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Skandalakis’ Surgical Anatomy > Chapter 20. Extrahepatic Biliary Tract and Gallbladder >

History

The anatomic and surgical history of the extrahepatic biliary tract and gallbladder is shown in Table 20-1.

Table 20-1. Anatomic and Surgical History of the Extrahepatic Biliary Tract and Gallbladder

Aristotle (384-322 B.C.)   Mentioned absence of gallbladder in animals
Galen (ca. A.D. 130-200)   Stated that humans have a single bile duct, or perhaps paired bile ducts
Berengario da Carpi 1522 Agreed with Galen. Wrote, “Sometimes a man lacks a gallbladder; he is then of infirm health and a shorter life.”
De Laguna 1535 Agreed with Galen
Vesalius 1543 Did not accept concept of Galen
Fallopius 1606 Denied concept of Galen
Bergman 1701 First definite case of absence of human gallbladder
Vater 1723 First report of dilatation of common bile duct
Morgagni 1769 Reported deformations of the gallbladder; may have been first to see torsion of the gallbladder
Home 1813 Described biliary atresia
Bobbs 1867 Described hydrops of gallbladder and performed first successful removal of gallstones
Von Wyss 1870 Studied variations of the common bile duct
Nitze 1877 Introduction of cystoscope
Calot 1891 Original description of cholecystohepatic triangle (Triangle of Calot)
Swain 1894 Performed first successful operation for cystic dilatation of the bile duct, a cholecystojejunostomy
Eppinger 1902 Studied cholestasis
Dévé 1903 First description of gallbladder completely submerged in the liver substance (intrahepatic gallbladder)
Yllpö 1913 Reported extrahepatic biliary atresia due to embryonic developmental arrest
Reich 1918 Produced first roentgenography of biliary tree by injecting bismuth paste and petrolatum into an external fistula
Beall and Jagoda 1921 Obtained incidental opacification of the biliary tract during upper GI series performed with barium and buttermilk
Bakes 1923 First report of intraoperative endoscopic visualization of the bile ducts; used ampullary dilators which are now known as Bakes’ dilators
Neugebauer 1924 First preoperative diagnosis of cystic dilatation of the common bile duct
Boyden 1926 Studied duplication of the gallbladder
Ladd 1928 First successful repair of biliary atresia
Ginzburg and Benjamin; Gabriel 1930 Simultaneous studies of biliary tract with Lipiodol injections
Mirizzi 1931 First operative cholangiography
Boyden 1932 Reviewed reports from 1800-1932 of bile ducts entering the stomach
Hicken, Best, and Hunt 1936 Performed operative cholangiography through the cystic duct stump
Babcock 1937 Used cystoscope to visualize interior of gallbladder
McIver 1941 Visualization of bile duct, showing stone
Porcher and Caroli 1948 Designed device for operative cholangiography
Mirizzi 1948 Reported syndrome of a long cystic duct with impacted stone (Mirizzi’s syndrome)
Ahrens 1951 First description of intrahepatic biliary atresia
Mallet-Guy 1952 Attempted to establish operative cholangiography as a routine procedure
Wildegans 1953 Instrumental in development of observation choledochoscope and operating-observation choledochoscope
Healey and Schroy 1953 Studied intrahepatic anatomy of bile ducts
Boyden 1957 Described relationship of sphincter of Oddi to common bile duct
Kasai 1957 Described treatment of “noncorrectable” cases of biliary atresia by hepatic portoenterostomy. Report published in Japanese in 1957, in English in 1968.
Alonso-Lej et al. 1959 Presented first classification system for choledochal cysts (described 3 types)
Myers et al. 1962 Cinefluorographic observation of the common bile duct
Kune 1964 Described surgical anatomy of common bile duct
Klatskin 1965 Described adenocarcinoma at hepatic duct bifurcation (Klatskin tumors) [Altemeier had described same structures in 1957]
Hering 1972 Described the connecting link between bile canaliculi and ductules
Todani et al. 1977 Developed current standard classification of cystic dilatation of the common bile duct
Harlaftis et al. 1977 Reviewed the literature of gallbladder duplication
Northover and Terblanche 1978 First description of retroportal artery
Frimdberg 1978 Performed laparoscopic cholecystotomy in pigs
Toouli et al. 1982 to 1986 Studied normal and abnormal function of sphincter of Oddi
Filipi, Mall, and Reosma 1985 Performed first animal laparoscopic cholecystectomy
Mühe 1985 Successfully treated patients by laparoscopic cholecystectomy
Mouret 1987 Generally credited with first human laparoscopic cholecystectomy
Petelim 1991 Performed laparoscopic choledochocholithotomy
Cotton et al. 1991 Studied risks and benefits of endoscopic sphincterotomy for bile stones in elderly high-risk patients and healthy young patients with normal-sized ducts
1994
1995
O’Neill 1992 Wrote classic monograph on choledochal cysts
Hintze et al. 1997 Successfully treated post-gastrojejunostomy patients endoscopically for biliary disease

History table compiled by David A. McClusky III and John E. Skandalakis.

References

Cotton PB, Geenen JE, Sherman S, Cunningham JT, Howell D, Carr-Locke DL, Nickl NJ, Hawes RH, Lehman GA, Ferrari A, Slivka A, Lichtenstein DR, Baillie J, Jowell PS, Lail LM, Evangelou H, Bosco JJ, Hanson BL, Hoffman BJ, Rahaman SM, Male R. Endoscopic sphincterotomy for stones by experts is safe, even in younger patients with normal ducts. Ann Surg 1998;227:201-204.

Davis CJ. A history of endoscopic surgery. Surg Laparosc Endosc 1992;2(1):16-23.

Diekhoff EJ. Altemeier tumors? [letter] Am J Surg 1993;166:570-571.

Hintze RE, Adler A, Veltzke W, Abou-Rebyeh H. Endoscopic access to the papilla of Vater for endoscopic retrograde cholangiopancreatography in patients with Billroth II or Roux-en-Y gastrojejunostomy. Endoscopy 1997;29:68-73.

Hintze RE, Veltzke W, Adler A, Abou-Rebyeh H. Endoscopic sphincterotomy using an S-shaped sphincterotome in patients with Billroth II or Roux-en-Y gastrojejunostomy. Endoscopy 1997;29:74-78.

LaRusso NF (ed). Gallbladder and Bile Ducts. Philadelphia: Current Medicine, 1997.

Nagy AG, Poulin EC, Girotti MJ, Litwin DEM, Mamazza J. History of laparoscopic surgery. Can J Surg 1992;35:271-274.

Popper H. Vienna and the liver. In: Brunner H, Thaler H (eds). Hepatology: A Festschrift for Hans Popper. New York: Raven Press, 1985, pp. 1-14.

Schein CJ, Stern WZ, Jacobson HG. The Common Bile Duct. Springfield IL: Charles C Thomas, 1966.

Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994.

Toouli J (ed). Surgery of the Biliary Tract. New York: Churchill Livingstone, 1993.

Embryogenesis

Normal Development

The genesis of the extrahepatic biliary duct system and gallbladder may, perhaps, be the responsibility of the distal portion of the hepatic diverticulum. By the end of the 4th week, it has produced the cystic duct and gallbladder primordium. The common bile duct and the hepatic ducts may be seen at the beginning of the 5th week. The solid stage of the ducts takes place during the 5th week. The ducts elongate to reach the liver, progressively forming at this time. Slow ductal recanalization occurs approximately from the 6th through 12th weeks. Human fetal gallbladder contractility in the second half of pregnancy has been reported, although its physiological role is unknown.3

Gallstones are among fetal gallbladder anomalies that have been reported.4

Variations and Congenital Anomalies of the Gallbladder

In an ultrasonographic study of 1823 patients, Senecail et al.5 found morphologic variations and abnormalities in more than 33% of gallbladders, topographic variations in approximately 3.5%, and 3 cases of duplication.

Sites of potential malformations of the extrahepatic biliary tract and common bile duct are shown in Fig. 20-1. Anomalies are shown in Tables 20-2 and 20-3.

Table 20-2. Anomalies of the Extrahepatic Biliary Ducts and the Gallbladder

Anomaly Prenatal Age at Onset First Appearance Sex Chiefly Affected Relative Frequency Remarks
Extrahepatic biliary atresia Acquired Soon after birth Equal Rare Most likely infectious or environmental; not genetic or congenital
Variation of the hepatic ducts 5th week None Equal Very common  
Accessory hepatic duct 4th week? None Equal Common  
Duplication of common hepatic duct 4th week? None ? ?  
Subvesicular and hepatocystic ducts 6th week None ? Rare Anomaly not well established
Variations of the common bile duct 4th week None ? Common  
Cystic dilatations of common bile duct Unknown Any age Female Rare (most common in Japanese)  
Duplication of common bile duct 4th-5th week None ? Very rare  
Absence of gallbladder 4th week Adulthood, if ever Female Rare  
Duplication of gallbladder 4th week None Equal Rare  
Deformation of gallbladder 6th week None Equal Uncommon  
Left-sided gallbladder 4th week? None ? Very rare  
Intrahepatic gallbladder 2nd month None ? Rare  
Mobile gallbladder 2nd month Late adulthood, if ever Female Rare Symptoms result from torsion
Heterotopic mucosa in gallbladder 4th week? None ? Very rare  
Adenomyoma of gallbladder 6th week? Late adulthood, if ever Female Rare  
Anomalies of cystic duct 5th week None ? Common  

Source: Skandalakis JE, Gray SW (Eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.

Table 20-3. Symptoms, Diagnosis, and Treatment of Anomalies of the Biliary Tract

Anomaly Pathology Symptoms Diagnosis Treatment Remarks
Extrahepatic biliary atresia   Early: Persistent progressive jaundice Elevated serum billirubin; biopsy to confirm presence of intrahepatic or Kasai portoenterostomy cholangiogram Anastomosis where possible: Hepatocholedochostomy; Choledochoduodenostomy; Cholecystoduodenostomy or Kasai portoenterostomy (various modifications) 80% will ultimately require liver transplant
Late: Enlarging abdomen; white stools
Variations of hepatic ducts   Asymptomatic Incidental radiographic or surgical finding None required  
Accessory hepatic duct   Asymptomatic Incidental radiographic or surgical finding None required  
Duplication of common hepatic duct   Asymptomatic or surgical finding Incidental radiographic    
Subvesicular and hepatocystic ducts   Abdominal distension Identified only at autopsy   Possible source of hepatic cysts
Variations of common bile duct   Asymptomatic Incidental radiographic or surgical finding    
Cystic dilatation of hepatic and common bile ducts   Early: jaundice IV cholangiogram, abdominal ultrasound; ERCP Cystectomy with Roux-en-Y; common hepaticojejunostomy Source of malignancy if not totally resected
Duplication of common bile duct   Asymptomatic Incidental radiographic or surgical finding    
Ectopic orifice of common bile duct   Asymptomatic Usually at surgery or autopsy    
Absence of gallbladder   Asymptomatic Absence on x-ray film not diagnostic; preoperative diagnosis not possible    
Duplication of gallbladder   Asymptomatic Recognizable on radiography    
Deformations of gallbladder   Asymptomatic May be recognized on radiography   May be result of cholecystitis and not of congenital origin
Abnormal positions of gallbladder          
  Left sided   Asymptomatic May be outside the radiographic field, hence not visualized    
  Intrahepatic   Asymptomatic Visualized radiographically; apparently absent at operation    
  Mobile   Symptoms of torsion or strangulation At surgery    
Absence of cystic duct (sessile gallbladder)   Asymptomatic Incidental radiographic or surgical finding    
Anomalies of junction of cystic and common bile ducts   Asymptomatic Incidental finding at surgery   May predispose to lithiasis

ERCP, endoscopic retrograde cholangiopancreatography

Source: Skandalakis JE, Gray SW (Eds). Embryology for Surgeons, 2nd Ed. Baltimore: Williams & Wilkins, 1994; with permission.

Fig. 20-1.

Sites of potential biliary tract malformations. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

Absence of the Gallbladder

Occasionally the gallbladder (and usually the cystic duct as well) is absent or vestigial (Fig. 20-2). The absence must be confirmed by ruling out an intrahepatic gallbladder or a left-sided gallbladder. A history of gallbladder disease with previous cholecystectomy is not in itself sufficient to establish absence of the organ. In at least three cases, a gallbladder was removed and the incision closed without discovery of the presence of a second gallbladder.2

Fig. 20-2.

Anomalies of gallbladder. A, Complete absence of gallbladder and cystic duct. B, Vestigial gallbladder and cystic duct atresia. C, Blind, dilated cystic duct without gallbladder.

Di Vita et al.7 reported agenesis of the gallbladder associated with lithiasis of the common bile duct. This rare congenital malformation is frequently associated with other anomalies.

It was suggested by Wilson and Deitrich8 that absence of the gallbladder may be a familial trait. Ultrasonography now makes it possible to detect the absence of the organ in individuals without gallbladder disease. Sarli et al.9 recommend preoperative cholangiography and laparoscopic exploration completed by laparoscopic sonography as adequate modalities to diagnose gallbladder agenesis. Gotohda et al.10 stated that if the gallbladder is not visualized by imaging techniques, laparoscopy should be performed before laparotomy.

Multiple Gallbladders

A double gallbladder in a human was found at autopsy by Blasius in 167411; the first such anomaly to be recorded from observation of a living patient was in 1911.12 Harlaftis et al. reviewed 297 reports of double gallbladder and eight reports of triple gallbladder.6 Of these anomalies, 142 were described adequately. Triple gallbladders can each have an individual cystic duct or all share the same duct. Variably, two of the gallbladders can share a duct, and the third have a separate duct.

Multiple gallbladders form a continuous spectrum of malformations, from an externally normal organ with an internal longitudinal septum to the most widely separated accessory gallbladders. For practical purposes, the anomalies can be categorized into six basic types.6,13,14 Three types belong to the split primordium group and three belong to the accessory gallbladder group. All are described below.

Split Primordium Group

In a split primordium, multiple gallbladder elements drain to the common bile duct by means of a single cystic duct. The three types follow.

 

Septate gallbladder. A longitudinal septum divides the gallbladder into two chambers. There may be no external trace of the septum or there may be a fundic cleft extending toward the neck (11.3%) (Figs. 20-3A, 20-3B).

Bilobate “V” gallbladder. Two gallbladders, separated at the fundus, are joined at the neck by a single, normal cystic duct (8.5%) (Fig. 20-3C).

“Y” duplication. Two separate gallbladders are present. Their respective cystic ducts join to form a common cystic duct before entering the common bile duct (25.3%) (Figs. 20-3D, 20-3E).

Fig. 20-3.

Types of double gallbladder arising from a split primordium. See text for explanation. (Modified from Colborn GL, Skandalakis LJ, Gray SW, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 5: Variations and anomalies. Contemp Surg 1987;31(2):27-39; with permission.)

Accessory Gallbladder Group

 

Ductular “H” duplication. The cystic duct and accessory cystic duct enter the common bile duct separately. This is the most frequent type (47.2%) (Figs. 20-4A – 20-4C).

Trabecular duplication. The accessory cystic duct enters a branch of the right hepatic duct within the liver (2.1%) (Fig. 20-4D). Rarely, the cystic duct is duplicated without duplication of the gallbladder (Fig. 20-4E).

Triple gallbladder. Various combinations may be present (5.6%).

Fig. 20-4.

Types of “accessory” gallbladder. See text for explanation. (Modified from Colborn GL, Skandalakis LJ, Gray SW, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 5: Variations and anomalies. Contemp Surg 1987;31(2): 27-39; with permission.)

Gallbladder duplication is reported more often in women than in men (1.7:1), but the incidence of duplication is probably more nearly equal. The disparity might be attributed to the greater incidence of gallbladder disease in women. When disease is present, both gallbladders are usually affected if they are intimately connected, less frequently if separation is complete.

Ultrasound is the best diagnostic test for double gallbladder and is useful in both healthy and diseased states.15 Previously, oral or intravenous cholecystogram failed to detect duplication preoperatively in 60% of cases.6 Nuclear medicine scan may identify double gallbladder, but if cystic duct obstruction is present it will fail to demonstrate one or both organs. Symptoms of gallbladder disease in a patient who has previously undergone cholecystectomy can suggest the presence of a second organ or of cystic duct remnant syndrome.16

Left-Sided Gallbladder

Rarely, a gallbladder is found on the inferior surface of the left lobe of the liver. In such cases, the cystic duct enters the common bile duct from the left. There is no associated functional disorder. Ultrasonography should detect this anomaly, but the radiologist must be alert.

