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neoplasm.

2.The varices are generally limited to the stomach (gastric varices) and therefore are curable by splenectomy.

L

Ascites is a complication of hepatic disease.

1.Etiology. It results from sinusoidal hypertension, hypoalbuminemia, abnormal hepatic and abdominal lymph production, and abnormal salt and water retention by the kidneys.

a.Salt and water retention are due to hyperaldosteronism, which is related to decreased breakdown of aldosterone by the liver.

b.Ascites may be worsened by portosystemic shunts with exception of side-to-side portacaval and mesocaval shunts (see II H 3 b, c).

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2.Medical management of ascites is efficacious and involves salt and water restriction and diuretics, especially the aldosterone antagonists.

3.Peritoneal-jugular shunting may be used to treat ascites that is refractory to medical management. Its efficacy in either controlling ascites or improving survival has not yet been definitely demonstrated.

a.A plastic tube is implanted surgically, originating in the peritoneal cavity and terminating in the jugular vein. A valve in the tubing controls the direction of flow out of the peritoneal cavity.

b.Diuretics should be continued for optimal shunt results.

c.Peritoneal-jugular shunts may result in bleeding due to the presence of factors in ascitic fluid that stimulate the development of disseminated intravascular coagulation.

4.TIPS (see II E 3 e) has also been found effective in controlling refractory ascites.

IIIGallbladder and Extrahepatic Biliary Tree

AOverview

1.Embryology

a.Development of the liver and biliary structures begins during the fourth week of fetal life.

b.The hepatic diverticulum forms as an outpouching of the foregut.

1.The cranial portion forms the liver, the larger branches of the intrahepatic ducts, and the proximal extrahepatic biliary tree.

2.The caudal portion forms the gallbladder, cystic duct, and common bile duct.

2.Anatomy (Fig. 14-13)

a.Extrahepatic biliary tree

1.Structure

a.The left and right hepatic ducts join together after leaving the liver. This confluence forms the common hepatic duct (3–4 cm in length).

b.The common hepatic duct is joined at an acute angle by the cystic duct to form the common bile duct (10 cm in length; 3–10 mm in diameter).

FIGURE 14-13 Gallbladder and extrahepatic biliary tree.

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c.The common bile duct is lateral to the common hepatic artery and anterior to the portal vein. The distal one third of the common bile duct passes behind the pancreas to the ampulla of Vater, also called the papilla.

d.The common bile duct joins the pancreatic duct in one of three ways.

i.Most commonly, the ducts unite outside the duodenum and traverse the duodenal wall and papilla as a single duct.

ii.They may join within the duodenal wall and have a short common channel.

iii.Least commonly, they enter the duodenum independently.

2.The sphincter of Oddi surrounds the common bile duct as it traverses the ampulla of Vater and controls bile flow.

3.Blood supply to the ducts

a.The hilar ducts within the liver parenchyma are supplied primarily from the hepatic arteries.

b.The blood supply to the supraduodenal common bile duct is variable, but generally blood flows superiorly. The most important vessels (the “three o'clock” and “nine o'clock” arteries) run along the sides of the duct, as their names imply.

b.The gallbladder is located on the inferior aspect of the liver and marks the division of the liver into its right and left lobes.

1.Anatomic portions

a.Fundus (most anterior)

b.Body, which serves as the storage area

c.Infundibulum (Hartmann's pouch), located between the neck and the body (most posterior)

d.Neck, which connects with the cystic duct

2.The wall of the gallbladder is composed of smooth muscle and fibrous tissue; the lumen is lined with high columnar epithelium.

3.Vasculature

a.Arterial supply. The gallbladder is supplied by the cystic artery, which is usually (95% of the time) a branch of the right hepatic artery that passes behind the cystic duct.

b.Venous return is via cystic veins to the portal vein and small veins that drain directly into the liver.

c.Lymphatic drainage from the gallbladder goes both to the liver and to hilar nodes.

4.Innervation is from the celiac plexus.

a.Motor innervation travels via vagal postganglionic fibers from the celiac ganglia. The preganglionic sympathetic level is T8–T9.

b.Sensory innervation travels from sympathetic fibers coursing to the celiac plexus through the right posterior root ganglion at levels T8–T9.

5.The valves of Heister are mucosal folds in the cystic duct. Despite their name, they have no valvular function.

c.Anomalies of the arterial and biliary systems are common. Because “normal” anatomy occurs in fewer than 50% of individuals, the surgeon must have a thorough knowledge of both normal and anomalous anatomy.

