Chapter 45-Cirrhosis and Portal HTN

scar tissue

Cirrhosis

Increased resistance to blood flow

Portal hypertension

Portosystemic shunts

Acute or chronic liver injury

Destruction and regeneration of hepatocytes, bile ducts, and endothelial cells

Stellate cell (Ito cell)

Perisinusoidal space of Disse

Storage of vitamin A

Pro-proliferative cytokines

Fibrotic scar formation

Perisinusoidal space

Nutrient depletion from hepatocytes

Nodules smaller than 3 mm uniformly distributed

Early stage cirrhosis

Nodules larger than 3 mm

Posthepatitis or postnecrotic changes

Both micronodular and macronodular nodules in equal proportions

Alcohol abuse

Micronodular cirrhosis

10% to 30%

Acetaldehyde

Viral hepatitis

Hepatitis B, C, and D

<5%

10% to 20%

<1%

90%

60%

30%

10%

Interferon-based therapy

Hepatitis B virus (HBV)

80%

Nonalcoholic steatohepatitis

Hemolytic anemia, cystic fibrosis, glycogen storage diseases, α1-antitrypsin deficiency

Decreased bile flow into the duodenum

Primary biliary cirrhosis, primary sclerosing cholangitis, lymphoma, amyloidosis, Alagille syndrome, cystic fibrosis

Choledocholithiasis, pancreatic cancer, cholangiocarcinoma, pancreatic and choledochal cystic disease, AIDS, bile duct strictures, biliary atresia

Alcoholic hepatitis, viral hepatitis, inherited deficiencies

95%

Antimitochondrial antibody

Autoimmune hepatitis

Carbon tetrachloride, beryllium, vinyl chloride

Sub-Saharan Africa

Long-term total parenteral nutrition

Obstruction of the hepatic veins

Chronic right-sided heart failure, constrictive pericarditis, Budd–Chiari syndrome

Hemochromatosis

Wilson’s disease

A chronic disease process

Patient history and awareness of diagnosis

Jaundice, dark urine, muscle wasting, ascites, edema, purpura, encephalopathy, splenomegaly, spider angiomata, caput medusae, asterixis, gynecomastia, testicular atrophy, venous hum, palmar erythema, loss of body hair, Dupuytren’s contractures

Vascular congestion or chronic disease

Hemorrhoids

Excess conjugated bilirubin due to overproduction or underexcretion

Excess unconjugated bilirubin from enzymatic deficiency

Greater than 2 mg/dl

By the kidney, since it is water soluble

Bone, placenta, and liver

In bile

Obstruction of bile ducts

Aspartate aminotransferase (AST) and alanine aminotransferase (ALT)

ALT > AST

AST > ALT

Yes, even during acute exacerbation

Albumin

They decrease

Production of fibrinogen, prothrombin, and clotting factors V, VII, IX, X

Fat and vitamin K malabsorption or hepatocellular insufficiency

Hypersplenism and portal hypertension

Nodular irregularities and hepatic ductal anatomy

Up to 90%

Liver size, ascites, and presence of varices

Hepatic artery pressures and portal vein flow

Assessing portal/systemic vessel patency and hepatobiliary pathology

To permit histologic diagnosis

Coagulopathy, thrombocytopenia, cholangitis, tense ascites

Bile leak, peritonitis, pneumothorax, bleeding, pain

To relieve dyspnea and anorexia from increased intraabdominal pressure

Cause of ascites and presence of spontaneous bacterial peritonitis

Infection, bleeding, perforation of viscus

It acts as the metabolic clearinghouse regulating almost every aspect of metabolism

Portal hypertension, lymphatic obstruction, hypoalbuminemia, hyperaldosteronism, and increased ADH

By increasing hydrostatic pressure

It allows fluid to leak (weep) from the liver surface

By lowering oncotic pressure and promoting fluid loss into the extravascular space

Increased aldosterone due to impaired liver function

It increases total body sodium and water by enhancing sodium resorption in the distal tubule

Due to perceived hypovolemia sensed by the carotid body and CNS

Decreased free water clearance

High cardiac output with low systemic vascular resistance

Peripheral shunting and vasodilatory agents

Prostaglandins, GABA, VIP, substance P, insulin, glucagon, bile acids

Decreased metabolism may contribute to vasodilation

Phenylethylamine, tyramine, octopamine

They displace sympathetic transmitters like norepinephrine

Renal failure in cirrhosis with oliguria, increased BUN and creatinine

Resolves with relief of ascites and improved renal perfusion

Resolves with improved liver function and increased vascular resistance

Urine sodium concentration less than 10 mEq/L

Normal or low

Increased

Normal or decreased

Increased

Normal or increased

Decreased

Low

Normal

Less than 10 mEq/L

Effective hypovolemia

Maldistribution of blood flow and portorenal reflex

Intractable ascites and hepatic encephalopathy

High hepatic vein wedge pressure

Volume infusion, β-adrenergic agents, levodopa

Only when hepatic function improves

Ascites reinfusion

Peritoneal-atrial shunt and side-to-side portal decompression

Gastrointestinal hemorrhage, portosystemic shunting, infection, excessive dietary protein, constipation, narcotics, and sedatives