Intrahepatic Gallbladder

An intrahepatic gallbladder is submerged in the liver and gives the appearance of absence of the gallbladder. CT scan or ultrasonography may provide its only evidence. A high percentage of occurrence of lithiasis is associated with this anomaly.

Mobile Gallbladder

At the opposite extreme from intrahepatic gallbladder is the occasional mobile gallbladder, attached to the liver by a mesentery. Such a gallbladder is susceptible to torsion and strangulation. Otherwise, it causes no symptoms.

Vascular Anomalies

Congenital Portocaval Shunt

A portal vein entering the inferior vena cava was first publicly described in 1793.17 This “natural” portocaval shunt is, perhaps, the result of persisting supracardinal veins18 and is an anomaly of the formation of the vena cava rather than of portal vein development. The condition is compatible with life.

Preduodenal Portal Vein

In 1921, Knight19 described a patient in whom the portal vein crossed the duodenum anteriorly instead of posteriorly. In the next 40 years, 13 more cases were recorded. In Knight’s case, there was no history of symptoms; however, duodenal compression has resulted from such an anomalous vein.20

The portal vein develops from the primitive paired vitelline veins (Fig. 20-5A) that arise on the yolk sac and pass up the body stalk to enter the developing heart. They reach their greatest development in the fourth week. Two extrahepatic cross-connections develop between the paired vessels. The cranial anastomosis lies behind the duodenum and the caudal anastomosis passes in front of the duodenum. Normally the cranial, retroduodenal anastomosis persists as the portal vein (Fig. 20-5B). Abnormally the caudal, preduodenal anastomosis can become the portal vein (Fig. 20-5C).

Fig. 20-5.

Embryonic origin of preduodenal portal vein. A, Two extrahepatic communications between vitelline veins early in sixth week of gestation. B, Normal development. Cranial, postduodenal communicating vein persists as part of portal vein. C, Anomalous development. Caudal, preduodenal communicating vein persists while cranial vein disappears.

Failure of Portal Vein to Bifurcate

Hardy and Jones21 reported failure of the portal vein to bifurcate and emphasized the surgical significance of this anomaly.

Congenital Absence of Portal Vein

Congenital absence of the portal vein is a very rare anomaly in which the intestinal and splenic venous drainage bypasses the liver, draining into the inferior vena cava. The absence of portal flow may cause nodular regenerative hyperplasia of the liver.22

Anomalous Pulmonary Veins

Anomalous pulmonary veins that pierce the diaphragm and enter the portal system are found occasionally. At least 37 cases were reported by Leal del Rosal and colleagues.23 Such veins compose about 15% of all anomalous pulmonary vein drainage. This anomaly results in a left-to-right shunt that is usually compensated for by a patent foramen ovale providing a right-to-left shunt. This malformation is caused by failure of the pulmonary vein to tap the pulmonary plexus, combined with persistence of a connection with the splanchnic plexus in the fifth week.24 Successful correction of this anomaly by anastomosing the pulmonary channel to the left atrium was reported by Woodwark and colleagues.25

Variations and Anomalies of the Biliary Ducts

Extrahepatic Biliary Atresia

Congenital biliary atresia is the most serious malformation of the biliary tract. A short segment, an entire duct, or the whole system may be atretic. All possible combinations may be encountered. Most of these have been described by Thompson26 and Holmes27 (Fig. 20-6). The atretic duct may be hypoplastic,28 stenosed, or reduced to a fibrous band that is easily overlooked by the surgeon.

Fig. 20-6.

Atresias of biliary tract. A-F, Extrahepatic biliary atresias. G, Intrahepatic atresia with normal extrahepatic ducts. Defects A-C are “correctable”; at least one patent duct emerges from the liver. D-G are termed “noncorrectable.” (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons. 2nd ed. Baltimore: Williams & Wilkins, 1994; with permission.)

From a purely embryologic viewpoint, if a liver has formed from the hepatic primordium, agenesis of structures other than those of the cystic diverticulum (the gallbladder and cystic ducts) is hard to imagine. In other words, the hepatic ducts and the common hepatic ducts have formed, even if in a greatly reduced state. Even when no remnant of the hepatic ducts can be identified, no true “agenesis” of these ducts has occurred.

Hepatic biliary ductular atresias may be divided into three groups:

 

The first type includes patent proximal hepatic ducts and occluded distal ducts. Patency may occur in any portion of the right or left hepatic duct as it emerges from the liver. This atresia is called “correctable” (Figs. 20-6A-C).

The second type includes occluded proximal ducts. No portion of the emerging hepatic duct is patent. This atresia is called “noncorrectable” (Figs. 20-6D-F).

The third type includes the presence of intrahepatic atresia. In this form of atresia, the extrahepatic ducts may be present or absent. The mechanism of intrahepatic atresia remains obscure29 and the condition is as yet noncorrectable. It requires early liver transplantation (Fig. 20-6G).

Three explanations may be offered to explain biliary atresia.

 

Recanalization of the solid cords of epithelium may fail. This developmental arrest of the duct system occurs in the sixth prenatal week.30

The epithelium may fail to proliferate fast enough to keep up with the elongation of the ducts during the fifth week. The ducts become attenuated and finally break, resulting in a complete loss of ductal continuity.24

Late prenatal or early postnatal inflammatory liver disease can result in fibrosis of part or all of the duct system.31

Surgery is the only treatment for unfortunate children with extrahepatic biliary atresia. The surgical procedure is decided upon in the operating room.

Hashimoto et al.32 reported their modification of hepatic portoenterostomy (Kasai operation) for biliary atresia, using the Cavitron ultrasonic suction aspirator. Persistent biliary drainage resulted in 77% of their cases.

Congenital Dilatation of the Common Bile Duct (Choledochal Cysts)

A local balloon-shaped or cylindrical enlargement of the common bile duct is probably congenital. Symptoms of obstruction are the result of the dilatation rather than its cause. Several explanations for these dilatations have been offered. None seems adequate.24

The first classification of these dilatations is that of Alonso-Lej et al.33 in 1959, who described three types of choledochal cysts. In 1984, Todani26 described a modification of this system that included five types (Fig. 20-7). A classic monograph on the topic was written by O’Neill35 in 1992; we urge the interested student to study O’Neill’s excellent work.

Fig. 20-7.

Five general forms of choledochal cyst found by cholangiography as originally described by Todani.34 (Modified from Taylor LA, Ross AJ III. Abdominal masses. In Walker WA, Durie PR, Hamilton JR, Walker-Smith JA, Walkins JB (eds). Pediatric Gastrointestinal Disease (2nd ed). St. Louis: Mosby, 1996;227-240; with permission.)

Todani’s classification of five types of choledochal cysts is summarized as follows.

 

I, Solitary fusiform extrahepatic cyst. Single cystic dilatation of the common bile duct (80-90% of cases)

II, Extrahepatic supraduodenal diverticulum. Double gallbladder, with one element sessile without cystic duct. Epithelial lining is that of normal gallbladder, according to Vohman and Brown [personal communication from Vohman and Brown to J.E. Skandalakis, 1987] (3%)

III, Intraduodenal diverticulum/choledochocele. Cystic biliary dilatation within the duodenal wall (5%)

IV, Any combination of multiple cysts, i.e., types I, II, III (10%)

 

IVA, Fusiform extra- and intrahepatic cysts. Combination of types I and II

IVB, Multiple extrahepatic cysts. Combination of type I with multiple intrahepatic cysts

V, Caroli’s disease/multiple intrahepatic cysts (very rare)

Among 58 patients with choledochal cysts reported by Todani and colleagues,34 46 had cystic dilatations (type I). The enlargements were cylindrical in 12 patients. The pancreaticocholedochal junction was abnormal in most of these patients.

Type I is the most common (90-95%), according to O’Neill.36 These cysts are either saccular or fusiform dilatations of the extrahepatic biliary ductal system. O’Neill wrote that choledochoceles, which are type III, have two forms, as shown in Figure 20-8. They are more commonly found in the duodenum, but occasionally occur in the head of the pancreas.

Fig. 20-8.

Two generally encountered forms of choledochocele (type I more common). (Modified from O’Neill JA Jr. Choledochal cyst. Curr Probl Surg 1992;29:361-410; with permission.)

Histopathologically, choledochal cysts have the following characteristics according to O’Neill36:

 

Thick-walled structure of dense connective tissue with some strands of smooth muscle

Chronic inflammatory process in older patients, but minimal in patients younger than 8-10 years

The biliary mucosa is acellular and in rare cases sparse islands of columnar epithelium and microscopic bile ducts are present

Malignancy is rare in childhood but common in adults as a form of adenosquamous carcinoma or occasionally small cell cancer

It is probable that the two most common causes of choledochal cyst formation are, according to O’Neill,36

 

Congenital abnormal insertion of the pancreatic duct into the common bile duct resulting in reflux of trypsin and other pancreatic enzymes into the common bile duct (CBD)

Obstruction of the distal CBD, perhaps with primary weakening

For adult patients with anomalous junction of pancreaticobiliary ductal system (AJPBDS) without bile duct dilatation, Tanaka et al.37 recommended prophylactic cholecystectomy even if no malignant lesion is found in the gallbladder. They make this recommendation because patients with AJPBDS have a high incidence of gallbladder cancer as well as poor prognosis. Tuech et al.38 reported a case of gallbladder carcinoma in a patient with pancreatobiliary maljunction without dilatation of the biliary tract. They urged resection of the extrahepatic biliary tract rather than cholecystectomy alone to prevent bile duct carcinoma in these patients.

Caudle and Dimler39 pointed out that the classic symptoms of pain, jaundice, and palpable mass are often absent in ductular dilatation. Diagnosis may be attained easily by sonography, endoscopic retrograde cholangiopancreatography (ERCP), and iminodiacetic acid scans. These authors also remarked on the occurrence of anomalies of the junction of the bile duct and the pancreatic ducts. They are not convinced that these are of etiologic significance.

Sugiyama et al.40 cautioned that associated pancreatic disease and an abnormal pancreatogram may be associated with anomalous pancreaticobiliary junction (APBJ). While cholecystectomy alone may be adequate for APBJ without choledochal cyst, APBJ with cyst requires cyst excision.

Remember

Choledochal cysts are most common in adult females, who complain about biliary tract symptomatology or perhaps pancreatitis. A right upper quadrant mass with pain and jaundice in infants suggests a choledochal cyst. Diagnosis is established by ultrasonography, CT scan, and cholangiography.41

The following questions about choledochal cysts remain unanswered.

 

Why are there so many cases in Asia?

Do Asians living in the West have a higher incidence than the general population?

Why do some cases of abnormal junction show no dilatation of the common bile duct?

Since the sphincteric apparatus of Boyden does not exist in an abnormal junction, why is there no clinical picture of pancreatitis and histologic changes in the pancreas in the first month of life?

Is type II a congenital dilatation or a double gallbladder with minimal cystic duct or without cystic duct?

Yoshida et al.42 stated that the congenital anomaly of APBJ outside the sphincter of Oddi without dilatation of the extrahepatic biliary system appears to be an important risk factor responsible for the genesis of carcinoma of the gallbladder. There have been some favorable outcomes for patients with gallbladder carcinoma associated with APBJ. However, Vitetta et al.43 raised the possibility that carcinoma of the gallbladder is an age-dependent malignancy, present mostly in females, intimately associated with long term benign gallstone disease.

Miscellaneous Asymptomatic Anomalies

Some of the many variations encountered in the biliary tract are shown in Figures 20-9, 20-10, 20-11, 20-12, 20-13, 20-14, and 20-15. Some of these variations may be more prone to lithiasis than the normal configuration. Their chief interest is to the surgeon, who must be aware of the possible occurrence of these and other variations rather than trying to make the findings at operation fit a “normal” pattern. An anomaly or variation must be recognized as such; the surgeon should never attempt to explain abnormal findings as “normal.” This is especially critical in laparoscopic surgery and reinforces the importance of cholangiography.

Fig. 20-9.

Variations of hepatic ducts. A, Intrahepatic union of right and left hepatic ducts. B, Extrahepatic (normal) union of hepatic ducts. C, Distal union of hepatic ducts resulting in absence of common hepatic duct. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons. 2nd ed. Baltimore: Williams & Wilkins, 1994; with permission.)

Fig. 20-10.

Accessory hepatic ducts.

Fig. 20-11.

Variations of common bile duct. A, Low junction of cystic and common hepatic ducts results in shortened common bile duct. B, Absence of a common bile duct. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

Fig. 20-12.

A, Duplication of common hepatic duct; case of Michels.44B, Duplication of common hepatic duct; case of Nygren and Barnes.229 Duplication is patent. Normally located duct is atretic. C, May be called “absence” of common hepatic duct or “duplication” of common bile duct.

Fig. 20-13.

Duplications of common bile duct. A, Double and parallel lumina of common bile duct. B, “X” type of anastomosis between duplicated bile ducts. C, “X” and “H” types of anastomosis between duplicated bile ducts.

Fig. 20-14.

Duplications of cystic duct without duplication of gallbladder. A, Both cystic ducts enter common hepatic duct. B, Accessory cystic duct opening into right hepatic duct. C, Double-barreled duplication of cystic duct.

Fig. 20-15.

A, Absence of cystic duct, with sessile gallbladder. B, Atretic cystic duct with normal gallbladder.

Remember

 

In most cases, the portal vein, hepatic artery, and biliary duct are fellow travelers within the hepatic parenchyma.

The hepatic veins do not follow the triad within the liver parenchyma: they pass between segments or subsegments.

The triad is enveloped extrahepatically and intrahepatically by a thin fibrous sheath. This structure is a continuation of the endoabdominal fascia. Characteristically, the hepatic veins are not protected by this special envelope. This explains their tendency to tear easily. The connective tissue envelope also allows one to differentiate the former structures from hepatic veins by ultrasound and MRI (magnetic resonance imaging).

The right hepatic vein can be exposed by division of the retrocaval ligament which connects segments I and VII.

Lumbar veins do not enter the retrohepatic part of the IVC.

The line of Rex (gallbladder to IVC) divides the liver into two equal functional lobes.

There are no external landmarks for the division created by the line of Rex.

There is confusion in the literature about the true anatomy of the quadrate and caudate lobes. All the various opinions may be correct from a surgical standpoint. However, in a right functional lobectomy, large parts of both the caudate and the quadrate lobes are transected. For all practical purposes, the caudate lobe (segment I) belongs to both the right and left functional lobes. The quadrate lobe belongs to the medial segment of the left lobe (segment IV).

The right and left coronary ligaments are quite different. The right is composed of two leaflets, anterior and posterior. The left is composed only of a seemingly singular leaflet. The left anterior and posterior leaflets are either fused or separated by a small layer of fibrofatty tissue containing small vessels and bile ducts. Therefore, always ligate the left triangular and coronary ligaments. Also, remember that the left hepatic vein can be injured during the division of the left ligament, resulting in massive hemorrhage and a fatal outcome.

Surgical Anatomy

Extrahepatic Triad and Extrahepatic Hepatic Veins

The extrahepatic triad consists of the hepatic artery, hepatic portal vein, and hepatic duct (Fig. 20-16). The course of the cystic artery and variations of the cystic artery are considered in the section “Vessels of the Gallbladder and Biliary Tract.”

Fig. 20-16.

Origin and branches of the celiac trunk. (Modified from Gray SW, Skandalakis JE. Atlas of Surgical Anatomy for General Surgeons. Baltimore: Williams & Wilkins, 1983; with permission.)

Blood Vessels

Hepatic Artery, Common Hepatic Artery, and Proper Hepatic Artery

The hepatic artery (Fig. 20-16) provides 25% of the afferent blood supply to the liver, as well as about 50% of the oxygen. The hepatic arterial supply is derived from the celiac trunk in 55% of subjects.44 In 45%, the common hepatic artery, the right hepatic, or the left hepatic may arise from vessels other than the celiac trunk (aberrant hepatic arteries).

The common hepatic artery takes origin from the celiac trunk in the majority of individuals: 83.2% according to Daseler and colleagues;45 86% according to Van Damme and Bonte (Figs. 20-17 and 20-18).46 In other cases, it may arise from the superior mesenteric artery (2.9%), from the aorta (1.1%), from the left gastric artery (0.54%), or even from rarer sources, according to Van Damme and Bonte.

Fig. 20-17.

Division of celiac trunk. (Lit.), reported in medical literature. (Modified from Van Damme JP, Bonte J. Atresia splenica and the blood supply of the spleen (splen). Probl Gen Surg 1990;7:18-27, with permission.)

Fig. 20-18.

Variations of hepatic artery. A, Normal pattern, 82%. B-D, Absence of proper hepatic artery, 14%. E, Absence of common hepatic artery and proper hepatic artery, 4%. (Modified from Van Damme JP, Bonte J. Vascular Anatomy in Abdominal Surgery. New York: Thieme, 1990; with permission.)