3.Physiology. Bile is produced by the liver and is transported via the extrahepatic ducts to the gallbladder, where it is concentrated and released in response to humoral and neural control.

a.Hepatic production of bile is under neural and humoral control. Vagal and splanchnic stimulation, secretin, theophylline, phenobarbital, and steroids all increase bile flow. Approximately 600 mL of bile are produced daily (normal range: 250–1,000 mL/day).

b.Composition of bile. Because the electrolyte concentration of bile approximates that of plasma, lactated Ringer's solution is a good replacement fluid for biliary losses. Bile is composed of:

1.Electrolytes and water

2.Bile pigments

3.Protein

4.Lipids

a.Phospholipids, primarily lecithin

b.Cholesterol

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c.Bile acids (bile salts); chenodeoxycholic acid and cholic acid conjugated with taurine and glycine

c.Functions of the gallbladder include:

1.Storage of bile

2.Concentration of bile

a.The absorption of water and electrolytes by the gallbladder mucosa results in a 10-fold increased concentration of lipids, bile salts, and bile pigments compared with hepatic bile.

b.The secretion of mucus protects the gallbladder mucosa from the irritant effects of bile and facilitates the passage of bile through the cystic duct. This mucus secretion represents the “white

bile” seen with hydrops of the gallbladder, which results from cystic duct obstruction.

3.Release of bile

a.The coordinated release of bile requires simultaneous contraction of the gallbladder and relaxation of the sphincter of Oddi.

b.This process is predominantly under humoral control (via cholecystokinin [CCK]), but vagal and splanchnic nerves also play a role.

B Radiologic diagnosis of biliary tract disease

1.Plain abdominal films demonstrate the 15% of gallstones that are radiopaque.

2.Real-time ultrasonography has a 90%–95% accuracy in identifying calculi. It is also useful in determining the presence of biliary ductal dilation, gallbladder wall thickening, and the presence of pericholecystic fluid.

a.Ultrasonography can be performed in a jaundiced patient.

b.It is usually the initial test obtained in the workup of a patient with biliary tract disease.

3.Oral cholecystography (OCG) is an alternative method for demonstrating biliary calculi in patients with an equivocal gallbladder sonogram. It is rarely used today.

a.This technique identifies abnormalities (visualization of stones or nonvisualization of the gallbladder) with a 95%– 98% accuracy.

b.The patient must ingest iopanoic acid tablets on the evening before the study. The chief disadvantages lie in its reliance on:

1.Absorption of contrast medium from the gastrointestinal tract

2.Uptake and excretion of contrast medium from the hepatocytes

3.Concentration of contrast medium in the gallbladder

4.Patency of hepatic and cystic ducts

c.Cholecystokinin stimulation is used to diagnose gallbladder disease in symptomatic patients with a normal OCG. A positive study is presented by either of the following:

1.Failure of the gallbladder to contract more than 40% at 20 minutes after CCK injection

2.Reproduction of the patient's pain after CCK injection

4.Hepatobiliary iminodiacetic acid (HIDA) scan (cholescintigraphy) makes use of a gamma-ray–emitting radioisotope (i.e., 99mTc) attached to a variety of lidocaine analogs bound to iminodiacetic acid, which is excreted in the bile.

a.A HIDA scan provides images of the liver, the biliary tree, and the intestinal transit of bile.

b.The HIDA scan is useful in the diagnosis of acute cholecystitis, choledochal cyst, bile leak (after laparoscopic cholecystectomy), and common bile duct obstruction.

c.A HIDA scan in conjunction with a CCK injection and subsequent ejection fraction calculation (normal is >35%) may be of value in diagnosing biliary dyskinesia and calculous and acalculous cholecystitis. In acute cholecystitis, the gallbladder cannot be visualized due to obstruction of the cystic duct. In common duct obstruction, the nuclide fails to enter the duodenum.

5.Endoscopic retrograde cholangiopancreatography (ERCP) is also useful in evaluating a patient with biliary tract disease. The procedure is both diagnostic and therapeutic.

a.This procedure permits evaluation of the stomach, duodenum, ampulla of Vater, pancreatic duct, and common bile duct.

b.If stones are present within the common bile duct, endoscopic papillotomy can be performed along with extraction of the stones. This procedure has a 90%–95% success rate.

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c.If a stricture is present, a stent can be inserted.

d.Complications include pancreatitis, bleeding, and duodenal perforation. The complication rate is approximately 10%, with a mortality rate of 1%.

6.Percutaneous transhepatic cholangiography (PTHC) is useful in evaluating a jaundiced patient. It can localize the site of the obstruction and also allows the placement of biliary drainage catheters. PTHC is usually performed when ERCP cannot be performed or when ERCP cannot visualize the proximal biliary systems because of a near-complete obstruction secondary to tumor, stone, or stricture.

7.CT and MRI are expensive, but they delineate dilated ducts as well as retroperitoneal lymphadenopathy and lesions of the pancreas and liver.

8.Intravenous cholangiography is no longer performed.

