Liver Review

Vic Vernenkar, D.O. St. Barnabas Hospital Bronx, NY

Major Structures and Landmarks

Glissons capsule: the peritoneal lining that surrounds the liver. Bare area: posterior surface of the liver not covered. Coronary ligaments: reflections of peritoneum on the posterior surface.

Major Structures and Landmarks

Triangular ligaments: lateral extensions of the coronary ligaments. Falciform: from umbilicus to diaphragm, contains obliterated umbilical vein. Ligamentum teres, extends from falciform on undersurface of liver.

Anatomy
Eight segments, based on arterial and portal venous inflow. Segment 1 is the caudate lobe of the liver. Segments 2-4 are segments of the left lobe resected during left hepatic lobectomy. Segments 5-8 are segments of the right lobe resected during right hepatic lobectomy.

Segments

Anatomy
Falciform ligament does not divide right and left lobes of liver, the portal fissure or Cantlies line is a plane passing from the left side of the gallbladder fossa to the left side of the IVC. It defines the physiologic division between left and right lobes of liver. It does separate medial and lateral segments of left lobe

Anatomy
A right trisegmentectomy includes a resection of the right lobe plus segment 4. A left lateral segmentectomy includes resection of segments 2 and 3 to the left of the falciform. Resection of 80% of parenchyma is compatible with life.

Anatomy
Portal vein is a valveless vein formed by SMV and splenic vein behind head of pancreas. Passes posteriorly to the bile duct and hepatic artery in the hepatoduodenal ligament. 75% of livers blood supply.

Anatomy
Portal vein drains blood from the small and large intestines, stomach, spleen, pancreas,and gallbladder. The portal trunk divides in to 2 lobar veins, the right drains the cystic vein, the left receives umbilical and paraumbilical veins that enlarge to form the caput medusae. The coronary vein drains the distal esophagus, which also enlarge in PHTN.

Anatomy
Common hepatic artery arises from the celiac artery and becomes the proper hepatic artery after the GD branches. Passes medial to the bile duct and anterior to portal vein. Bifurcates into right and left hepatics in liver parenchyma. Can come off SMA (right) or Left gastric (left). Pringle maneuver.

Infections of Liver
Pyogenic liver abscesses (80% of all liver abscesses). Routes of infection are portal, ascending biliary tree, bacteremia via hepatic artery, direct extension (appendicitis), primary infection post trauma. Intra-abdominal infection most common identifiable source (biliary, colonic). ABX plus drainage, look for source.

Infections of Liver
Amebic Liver abscess, entamoeba histolytica. Via portal venous system after intestinal infection after a trophozoite is ingested. Contains necrotic tissue and blood, anchovy paste. Right lobe (80%), solitary (80%). CT scan (? One?) Antibody test specific. Non surgical, Flagyl. Surgery if rupture or secondary infection.

Infections of Liver
Hydatid Liver Cysts are rare liver cysts, right lobe, echinococcal, dogs that eat sheep (carrier). Vague abdominal pain, jaundice. Ct characteristic (calcified wall), ELISA test for antibody >90%, eosinophilia (10-30%). Surgical drainage, hypertonic saline, removal of cyst wall, dont spill it! anaphylaxis. Mebendazole

Benign Tumors
Hemangiomas (most common). Symptomatic, Surgical. Rupture rare, most asympt.Women. Adenomas (exclusively in women 30-50, OCP risk factor). 10% malig trans, rupture. Surgical. Focal nodular hyperplasia (FNH).Women 2050, stellate scar on CT. Kupffer cells on scan.Non surgical. Simple Cysts. Surgical if sympt, rupture, infection, bleed, or suspicious. Unroof, oversew. Polycystic liver disease associated with renal failure. Women 30-80, 50% PC kidneys as well.

Malignant Tumors
Hepatocellular carcinoma (HCC) most common, men, 40-70. Risks: cirrhosis, Hep B, Hep C, carcinogens, hemachromatosis, tyrosinemia, glycogen storage, Wilsons, adenoma, schistosomiasis, alpha-1 antitrypsin deficiency, blood group B.

Malignant Tumors
Dx: AFP (elevated 40-70%), US, CT, MRI TX: 5-y survival 31% for resectable tumors. With no treatment, 1-4 months,11% operative mortality, cirrhosis is the limiting factor, recurrence 50%, so transplant an option. Chemo is no benefit, transarterial embolization, ethanol injection may help.