In 75% of the 200 specimens of Michels,44 the gastroduodenal artery arose from the distal horizontal portion of the common hepatic artery. The right gastric artery arose from the common or proper hepatic in about 40% of these cases and from the left hepatic artery with similar frequency. In other specimens, the right gastric artery took origin from another hepatic branch (11%) or from the gastroduodenal artery (8%).

Concerning the overall behavior of the normal hepatic arteries, Van Damme wrote the following;47 we concur with his rules.

By definition, the normal common hepatic artery becomes the proper hepatic artery at the point where the gastroduodenal artery begins. According to most textbooks, the proper hepatic artery divides into a right and a left hepatic branch but variations are legion. We find no reason to consider a middle hepatic branch as Michels44 did, because this only increases the confusion. We have summarized the behavior of the hepatic artery in three rules. First, the hepatic artery may divide into its right and left hepatic branches at any point between the liver hilum and the origin of the hepatic artery itself [Fig. 20-18]. If it divides exactly at the site of origin of the gastroduodenal artery, there is no proper hepatic artery. If it splits at the origin of the hepatic artery itself, there is not even a common hepatic artery.

Second, the gastroduodenal artery always arises at a fixed point at the transition of the mobile and fixed segments of the first part of the duodenum. Consequently, the origin of the gastroduodenal artery is determined by the hepatic vessel that passes at this site, whatever the divisional pattern of the hepatic artery may be. Third, if a normal common hepatic artery bifurcates very early, medial to the portal vein [Fig. 20-18], the right branch will pass behind the portal vein; the pulsations can be palpated through the hiatus of Winslow.

When arising from the common source, the typical common hepatic artery (Fig. 20-19A) runs horizontally along the upper border of the head of the pancreas and then turns upward to ascend between the layers of the lesser omentum. The peritoneum of the posterior wall of the omental bursa covers the horizontal portion of the artery. The hepatoduodenal ligament envelops the ascending portion, which lies in front of the epiploic foramen (of Winslow) to the left of the common bile duct and anterior to the portal vein.

Fig. 20-19.

Aberrant hepatic arteries. A, “Normal” hepatic artery arises from celiac trunk. B, “Accessory” left hepatic artery arises from left gastric artery. C, “Replacing” common hepatic artery arises from superior mesenteric artery. D, “Replacing” right hepatic artery arises from superior mesenteric artery.

Aberrant Hepatic Arteries

There is confusion in the literature regarding the terms aberrant, replacing, and accessory arteries. Aberrant hepatic arteries occur frequently (46% according to Van Damme;47 45% according to Suzuki et al;48 43% according to Healey et al;49 41.5% according to Michels44) as shown in Figs. 20-19B-D. Aberrant or atypical hepatic arteries are often described as “replacing” arteries if the artery arises entirely from some source other than the celiac arterial distribution. In such cases, the replacing artery can supply the entire liver or an entire lobe of the liver. Atypical hepatic arteries are often, if erroneously, referred to as “accessory” hepatic arteries if they arise from some aberrant source and are additive to lobar branches derived from the celiac hepatic arteries (Fig. 20-19B). Except in unusual cases, truly “accessory” arteries do not exist, because they are providing the primary arterial supply to a specific part of the liver, whether it be a lobe, segment, or subsegment of parenchyma.

The common hepatic artery may arise from the superior mesenteric, the aorta, the left gastric, or other sources, as noted above. The left hepatic artery arises in 25-30% of cases from the left gastric artery.46,50 These include a totally “replacing” left hepatic artery in 10% and an “accessory” left hepatic artery in about 15% of cases.

The right hepatic artery originates from the superior mesenteric in about 17%50,51 of cases. Of these, 11% represent total replacement (Fig. 20-19D), and about 7% are “accessory” in nature. The middle hepatic artery arises with nearly equal frequency from the left or right hepatic artery, although it is more often depicted as arising from the left hepatic artery.52,53

As one might reasonably predict, various combinations of “replacing” or “accessory” hepatic arteries can occur in the same individual. For instance, in 2% of cases a replaced right hepatic may exist together with an accessory left hepatic in the same person, or the configuration may be reversed.50

Feigl and colleagues54 distinguished the following types of anastomoses between the celiac artery and the superior mesenteric artery: 1) direct connection; 2) anastomoses with the hepatic artery; 3) anastomoses following pre- or postnatal stenosis; and 4) the pancreatic arcades. Two of the authors of this chapter (JES and GLC) have independently observed instances of an accessory right hepatic artery that arose from the superior mesenteric artery and terminated in a normal right hepatic artery of celiac origin. It must be emphasized, however, that such collateral vessels are seen only infrequently. Almost all “accessory” hepatic arteries exposed surgically should be considered functionally essential to the survival of liver tissue.

In a study of the anatomic variations in the vascular supply to the liver in 1000 donor liver arteries used for transplantation, Hiatt et al.55 reported the arterial patterns in order of frequency as follows:

 

Normal type (common hepatic artery arising from the celiac axis to form the gastroduodenal and proper hepatic arteries, and the proper hepatic dividing distally into right and left branches): 757 cases

Replaced or accessory right hepatic from SMA: 106 cases

Replaced or accessory left hepatic from left gastric: 97 cases

Both right hepatic (from SMA) and left hepatic (from left gastric) arising abnormally: 23 cases

Entire common hepatic artery from SMA: 15 cases

Common hepatic artery from aorta: 2 cases

Weimann et al.56 stated that an aberrant left hepatic artery arising from the left gastric artery may be protected if the left gastric artery is ligated distal to the origin of the hepatic branch.

If one traces aberrant arteries backward, that is, from within the liver, the path will reveal the “replacing” arteries to be lobar arteries with aberrant origin but with normal distribution.

Van Damme’s47 findings and thoughts about aberrant hepatic arteries follow:

Aberrant hepatic branches are found in 46% of the preparations [dissection, postmortem arteriography, and corrosion]: a right one in 24% and a left one in 30%; in 8% there is both a right and a left aberrant hepatic branch. We do not follow Michels44 in distinguishing between accessory and replaced aberrant hepatic branches, because this distinction is very difficult to make during surgery and because even the “accessory” branches are usually the only supply for a specific segment. An aberrant right hepatic branch from the superior mesenteric artery (20%) always runs behind the pancreas and behind the portal vein and always supplies a cystic artery. Its ligation should always be followed by cholecystectomy. From behind the portal vein it runs through the intercholedochohepatic triangle and usually crosses under the bile ducts before it enters the liver posterolateral to the hepatic duct [Fig. 20-20A]. Exceptionally, it may turn in the intercholedochohepatic triangle toward the anterior side of the portal vein and continue like a normal hepatic artery [Fig. 20-20B]. During surgery, this aberrant branch is to be found in the intercholedochohepatic triangle and in the triangle between the cystic and hepatic ducts. Through the hiatus of Winslow it can be palpated behind the portal vein. After a Kocher maneuver its pulsations can be felt behind the head.

Fig. 20-20.

Aberrant right hepatic branch from superior mesenteric artery runs behind pancreas and behind portal vein. A, Branch appears in intercholedochohepatic area and continues behind choledochus. B, Same branch turns upward to run upon portal vein, behaving like normal right hepatic branch. (Modified from Van Damme JP, Bonte J. Vascular Anatomy in Abdominal Surgery. New York: Thieme, 1990; with permission.)

The aberrant left hepatic branch (30%) always arises from the left gastric artery. It runs in the cranial part of the lesser omentum where it is endangered during gastrectomy and hiatal hernia repair. It enters the liver through the fissure of the venous ligament. It often gives off branches to the stomach and to the esophagus.

We quote from Rygaard et al.57:

From a surgical point of view it is important to know the gross anatomy of the hepatic arteries before an intervention on the liver and pancreas. Thus, when the right hepatic artery arises from the superior mesenteric artery, it may pass through the pancreatic head. Particulars about this variant are of great value prior to pancreatectomy and hemihepatectomy. Information to the effect that the left hepatic artery originates from the left gastric artery may allow rapid dissection of the porta hepatis in hemihepatectomy. Ligation or embolization of hepatic arteries in the treatment of liver trauma, hepatic tumor or lesions of the hepatic vessels such as aneurysm, arteriovenous fistula or hemobilia require detailed angiographic analysis.

Hepatic Portal Vein

The hepatic portal vein provides 75% of the blood and about 50% of the oxygen reaching the liver. The portal vein (Fig. 20-21) is formed by the confluence of the superior mesenteric vein and the splenic vein behind the neck of the pancreas. However, the inferior mesenteric vein may enter the splenic vein, superior mesenteric vein, or their junction. In these cases the portal vein is thought of as being formed by the junction of all three. Table 20-4 indicates some studies of these variations.

Table 20-4. Participation of the Inferior Mesenteric Vein in the Formation of the Hepatic Portal Vein

  Inferior Mesenteric Vein Enters:
Investigator, # of Cases Splenic v. SMV Junction of Splenic/SMV Other
Treves (100) 18% 36% 44% 2%
Douglass et al. (92) 38% 29.3% 32.7%
Purcell et al. (100) 28% 53% 3% 16%

SMV, Superior mesenteric vein.

Data from Hollinshead WH. Anatomy for Surgeons, Vol. 2. New York: Hoeber-Harper, 1961, pp. 454-455.

Fig. 20-21.

Portal vein and major tributaries. (Modified from O’Rahilly RO. Gardner-Gray-O’Rahilly Anatomy (5th ed). Philadelphia: WB Saunders, 1986; with permission.)

Toward the liver, the portal vein lies in front of the inferior vena cava. The common bile duct is on the right, and the proper hepatic artery is on the left. In the absence of disease, the portal vein and the superior mesenteric vein can be easily separated from the posterior surface of the pancreas.

The portal vein is 7-10 cm long and 0.8-1.4 cm in diameter and is without valves. At the porta hepatis, it bifurcates into right and left portal veins. Its further course in the liver is discussed in the chapter on the liver in the section on hepatic portal veins.

The inferior mesenteric vein ends with approximately equal frequency in the splenic vein, the superior mesenteric vein, or the portal vein. Either the splenic vein or the portal vein receives the coronary (left gastric) vein as well. The portal vein receives an accessory pancreatic vein on the left and the superior pancreaticoduodenal and the pyloric veins on the right.

In 17 of 23 subjects the senior author of this chapter (JES) dissected, the left gastric vein entered the portal vein; in six, it entered the splenic vein. Healey and Schwartz51 observed a portal termination of the left gastric vein in 83% of their specimens. Where drainage was into the portal vein, the left gastric vein lay in the hepatogastric ligament.

Hepatic Veins (Upper Portas)

The liver is drained by a series of dorsal hepatic veins. They are located in the area aptly called “the upper hilum”58 by Rodney Smith. There are 3 major veins —the right, middle, and left hepatic— and from 10 to 50 smaller veins opening into the inferior vena cava.59

The extrahepatic length of the three major veins varies from 0.5 cm to 1.5 cm. The right hepatic vein (Fig. 20-22) is the largest. It lies in the right segmental fissure, draining the entire posterior segment and the superior area of the anterior segment of the right lobe.

Fig. 20-22.

Portal venous supply. (Modified from Healy JE Jr, Hodge J. Surgical Anatomy (2nd ed). Philadelphia: Decker, 1990; with permission.)

The middle hepatic vein lies in the main lobar fissure. It drains the inferior area of the anterior segment of the right lobe and the inferior area of the medial segment of the left lobe.

The left hepatic vein lies in the upper part of the left segmental fissure. It drains the superior area of the medial segment and all of the lateral segment. In about 60% of individuals, the left and middle veins unite to enter the inferior vena cava as a single vein.51 The length of the common trunk is 1-2 cm. Nakamura and Tsuzuki59 found a common trunk in 70 of 83 autopsies. They state that 1 cm of vein without tributaries was sufficient for successful ligation. By their standards, the right vein could have been ligated in 60% of the cadavers examined. The middle and left veins could have been ligated in only 11%. Any surgeon contemplating procedures in this area should study Nakamura and Tsuzuki’s findings.

The right hepatic vein enters the inferior vena cava. In some individuals a significant segment of the right vein may course in a retrohepatic position, where it is especially vulnerable to posterior incisions at the level of the 12th rib or other surgical approaches designed to treat upper posterior abdominal injuries or pathology. The left hepatic vein may also enter the inferior vena cava directly. This vein may be torn during operations at the gastroesophageal junction when the left triangular ligament is incised. The middle hepatic vein enters into the left hepatic vein.

Of the smaller veins, one or two constant vessels drain the caudate lobe and enter the inferior vena cava on the left side. Several inconstant veins draining the posterior segment of the right lobe enter the right posterolateral aspect of the inferior vena cava.60

As noted previously, the number of these small veins may vary from 10 to as many as 50. Between 5 and 10 of these will require ligation during hepatic resections.59

Cavalcanti et al.61 reported a large number of muscular and collagenous fibers present on the walls of the hepatic veins at the level of the junction with the inferior vena cava. They consider this a sphincterlike formation that may play some physiological role in controlling hepatic circulation.

Extrahepatic Biliary Tract

The right and left lobes of the liver are drained by ducts originating as bile canaliculi in the lobules. The canaliculi empty into the canals of Hering in the interlobular triads. The canals of Hering are collected into ducts draining the hepatic areas, the four hepatic segment ducts, and finally, outside the liver, the right and left hepatic ducts.

Right Hepatic Duct

The right hepatic duct is formed by the union of the anterior and posterior segment ducts at the porta hepatis. This pattern was present in 72% of specimens examined by Healey and Schroy62 as shown in Fig. 20-23A. In the remainder, the posterior segment duct (or, rarely, the anterior segment duct) (Figs. 20-23B, 20-23C) crossed the segmental fissure to empty into the left hepatic duct or one of its tributaries. In these cases, the right hepatic duct is absent. The average length of the right hepatic duct, when present, is 0.9 cm.

Fig. 20-23.

Variations in tributaries to right hepatic duct. A, Usual pattern. Right hepatic duct receives anterior and posterior segment ducts. B, Alternate pattern. Posteroinferior area duct enters common hepatic duct. C, Anterior and posterior segment ducts enter left hepatic duct. Right hepatic duct absent. (Modified from Colborn GL, Skandalakis LJ, Gray SW, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 3: Surgical anatomy of the liver. Contemp Surg 1987;30(6):15-23; with permission.)

Left Hepatic Duct

The left hepatic duct is usually (67% of Healey and Schroy’s62 specimens) formed by the union of the medial and lateral segment ducts (Fig. 20-24A), although the medial segment duct sometimes enters the inferolateral duct (Fig. 20-24B). The union of the two area ducts is in line with the left segmental fissure (50%), to the right of the fissure (42%), or to the left of the fissure (8%).

Fig. 20-24.

Variations of left hepatic duct. A, Usual pattern. Left hepatic duct forms by confluence of medial and lateral segment ducts. B, Medial segment duct may enter inferolateral duct. Medial segment duct is usually double. (Modified from Colborn GL, Skandalakis LJ, Gray SW, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 3: Surgical anatomy of the liver. Contemp Surg 1987;30 (6):15-23; with permission.)

The average length of the left hepatic duct is 1.7 cm.62 Usually the right and left hepatic ducts are of equal size. In patients with chronic obstructive biliary disease, the left duct, for unknown reasons, is larger than the right duct.63 Drainage of the medial segment duct is shown in Fig. 20-25.

Fig. 20-25.

Variations of sites of drainage of medial segment duct. CHD, Common hepatic duct; RHD, Right hepatic duct; LHD, Left hepatic duct; LS, Lateral segment duct; MS, Medial segment duct; LSA, Lateral superior area duct; LIA, Lateral inferior area duct. (Modified from Healey JE Jr, Schroy PC. Anatomy of the biliary ducts within the human liver: analysis of the prevailing pattern of branchings and the major variations of the biliary ducts. Arch Surg 1953;66:599; with permission.)

Common Hepatic Duct

The common hepatic duct (Fig. 20-26) is formed by the union of the right and left hepatic ducts in the porta at the transverse fissure of the liver. Its lower end is defined as its junction with the cystic duct. The distance between these points varies from 1.0 cm to 7.5 cm. The diameter of the duct is about 0.4 cm.

Fig. 20-26.

Location of common hepatic duct. (After O’Rahilly RO. Gardner-Gray-O’Rahilly Anatomy (5th ed). Philadelphia: WB Saunders, 1986; with permission.)

Several arteries are found in relation to the extrahepatic biliary tract. Many of these may lie anterior or posterior to the ducts. The frequency with which they lie anterior to the ducts is summarized in Table 20-5.