Spontaneous bacterial peritonitis

It increases ammonia levels, exacerbating encephalopathy

It may increase ammonia absorption from the gut

They can exacerbate the condition by altering mental status and reducing liver function

Because cirrhosis can lead to complications that increase surgical risk

Prophylactic treatment for complications of cirrhosis

To serve as a prognostic guide and estimate surgical risk

Through preoperative interventions like nutritional support and bowel preparation

Improved liver function and reduced surgical risk

Because cirrhosis can lead to complications that increase surgical risk

Prophylactic treatment for complications of cirrhosis

To serve as a prognostic guide and estimate surgical risk

Through preoperative interventions like nutritional support and bowel preparation

Improved liver function and reduced surgical risk

The severity of cirrhosis and surgical risk

Ascites, bilirubin, encephalopathy, prothrombin time, and albumin

Less than or equal to 2.0 mg/dl

Greater than or equal to 3.0 mg/dl

None

Minimal

Less than or equal to 3.0 g/dl

4–6 seconds

5–6 points

10–15 points

5 to 7 points

8 to 10 points

11 points or more

2%

10%

50%

Ascites, variceal bleeding, encephalopathy, and hepatorenal failure

To manage fluid and electrolyte balance

Intravascular dehydration and prerenal acute renal failure

1.1 g protein/kg/day

A total parenteral nutrition solution high in branched-chain amino acids and low in aromatic amino acids

Low-sodium enteral diet

It increases intraluminal protein load

H2 blockers

It decreases intraluminal bacterial counts

It converts NH3 to poorly absorbed NH4 by lowering colonic pH

10%

20% to 70%

Up to 30%

20% to 50%

30%

Up to 70%

Greater than 12 mm Hg

Nasogastric lavage

Esophagogastroduodenoscopy

50% to 90%

Mallory–Weiss tears, portal hypertensive gastropathy, peptic ulcers, neoplasms

Airway protection

Nasogastric tube with saline lavage

Crystalloid resuscitation

Packed red blood cells, fresh frozen plasma, cryoprecipitate, platelets

250 μg IV bolus

25 to 50 μg/hr for 2 to 4 days

20 units IV over 20 minutes

0.2 to 0.4 units/min

Nitroglycerin

Sclerosant injection and band ligation

Variceal banding

Esophageal stricture, chest pain, perforation, hemorrhagic ulceration, bacteremia

Sengstaken–Blakemore or Minnesota tube

40 to 50 ml

200 to 300 ml

35 to 40 mm Hg

Gastric erosion, perforation, aspiration pneumonia

20%

Transjugular Intrahepatic Portosystemic Shunt

90%

10%

Hepatic encephalopathy (25%), accelerated liver failure (5%)

Surgical decompression

Portosystemic shunt, esophagogastric devascularization, liver transplant

Hepatic encephalopathy

One that eliminates all portal flow, like portacaval shunt

Portacaval end-to-side shunt (Eck fistula) or side-to-side portacaval shunt

Surgical patients had significantly lower rebleeding rates (9–25% vs. 68–98%).

No, current data do not show a statistically significant survival benefit.

90% effective

15% to 30%

Hepatic failure (13–18%)

Lack of significant survival benefit

End-to-side shunt for acute hemorrhage and side-to-side shunt for refractory ascites

Budd–Chiari syndrome, liver transplant anticipation, refractory ascites

Mesocaval, portacaval, and mesorenal shunts using a graft

Grafts >10 mm are considered total shunts

Higher rate of late thrombosis

They are useful in liver transplant candidates

Splenectomy with anastomosis of splenic vein to left renal vein

Physiologically similar to side-to-side portacaval shunt

Probably has a higher thrombosis rate compared to portacaval shunts

Splenectomy with anastomosis of the portal side of the splenic vein to the left renal vein

It is similar to a side-to-side portacaval shunt

Probably has a greater thrombosis rate

Portal venous flow to the liver via the mesenteric veins

A selective shunt involving ligation of the splenic vein and end-to-side anastomosis to the left renal vein

Via the short gastric veins

Maintains portal perfusion in 90% of patients

7–10%

Improved survival in nonalcoholic cirrhosis

Possibly lower incidence of hepatic failure and encephalopathy

60% 5-year survival rate

Rebleeding is more common in sclerotherapy; shunting may cause liver dysfunction

Splenic vein >7 mm and absence or control of ascites

Sugiura procedure

Japan

Orthotopic liver transplantation

Donor availability

70%

To preserve portal anatomy for transplantation

Banding, sclerotherapy, TIPS, or selective shunting

Anastomosis of spleen to lung through diaphragm to decompress varices through pulmonary circulation

Peritoneovenous shunt

Directly into the superior vena cava

A one-way valve that opens when intraabdominal pressure exceeds 3 cm H2O

It has a subcutaneous pump to prevent clogging by active pumping

Sepsis, CHF, DIC, hypokalemia, shunt malfunction, air embolism, and SVC thrombosis

With serial fibrinogen levels, fibrin degradation products, and platelet counts

The shunt must be ligated