Malignant Tumors
Liver metastases are most common tumors of liver! Much more frequent than primary tumors. Colon, lung, breast, melanoma, carcinoid, renal cell. DX: CEA a reliable indicator for recurrence of colon cancer previously treated. CT scan, IOUS.

Malignant Tumors
TX: Liver resection other than for colon cancer show no reliable benefit. 5-y survival post resection 30-35%(colorectal). Untreated <5%. 5% operative mortality. Size, number, location, extent of primary tumor, resectable lesions are a small minority of patients. If mets to other areas of body, contraindicated.

Malignant Tumors
Hepatoblastomas are primary malignant tumors of liver seen in boys younger than 2 years old. Cholangiocarcinomas are primary malignant tumors of biliary ductal epithelium, can present as intrahepatic or extrahepatic lesions.

Portal Hypertension

Background
Portal pressure gradient 12 mmHg or more Often associated with varices and ascites. Many conditions are associated with it, the most common being cirrhosis of the liver.

Causes of Portal HTN

Four Major Consequences

Ascites Portosystemic venous shunts and varices. Congestive splenomegaly Hepatic encephalopathy

Mortality/Morbidity
Variceal hemorrhage most common complication 90% with cirrhosis develop varices. 30% of these bleed. The first episode is estimated to carry a mortality of 30-50%.

Pathophysiology
P=FR, where P is pressure gradient thru the portal system, F is the volume of blood flowing thru the system, R is the resistance to flow. Changes in either F or R affect the pressure. In most types of portal hypertension, both flow and resistance are altered.

History
Directed towards determining the cause, the presence of complications of portal hypertension. Jaundice, transfusions, IVDA, pruritis, hereditary liver disease, ETOH? Hematemesis, melena, mental status, abdominal girth, pain, fever, hematochezia?

Physical
Signs of portosystemic collateral formation. Dilated veins in abdominal wall Caput medusa Rectal hemorrhoids Ascites Umbilical hernia

Signs of Liver Disease

Ascites Jaundice Palmar erythema Asterixis Testicular atrophy, gynecomastia Muscle wasting, Dupuytren contracture Splenomegaly

Caput Medusa

Lab Studies
LFTs PT/PTT Albumin Hepatitis serology Platelets ANA, Antimitochondrial antibodies Alpha 1-antitrypsin deficiency

Imaging Studies
Duplex is safe, noninvasive. Demonstrates portal flow, portal vein thrombosis, splenic vein thrombosis Nodular liver surface, splenomegaly, presence of collateral circulation. Limitations include meals, meds, sympathetic nervous system affect flow.

Imaging Studies
CT scan when US inconclusive Look for collaterals from portal system Dilatation of the vena cava suggests portal hypertension. Limitations include not being able to use IV contrast in allergic patients or with renal failure.

Incidental Finding on Barium Swallow

Procedures
Hemodynamic measurement of pressure, usually not performed due to invasive nature. Measures hepatic venous pressure gradient (HVPG). Similar to Swan Ganz, where balloon is inflated measuring wedged hepatic venous pressure, minus the unoccluded pressure is the HVPG.

Procedures
Endoscopy is performed to screen for varices. Gastroesophageal varices confirms diagnosis of portal hypertension, absence does not rule it out. Many times an incidental finding when scoped for something else.

Varices on EGD

Varix Banding

Medical Care
Treatment is directed at cause. Emergent treatment Primary prophylaxis Elective treatment

Emergent Treatment
Bleeding from varices ceases spontaneously in 40%. Rebleed in 40% within 6 weeks. Following resuscitation, treatment includes control of bleeding, prevention of recurrence, blood replacement, avoid over expansion of volume status. Diagnose source of bleed, specific treatment of bleeding lesion.

Emergent Treatment
All patients with cirrhosis and upper GI bleed are at risk for severe bacterial infections, which are associated with early rebleed. Use of antibiotics shown to increase survival, decrease rate of infection. Thus prophylactic use of antibiotics in acute bleeding is recommended.

Pharmacologic Therapy
Somatostatin-decreases portal flow, splanchnic vasoconstriction. Octreotide- 50mcg/h shown to reduce complications of bleeding after sclerotherapy. Vasopressin- reduces blood flow to all splanchnic organs, decreases portal pressure, venous blood flow. Use nitroglycerin with it! Its the most potent splanchnic vasoconstrictor.