Table 20-5. Segments of the Biliary Tract and the Frequency of Arteries Lying Anterior to Them

Segment Artery Anterior Percent Frequency
Right and left hepatic ducts Right hepatic artery 12-15
Cystic artery <5
Common hepatic duct Cystic artery 15-24
Right hepatic artery 11-19
Common hepatic artery <5
Supraduodenal common bile duct Anterior artery to CBD 50
Posterosuperior pancreaticoduodenal artery 12.5
Gastroduodenal artery 5.7-20*
Right gastric artery <5
Common hepatic artery <5
Cystic artery <5
Right hepatic artery <5
Retroduodenal common bile duct Posterosuperior pancreaticoduodenal artery 76-87.5
Supraduodenal artery 11.4

*In another 36 percent, the gastroduodenal artery lay on the left border of the common bile duct (Maingot, 1974).

CBD, Common bile duct.

Source: Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983. Data from Johnston and Anson. Surg Gynecol Obstet 94:669, 1952, and others; with permission.

Cystic Duct

The cystic duct contains a series of 5 to 12 crescent-shaped folds of mucosa similar to those seen in the neck of the gallbladder. These form the so-called spiral valve of Heister. The length of the cystic duct and the manner in which it joins the common hepatic duct vary.

The pressure of secretion from the mucous glands in the cystic duct is higher than the secretion pressure of bile. The intracholecystic result of prolonged obstruction of the extrahepatic biliary tree proximal to the cystic duct is white “bile,” composed only of mucus.

The cystic duct joins the hepatic duct at an angle of about 40° in 64-75% of individuals (Fig. 20-27A). In 17-23%, the cystic duct parallels the hepatic duct for a longer or shorter distance and may even enter the duodenum separately. This is called “absence” of the common bile duct, and is shown in Fig. 20-27F. In 8-13%, the cystic duct may pass inferior to or superior to the common hepatic duct to enter the latter on the left side64-66 as shown in Figs. 20-27B, C. In the parallel type of junction, the common duct is at risk from the surgeon attempting to ligate the cystic duct. If the long parallel portion of the cystic duct is left in place, cystic duct remnant syndrome with various sequelae may result. Less frequently, the gallbladder is sessile with little or no cystic duct (Figs. 20-27D, E).

Fig. 20-27.

Variations of cystic duct. A, Cystic duct parallels common bile duct before entering it. B-C, Cystic duct crosses common bile duct and enters it on left. D-E, Short cystic duct. F, Long cystic duct enters duodenum. This can also be called absence of common bile duct (separate entrance of common hepatic duct and cystic duct into duodenum). (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

The cystic duct should be prepared well. The duct should be ligated such that it avoids a long cystic duct remnant, but at the same time avoiding ligation so close that the common bile duct is injured.

In his doctoral thesis about the cystic duct remnant and the postcholecystectomy syndrome, Droulias16 concluded:

 

1. A relatively long cystic duct remnant can be the cause of postcholecystectomy symptoms, sometimes quite severe, by being the site of chronic inflammation, lithiasis or neuroma formation. Rarely, it can cause kinking of the common bile duct or reflex spasm of Oddi.

2. Re-exploration and excision of the remnant is indicated after thorough study of the patient, provided the symptoms are severe enough to interfere with normal life and work.

3. Should the remnant be found quite long or diseased during re-operations on the biliary tree or pancreas it must be excised.

4. Prevention can be achieved by meticulous dissection of the cystic duct at cholecystectomy and ligation 2-3 mm from the junction with the common bile duct.

5. It seems probable that regeneration of the gallbladder after complete cholecystectomy in humans, dogs and monkeys does not take place.

Gallbladder

The gallbladder is 7-10 cm long and has a capacity of 30-50 ml. It is located on the visceral surface of the liver in a shallow fossa at the plane dividing the right lobe from the medial segment of the left lobe (the GB-IVC line). In other words, the gallbladder fossa is found at the junction of the quadrate lobe (segment IV) and the right lobe of the liver along the line of Rex. The gallbladder is separated from the liver by the connective tissue of Glisson’s capsule. Anteriorly, the peritoneum of the gallbladder is continuous with that of the liver.

The gallbladder can be divided into fundus, body, infundibulum, neck, and cystic duct (Fig. 20-28). However, these divisions are arbitrary and imprecise; some classifications omit the infundibulum. From a surgical standpoint (when performing cholecystectomy, cholangiogram, etc.), it makes no difference which classification you choose. The following paragraphs describe the fundus, body, infundibulum, and neck; the cystic duct was described above.

Fig. 20-28.

Arbitrary divisions of gallbladder. (Modified from Skandalakis LJ, Gray SW, Colborn GL, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 4: Surgical anatomy of the hepatic vessels and the extrahepatic biliary tract. Contemp Surg 1987;31(1):25-36; with permission.)

Fundus

The fundus is usually located at the angle of the ninth costal cartilage with the right border of the rectus sheath and to the left of the hepatic flexure of the colon. It is completely covered by peritoneum, because it projects beyond the lower border of the liver.

A partial folding of the fundus may result in the “Phrygian cap” deformity (Fig. 20-29A), named by Bartel67 after the Greek term for the liberty cap, the widely used symbol of the French Revolution. Two to six percent of gallbladders have this shape. The deformation may or may not be visible from the outside. When seen radiographically, many cases appear to be caused by defective musculature of the fundus.66 It was suggested that such gallbladders may be at higher risk for lithiasis,68 but this has not been confirmed.

Fig. 20-29.

Deformations of gallbladder. A, “Phrygian cap” deformity, showing partial folding of tip of fundus. B, Hartmann’s pouch of infundibulum. (Modified from Skandalakis JE, Gray SW. Embryology for Surgeons (2nd ed). Baltimore: Williams & Wilkins, 1994; with permission.)

Body

The body of the gallbladder is in contact with the first and second portions of the duodenum and occupies the gallbladder fossa of the liver. The body is also related to the transverse colon. Only in the rare presence of a mesentery (wandering gallbladder), a prerequisite for acute torsion, is the body completely covered by peritoneum.

Occasionally in the operating room and in the laboratory, we have seen several inconstant or anomalous peritoneal (lesser omental) folds from the gallbladder to the duodenum, colon, or stomach (Fig. 20-30) in that order of frequency.

Fig. 20-30.

Inconstant or rare peritoneal folds of gallbladder to duodenum, colon, or stomach. Their presence is often associated with biliary fistulas. (Modified from Skandalakis JE, Gray SW, Skandalakis LJ. Surgical anatomy of intestinal obstruction. In: Fielding LP, Welch J (eds). Intestinal Obstruction. New York, Churchill Livingstone, 1987, pp. 14-32; with permission.)

The peritoneal folds may be associated with the pathway of a large gallstone ulcerating from the gallbladder into the intestinal tract. The duodenal path is the most common; the gastric path is the rarest. We do not know if there is a relationship between these folds and the corresponding fistulous tracts of gallstone ileus. However, it is possible that the folds predispose to fistulas.69

Infundibulum

The infundibulum is the angulated posterior portion of the body between the neck and the point of entrance of the cystic artery. When this portion is dilated, with eccentric bulging of its medial aspect, it is called a Hartmann’s pouch (Fig. 20-29B) (though it was originally described by Broca). Many have regarded it as a constant feature; Kaiser70 considered it to be a normal constitutional characteristic of a short stocky habitus. Davies and Harding71 have determined that it is consistently a sequela of pathological states, especially dilatation. It may be important to note that when this pouch achieves considerable size, the cystic duct arises from its upper left aspect rather than from what appears to be the apex of the gallbladder. The pouch is often associated with chronic or acute inflammation due to lithiasis and often accompanies a stone impacted in the infundibulum.

Neck

The narrow neck (cervix) curves up and forward and then sharply back and downward forming an S to become the cystic duct. The junction of the neck and the cystic duct is said to be indicated by a constriction.72 The cystic artery is found in this region coursing in the loose connective tissue that attaches the neck of the gallbladder to the liver.

The mucosa lining the neck is a spiral ridge said to be a spiral valve, but not to be confused with the spiral valve of the cystic duct (the valve of Heister). When the neck becomes distended, this spiral gives its surface a spiral groove. The neck lies in the free border of the hepatoduodenal ligament. The ridges of the valve of Heister, in addition to the previously mentioned constriction, interfere with the passage of an instrument and may stop the passage of gallstones.

Following removal of the gallbladder, there is sometimes leakage of bile from small bile ducts in the gallbladder bed. (There has been disagreement as to whether these ducts [hepatocystic ducts] enter the gallbladder. Michels44 was unable to find such ducts in his 500 carefully dissected specimens. He found branches from the right hepatic duct in the gallbladder bed but the branches did not communicate with the gallbladder.) The small bile ducts may cause postoperative bile leakage if they are injured.

Lindner and Green73 and Wayson and Foster74 expressed opposing views on the existence of hepatocystic ducts, citing personal experience and hepatic embryology to prove their cases. Because the presence of a cystic vein is an extremely rare phenomenon, Lindner and Green state that there are multiple small veins that drain into the liver parenchyma. They indicate that minute bile canaliculi may drain directly from the hepatic parenchyma into the gallbladder. Wayson and Foster considered these vessels to be postinflammatory artifacts.

Common Bile Duct (Ductus Choledochus)

The common bile duct begins at the union of the cystic and common hepatic ducts and ends at the papilla of Vater in the second part of the duodenum. It varies in length from 5 cm to 15 cm, depending on the actual position of the ductal union. In 22%, the common hepatic and cystic ducts, on average, run parallel for 17 mm before the ducts actually unite.66 The average diameter is about 6 mm.

The common bile duct can be divided into four portions or segments (Fig. 20-31): supraduodenal, retroduodenal, pancreatic, and intramural.

Fig. 20-31.

Four portions of common bile duct. (Modified from Skandalakis LJ, Gray SW, Colborn GL, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 4: Surgical anatomy of the hepatic vessels and the extrahepatic biliary tract. Contemp Surg 1987;31(1):25-36; with permission.)

The supraduodenal portion of the common bile duct lies between the layers of the hepatoduodenal ligament in front of the epiploic foramen of Winslow, to the right or left of the hepatic artery, and anterior to the portal vein. Its length is 2-5 cm.73

The distal part of the supraduodenal portion is related to the posterior superior pancreaticoduodenal (PSPD) artery, which has a retroduodenal location and which crosses the duct first anteriorly and then posteriorly. This artery is not to be confused with the supraduodenal artery, which also may pass anterior to the common bile duct. In the majority of cases the retroportal artery joins the PSPD artery, but it may join the right hepatic artery directly and send branches to the common duct en route. The PSPD artery is easily injured while exploring the common duct.44

If the junction of the cystic and common hepatic ducts is low, the supraduodenal segment is short or even absent. Large lymph nodes may be fixed to the right side of the supraduodenal segment.

The retroduodenal portion of the common bile duct is between the superior margin of the first portion of the duodenum and the superior margin of the head of the pancreas. It is 1-3.5 cm long. The duct may be free or partially fixed to the duodenum.

The gastroduodenal artery lies to the left. The PSPD artery lies anterior to the common bile duct. The middle colic artery lies anterior to the common bile duct and other arteries.

Prudhomme et al.75 reported the following relationships of the bile duct and retroduodenal arteries after studying 35 bloc specimens of normal cadavers.

The distances between the gastroduodenal artery (GDA), the pylorus, and the bile duct were measured in the sagittal plane. The origin and course of the posterior superior pancreaticoduodenal artery (PSPD) in relation to the bile duct were studied. The relation of the GDA and the bile duct were divisible into four types: in Type 1 (n=22) the two structures separated progressively, the artery being on the left of the bile ducts; in Type 2: (n=7) the structures approached each other without crossing; Type 3: (n=5) the GDA crossed in front of the bile duct at the level of the first part of the duodenum (D1); Type 4: (n=1) the GDA crossed the bile duct below D1 and ran along its right border. The PSPD originated at the posterior face of D1 in 20% of cases (n=7) and crossed the anterior surface of the bile duct at the posterior surface of D1. In four cases there was no pancreatic tissue between the PSPD and the bile duct. It follows that the risk of injury to the bile duct when securing hemostasis by transfixing a bleeding duodenal ulcer in the D1 segment is great when the arterial structures (GDA and PSPD) cross the bile duct. This risk is increased when there is no pancreatic tissue between them.

Dorrance et al.76 reported that acquired absence of the cystic duct secondary to inflammatory process of an impacted gallstone in Hartmann’s pouch may occur with some frequency. Therefore, the surgeon should be extremely careful to avoid injuring the common bile duct. However, a problem remains if the cystic duct is congenitally absent or has become obliterated secondary to inflammatory processes.

The pancreatic portion of the common bile duct extends from the upper margin of the head of the pancreas to the point of entrance into the duodenum. It passes downward to the right, posterior to the pancreas or within the pancreatic parenchyma.

From a series of 200 specimens, Smanio77 described five patterns of the relation of the common bile duct and the pancreas (Fig. 20-32). Other variations include a prepancreatic common bile duct; seven cases were found among 550 bodies examined.44 The senior author of this chapter (JES) has seen a case in which the bile duct was completely extrapancreatic and near the renal vein.

Fig. 20-32.

Five variations of third portion of common bile duct to pancreas. A-B, Bile duct partially covered by tongue of pancreatic tissue (44%). C, Bile duct completely covered by pancreas (30%). D, Bile duct completely uncovered. It lies on posterior surface of pancreas (16.5%). E, Bile duct covered by two tongues of pancreatic tissue (9%). (After Smanio T. Varying relations of the common bile duct with the posterior face of the pancreas in negroes and white persons. J Int Coll Surg 1954;22:150-173. Modified from Skandalakis JE, Gray SW. Embryology for Surgeons, 2nd ed. Baltimore: Williams & Wilkins, 1994; with permission.)

The PSPD artery crosses the pancreatic portion of the common bile duct. It first passes ventral to the duct at the point of origin of the artery from the gastroduodenal artery, and then passes dorsal to the duct just before the latter reaches the pancreas.

The duct may be in intimate contact with the duodenum for 0.8-2.2 cm before entering the wall.78 Lytle79 reported that the pancreatic groove or tunnel occupied by the duct may be palpated using the Kocher maneuver. The groove is located in front of the right renal vein.

The intramural portion of the common bile duct takes an oblique path averaging 1.5 cm through the duodenal wall80 (Fig. 20-33). Here it receives the main pancreatic duct inferiorly. The two ducts usually lie side-by-side with a common adventitia for several millimeters. The diameter of both ducts decreases within the duodenal wall.80 The septum between the ducts is reduced to a thin mucosal membrane before the ducts become confluent.

Fig. 20-33.

Choledochoduodenal junction. The sphincteric muscle is predominately circular in orientation. It extends beyond the wall of the duodenum and for a short distance along the pancreatic duct. (After Toouli J. Sphincter of Oddi motility. Br J Surg 1984;71:251-256; with permission.)

The common bile duct and the pancreatic duct end at the papilla of Vater on the posteromedial wall of the second part of the duodenum, just to the right of the second or third lumbar vertebra. Rarely, the bile duct enters at another location (Fig. 20-34).

Fig. 20-34.

Duplication of common bile duct. One duct enters stomach. A, Case of Vesalius.230B, Case of Everett and Macumber.231 Gallbladder and cystic duct absent. C, Sites of ectopic openings of common bile duct.232

Variations in the distance between the pancreaticobiliary junction and the tip of the papilla are the result of developmental processes.81 In the embryo, the main pancreatic duct arises as a branch of the common bile duct that, in turn, arises from the duodenum. As the duodenum increases in size, it absorbs the proximal bile duct up to its junction with the pancreatic duct. When the resorption is minimal, there is a long ampulla and the junction is high or even extramural. Increased resorption shortens the ampulla; maximum resorption results in separate orifices for the common bile and pancreatic ducts. Michels44 classified the types of junctions, as shown in Figure 20-35.

Fig. 20-35.

Variations of opening of common bile duct and pancreatic duct into duodenum. A, Junction of ducts is high. Common channel may or may not be dilated to form ampulla (85%). B, Common channel is short. No ampulla present (5%). C, Common bile and pancreatic ducts enter duodenum separately. No ampulla present (9%). (Modified from Skandalakis LJ, Gray SW, Colborn GL, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 4: Surgical anatomy of the hepatic vessels and the extrahepatic biliary tract. Contemp Surg 1987;31(1):25-36; with permission.)

