10% of people with ascites

- mortality is 10-20%

Question 14

wha is the management of bacterial peritonitis?

Answer 14

• Take an ascitic culture prior to giving antibiotics

- Usually treated with an IV cephalosporin such as cefotaxime

Question 15

what is the presentation of bacterial perotinits?

Answer 15

Can be asymptomatic so have a low threshold for ascitic fluid culture

• Fever
• Abdominal pain
• Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
• Ileus
• Hypotension

Question 16

what is the pathophysiology of hepatorenal syndrome?

Answer 16

portal hypertension occurs due to cirrhosis which leads to pooling off blood in the portal system and a reduction is circultating blood volume

hypotension leads to activation of RAAS and renal vasoconstriction, which combined with low circulating volume leads to renal starvation

this leads to rapid deterioration of kidney function-> fatal within a week, unless transplant is preformed

Question 17

what is the pathophysiology of hepatic encephalopathy?

Answer 17

• build up of ammonia in the systemic circulation because the liver is unable to metabolise it
• can cross the blood brain barrier and metabolised by astrocytes to make glutamine from glutamate
• more glutamine in the astrocytes causes an increase in the oncotic pressure and astrocyte swells
• hepatic encephalopathy can be acute or it can be caused by a number of triggers in someone with chronic liver failure?

Question 18

what are the triggering factors for hepatic encephalopathy?

Answer 18

1. excessive nitrogen load: due to kidney failure or GI bleeding
2. metabolic disturbance- hyper/hypokalaemia
3. drugs: benzodiazepines and antipsychotics
4. infections- Spontaneous bacterial peritonitis
5. surgery- TIPS

Question 19

how is hepatic encephalopathy staged?

Answer 19

using west haven criteria

Question 20

what are clinical features of hepatic encephalopathy?

Answer 20

• asterixis (liver flap)
• clonus
• seizures
• positive babinski sign
• musty breath- Fetor hepaticus

Question 21

how is hepatic encephalopathy diagnosed?

Answer 21

• there may be elevated serum ammonia levels
• cerebral oedema seen on CT in last stage
• but it is a diagnosis of exclusion

must exclude…

• cerebral haemorrhage
• seizures
• meningitis encephalitis
• Wilsons disease

Question 22

what is the management of hepatic encephalopathy?

Answer 22

• Laxatives (i.e. lactulose) promote the excretion of ammonia. The aim is 2-3 soft motions daily. They may require enemas initially.
• Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia. Rifaximin is useful as it is poorly absorbed and so stays in the GI tract.
• Nutritional support. They may need nasogastric feeding.
• later stages may require airway management

Question 23

what is the SAAG and what do the different numbers mean?

Answer 23

SAAG = serum albumin - ascitic fluid albumin.

A high SAAG (>11g/L) indicates portal hypertension and the ascitic fluid is a transudate. Causes of this include liver cirrhosis, hepatic failure, venous occlusion (e.g. Budd Chiari syndrome), alcoholic hepatitis, and kwashiorkor malnutrition.

A low SAAG (<11g/L) suggests the ascitic fluid is an exudate. Causes of this include malignancy, infection, pancreatitis and nephrotic syndrome.

Question 24

how would spontaneous bacterial peritonitis be diagnosed?

Answer 24

paracentesis: neutrophil count > 250 cells/ul

the most common organism found on ascitic fluid culture is E. coli

Question 25

when should abx prophylaxis be given to patients with ascites?

Answer 25

• had an episode of SBP
• patients who have had an episode of SBP
  patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
• NICE recommend: ‘Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less until the ascites has resolved’