Endoscopic Therapy(EST, EVL)

Hemostasis in 80%, declines to 70% at day 5 due to very early rebleeding. No more than 2 sessions before deciding on TIPS or surgery. Complications include fever, stricture, perforation, mediastinitis, ulceration, pleural effusion. EVL and EST comparable in control of bleeding EST associated with more complications.

Minnesota Tube
Balloon tamponade only in massive bleeding as a temporizing measure. Complications Has 4 lumens, 1 for gastric aspiration, 2 to inflate the balloons, 1 above the esophageal balloon to prevent aspiration. Usually only need to inflate gastric balloon.

Sengstaken Tube

Prophylaxis
Beta-blockers (propanolol, nadolol) are non cardioselective, reduce portal and collateral blood flow. Also reduces cardiac output, splanchnic vasoconstriction. First bleeding rates significantly reduced, mortality rates lower as well

Prophylaxis
No role for sclerotherapy in primary prophylaxis. EVL is more effective than no treatment to prevent first bleed. Similar efficacy to beta-blockers, with more adverse effects. Not recommended for primary prophylaxis except perhaps in patients with very large varices.

Elective Treatment
This is for prevention of rebleeding (2 year recurrence rate of 80%). Propanolol and nadolol, reduce rebleed, increase survival. Beta blockers vs sclerotherapy have comparable rates of prevention EVL is considered treatment of choice in prevention of rebleeding, may combine with drugs.

Surgical Treatment (Shunts)

Total Portosystemic shunts include any shunt larger than 10mm between portal vein and IVC. Includes Eck (end to side) and side to side portocaval shunts. Eck fistula controls bleeding, but ascites unrelieved. Side to side controls bleeding and ascites, but encephalopathy a problem (40-50%).

Surgical Shunts
Partial portal systemic shunts reduce the size to 8mm in diameter. Use an interposition graft between portal vein and IVC. 90% control of bleeding, decreased incidence of encephalopathy and liver failure.

Surgical Shunts
Selective shunts aim to decompress varices whilst maintaining portal hypertension to maintain portal flow to liver. Warren distal splenorenal shunt, the most commonly used for patients with refractory bleeding and good liver function. Decompresses GE varices thru short gastrics, spleen, splenic vein to left renal vein. Lower incidence of encephalopathy (15%), preserves some liver function. It does produce ascites.

Splenorenal Shunt

Devascularization Procedures
Include splenectomy, gastroesophageal devascularization, esophageal transection. Incidence of encephalopathy is low, because of maintenance of portal flow. Used in patients who are not candidates for decompression in whom 1st line therapy has failed. This includes pts with splenic or portal vein thrombosis in addition to cirrhosis

Denver and Leveen Shunts

Subcutaneous shunts that drain ascitic fluid from the abdomen into the central venous system. Come with pressure valves. DIC is a known complication of peritoneovenous shunting of ascitic fluid.

Devascularizaton
Splenectomy- the spleen is a major inflow path to GE varices. Splenectomy gives better access to fundus and distal esophagus to complete the devascularization. Complicated by portal vein thrombosis, and ascites.

Devascularization
Sugiura procedure- devascularizes whole greater curve from pylorus to esophagus, upper two thirds of lesser curve. The esophagus is devascularized a minimum of 7 cm.

Liver Transplant
The ultimate shunt, as it relieves portal hypertension, prevents bleeding, manages ascites and encephalopathy by restoring liver function. Child class A: shunt surgery Child class B: shunt or TIPS Child class C: TIPS or liver transplant

Childs Classification
A: 2% mortality B: 10% mortality C: 50% mortality

Tips
For continued bleeding despite medical and endoscopic treatment in patients with Child C disease and selected Child B disease. It is only useful in portal hypertension of hepatic origin. Internal jugular to hepatic vein thru hepatic parenchyma to portal vein. Tract dilated and stented.

TIPS

Accepted Indications
Active bleeding despite endoscopic or pharmacologic treatment Recurrent variceal bleeding despite adequate endoscopic treatment. Potential indications include bleeding gastric fundic varices, refractory ascites. A bridge to transplantation.

Complications of TIPS
Hematoma, cardiac arrythmias, bacteremia Perihepatic hematoma, rupture of liver capsule Extrahepatic punture of portal vein Arterioportal fistula, portobiliary fistula Encephalopathy (30%) Liver failure

Overview of Treatments

Splenic Vein Thrombosis

Can lead to isolated gastric varices without elevation of pressure in portal system These gastric varices can bleed Most often caused by pancreatitis Treatment is splenectomy.