Opie82 suggested that a gallstone impacted in the papilla might, in the presence of a long ampulla, permit bile to reflux into the pancreatic duct and produce pancreatitis. This “common channel” theory was supported by Dragstedt and colleagues83 and revived by Doubilet and Mulholland.84 Silen85 questioned the frequency of this cause of pancreatitis. He observed that the pancreatic secretory pressure is usually higher than that of the liver. Although reflux pancreatitis is real, the frequency of its origin from ampullary obstruction is still controversial and largely unsupported by animal models.

Fuzhou et al.86 reported that anomalous junction of pancreaticobiliary ducts (AJPB) is related to pancreatitis. They conclude that AJPB is an anatomic factor inducing pancreatitis. Another study by Fuzhou et al.87 found that endoscopic nasobiliary drainage (ENBD) can prevent the development of severe acute pancreatitis in patients with mild acute pancreatitis. A thin tube is inserted into the bile duct with the help of a duodenoscope (Fig. 20-36A). According to the researchers, the gallstones leave the common pancreaticobiliary channels (Fig. 20-36B), and the bile drains directly into the duodenum (Fig. 20-36C). They speculate that because the tube curves in a U-shaped course around the ampulla of Vater (Fig. 20-36D), the tube pulls the ampulla to relieve its obstruction resulting from edema, inflammation, or stricture.

Fig. 20-36.

Endoscopic nasobiliary drainage (ENBD). See text for description of procedure.

Richer et al.88 advised that a long common channel in excess of 15 mm is associated with a higher incidence of carcinoma of the gallbladder or the bile duct.

Vessels of the Gallbladder and Biliary Tract

Arteries

The cystic artery usually arises from the right hepatic artery as it traverses the hepatocystic triangle to the right of the common hepatic duct (Fig. 20-37A). The lymph node of Calot usually lies just superficial to the position of the cystic artery in the cystic triangle, and can be a good guide to finding and ligating it. Reaching the gallbladder behind the common hepatic duct, the cystic artery usually branches into an anterior superficial branch and a posterior deep branch. These branches anastomose and send arterial twigs to the adjacent liver. Remember in this context that in approximately one third of cases the right hepatic artery arises from the superior mesenteric artery. The cystic artery may arise from the left hepatic artery (Fig. 20-37B) or the gastroduodenal artery (Fig. 20-37C).

Fig. 20-37.

Variations of origin and course of cystic artery. A, Cystic artery arises from right hepatic artery (74.7%). B, Cystic artery arises from left hepatic artery and passes anterior to common hepatic duct (20.5%). C, Cystic artery arises from gastroduodenal artery (2.5%). D-E, Recurrent cystic arteries reach fundus of gallbladder and descend toward neck (rare). In the remainder (approximately 2.3%, not shown), cystic artery arises from a variety of other arteries. (Modified from Skandalakis LJ, Gray SW, Colborn GL, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 4: Surgical anatomy of the hepatic vessels and the extrahepatic biliary tract. Contemp Surg 1987;31(1):25-36; with permission.)

In approximately 25% of subjects, the superficial and deep branches arise separately (Fig. 20-37D). The deep branch usually comes from the right hepatic artery, but two of the authors of this chapter (GLC and JES) have observed a number of cases in which it arose directly from the superior mesenteric artery. The superficial branch may spring from the right hepatic, left hepatic, gastroduodenal, or retroduodenal artery.89 Each possible origin and its frequency are shown in Table 20-6.

Table 20-6. Origin of the Cystic Artery

Origin Anson (676) Michels (200) Moosman (482)
  Percent
Right hepatic artery      
  Normal 61.4 76 72
  Aberrant (accessory) 10.2 13.5 15
  Aberrant (replacing) 3.1
Left hepatic artery 5.9 4 3
Common hepatic artery 14.9* 3 5
Gastroduodenal artery 2.5 4 2
Other 1.0 rare 3
  100.5 99 100

*Includes “bifurcation” of artery.

Source: Skandalakis LJ, Gray SW, Colborn GL, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Contemp Surg 31(4):25-36, 1987; with permission.

In an exhaustive study of the cystic artery, Michels44 described 12 types of double cystic arteries; consult his book for details. Less common than duplications is a recurrence of the superficial branch. The artery first supplies the fundus, then turns downward to branch over the body of the gallbladder90 as shown in Figs. 20-37D, E.

Again we wish to quote Van Damme.47 This time we present his beautiful description of the behavior of the cystic artery.

The behavior of the cystic artery can be summarized using the following three general rules.

 

A cystic artery arising to the right of the bile ducts from the right hepatic branch is found in the triangle between the hepatic and cystic ducts.

A second cystic artery that arises to the left of the bile ducts usually runs anterior to the bile ducts.

If the posterior pancreaticoduodenal arcade arises from a normal gastroduodenal artery, it lies in front of the ductus choledochus. If it arises from a vessel behind the pancreatic head, it also passes behind the ductus choledochus. This is important to remember during choledochotomy and pancreaticoduodenectomy.

Balija et al.91 presented a laparoscopic visualization and classification of the cystic artery (Figs. 20-38, 20-39, 20-40, 20-41, and 20-42).

Fig. 20-38.

Normal position of the cystic artery. A, Conventional visualization. B, Laparoscopic visualization. a, Common hepatic artery; b, Right hepatic artery; c, Cystic artery; d, Cystic duct. (Modified from Balija M, Huis M, Nikolić V, Štulhofer M. Laparoscopic visualization of the cystic artery anatomy. World J Surg 1999;23:703-707; with permission.)

Fig. 20-39.

Double cystic artery. A, Conventional visualization. B, Laparoscopic visualization. a, Double cystic arteries; b, Cystic duct. (Modified from Balija M, Huis M, Nikolić V, Štulhofer M. Laparoscopic visualization of the cystic artery anatomy. World J Surg 1999;23:703-707; with permission.)

Fig. 20-40.

“Large cystic artery.” A, Conventional visualization. B, Laparoscopic visualization. a, Cystic artery (or cystic arteries); b, Aberrant right hepatic artery; c, Cystic duct. (Modified from Balija M, Huis M, Nikolić V, Štulhofer M. Laparoscopic visualization of the cystic artery anatomy. World J Surg 1999;23:703-707; with permission.)

Fig. 20-41.

Cystic artery originating from the gastroduodenal artery. A, Conventional visualization. B, Laparoscopic visualization. a, Cystic artery; b, Cystic duct. (Modified from Balija M, Huis M, Nikolić V, Štulhofer M. Laparoscopic visualization of the cystic artery anatomy. World J Surg 1999; 23:703-707; with permission.)

Fig. 20-42.

Cystic artery originating from the left hepatic artery. A, Conventional visualization. B, Laparoscopic visualization. a, Cystic artery originating from the left hepatic artery; b, Left hepatic artery; c, Cystic duct. (Modified from Balija M, Huis M, Nikolić V, Štulhofer M. Laparoscopic visualization of the cystic artery anatomy. World J Surg 1999;23:703-707; with permission.)

Chen et al.92 reported autopsy findings on the origin and course of the cystic artery:

The cystic artery arises from many possible origins; the right hepatic artery is the most common origin (76.6%). The Calot triangle (hepatocystic triangle), which is an important imaginary referent area for biliary surgery, is bounded by the common hepatic duct (CHD), the cystic duct, and the cystic artery. Of all the cystic arteries, 86.1% coursed through the Calot triangle, and 100% of the cystic arteries originating from the right hepatic artery coursed through the Calot triangle. However, only 54% of the cystic arteries that originated from the left, bifurcation, proper, and common hepatic arteries ran through the triangle. None of the cystic arteries that originated from the gastroduodenal, celiac, superior mesentery, or superior pancreaticoduodenal arteries passed through the triangle. Furthermore, 72.7% of the cystic arteries that originated from the right hepatic artery ran beneath the CHD as they entered the Calot triangle; the others ran anterior to the CHD. Of the cystic arteries that arose from locations other than the right hepatic artery, 29.4% ran posterior to the CHD, and 11.8% ran anterior to the CHD.

The extrahepatic bile ducts in most individuals are supplied from the cystic artery above and from the posterior superior pancreaticoduodenal artery below. Shapiro and Robillard93 described several variations in this pattern. The upper supply from the cystic artery is relatively constant. The lower supply may be from the hepatic, gastroduodenal, or supraduodenal arteries.

The epicholedochal arterial plexus of the common bile duct is derived from the retroduodenal or posterior superior pancreaticoduodenal arteries94 (Figs. 20-43, 20-44). The collateral circulation is enhanced by two intramural plexuses (Fig. 20-45). These may be compressed between the edematous mucosa and the external tough fibrous coat in pathologic conditions such as cholangitis or common bile duct obstruction secondary to choledocholithiasis. Appleby95 emphasized that the surface of the common bile duct should be protected to prevent iatrogenic ischemia as well as to avoid venous bleeding.

Fig. 20-43.

Arterial blood supply of extrahepatic biliary tract showing epicholedochal arterial plexus. HA, Hepatic artery. (Modified from Toouli J (ed). Surgery of the Biliary Tract. New York: Churchill Livingstone, 1993; with permission.)

Fig. 20-44.

Course of retroduodenal and retroportal arteries (posterior view). PV, Portal vein. LHA, Left hepatic artery. RHA, Right hepatic artery. SV, Splenic vein. IMV, Inferior mesenteric vein. SMA, Superior mesenteric artery. IPDA, Inferior pancreaticoduodenal artery. (Modified from Toouli J (ed). Surgery of the Biliary Tract. New York: Churchill Livingstone, 1993; with permission.)

Fig. 20-45.

Arterial blood supply of extrahepatic biliary tract showing epicholedochal arterial plexus. (Modified from Toouli J (ed). Surgery of the Biliary Tract. New York: Churchill Livingstone, 1993; with permission.)

Veins

The hepatic surface of the gallbladder is drained by numerous small veins passing through the gallbladder bed that break up into capillaries within the liver. They do not form a single “cystic vein.” Veins from the hepatic surface drain directly into the liver. Veins on the free surface open directly or follow the hepatic ducts into the liver.

From the peritoneal surface, one vein usually drains the fundus and body and other veins drain the neck and upper portions of the cystic duct as well as the hepatic ducts. These small veins enter the liver together with ascending veins from the common bile duct96 as shown in Fig. 20-46. These veins rarely open into extrahepatic portal veins.97 This is not an important portosystemic shunt.

Fig. 20-46.

Venous drainage of gallbladder and cystic duct. (Modified from Skandalakis LJ, Gray SW, Colborn GL, Skandalakis JE. Surgical anatomy of the liver and associated extrahepatic structures. Part 4: Surgical anatomy of the hepatic vessels and the extrahepatic biliary tract. Contemp Surg 1987;31(1):25-36; with permission.)

Sugita et al.98 recommended the use of computed tomography during angiography to detect cystic vein inflow portions of the intrahepatic vessels, identifying possible areas of micrometastasis of gallbladder cancer.

Lymphatics of the Biliary Tract

The lymphatic drainage of the gallbladder has been well documented from the studies by Clermont,99 Rouviere,100 Fahim and colleagues,101 and Ito et al.102

Long collecting trunks drain the lymphatic plexus of the fundus and body of the gallbladder (Figs. 20-47 and 20-48). The trunks are on the right and left borders (lateral and medial borders of the gallbladder wall) and are connected by an oblique trunk to form a large “N” on the surface. The trunks on the left drain into the cystic node, which lies in the angle formed by the cystic and common hepatic ducts. The trunks on the right follow the cystic duct, passing without entering the cystic node. These vessels and the efferent vessels of the cystic node drain to the node of the anterior border of the epiploic foramen, called the “hiatal node” by Fahim et al.,101 and to the superior pancreaticoduodenal nodes on the common bile duct. As shown in Fig. 20-48, there is no drainage upward to the liver.99 For all practical purposes, lymphatics of the gallbladder and hepatic ducts have the same lymphatic drainage.

Fig. 20-47.

Intra- and extrahepatic lymphatic drainage of gallbladder. (Modified from Toouli J (ed). Surgery of the Biliary Tract. New York: Churchill Livingstone, 1993; with permission.)

Fig. 20-48.

Lymphatic drainage of gallbladder and biliary tract. Left lateral wall of gallbladder drains to cystic node and then to “node of the hiatus.” Right lateral wall drains directly to hiatal node. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Ito et al.102 divided the lymphatic drainage of the gallbladder into the following three pathways.

 

The cholecystoretropancreatic pathway is the main pathway. It terminates in a large node at the retroportal segment, designated as the principal retroportal lymph node.

The cholecystoceliac pathway at the left of the hepatoduodenal ligament ends at the celiac nodes.

The cholecystomesenteric pathway passes to the left and front of the portal vein and terminates at the superior mesenteric lymph nodes.

Near the left renal vein all pathways converge with the abdomino-aortic lymph nodes.

The hiatal node also drains the wall of the extrahepatic bile ducts and the right lobe of the liver. It, in turn, drains to the superior pancreaticoduodenal node. From the latter node, efferents pass to preaortic and celiac nodes or, by way of several small posterior pancreaticoduodenal nodes, to reach nodes at the origin of the superior mesenteric artery from the aorta.

Enlarged metastatic lymph nodes may cause jaundice by obstructing the common bile duct.45 However, the likelihood of this is minimized by some writers.103

Kurosaki et al.104 reported the following results about the mode of lymphatic spread in carcinoma of the bile duct.

The frequency of lymphatic spread of carcinomas in the proximal, middle, and distal bile ducts, excluding seven T1 tumors, was 48%, 67%, and 56%, respectively. With regard to the mode of lymphatic spread: (1) a metastatic pathway along the common hepatic artery predominated over that to the retropancreatic area in the proximal duct carcinoma group; (2) in the middle duct carcinoma group, metastatic lymph nodes were distributed widely, involving nodes around the superior mesenteric artery or at the para-aortic area; and (3) in the distal duct carcinoma group, metastatic nodes generally were localized around the head of the pancreas (Figs. 20-49, 20-50).

Fig. 20-49.

Anatomic configuration of lymph nodes around head of pancreas and in hepatoduodenal ligament. Nodes along superior mesenteric artery are subdivided into four groups: * Node near origin of superior mesenteric artery; ** Node around origin of inferior pancreaticoduodenal artery; *** Node around origin of middle colic artery; **** Node around origin of first jejunal artery. (Modified from Kurosaki I, Tsukada K, Hatakeyama K, Muto T. The mode of lymphatic spread in carcinoma of the bile duct. Am J Surg 1996;172:239-243; with permission.)

Fig. 20-50.

Comparison of modes of lymphatic spread according to location of primary tumor (T1 tumors excluded). BDC-P, Proximal bile duct carcinoma. BDC-M, Middle bile duct carcinoma. BDC-D, Distal bile duct carcinoma. (Modified from Kurosaki I, Tsukada K, Hatakeyama K, Muto T. The mode of lymphatic spread in carcinoma of the bile duct. Am J Surg 1996;172:239-243; with permission.)

Malignancy of the hepatic duct confluence was studied by Jarnagin et al.105 Since complete excision of tumors in this area is not always possible, various palliative measures must be considered. Doglietto et al.106 found palliative endoscopic stenting a safe and efficient procedure for inoperable extrahepatic bile duct cancer. Kobayashi et al.107 found that residual bile duct carcinoma occurred in patients with pancreaticobiliary maljunction who had undergone excision of extrahepatic bile ducts, and recommended careful long-term follow-up.

Innervation of the Gallbladder and Biliary Tract

Parasympathetic (vagal) and general visceral sensory fibers from the hepatic division of the anterior vagal trunk and the celiac division of the posterior vagal trunk follow the hepatic artery and its branches to the extrahepatic bile ducts and the gallbladder.

Preganglionic sympathetics and visceral afferent fibers for pain reach the celiac plexus by way of the greater thoracic splanchnic nerves. The autonomic fibers synapse in the celiac ganglia, and postganglionic and sensory fibers pass into the hepatic plexuses to reach the liver.

Fibers from the right phrenic nerve travel by way of the phrenic, celiac, and hepatic plexuses to reach the gallbladder. Many of these fibers are afferent and may account for the pain referred to the right hypochondrium and radiating to the back between the shoulder blades in some patients with gallbladder diseases.

Burnett and associates108 demonstrated three nerve plexuses: subserous, muscular, and mucosal. The ganglion cells in each nerve plexus decrease in number from subserous to mucosal levels. In comparison with the myenteric plexus of the gut, the subserous plexus ganglia are larger and spaced farther apart. In spite of this well developed nerve supply, there are relatively few smooth muscle cells in the ducts.109 Petkov110 reported a distinct nerve to the sphincter of the common bile duct in 92% of the cases he studied.