C Cholelithiasis (gallstones)

1.Types and mode of formation. Gallstones form as a result of biliary solids precipitating out of the solution. Most stones (70%) are made up of cholesterol, bilirubin, and calcium, with cholesterol as the major component.

a.Cholesterol stones are large and smooth.

1.The solubility of cholesterol in bile depends on the concentration of bile salts, lecithin, and cholesterol. Lecithin and cholesterol are insoluble in aqueous solution but dissolve in bile salt–lecithin micelles.

2.Failure of the liver to maintain a micellar liquid can be caused by an increase in the concentration of cholesterol or a decrease in the concentration of bile salts or lecithin; either can result in cholesterol stone formation.

3.Conversely, increasing the biliary concentration of lecithin and bile salts should hinder cholesterol stone formation.

a.This theory has been investigated by treating patients with cholesterol stones with oral bile salts.

b.In the National Cooperative Gallstone Study, patients with cholesterol gallstones were treated with chenodeoxycholic acid over a 2-year period. Complete resolution of stones was found in 13% of the patients, and partial dissolution in 41%. The recurrence rate is 50% at 5 years.

b.Pure pigment (bilirubin) stones are smooth and are green or black in color; they are associated with hemolytic disorders, such as sickle cell anemia or spherocytosis.

c.Calcium bilirubinate stones are associated with infection or inflammation of the biliary tree.

1.Infection results in an increase in biliary calcium as well as an increase in β-glucuronidase (which converts conjugated bilirubin to the unconjugated form).

2.The calcium binds to the unconjugated bilirubin and precipitates to form calcium bilirubinate stones.

3.Normal bile contains glucaro-1,4-lactone, which inhibits the conversion of conjugated to unconjugated bilirubin, and thus deters calcium bilirubinate stone formation.

2.Clinical presentation of cholelithiasis varies. It can present as (in increasing order of severity):

a.Asymptomatic cholelithiasis

b.Chronic cholecystitis

c.Acute cholecystitis

d.Complications of cholecystitis

e.Choledocholithiasis (common bile duct stones)

3.Asymptomatic cholelithiasis. The treatment of asymptomatic cholelithiasis is somewhat controversial.

a.Each year, approximately 1%–4% of patients with asymptomatic gallstones develop symptoms or complications

of their disease. Most patients do develop symptoms before developing a severe complication of cholelithiasis.

b.There is little evidence that prophylactic treatment is justified in the management of cholelithiasis, with the exception of calcified or porcelain gallbladder, which should be removed because the risk of malignancy exceeds 25%.

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c.The National Institutes of Health Consensus Conference on Gallstone and Laparoscopic Cholecystectomy, held in September 1992, does not recommend cholecystectomy for asymptomatic diabetic patients with gallstones. The opposite was widely practiced until recently.

D

Cholecystitis is inflammation of the gallbladder. In 85%–90% of patients, cholecystitis is caused by calculi, bile stasis, and bacteria; pancreatic juice irritation may play a lesser role.

1.Chronic cholecystitis

a.Clinical presentation. The patient complains of moderate intermittent pain in the right upper quadrant and epigastric region, nausea, and vomiting. The pain may radiate to the back or right scapular region. Symptoms may be associated with eating fatty foods.

b.Diagnosis. Laboratory studies are generally normal. With an OCG, the gallbladder fails to appear or shows filling defects. Ultrasonography reveals stones.

c.Treatment is elective cholecystectomy. Approximately 95% of patients receiving surgery for cholecystitis secondary to cholelithiasis are completely relieved of their symptoms. Approximately 5% of patients retain mild symptoms that presumably are unrelated to the biliary tree.

d.Nonoperative treatment (e.g., oral bile salts, lithotripsy) may be appropriate for patients with small stones and functioning gallbladders (determined by OCG) who are not operative candidates or who refuse surgery.

2.Acute cholecystitis

a.Pathophysiology

1.Most cases are due to an impacted stone in the gallbladder neck or the cystic duct with resultant obstruction. Direct pressure from the stone on the mucosa or duct obstruction causes ischemia, ulceration, edema, and impaired venous return, all of which lead to extensive inflammation in and around the gallbladder.

2.In 75% of cases, bacterial infection of the bile and gallbladder wall occurs.

3.Unchecked, these changes can lead to complications of acute cholecystitis.

b.Clinical presentation

1.The greatest incidence of acute cholecystitis is in adults 30–80 years old; women are affected more often than men.

2.Most patients give a history consistent with prior chronic cholecystitis, except this episode is worse or lasts longer.

3.Fever, nausea, and vomiting; right upper quadrant tenderness with or without rebound tenderness; and Murphy's sign are common. The gallbladder may be palpable.

c.The differential diagnosis includes:

1.Perforated or penetrating peptic ulcer

2.Myocardial infarction

3.Pancreatitis

4.Hiatal hernia