Hepatocystic Triangle, Triangle of Calot, and Area of Moosman

The hepatocystic triangle is formed by the proximal part of the gallbladder and cystic duct to the right, the common hepatic duct to the left, and the margin of the right lobe of the liver superiorly. The triangle originally described by Calot111 defined the upper boundary as the cystic artery. The area included in the triangle has enlarged over the years112 as shown in Fig. 20-51. The area of Moosman113 is a circular area 30 mm in diameter; it fits into the hepatocystic duct angle.114

Fig. 20-51.

Hepatocystic triangle and triangle of Calot. Upper boundary of hepatocystic triangle is inferior border of liver. CA, Cystic artery. CD, Cystic duct. CHD, Common hepatic duct. CBD, Common bile duct. LHA/RHA, Left and right hepatic arteries. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Within the boundaries of the triangle as it is now defined and of Moosman’s area are several structures that must be identified before they are ligated and sectioned: the right hepatic artery, common bile duct, aberrant hepatic artery (if present), and cystic artery.

After its origin from the proper hepatic, the right hepatic artery enters the hepatocystic triangle by crossing posterior to the common hepatic duct in 85% of cases. The right hepatic artery or one of its branches passes anterior to the duct in 15%.44,51 It lies parallel with the cystic duct for a short distance, then turns upward to enter the liver. Saint115 emphasized the presence of an epicholodochal venous plexus that helps the surgeon to identify the common bile duct. There is no such venous plexus on the surface of the cystic duct. The right hepatic artery lay within 1 cm of the duct in 20% of cadavers examined by Moosman116 and might have been mistaken for the cystic artery. As a general rule, no artery more than 0.3 cm in diameter in the triangle will be a cystic artery.

An aberrant right hepatic artery was present in 18% of Moosman’s116 specimens. In 83% of these, the aberrant artery gave rise to the cystic artery within the triangle.

In most individuals (96%), the cystic artery is found in the hepatocystic triangle.116 In 80%, the origin of the artery from a normal or aberrant right hepatic artery is within the triangle.44 In a few cases, the origin of the right hepatic artery is to the left of the common hepatic duct. Hence, it enters the triangle by passing in front of the duct. A similar course is followed in the rare cases in which the cystic artery originates in the left hepatic artery. Where the artery arises from the common hepatic artery or gastroduodenal artery, it enters the triangle from below.

Among 220 cadavers examined by Michels,44 the cystic artery was double in 50 and triple in one. Michels described 20 possible patterns of the origin of double cystic arteries. Three of the possible arrangements have never been reported.

Bergamaschi and Ignjatovic117 reported on the surgical ramifications of the occurrence of multiple anatomic structures within Calot’s triangle. Inadvertent ligation of variant veins or bile ducts may complicate laparoscopic cholecystectomy.

Stremple114 estimated that 85% of all variations in the hepatic pedicle are found in Moosman’s area, and 50% of these variations are a potential hazard during cholecystectomy.

Histology

The bile ducts are composed of an external fibrous layer of connective tissue, a few thin smooth muscle layers (longitudinal, oblique, and circular), and an internal layer of mucosa of columnar epithelium.

Opening into the cystic duct are the true ducts of Luschka. These are found in the connective tissue between the neck of the gallbladder and liver, but they open into the lumen of the cystic duct, not that of the gallbladder. These are histologically the same as intrahepatic bile ducts and may be the remnants of aberrant embryonic ducts.

The gallbladder wall is formed, from external to internal, by the following layers:

 

Serosa

Adventitia

Fibromuscular layers

Mucosa

Serosa is the typical visceral peritoneum formed by mesothelium on the surface with loose connective tissue directly beneath.

Adventitia is a layer of dense connective tissue that is found external to the muscularis externa where the gallbladder is attached to the surface of the liver. The adventitia contains large blood vessels, autonomic fibers for innervation of muscularis externa and blood vessels, a rich lymphatic network, and a plethora of elastic fibers and adipose tissue.

Fibromuscular layers comprise many elastic and collagen fibers among bundles of smooth muscle cells. No muscularis mucosa or submucosa is found in the gallbladder.

Mucosa is distinguished by having very tall, slender columnar epithelial cells. While no glands are found in the mucosa, this layer is thrown into elaborate folds which on first inspection give the impression of glands. These folds form deep diverticula of the mucosa and have been identified as “Rokitansky-Aschoff sinuses”; in some cases, these extend through the muscularis externa. Bacteria have been known to accumulate in these folds, and chronic inflammation may develop.

Physiology

Bile, produced by hepatocytes, drains into the hepatic canaliculi. It travels from the terminal bile ducts to the right and left hepatic ducts. Then it moves to the common hepatic duct. The majority of the bile goes from the common hepatic duct through the cystic duct to the gallbladder, drains to the common bile duct, and then to the duodenum. The remainder of the bile goes to the common bile duct, then to the duodenum, bypassing the gallbladder.

Bile production is such that 250 ml to 1,500 ml of bile enters the duodenum each day. The gallbladder has a capacity ranging from 15 to 60 ml (average approximately 35 ml). The gallbladder concentrates bile by absorbing sodium, chloride, and bicarbonate ions and water such that bile salts can be concentrated 5 to 250 times. Potassium ions are concentrated as the water is absorbed; further concentration results from simple diffusion. Bile contains significant amounts of carbonate and calcium ions. The epithelium secretes hydrogen ions, and the carbonate ions are converted to bicarbonate. Calcium and bicarbonate ions are absorbed by the epithelial cells and, thus, calcium carbonate precipitation in the gallbladder is avoided.

The hormone cholecystokinin causes contraction of the gallbladder muscle, forcing bile out. Stimulation from the vagus nerve also causes the gallbladder to contract. The sphincteric apparatus of Oddi becomes inhibited in the presence of cholecystokinin and relaxes as a reaction to gallbladder contraction.118 All of these actions force bile into the common bile duct and the duodenum.

Surgery of the Extrahepatic Biliary Tract and Gallbladder

Prior to surgery, if possible, the gallbladder should be studied and diagnosis of the disease should be made using some of the following tools:

 

Abdominal x-rays

Oral cholecystogram

Abdominal ultrasonography

Hepatobiliary scintigraph

While transabdominal ultrasonography will demonstrate polypoid lesions of the gallbladder, Azuma and colleagues119 recommend endoscopic ultrasonography for differential diagnosis of gallbladder polyps.

Exploration of the Gallbladder and Ducts

To explore the gallbladder and ducts first inspect and palpate the liver. Then place the patient in a reversed Trendelenburg position to permit the viscera to descend. Gallstones in the gallbladder can be felt because they will be in the most dependent position.

When the hepatic triad and lesser omentum are palpated, enlarged lymph nodes may be found. Large stones in the common bile duct can occasionally be felt. Tumors of the porta hepatis or of the head of the pancreas can be discovered with careful palpation. The pulsation of the hepatic artery and a normal or dilated common bile duct can be seen. Remember that obstruction can be present without dilatation of the duct.120

To palpate the distal common bile duct, kocherization of the duodenum is necessary. This is accomplished by mobilizing the hepatic flexure of the colon and incising the peritoneum lateral to the second part of the duodenum. The left index and middle fingers are inserted posteriorly while the left thumb is positioned anteriorly. In this way, the common duct and a possible stone or tumor can be palpated, and the duodenum and the head of the pancreas can be evaluated (Table 20-7).

Table 20-7. the Anatomy of Differential Diagnosis in the Operating Room

Pathology Pancreas Gallbladder/Common Bile Duct
Carcinoma of the pancreas Discrete mass in head (67%); less often in body or tail (33%). Body and tail distal to tumor are pale, indurated, rounder; tail is retracted from splenic hilum. Distal pancreatic duct is dilated and palpable along ventral surface of gland. With more ductal dilation, duct of Wirsung becomes centrally located. With carcinoma (CA) of head, common duct is dilated, thin-walled and bluish. Gallbladder is usually distended with distal CA, common duct is not involved.
Carcinoma of ampulla of Vater Marble-like structure projecting from medial wall of duodenum. If duct of Wirsung is obstructed (20-25%) then pancreas is as above. Same as above
Chronic pancreatitis If the duct of Wirsung is obstructed, then the duct is palpable and the pancreas is rounded, pale and indurated as in cancer If jaundice is present, then the gallbladder and common bile duct are distended, thick-walled, edematous and pale. Hepatogastric ligament is inflamed.
Penetrating duodenal ulcer Localized induration in the head of the pancreas, without obstruction of the pancreatic duct. No pancreatic changes. No jaundice. No dilation of gallbladder or common bile duct.
Impacted stone Stone in the head of the pancreas without projecting into the lumen of the duodenal induration around the stone. No pancreatic changes. Gallstones in 93% cases. Gallbladder and common bile duct rarely distended.

Source: Skandalakis JE, Gray SW, Rowe JS, Skandalakis LJ. Anatomical complications of pancreatic surgery, Part 2. Contemp Surg 15(6):21-50, 1979; with permission.

Surgical Procedures

Open Cholecystectomy

Routinely, the anterior leaf of the hepatoduodenal ligament is incised over the hepatocystic triangle and the underlying structures are revealed. In more difficult cases, where adhesions from inflammation or previous surgery have obscured normal relationships, greater efforts are required. Three techniques follow.

 

The hepatic flexure of the colon and the duodenum may be mobilized to the left.

The liver may be retracted to the right. This puts slight tension on the biliary ducts and opens the epiploic foramen of Winslow, providing better orientation of the field.

When dissecting the gallbladder away from the liver bed, one may expose the cystic artery by rotating the gallbladder to the left. This also exposes the common hepatic duct, the right and left hepatic ducts, and the cystic duct. Performing this maneuver provides one of the advantages of removing the gallbladder from the fundus downward.

Occasionally the gallbladder bed bleeds profusely. The use of suction and diathermy is advisable. The gallbladder bed may be filled with omentum and a drain placed over the omentum (not between the bed and the omentum).

Subserous excision of the gallbladder, first advocated by Bickham,121 is still a useful procedure.122 In this procedure, the lamina propria of loose connective tissue is used as the plane of dissection. This at once removes the entire mucosa and leaves the surface of the liver uninjured.

Many surgeons, when removing the gallbladder, prefer to begin in the hepatocystic triangle. After incision of the anterior leaf of the hepatoduodenal ligament, the cystic artery and duct are identified, ligated, and transected. The gallbladder can then be dissected from its bed from below upward. This procedure has the following advantages:

 

Early identification and ligation of the cystic duct prevents cystic or gallbladder stones from being milked into the common bile duct

Early ligation of the cystic artery reduces blood loss to a minimum

An alternative procedure is to begin at the fundus of the gallbladder and dissect downward toward the neck. Blood loss may be reduced if branches of the cystic artery and veins are clamped or cauterized. When freeing up the cystic artery, one must be aware of a small branch from it to the cystic duct that can occasion bleeding if avulsed. Similarly, stones may be kept from descending by early ligation of the cystic duct. When there is doubt about the anatomy, an operating room cholangiogram is indicated.

Herman123 advocated the following procedure for cholecystectomy.

 

1. Dissection of the gallbladder

2. Exposure of the cystic duct and its union with the common bile duct

3. An operating room cholangiogram

4. Dissection and ligation of the cystic duct and removal of the gallbladder

Regardless of the direction of the procedure, the junction of the cystic and common hepatic ducts should be identified. A short cystic duct may cause inadvertent injury to the common bile duct, but a long cystic duct remnant may produce the cystic duct remnant syndrome, which is similar to gallbladder disease secondary to lithiasis.

Seale and Ledet124 reported good results with primary closure of the common bile duct following minicholecystectomy.

Davis et al.125 advised percutaneous cholecystostomy for the treatment of patients with suspected acute cholecystitis. Kim et al.126 found percutaneous gallbladder drainage a safe and effective emergency procedure for acute cholecystitis, allowing delayed laparoscopic cholecystectomy.

Bouvert’s syndrome, which is obstruction of the gastric outlet or the first and (partially) second part of the duodenum including the duodenal bulb by a giant gallstone, occurs in 1-3% of all cholecystoenteric fistulas.127

Routine drainage of the subhepatic space after cholecystectomy has been debated in the past. Some authors have supported the practice as preventative against postoperative bile collection. Recent studies show that routine drainage results in increased hospital stay, higher postoperative fever, slower progression to a regular diet, and a higher rate of postoperative complications. Ronaghan and colleagues128 showed that drainage should be used only where contamination, hemorrhage, bile leakage, or inflammation are present. Henry and Carey129 emphasized that the proper timing of drainage is important. Attempting drainage too early fails to solve the problem and waiting too long exposes the patient to excess risk of systemic infection.

When carcinoma of the gallbladder is present, Ogura et al.130 have recommended extensive hepatic resection if the malignancy invades the liver at the gallbladder fossa. Chijiwa et al.131 urged radical surgery to treat T2 carcinoma of the gallbladder, with the presence of lymph node metastasis and/or perineural invasion suggesting a need for further post-surgical treatment. Azuma et al.132 stated that intraoperative ultrasonography and frozen section examination are useful in the diagnosis of the depth of invasion of carcinoma of the gallbladder. Furukawa et al.133 stated that differentiation between benign and malignant polypoid lesions in the gallbladder may be reliably identified, therefore cholecystectomy is not necessary. This may be so, but the authors of this chapter advise cholecystectomy.

According to Patiño and Quintero,134 patients with asymptomatic cholelithiasis may have elective cholecystectomy, a safe procedure with low morbidity and mortality. Some patients, however, are at high risk for developing complications of their asymptomatic disease, and surgery in these patients may be technically difficult and involve high morbidity and mortality. The authors present the following criteria for identifying those high-risk patients:

 

Life expectancy >20 years

Calculi >2 cm in diameter

Calculi <3 mm and patent cystic duct

Radiopaque calculi

Polyps in the gallbladder

Nonfunctioning gallbladder

Calcified gallbladder

Concomitant diabetes

Women <60 years

Individuals in geographic regions with a high prevalence of gallbladder cancer

We quote from Merriam et al.:135 “Older male patients (age older than 50 years) with history of cardiovascular disease, leukocytosis greater than 17,000 white blood cells/mL, and acute cholecystitis have increased risk of gallbladder gangrene and conversion of laparoscopic cholecystectomy to open cholecystectomy.”

 Read an Editorial Comment

Laparoscopic Cholecystectomy

It should always be remembered that a well performed operation outside a trial setting is always more beneficial than a poorly conducted operation within a trial setting.—Alastair R. Brown139

Regarding the earliest history of laparoscopic cholecystectomy, McKernan140 has written:

The first laparoscopic cholecystectomy was done by a German shortly after Semm performed laparoscopic appendectomy in 1982. On September 12, 1985, Erich Muhe, in Boblingen, Germany, performed a laparoscopic cholecystectomy by looking through the scope (without video optics). A piece of bicycle tubing was used as a large cannula through which the gallbladder was removed. His license was revoked shortly thereafter.

Laparoscopic cholecystectomy was reintroduced to the surgical profession by DuBois, Mouret, and Périssat in 1988.141 Since then, the laparoscopic technique has become the treatment of choice for symptomatic gallstones. Lujan et al.142 stated that laparoscopic cholecystectomy for the treatment of acute cholecystitis is a safe and valid procedure with a low rate of complications.

Perissat143 stated:

The end of this century has witnessed a profound and definitive change in our surgical profession, a true revolution indeed. This change is comparable to that experienced by our elders by the end of the nineteenth century when surgery started to obey the laws of asepsis. Laparoscopic cholecystectomy, born during the years 1987-1988, will be remembered as the discovery that triggered this revolution.144

The role of laparoscopic cholecystectomy in the treatment of gallbladder cancer is still evolving. Whalen et al.145 reported the following about patients whose cancer was accidentally resected between 1985 and 1988 (immediate prelaparoscopic era) and from 1992 to 1995 (when laparoscopic cholecystectomy was well established):

The widespread adoption of laparoscopic cholecystectomy did not worsen the survival of patients with gallbladder cancer, and patients with serendipitously treated gallbladder cancers did not have a worse survival after laparoscopic manipulation than after a standard open cholecystectomy. The laparoscopic aspects of operative manipulation of a gallbladder with cancer in it do not appear to be a proximate cause of the poor prognosis of this disease.

Schwesinger et al.146 presented the algorithm shown in Fig. 20-52 which includes laparoscopic management of acute cholecystitis.

Fig. 20-52.

Simplified algorithmic approach to the management of patients with acute cholecystitis. The dotted line represents an acceptable alternative strategy. PCC, percutaneous cholecystostomy. LC, laparoscopic cholecystectomy. (From Schwesinger WH, Sirinek KR, Strodel III WE. Laparoscopic cholecystectomy for biliary tract emergencies: State of the art. World J Surg 1999;23:334-342; with permission.)

In reference to laparoscopic common bile duct exploration, Crawford and Phillips147 stated:

Although still controversial, laparoscopic common bile duct exploration has been shown to be safe, applicable, and cost-effective in the treatment of choledocholithiasis.

Jawad et al.148 advised laparoscopic cholecystectomy for infants and children as the procedure of choice for gallstones.

Cholecystostomy is performed rarely today, but occasionally it is a necessity. As was emphasized several years ago by Skandalakis and Jones:149 “Cholecystostomy should not be considered a mark of inferior surgical skill, but rather a sign of mature surgical judgment.”

Sugiyama et al.150 reported that cholecystostomy may be a definitive procedure for acalculus cholecystitis in elderly patients.

A study by Misawa et al.151 found that patients “with large branches of the middle hepatic vein close to the gallbladder bed are at risk of hemorrhage during laparoscopic cholecystectomy and should be identified preoperatively with ultrasound.”

Common Bile Duct Surgery

Although the diameter of the common bile duct increases in the presence of obstruction, there is no sharp dividing line between normal and obstructed ducts that can be applied in all cases.

Madden152 provided good indicators for cholangiography or exploration of the duct in stone disease. The following list is based on his indicators:

 

Recent or present jaundice (cholangiography)

Dilatation of the common bile duct (7 mm ultrasonographically or 10 mm at direct visualization) (cholangiography)

Multiple stones in the gallbladder together with a large cystic duct (cholangiography)

Aspiration of murky bile from the duct (cholangiography)

Presence of a palpable stone (exploration)

Roentgenographic visualization of a stone (exploration)

When in doubt, explore!

The ability to mobilize the common bile duct depends on the pathology and the scarring from previous operations. Lahey and Pyrtek153 were able to obtain 2-5 cm in length by mobilizing the distal common bile duct from the undersurface of the pancreas. Since the duct may be intrapancreatic (see Fig. 20-32), the pancreas and duodenum should be mobilized. In about 70 percent of patients, the duct is free on the surface of the pancreas or is covered by a tongue of pancreatic tissue that leaves a cleavage plane between pancreas and duct (Figs. 20-32B-E). In the remaining cases, the pancreas may have to be mobilized because the duct is entirely covered by pancreatic tissue.

Cole and associates154 were skeptical of mobilization of the distal common bile duct as a means of repairing strictures. They avoided all end-to-end anastomosis in favor of a Roux-en-Y procedure when more than 1 cm of the duct needed replacement. Avoidance of end-to-end anastomosis has become current standard practice, using instead a Roux-en-Y hepato- or choledochojejunostomy in virtually all bile duct reconstructions.

As to common bile duct malignant processes, Gerhards et al.155 reported that absence of multifocality, diploid-type tumors and negative proximal bile duct margin histopathologies are significant factors prognostic of long-term survival for patients with carcinoma of the proximal bile duct (Klatskin tumors).

We quote from Blom and Schwartz156 on the surgical treatment of Klatskin tumors:

Curative resection could be achieved in approximately one third of patients who had cholangiocarcinoma, and should be the goal of treatment. Survival is significantly improved in those patients who are considered to have resectable tumors and who undergo removal of all gross disease. Palliative surgical treatments also revealed a survival advantage over nonoperative therapies.

Sutherland et al.157 stated that the Hepp-Couinaud hepaticojejunostomy without stenting is a reliable procedure for repair of postcholecystectomy stricture of bile ducts.

Nakayama et al.158 advised that because it is usually not possible to determine whether strictures of the proximal bile duct are malignant or benign, they should be presumed malignant and treated accordingly.

Common Bile Duct Stones

Thistle159 presents the pathophysiology of bile duct stones as follows:

 

Primary stones (less common, frequent recurrence, no pharmacologic response, difficult surgery)

 

– Intrahepatic

 

“Pure” cholesterol

Black mixed cholesterol

Brown

 

– Extrahepatic

 

Brown

Secondary stones (common, easy to treat surgically)

 

Black bilirubin polymer

“Pure” cholesterol

Mixed cholesterol

Brown and other rare

Liu et al.160 reported that the treatment of primary biliary stones was satisfactorily achieved by a systematic, aggressive approach consisting of hepatic resection, frequent construction of a hepaticocutaneous jejunostomy, and postoperative choledochoscopy.

González-Koch and Nervi161 reported that although there is no primary indication to use solvents (chenodeoxycholic acid, ursodeoxycholic acid, monooctanoin, methyl tert-butyl ether) on common bile duct stones, due to their adverse reaction and their limited success in comparison with lithotripsy, the use of solvents may be indicated in a small group of patients in whom invasive or surgical treatment is risky or may fail.

Raraty et al.162 advised that the treatment of acute cholangitis and pancreatitis secondary to common bile duct stones consists of systemic antibiotics and early removal of the obstructing stones by endoscopic retrograde cholangiopancreatography and endoscopic sphincterotomy. Cholecystectomy may be used prophylactically to prevent recurring episodes of gallstone pancreatitis.

We quote from Poon et al.163:

Endoscopic sphincterotomy for biliary drainage and stone removal, followed by interval laparoscopic cholecystectomy, is a safe and effective approach for managing gallstone cholangitis. Patients with gallbladder left in situ after endoscopic sphincterotomy have an increased risk of biliary symptoms. Laparoscopic cholecystectomy should be recommended after endoscopic management of cholangitis except in patients with prohibitive surgical risks.

De Aretxabala and Bahamondes164 advised that side-to-side choledochoduodenostomy with wide stoma is a safe procedure in selected patients with common bile duct stones and with minimal complications (5%). One complication is sump syndrome, which consists of bile duct contamination, cholangitis, and even secondary biliary cirrhosis.

Stuart et al.165 stated that laparoscopic cholangiogram is safe, quick, and detects common bile duct stones.

Csendes et al.166 stated that open choledochostomy has a definite place for the surgical treatment of bile duct stones, together with endoscopic retrograde cholangiopancreatography, papillotomy, and laparoscopic common bile duct exploration.

Navarrete et al.167 reported their experience with 373 patients in whom residual choledocholithiasis was effectively treated by the percutaneous approach in the presence of a T-tube, with low morbidity and mortality.

Seitz et al.168 reported that therapeutic endoscopic papillary balloon dilatation is an alternative procedure to endoscopic papillotomy for extraction of small common bile duct stones, but that further study is required before its routine use can be recommended.

Both Giurgiu et al.169 and Shuchlieb et al.170 reported that laparoscopic common bile duct exploration is an effective method for treatment of choledocholithiasis, the latter stressing the necessity of a laparoscopist who is skillful and who has good equipment. In his commentary on Shuchlieb, Fielding171 stated, “Laparoscopic common bile duct exploration is the logical extension of the great revolution of laparoscopic cholecystectomy. It provides an all-in-one treatment for most patients with common bile duct (CBD) stones and avoids the need for preoperative endoscopic retrograde cholangiopancreatography (ERCP) in most patients.”

Choledochal Cyst Surgery

For treatment of choledochal cysts type I, the preferred procedure is excision of the cyst and Roux-en-Y hepaticojejunostomy (Figs. 20-53, 20-54).

Fig. 20-53.

Surgical options for treatment of choledochal cysts. (Preferred treatment in capital letters.) (Modified from Nagorney DM. Choledochal cysts in adult life. In: Blumgart LH (ed). Surgery of the Liver and Biliary Tract, vol 2. New York: Churchill Livingstone, 1988; with permission.)

Fig. 20-54.

Choledochal cyst excision with Roux-en-Y hepaticojejunostomy, the preferred method of operative management. (Modified from O’Neill JA Jr. Choledochal cyst. Curr Prob Surg 1992;19:361-410; with permission.)

Excision of the diverticulum only is the the accepted procedure of choice today for the treatment of type II choledochal cysts.

Duodenal choledochoceles (type III) are treated by duodenotomy with unroofing of the cyst, reapproximation of the mucosa with interrupted absorbable sutures, and sphincteroplasty. Pancreatic choledochoceles may require pancreaticoduodenectomy.

For type IV cysts, the treatment of choice is complete excision or hepatic lobectomy.

Caroli’s disease (type V cyst) is treated by partial hepatic lobectomy when localized. Unroofing and drainage into a Roux loop should be performed as needed. Conservative treatment is advised when diffuse cystic disease is present.

When intrahepatic bile duct stenosis is present in patients with choledochal cysts, Ando et al.172 advised resection of the stenotic ducts and performing a Roux-en-Y end-to-side anastomosis.

Ishibashi et al.173 reported that malignant change was not observed after total or subtotal excision in their series studying 48 patients over a 21-year period.

Hamada et al.174 reported a case of choledochal cyst diagnosed at the 29th week of gestation with rapid cystic enlargement and gastric outlet obstruction after delivery. Temporary external drainage was performed and, at the age of 81 days, cystic excision and hepaticoduodenostomy.

Weyant et al.175 review the literature on choledochal cysts in adults and describe two cases. They emphasize that, if possible, complete excision of the cyst should be performed to prevent malignancy.

Tanaka et al.37 recommended prophylactic cholecystectomy in patients with anomalous junction of the pancreatobiliary ductal system but without dilatation. This recommendation is made to avoid future malignancy in a population that has a relatively high risk of developing biliary tract cancer.

Multiple carcinomas of the biliary tract in a patient with pancreaticobiliary maljunction and congenital choledochal dilatation have been reported.176

Although we have recommended the writings of O’Neill35,36 previously, they cannot be praised highly enough. They are a storehouse of information, and should be consulted by the surgeon of the extrahepatic biliary tract.

Portal Hypertension

By definition, portal hypertension is produced by an increase in resistance of the portal blood flow secondary to cirrhosis of the liver in most cases, or secondary to splenic vein thrombosis (Fig. 20-55), with formation of collateral circulation between the portal and systemic venous networks.

Fig. 20-55.

Diagrammatic representation of collateral circulation characteristic of isolated occlusion of the splenic vein. (Modified from Salam AA, Warren WD. Anatomic basis of the surgical treatment of portal hypertension. Surg Clin North Am 1974;54:1247-1257; with permission.)

Anatomically, submucosal varices are developed in the proximal stomach and distal esophagus. Hematemesis, ascites, hypersplenism, and encephalopathy may be the sequelae of this clinical entity. Among the choice of treatments are selective distal splenorenal shunt (Fig. 20-56), mesorenal interposition shunt (Fig. 20-57), and several other procedures.

Fig. 20-56.

Diagrammatic illustration of the selective distal splenorenal shunt. (Modified from Salam AA, Warren WD. Anatomic basis of the surgical treatment of portal hypertension. Surg Clin North Am 1974;54:1247-1257; with permission.)

Fig. 20-57.

Diagrammatic illustration of the mesorenal interposition shunt. (Modified from Salam AA, Warren WD. Anatomic basis of the surgical treatment of portal hypertension. Surg Clin North Am 1974;54:1247-1257; with permission.)

Wind et al.177 reported that with portal hypertension there are splenorenal and gastrorenal anastomoses, some of which are situated posteriorly in the left subphrenic compartment. The incidence of spontaneous splenorenal shunts is approximately 17%, and their anatomic pathway is as follows: the gastric collateral vein is connected to the left renal vein via the inferior vein of the left crus of the diaphragm and the middle capsular vein.

Anatomic Complications

Diagnostic Procedures

For complications of open (wedge) biopsy and percutaneous (needle) biopsy, please consult the chapter on the liver.

Percutaneous Transhepatic Cholangiography (PTC)

Most of the organs that may be injured by needle biopsy are also at risk from percutaneous transhepatic cholangiography (PTC). Hemorrhage, bile peritonitis, and septicemia are the chief dangers.

Endoscopic Retrograde Cholangiopancreatography (ERCP)

Cholangitis,178 duodenal perforation, pancreatitis, pancreatic sepsis, and pseudocyst formation are among possible complications of endoscopic retrograde cholangiopancreatography (ERCP). The instrument may injure the common bile duct, the main pancreatic duct, or the duodenal papilla.

Angiography

Although duplex Doppler sonography and MRI have lessened the need for invasive investigation, angiography still provides critical diagnostic information for carefully selected patients. Angiography may increase ongoing gastrointestinal bleeding and may increase existing renal or hepatic insufficiency. Contrast medium should not exceed 1 g of iodine per kilogram of body weight.179

Choledochoscopy (Cholangioscopy)

Injury to bile ducts, duodenum, pancreas, or liver is always possible, though uncommon, during choledochoscopy. The incidence of wound infection is not increased by endoscopy. Schebesta and colleagues180 reported a case of operative choledochoscopy resulting in aspiration of gastric contents into the tracheobronchial apparatus.

Peritoneoscopy

Reynolds and Cowan181 list the following complications from peritoneoscopy:

 

Air embolism by accidental injection of air into liver or large abdominal veins

Internal bleeding from vessels at puncture site or from vessels in adhesions

Bleeding from associated liver biopsy

Perforation of intestines adherent to the anterior body wall

Injury to abdominal viscera

Tearing of an adhesion containing a large blood vessel

Puncture of an unsuspected ovarian cyst

Reynolds and Cowan reported only twelve major complications among 2400 peritoneoscopies over 30 years (0.5 percent). Other large series182 had complication rates as high as 2.5 percent.

Surgical Procedures

Cholecystectomy, Common Bile Duct Surgery, and Sphincteroplasty

General Considerations

Matolo183 estimated that about 500,000 operations for biliary tract disease are performed in the United States each year, and he wrote that “nearly 10,000 deaths result from complications or treatment of diseases of the biliary system.” A great many of these deaths result from anatomic complications following surgery in elderly patients with comorbid conditions.

Procedures of biliary tract surgery are many and complicated. The hazards in each procedure are similar, however. Here we consider the anatomic complications that are common to the following three procedures: cholecystectomy, surgery of the common bile duct, and sphincteroplasty.

Remember

 

Isolate and study the structure you intend to cut or ligate.

Identify the common hepatic duct, the cystic duct, and the common bile duct.

Do a cholangiogram if in doubt.

Injuries associated with laparoscopic cholecystectomy will be presented later in this chapter.

Vascular Injury

The most obvious danger is that of hemorrhage from the many large blood vessels lying anterior to the biliary tree. Such vessels are inconstant in number and location. The posterior superior pancreaticoduodenal artery, anterior to the retroduodenal portion of the common bile duct, is the vessel most frequently encountered.

All the vessels listed in Table 20-5 are subject to possible injury.

The following list of variations in the cystic artery may help one avoid common pitfalls.

 

The cystic artery may be single or double, short or long.

It may pass anterior or posterior to the right and left hepatic ducts, the common hepatic duct, or the common bile duct.

It may be large, mimicking a small right hepatic artery.

It may bifurcate at the neck of the gallbladder, or the two arteries may have separate origins.

Injury to the portal vein184 or the inferior vena cava185 is a serious complication. These vessels must, of course, be repaired at once.

Bleeding from veins of the gallbladder bed or from veins of the common bile duct is a minor complication.

A second vascular complication of biliary surgery is ischemia to the liver from unintended ligation of the right hepatic artery or an accessory or replacing aberrant right hepatic artery. Interference with the blood supply of the common bile duct may result in ischemia and stricture.93,94 Other surgeons feel that the blood supply is good and that collateral circulation will prevent local ischemia.186

Parke and associates,94 working on fetal and neonatal specimens, concluded that in spite of an apparently abundant blood supply, the common bile duct should not be skeletonized for more than 2 cm. The combination of ischemia and bile leakage is a danger recognized decades ago by Dragstedt.187

Injury to the Biliary Tract

Jaundice, biliary fistula, and bile peritonitis with pain and fever will follow iatrogenic injury to the biliary ductal system (Fig. 20-58). Glenn188 reviewed 100 cases of such iatrogenic injury.

Fig. 20-58.

Possible iatrogenic injuries to biliary tract. A, Ligation of an accessory hepatic duct (a) together with cystic duct. B, Ligation of an accessory hepatic duct (a) instead of cystic duct. C, Ligation of right hepatic duct below anomalous entry of cystic duct. D, Short cystic duct under tension may angulate common bile duct. One or both limbs may be inadvertently ligated. (Modified from Skandalakis JE, Gray SW, Rowe JS Jr. Anatomical Complications in General Surgery. New York: McGraw-Hill, 1983; with permission.)

Injury to any part of the extrahepatic biliary tree may result in bile leakage, which leads to bile peritonitis. A small, insidious bile leak is probably a greater danger than leakage from an inadvertently cut major duct, because the small leak may go undetected. Small bile ducts in the bed of the gallbladder and small accessory hepatic ducts are easily overlooked and cut. Loosening of the ligation of the cystic duct stump is a possible source of postoperative bile peritonitis.189

The common bile duct itself may be injured if one attempts to pass a probe through it without a preoperative cholangiogram. Fixation of the duct from disease or adhesion from prior surgery may result in unexpected sharp angulation.190

An anatomic classification of bile duct strictures was presented by Bismuth:191

Since the length of the superior biliary stump is a determinant factor in biliary repair, a classification of postoperative biliary strictures according to the level where healthy biliary mucosa can be found may be proposed. Cholangiography is indispensable to precise knowledge of the level of the stricture. We have classified postoperative strictures of the common bile duct into five types (Fig. 20-59).

 

Type 1. Low common hepatic duct stricture: the hepatic stump is longer than 2 cm.

Type 2. Middle common hepatic duct stricture: the hepatic stump is less than 2 cm.

Type 3. High stricture or hilar stricture preserving the biliary confluence: the hepatic duct does not exist any more. The stricture reaches the confluence of the right and left hepatic ducts but communication between the two branches is preserved across the confluence.

Type 4. Hilar structure interrupts the confluence: communication between the left and right branches no longer exists. If the fibrotic scar joining the two branches is thin, then they may remain in continuity, but if the process has destroyed an important part of the ductal tissue, the right and left hepatic ducts may be separated by 1-2 cm.

Type 5. When the trauma has involved an anomalous distribution of the segmental right branches (‘convergence étagée,’ i.e., separate junction of posterior right sectorial duct below the major confluence), one of these two ducts can be separated from the biliary tract by the stricture.

Fig. 20-59.

The different types of postoperative strictures classified according to the length of the superior end. Three landmarks are used: 2 cm under the biliary confluence, the inferior level of the confluence, and roof of the confluence. Type 1: Low stricture. Type 2: Middle stricture. Type 3: High stricture (hilar stricture) preserving the biliary confluence. Type 4: High stricture (hilar stricture) interrupting the biliary confluence. Type 5: Apart, stricture on an anomalous union of the sectorial right branches. (Modified from Bismuth H. Postoperative strictures of the bile duct. In: Blumgart LH (ed). The Biliary Tract. Edinburgh: Churchill Livingstone, 1982, pp. 209-218; with permission.)

Lillimoe et al.192 summarized the treatment of postoperative biliary strictures:

Major bile duct injuries and postoperative bile duct strictures remain a considerable surgical challenge. Management with preoperative cholangiography to delineate the anatomy and placement of percutaneous biliary catheters, followed by surgical reconstruction with a Roux-en-Y hepaticojejunostomy, is associated with a successful outcome in up to 98% of patients.

Injury to Other Organs

Efforts to dissect the distal common bile duct from the pancreas or to mobilize it may result in injury to the pancreas. Retraction of the liver to obtain a better approach to the right and left hepatic duct may tear the liver. Other structures to be protected are the stomach, duodenum, and hepatic flexure of the colon.

Inadequate Procedures

The following inadequate procedures may result in iatrogenic injury.

 

Leaving a long cystic duct stump may lead to cystic duct remnant syndrome.

Failing to securely ligate the stump of the cystic duct may produce bile leakage.193

Failure to recognize a dilated common bile duct that contains stones may lead to cholangitis or pancreatitis.

Laparoscopic Cholecystectomy

The anatomic complications of laparoscopic cholecystectomy are similar to those of the open removal of the gallbladder. According to Morgenstern et al.,194 injury to the common bile duct was less than 0.2% with the open method. The same authors reported bile duct injuries with laparoscopic cholecystectomy of 0.58% in 1284 operations performed between 1989 and 1991, and 0.50% in 1143 operations performed between 1992 and 1994. Moore and Bennett of the Southern Surgeons Club195 stated that an individual surgeon had a 1.7% bile duct injury rate in his or her first 15-20 laparoscopic cholecystectomies, decreasing to 0.17% after 50 operations.

We agree with Morgenstern and colleagues194 that laparoscopic cholecystectomy will continue to pose a problem in biliary tract surgery. Certainly the “learning curve,” both institutional and individual, may explain some of the difference in outcome. The fact remains that the chance of injury to the bile duct is greater in laparoscopic cholecystectomy than in open gallbladder surgery.

The literature indicates differing views concerning operating room cholangiogram for recognition of bile duct injury. Morgenstern et al.194 stated, “The early recognition and repair of ductal injuries in our cases, with successful outcomes in all cases, lends emphasis to the importance of the operative cholangiogram.” Lorimer et al.196 reported that intraoperative cholangiography is not essential. We agree with Morgenstern’s analysis, while at the same time applauding Lorimer’s plea for “meticulous demonstration of anatomic detail at operation.”

We advocate routine fluoroscopic cholangiography in any surgeon’s first fifty laparoscopic cholecystectomies and subsequently in any case where inflammation, questionable anatomy, leak of golden “hepatic” bile, or “aberrant” structures are encountered. Woods et al.197 demonstrated that cholangiography can prevent a minor biliary injury from becoming a disastrous resection of the extrahepatic biliary tree —the “classic” laparoscopic cholecystectomy injury.

We quote from Organ and Porter:198

The role of laparoscopic surgery continues to be defined as data from outcomes research becomes available. Through a medical record review, Wherry and colleagues199 analysed the outcomes of laparoscopic cholecystectomies performed at 94 US military hospitals between January 1993 and May 1994. Of 10458 cholecystectomies, 9130 (87%) were performed laparoscopically. This is an increase from the 65.9% rate of cholecystectomies performed laparoscopically between July 1990 and May 1992 when the procedure was being introduced into the military health services system.200 Complete medical records were obtained for 9054 patients who underwent laparoscopic cholecystectomy. The conversion rate to an open procedure was slightly less than 10%. The 30-day postoperative morbidity rate, including bile duct, bowel, and vascular injuries, was 6.09%; the 30-day postoperative mortality rate was 0.13%

For all practical purposes the complications of laparoscopic cholecystectomy are the same as those of open cholecystectomy. However, the incidence of complications is higher in laparoscopic cholecystectomy and the severity of the bile duct injuries is greater.

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There is no question, as Hunter201 wrote, that cholecystectomy is a triumph of laparoscopic surgery. Nonetheless the procedure can be associated with tragic and catastrophic ductal injuries. These injuries take place because of the surgeon’s inexperience and because of congenital ductal anomalies and variations which are extremely difficult to recognize during the procedure. The extrahepatic biliary system is a topographicoanatomic area notorious for anomalies.

Sarli et al.202 reported 131 cases of gallbladder perforation during laparoscopic cholecystectomy out of 1127 cases (11.6%).

Aoki et al.203 advised that repair of the injured peritoneum at trocar sites during laparoscopic cholecystectomy may reduce the frequency of wound metastasis in cases of unexpected carcinoma of the gallbladder.

Z’graggen et al.204 stated that laparoscopic cholecystectomy on an undiagnosed adenocarcinoma of the gallbladder has a high incidence of recurrences at the port site, followed by death.

Aru et al.205 reported that endoscopic retrograde cholangiopancreatography (ERCP) resolves isolated bile leaks, but iatrogenic strictures after laparoscopic cholecystectomy often require surgical treatment after ERCP.

Hannan et al.206 recommended that “efforts be undertaken to carefully examine the choice of procedure for patients requiring cholecystectomies and to be sure that patients entering each hospital in which the procedure is performed have access to a sufficient number of surgeons trained to perform the procedure laparoscopically.”

Machi et al.207 recommended both laparoscopic ultrasonography and operative cholangiography during laparoscopic cholecystectomy.

Rosenthal et al.213 reported that the choice of technique (open or laparoscopic) used in management of choledocholithiasis depends on the patient’s condition, associated diseases, secondary complications of gallstones, and, above all, the good training and skill of the surgeon.

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Habib et al.214 concluded that gangrenous cholecystitis encountered in patients with acute cholecystitis was not a predictive factor in a laparoscopic approach being converted to open surgery.

Note

In the following material, repetition of information is intended to emphasize its importance.

Bile Duct Injuries

Extrahepatic bile duct injuries are iatrogenic and virtually all are preventable (Table 20-8). They may involve any part of the extrahepatic biliary tract. Local or generalized bile peritonitis is the result of these injuries.

Table 20-8. Techniques to Avoid Injury during Laparoscopic Cholecystectomy

Clear, unobstructed view of the infundibulum/triangle of Calot
Firm cephalad retraction of the fundus, inferior and lateral retraction of the infundibulum
Dissect fat/areolar tissue from infundibulum toward common duct, never vice versa
Visualize absolutely the cystic duct-gallbladder junction with no other intervening tissue
Cholangiography to confirm anatomy and rule out other pathology
Accessory/anomalous ducts are rare; do not over-call
A ductal structure wider than a standard clip is the common duct until proven otherwise
Never cauterize or clip blindly to control bleeding
Irrigate as often as necessary to clear the operative field and optimize visualization
Six to eight clips are the routine maximum; the need for more should lead to conversion
Asking oneself if one should convert to open surgery probably means one should

Source: Branum GD, Pappas TN. Complications of laparoscopic cholecystectomy. In Pappas TN, Schwartz LB, Eubanks S, eds. Atlas of Laparoscopic Surgery. Philadelphia: Current Medicine, 1996, pp. 2-11; with permission.

Careful dissection of the presumed cystic duct is essential. The surgeon should be familiar with this anatomic entity and able to identify both junctions of the cystic duct: the one to the gallbladder and, especially, the one to the common hepatic duct. The junction is exposed after dissecting approximately 1 cm above and 1 cm below the junction.

Nahrwold215 stated that the junction of the three ducts (common hepatic duct, cystic duct, common bile duct) should serve as the primary anatomic landmark for all biliary tract operations. Nahrwold also supports the use of intraoperative cholangiography.

Ductal injuries can be recognized during surgery, in the operating room after surgery by observing bile leak or cholangiogram, or after surgery by the formation of ascites secondary to bile peritonitis. If injury is recognized at the time of surgery, an incomplete transection may undergo primary repair over a stent or T tube.

After studying 12,397 patients who had undergone laparoscopic cholecystectomy, Scott et al.216 reported the following:

 

Major bile duct injury: 0.3%

Minor bile duct injury: 0.1%

Bile leak: 0.4%

Overall morbidity: 4%

Mortality: 0.08%

These rates compare favorably with published reports for open cholecystectomy and indicate that laparoscopic cholecystectomy offers a viable alternative to conventional cholecystectomy.

A classification of laparoscopic bile duct injuries provided by Strasberg et al.217 also includes 5 types, as follows (Figs. 20-60, 20-61).

 

Type A: Bile leak from a minor duct still in continuity with the common bile duct.

Type B: Occlusion of part of biliary tree.

Type C: Bile leak from duct not in communication with common bile duct.

Type D: Lateral injury to extrahepatic bile ducts.

Type E: Circumferential injury of major bile ducts (Bismuth class 1 to 5).

Fig. 20-60.

Proposed classification of laparoscopic injuries to the biliary tract. The injuries Type A to E are illustrated. Type E injuries are subdivided according to the Bismuth classification. Type A injuries originate from small bile ducts that are entered in the liver bed or from the cystic duct. Type B and C injuries almost always involve aberrant right hepatic ducts. Type A, C, D, and some E injuries may cause bilomas or fistulas. Type B and other Type E injuries occlude the biliary tree and bilomas do not occur. (Modified from Strasberg SM, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic cholecystectomy. J Am Coll Surg 1995;180:101-125; with permission.)

Fig. 20-61.

Patterns of biliary injury. [Note: Type E injuries are illustrated also in Fig. 20-60.] a, “classical” Type E injury in which the common duct is divided between clips (point X). The ductal system is divided again later to remove the gallbladder (point Y1). b and c are variants of the injury. d, e, and f represent variants of injury to aberrant right hepatic duct, producing Type B and C injuries. (Modified from Strasberg SM, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic cholecystectomy. J Am Coll Surg 1995;180:101-125; with permission.

Causes of laparoscopic biliary injuries as classified by Strasberg et al. are shown in Table 20-9.

Table 20-9. Classification of Causes of Laparoscopic Biliary Injuries

Misidentification of bile ducts as the cystic duct
  Misidentification of common bile duct as cystic duct*
  Misidentification of aberrant right duct as cystic duct*
Technical causes
  Failure to securely occlude cystic duct*
  Too deep plane of dissection on liver bed*
  Injudicious use of thermal energy* to dissect, control bleeding, or divide tissue
  Tenting injury of cystic duct
  Injudicious use of clips to control bleeding
  Injuries due to improper techniques of ductal exploration

*Common causes of injury in laparoscopic cholecystectomy.

Source: Strasbert SM, Hertl M, Soper NJ. An analysis of the problem of biliary injury during laparoscopic cholecystectomy. J Am Coll Surg 180:101-125, 1995; with permission.

Deziel et al.211 reported the following for treatment of laparoscopic cholecystectomy complications: Laparotomy for the treatment of complications was required by 1.2% of patients. The mean rate of bile duct injury (excluding the cystic duct) was 0.6%. The most lethal complications included bowel injuries in 0.14% and vascular injuries in 0.25%. The most common origin of postoperative bile leak (0.3%) was from the cystic duct.

Beyer et al.218 discussed the mode of treatment of biliary tract disease by minimally invasive procedures, emphasizing the nonoperative treatment of bile duct injuries, namely:

 

Cholangiography for diagnosis of the biliary tract injury

Balloon dilatation for treatment of the biliary stricture

Biliary drainage to allow decompression of the biliary system, which is essential for uncomplicated healing

Percutaneous drainage of fluid collections associated with bile duct injury

Remember

 

The gallbladder bed is the most common site of bile leakage.

Other potential sites of leakage are:

 

– Posterolateral surface of the common hepatic duct, near its junction with the cystic duct

– Posterior surface of the intrahepatic portion of the common bile duct

Both of these injuries are difficult to recognize at the time of surgery, according to Nahrwold.215

 

Liquidation or partial excision of the common hepatic duct or common bile duct are also iatrogenic injuries. They are caused by:

 

– Too much traction of the cystic duct

– Poor anatomic dissection

– Incorrect use of clamps to stop bleeding

If in doubt, perform an operating room cholangiogram and act as appropriate. You can:

 

– Remove the ligation and insert a T tube

– Perform primary repair (end to end anastomosis), or

– Perform Roux-en-Y choledochojejunostomy

Vascular Injuries

Ligate the cystic artery or its two branches (anterior and posterior) close to the gallbladder wall. Although there have been reports of ligation with good results, the hepatic artery and portal vein should be repaired immediately.215

Gallstone Spillage

Horton and Florence219 report abscess formation secondary to dropped gallstones complicating laparoscopic cholecystectomy. Eisenstat220 reported abdominal wall abscess secondary to gallstone spillage during laparoscopic cholecystectomy. According to Kakani and Bhullar,141 gallstone spillage can be avoided by removing the gallbladder intact. This avoids future intraabdominal abscess and such rare complications as cholelithoptosis or cholelithorrhea. Of course, small bowel adhesions are present. Gerlinzani et al.221 remind us that the loss of gallstones and their retention in the abdominal cavity should be noted in the description of the surgical procedure.

Rare Complications

Subcutaneous Emphysema

According to Kent,222 subcutaneous emphysema may be secondary to CO2 pneumoperitoneum. Hypercarbia and acidosis may also be present. Hyperventilation and elimination of the CO2 pneumoperitoneum is the treatment of choice. Rarely patients may require conversion to N2 insufflation. A chest film may reveal the presence of pneumothorax that, if present, should be treated by tube thoracostomy.

Hydrocele

Kauer et al.223 reported the formation of a hydrocele following laparoscopic cholecystectomy. The hydrocele was probably produced by high intraabdominal pressure. This resulted when extended pneumoperitoneum opened the obliterated processus vaginalis.

Subtotal Cholecystectomy

Inadvertent subtotal laparoscopic cholecystectomy with bilious ascites was reported by Blackard and Baron.224 Exploratory laparoscopy with removal of a gallbladder remnant containing stones and drainage of the biliary ascites was performed with good results. Cottier et al.225 and Bickel and Shtamler226 cited specific presurgical indications for the performance of subtotal laparoscopic cholecystectomy in selected high risk patients.

Retained Stones

Retained stones should be avoided if at all possible. An operating room cholangiogram will detect virtually all common bile duct stones. When stones are detected, common bile duct exploration and removal of the stones is the procedure of choice and may be accomplished by laparoscopic or open surgery.

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Trocar Insertion

Thompson et al.227 reported two instances of IVC injuries during insertion of trocar for laparoscopic cholecystectomy.

Suzuki et al.228 studied port site recurrence of carcinoma of the gallbladder after laparoscopic cholecystectomy.

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